Disaster Medicine, 3rd Edition

1600 John F. Kennedy Boulevard, Suite 1800 Philadelphia, PA 19103-2899 DISASTER MEDICINE Third Edition Copyright © 2006 by Mosby, Inc.

ISBN-13: 978-0-323--03253-7 ISBN-10: 0-323-03253-2

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NOTICE Knowledge and best practice in this field are constantly changing.As new research and experience broaden our knowledge, changes in practice, treatment and drug therapy may become necessary or appropriate. Readers are advised to check the most current information provided (i) on procedures featured or (ii) by the manufacturer of each product to be administered, to verify the recommended dose or formula, the method and duration of administration, and contraindications. It is the responsibility of the practitioner, relying on their own experience and knowledge of the patient, to make diagnoses, to determine dosages and the best treatment for each individual patient, and to take all appropriate safety precautions.To the fullest extent of the law, neither the Publisher nor the [Editors/Authors] [delete as appropriate] assumes any liability for any injury and/or damage to persons or property arising out or related to any use of the material contained in this book. Library of Congress Cataloging-in-Publication Data Disaster medicine/editor-in-chief, Gregory R. Ciottone; associate editors, Philip D. Anderson ... [et al.]; section editors, Kathryn Brinsfield ... [et al].–1st ed. p.; cm. Includes bibliographical references and index. ISBN 0-323-03253-2 1. Disaster medicine. I. Ciottone, Gregory R. [DNLM: 1. Disaster Planning–methods. 2. Accidents, Radiation–prevention & control. 3. Bioterrorism–prevention & control. 4. Emergency Medical Services–methods. 5. Natural Disasters. WA 295 D611 2006] RC86.7.D56 2006 362.18–dc22 2005047926 Acquisitions Editor: Todd Hummel Developmental Editior: Martha Limback Publishing Services Manager: Joan Sinclair Project Manager: Mary Stermel Design Direction: Karen O’Keefe Owens Marketing Manager: Dana Butler

Printed in the United States of America. Last digit is the print number: 9 8 7 6 5 4 3 2 1

Dedicated to victims and survivors of disasters everywhere and to the medical professionals who care for them.

A S S O C I A T E

E D I T O R S

Philip D. Anderson, MD Assistant Professor in Medicine, Harvard Medical School Director, Division of International Disaster and Emergency Medicine Attending Physician, Department of Emergency Medicine Beth Israel Deaconess Medical Center Boston, Massachusetts

Irving Jacoby, MD Professor of Medicine & Surgery University oif California, San Diego, School of Medicine La Jolla, California Attending Physician, Department of Emergency Medicine Hospital Medical Director for Emergency Preparedness and Response University of California, San Diego, California

Erik Auf Der Heide, MD, MPH, FACEP Medical Officer Agency for Toxic Substances and Disease Registry U.S. Department of Health and Human Services Atlanta, Georgia

Eric Noji, MD, MPH Senior Medical Officer Centers for Disease Control and Prevention Atlanta, Georgia

Robert G. Darling, MD, FACEP Captain, Medical Corps, Flight Surgeon, United States Navy Senior Medical Advisor, Navy Medicine Office of Homeland Security Specialty Advisor to the Chief of the Medical Corps for Homeland Security

Selim Suner, MD, MS, FACEP Assistant Professor Department of Emergency Medicine and Surgery Brown Medical School Director of Emergency Preparedness and Disaster Response Department of Emergency Medicine Chairman, Emergency Preparedness Committee Rhode Island Hospital Providence, Rhode Island

vii

S E C T I O N

E D I T O R S

KATHRYN BRINSFIELD, MD, MPH, FACEP Medical Director for Homeland Security Boston Emergency Medical Services Assistant Professor, Emergency Medicine and Environmental Health Boston University Schools of Medicine and Public Health Boston, Massachusetts JONATHAN L. BURSTEIN, MD, FACEP Director, Section of Disaster Medicine Division of Emergency Medicine Department of Medicine Harvard Medical School Associate Director for Science Harvard Center for Public Health Preparedness Harvard School of Public Health Boston, Massachusetts JOHN D. CAHILL, MD, DTM Assistant Professor Attending Physician in Emergency Medicine and Infectious Diseases St. Luke’s/Roosevelt Hospital New York, New York EDWARD W. CETARUK, MD Assistant Clinical Professor of Medicine University of Colorado Health Sciences Center Division of Toxicology and Clinical Pharmacology Toxicology Associates, L.L.C. Denver, Colorado FRANCESCO DELLA CORTE, MD Associate Professor Chair of Anesthesiology and Intensive Care Università del Piemonte Orientale Novara, Italy ERIC W. DICKSON, MD Head, Department of Emergency Medicine University of Iowa Carver College of Medicine Iowa City, Iowa

DAVID G. JARRETT, MD, FACEP Colonel, Medical Corps, Flight Surgeon, U.S.Army Director,Armed Forces Radiobiology Research Institute Bethesda, Maryland MARK E. KEIM, MD Medical Officer and Team Leader International Emergency and Refugee Health Branch National Center of Environmental Health U.S. Centers for Disease Control and Prevention Atlanta, Georgia Clinical Associate Professor Department of International Health and Development Tulane University School of Public Health and Tropical Medicine New Orleans, Louisiana Honorary Faculty Center for International, Emergency, Disaster and Refugee Studies Johns Hopkins University School of Medicine Baltimore, Maryland KATHARYN E. KENNEDY, MD Assistant Professor of Emergency Medicine Department of Emergency Medicine University of Massachusetts Medical School Director of Emergency Medicine, Marlborough Hospital Worcester, Massachusetts JAMES M. MADSEN, MD, MPH Colonel, Medical Corps, Flight Surgeon, U.S.Army Scientific Advisor, Chemical Casualty Care Division U.S.Army Medical Research Institute of Chemical Defense (USAMRICD) APG-EA, Maryland Associate Professor of Preventive Medicine and Biometrics, Uniformed Services University (USU) Assistant Professor of Pathology, of Military and Emergency Medicine, and of Emerging Infectious Diseases, USU Bethesda, Maryland

ROBERT L. FREITAS, MHA Program Director for Emergency Medicine Harvard Medical Faculty Physicians Boston, Massachusetts

ix

KEN MILLER, MD, PHD Medical Director Orange County Fire Authority Irvine, California Assistant Medical Director Orange County Healthcare Agency/Emergency Medical Services Santa Ana, California Medical Team Manager, DHS/FEMA Urban Search & Rescue CA Task Force-5 Team Leader, DHS/FEMA/NDMS Disaster Medical Assistance Team CA-1 Medical Officer DHS/FEMA Incident Support Team/Joint Management Team Washington, DC

LEON D. SANCHEZ, MD, MPH Department of Emergency Medicine Beth Israel Deaconess Medical Center Boston, Massachusetts

JERRY L. MOTHERSHEAD, MD, FACEP Assistant Professor Uniformed Services University of the Health Sciences Bethesda, Maryland Physician Advisor, Medical Readiness and Response Group Battelle Memorial Institute Columbus, Ohio

ERIC S. WEINSTEIN, MD, FACEP Medical Director of Emergency Services Colleton Medical Center Walterboro South Carolina Medical University of South Carolina Charleston, South Carolina Chair,ACEP Disaster Medicine Section SC-1 DMAT Emergency Physician

ROBERT PARTRIDGE, MD, MPH Associate Professor of Emergency Medicine Director, Division of International Emergency Medicine Department of Emergency Medicine Rhode Island Hospital Brown Medical School

x SECTION EDITORS

CHARLES STEWART, MD, FACEP, FAAEM Colorado Springs, Colorado GARY M. VILKE, MD, FACEP, FAAEM Associate Professor of Clinical Medicine Department of Emergency Medicine University of California, San Diego Medical Center Medical Director, San Diego County Emergency Medical Services San Diego, California

RICHARD D. ZANE, MD Vice Chair Department of Emergency Medicine Brigham and Women’s Hospital Harvard Medical School Boston, Massachusetts

C O N T R I B U T O R S

GEORGE A. ALEXANDER, MD Radiation Research Program National Cancer Institute National Institutes of Health Bethesda, Maryland

MATTHEW BERKMAN, MD Harvard Affiliated Emergency Medicine Residency Program Beth Israel Deaconess Medical Center Boston, Massachusetts

ANGELA C. ANDERSON, MD, FAAP Pediatric Emergency Medicine Clinical Toxicology and Pharmacology Hasbro Children’s Hospital Associate Professor of Pediatrics and Emergency Medicine Brown University Medical School Providence, Rhode Island

ANDREW I. BERN, MD, FACEP Attending Emergency Physician Delray Medical Center Delray Beach, Florida Hollywood Medical Center Hollywood, Florida

ANDREW W. ARTENSTEIN, MD, FACP Director, Center for Biodefense and Emerging Pathogens Division of Infectious Diseases Memorial Hospital of Rhode Island Pawtucket, Rhode Island

MILANA BOUKHMAN, MD Instructor of Medicine Disaster Medicine Fellow Harvard Medical School Attending Physician Emergency Medicine Department Beth Israel Deaconess Hospital Boston, Massachusetts

KAVITA BABU, MD Fellow in Toxicology Department of Emergency Medicine University of Massachusetts Medical School Worcester, Massachusetts

PETER BREWSTER Education,Training, and Exercise Program Manager EMSHG VA Medical Center Martinsburg,West Virginia

FERMIN BARRUETO, JR., MD Assistant Professor of Surgery/Division of Emergency Medicine University of Maryland Emergency Physicians Baltimore, Maryland CARRIE BARTON, MD Disaster Medicine Research Fellow Center for Disaster Preparedness Birmingham,Alabama BRUCE M. BECKER, MD, MPH Attending Physician Department of Emergency Medicine Rhode Island Hospital/Hasbro Children’s Hospital Associate Professor Department of Community Health Brown School of Medicine Providence, Rhode Island

CHURTON BUDD, RN, EMTP Systems Analyst III Clinical Informatics Medical College of Ohio Toledo, Ohio JAMES M. BURKE, MD Staff Physician, Glendale Adventist Medical Center Glendale, California Lieutenant Commander, U.S. Naval Reserve Fleet Hospital Fort Dix, New Jersey FREDERICK M. BURKLE, JR., MD, MPH, FAAP, FACEP Senior Scholar Scientist and Visiting Professor The Center for International Emergency, Disaster & Refugee Studies (CIERDS) Johns Hopkins University Medical Institutions Baltimore, Maryland Director CIEDRS Asia-Pacific Branch Kailu xi

LYNNE BARKLEY BURNETT, MD Medical Advisor Fresno County Sheriff’s Department Vice Chairman, Medical Ethics Community Medical Centers Adjunct Professor of Forensic Medicine and Forensic Pathology National University Adjunct Instructor EMS Operations and Planning for WMD Texas, A&M University Fresno, California NICHOLAS VINCENT CAGLIUSO, SR., PhD(C), MPH Emergency Preparedness Analyst Office of Emergency Management The Port Authority of New York and New Jersey Jersey City, New Jersey JOHN D. CAHILL, MD, DTM Assistant Professor Attending Physician in Emergency Medicine and Infectious Diseases St. Luke’s/Roosevelt Hospital New York, New York DUANE C. CANEVA, MD, FACEP Commander, U.S. Navy Adjunct Assistant Professor Department Military/Emergency Medicine Uniformed Services University of the Health Sciences (USUHS) Bethesda, Maryland JULIE ANN P. CASANI, MD, MPH Director Office of Public Health Preparedness and Response Maryland Department of Health and Mental Hygiene Baltimore, Maryland MARY W. CHAFFEE, SCD(H), MS, RN, CNAA, FAAN PhD Student, Graduate School of Nursing Uniformed Services University of the Health Sciences Bethesda, Maryland Formerly, Director Navy Medicine Office of Homeland Security Bureau of Medicine and Surgery Washington, DC HENRY C. CHANG, MD Department of Emergency Medicine North Shore University Hospital Manhasset, New York JAMES C. CHANG, CIH, BS, MS Emergency Management Coordinator Duke University Hospital Durham, North Carolina

xii CONTRIBUTORS

ANNA I. CHEH, MD Harvard Affiliated Emergency Medicine Residency Beth Israel Deaconess Medical Center Boston, Massachusetts ESTHER H. CHEN, MD Department of Emergency Medicine University of Pennsylvania Medical Center Philadelphia, Pennsylvania TERIGGI J. CICCONE, MD Chief Resident Harvard Affiliated Emergency Medicine Residency Program Beth Israel Deaconess Medical Center Boston, Massachusetts MARIANNE E. CINAT, MD UCI Regional Burn Center University of California Irvine Medical Center Orange, California GREGORY R. CIOTTONE, MD, FACEP Director, International Emergency Medicine Section Harvard Medical School Director, Division of Disaster Medicine Beth Israel Deaconess Medical Center Boston, Massachusetts ROBERT A. CIOTTONE, PhD Clinical Psychologist (ABPP) Professor of Psychology (Afil.), Clark University Associate in Psychiatry and Pediatrics University of Massachusetts Medical School Worcester, Massachusetts STEVEN T. COBERY, MD, MC, USNR Neurosurgery Resident Brown University Medical School Rhode Island Hospital Providence, Rhode Island JOANNE CONO, MD, SCM Deputy Associate Director for Science Coordinating Office for Terrorism Preparedness and Emergency Response Centers for Disease Control and Prevention Atlanta, Georgia KELLY J. CORRIGAN, MD, MA Instructor of Medicine, Harvard Medical School Attending Physician Beth Israel Deaconess Medical Center Boston, Massachusetts

FRANCESCO DELLA CORTE, MD Associate Professor Chair of Anesthesiology and Intensive Care Università del Piemonte Orientale Novara, Italy

ERIC W. DICKSON, MD, FAAEM Head, Department of Emergency Medicine University of Iowa Carver College of Medicine Iowa City, Iowa

CHRISTO C. COURBAN, MD Brigham and Women’s Hospital Cambridge Hospital Harvard Medical School Boston, Massachusetts

SHARON DILLING Consultant, University of Medicine and Dentistry of New Jersey Center for BioDefense Director of Communications New Jersey Credit Union League Hightstown, New Jersey

HILARIE CRANMER, MD, MPH Department of Emergency Medicine Brigham and Women’s Hospital Boston, Massachusetts STEPHEN O. CUNNION, MD, MPH, PhD Department of Emergency Medicine PENN Travel Medicine Hospital of the University of Pennsylvania Philadelphia, Pennsylvania ROBERT G. DARLING, MD, FACEP Captain, Medical Corps Flight Surgeon, U.S. Navy Senior Medical Advisor Navy Medicine Office of Homeland Security Specialty Advisor to the Chief of the Medical Corps for Homeland Security Washington, DC DAVID DAVIS, MD Duke University Medical Center Emergency Medicine Durham, North Carolina TIMOTHY DAVIS, MD, MPH Associate Professor Emory University School of Medicine Atlanta, Georgia JENNIFER E. DELAPENA, MD Beth Israel Deaconess Medical Center Boston, Massachusetts CHAYAN DEY, MD, FACEP Center for International Emergency, Disaster and Refugee Studies Department of Emergency Medicine The Johns Hopkins University School of Medicine Baltimore, Maryland

K. SOPHIA DYER, MD Assistant Professor Department of Emergency Medicine Boston University School of Medicine Attending Physician Department of Emergency Medicine Boston Medical Center Boston, Massachusetts JASON DYLIK, MD, EMT Emergency Division, Department of Surgery Duke University Hospital Durham, North Carolina JONATHAN A. EDLOW, MD, FACEP Vice-Chairman, Department of Emergency Medicine Beth Israel Deaconess Medical Center Associate Professor of Medicine, Harvard Medical School Boston, Massachusetts MARSHALL EIDENBERG, DO Chief, Initial Entry Training Division DCMT Medical Director Department of Combat Medic Training KHAMA D. ENNIS-HOLCOMB, MD, MPH Senior Resident, Department of Emergency Medicine Brigham & Women’s and Massachusetts General Hospital Boston, Massachusetts DENIS J. FITZGERALD, MD Chief Medical Officer Counter-Narcotics and Terrorism Operational Medical Support (CONTOMS) Program Casualty Care Research Center Uniformed Services University of the Health Sciences U.S. Department of Defense Washington, DC

WILLIAM E. DICKERSON, MD Colonel, U.S.Air Force, Medical Corps Head, Military Medicine Department Armed Forces Radiobiology Research Institute Bethesda, Maryland

CONTRIBUTORS xiii

KERRY FOSHER, BS, BA, MA New England Center for Emergency Preparedness Dartmouth Medical School Lebanon, New Hampshire Research and Practice Associate Institute for National Security and Counter-Terrorism Maxwell School of Citizenship and Public Affairs and College of Law Syracuse University Syracuse, New York ROBERT L. FREITAS, MHA Program Director of Emergency Medicine Harvard Medical Faculty Physicians Boston, Massachusetts RYAN FRIEDBERG, MD Harvard Affiliated Emergency Medicine Residency Program Beth Israel Deaconess Medical Center Boston, Massachusetts FRANKLIN D. FRIEDMAN, MD, MS Assistant Professor of Emergency Medicine Tufts University School of Medicine Director of Emergency Clinical Operations Tufts-New England Medical Center Department of Emergency Medicine Boston, Massachusetts FREDERICK FUNG, MD, MS Clinical Professor Department of Medicine, Division of Occupational Medicine University of California, Irvine Irvine, California Medical Director, Occupational Medicine Sharp Rees-Stealy Medical Centers Medical Director, Employee Health Sharp Health Care San Diego, California ROBERT D. FURBERG, BS, NREMTP Paramedic, EMS Education Parkwood Fire Rescue Research Triangle Park, North Carolina Adjunct Instructor, Emergency Health Sciences Department of Emergency Medicine The George Washington University Washington, DC WADE GAASCH, MD, FAAEM Assistant Professor Division of Emergency Medicine University of Maryland School of Medicine Director of Pre-Hospital Care Emergency Medicine University of Maryland Medical Center Chief Physician and Medical Director Baltimore City Fire Department Baltimore, Maryland xiv CONTRIBUTORS

FIONA E. GALLAHUE, MD Associate Residency Director Department of Emergency Medicine New York Methodist Hospital Brooklyn, New York LUCILLE GANS, MD Edmonton,Alberta, Canada ALESSANDRO GEDDO, MD Resident in Anaestesiology and ICU University of Eastern Piedmont Maggiore della Carità Hospital Novara, Italy JAMES GEILING, MD, FACP Associate Professor of Medicine Dartmouth Medical School Assistant Director, New England Center for Emergency Preparedness Dartmouth-Hitchcock Medical Center Hanover, New Hampshire Chief, Medical Service Veterans Affairs Medical Center White River Junction,Vermont PAUL GIANNONE, MPHORISE FELLOW Disaster Planner International Emergency and Refugee Health Branch National Center of Environmental Health U.S. Centers for Disease Control and Prevention Atlanta, Georgia WILLIAM GLUCKMAN, DO, EMT-P, FACEP Assistant Professor of Surgery New Jersey Medical School Attending Emergency Physician UMDNJ-University Hospital, Medical Director, University EMS Newark, New Jersey SUSAN E. GORMAN, PHARMD Associate Director for Science Strategic National Stockpile Program Centers for Disease Control and Prevention Atlanta, Georgia J. SCOTT GOUDIE, MD Harvard Affiliated Emergency Medicine Residency Program Beth Israel Deaconess Medical Center Boston, Massachusetts ROBERT M. GOUGELET, MD Assistant Professor Medicine (Emergency Medicine) Dartmouth Medical School Medical Director Emergency Response Dartmouth Hitchcock Medical Center Lebanon, New Hampshire

MARK A. GRABER, MD Associate Professor of Emergency Medicine and Family Medicine University of Iowa Carver College of Medicine Iowa City, Iowa JILL A. GRANT, MDCPT San Antonio Uniformed Services Health Education Consortium Emergency Medicine Residency Program Brooke Army Medical Center Fort Sam Houston,Texas MICHAEL I. GREENBERG, MD, MPH Clinical Professor of Emergency Medicine Temple University School of Medicine Professor of Emergency Medicine Professor of Public Health Drexel University College of Medicine Philadelphia, Pennsylvania P. GREGG GREENOUGH, MD, MPH Assistant Professor and Co-Director The Center for International Emergency, Disaster and Refugee Studies, Schools of Medicine and Public Health Johns Hopkins University Medical Institutions Baltimore, Maryland SHAMAI A. GROSSMAN, MD, MS, FACEP Director, The Clinical Decision Unit and Cardiac Emergency Center Department of Emergency Medicine Beth Israel Deaconess Medical Center Instructor of Medicine Harvard Medical School Boston, Massachusetts TEE L. GUIDOTTI, MD, MPH Professor Chair, Dept. of Environmental and Occupational Health Director, Division of Occupational Medicine and Toxicology (Department of Medicine) The George Washington University Medical Center Washington, DC DEBORAH GUTMAN, MD, MPH Clinical Assistant Professor Department of Emergency Medicine Brown Medical School Attending Physician Department of Emergency Medicine Rhode Island Hospital Providence, Rhode Island

DAN HANFLING, MD, FACEP Director, Emergency Management and Disaster Medicine Inova Health System Falls Church,Virginia Assistant Clinical Professor of Emergency Medicine George Washington University Washington, DC RACHEL HAROZ, MD Instructor in Emergency Medicine Department of Emergency Medicine Drexel University School of Medicine Philadelphia, Pennsylvania BONNIE H. HARTSTEIN, MD Associate Professor of Pediatrics Uniformed Services University of Health Sciences Bethesda, Maryland Department of Emergency Medicine Brooke Army Medical Center Fort Sam Houston,Texas JOHN L. HICK, MD, FACEP Assistant Professor of Emergency Medicine University of Minnesota Faculty Physician Hennepin County Medical Center Minneapolis, Minnesota STEPHEN F. HOOD, MA Public Administration/Public Policy Coordinator The George Washington University Response to Emergencies and Disasters Institute Ashburn,Virginia MICHAEL HOROWITZ, MD Resident in Emergency Medicine Department of Emergency Medicine Drexel University School of Medicine Philadelphia, Pennsylvania KURT R. HORST, MD University of Massachusetts School of Medicine UMass Memorial Medical Center Department of Emergency Medicine Worcester, Massachusetts HANS R. HOUSE, MD, DTMH Residency Director The Iowa Emergency Medicine Residency Assistant Professor of Emergency Medicine University of Iowa Carver College of Medicine Iowa City, Iowa

PINCHAS HALPERN, MD Director, Emergency Department Tel Aviv Sourasky Medical Center and the Sackler Faculty of Medicine Tel Aviv University Tel Aviv, Israel CONTRIBUTORS xv

CURTIS J. HUNTER, MD Assistant Professor Military and Emergency Medicine Uniformed Services University of the Health Sciences Bethesda, Maryland Chief, Department of Emergency Medicine Brooke Army Medical Center Fort Sam Houston,Texas Attending Faculty San Antonio Uniformed Services Health Education Consortium Emergency Medicine Residency San Antonio,Texas JASON IMPERATO, MD, MBA Attending Physician Beth Israel Deaconess Medical Center Boston, Massachusetts PIER LUIGI INGRASSIA, MD Resident in Anaestesiology and ICU University of Eastern Piedmont Maggiore della Carità Hospital Novara, Italy IRVING JACOBY, MD Professor of Medicine and Surgery University of California, San Diego, School of Medicine La Jolla, California Attending Physician, Department of Emergency Medicine Hospital Medical Director for Emergency Preparedness and Response University of California San Diego, California THEA JAMES, MD Clinical Instructor/Attending Physician Boston University School of Medicine Boston Medical Center Boston, Massachusetts DAVID JASLOW, MD, MPH, EMT-P, FAAEM Chief, Division of EMS, Operational Public Health and Disaster Medicine Co-Director, Center for Special Operations Department of Emergency Medicine Albert Einstein Medical Center Philadelphia, Pennsylvania GREGORY D. JAY, MD Associate Professor of Medicine Division of Engineering Brown Medical School Research Director, Associate Professor of Medicine and Emergency Medicine Department of Emergency Medicine Rhode Island Hospital Providence, Rhode Island

xvi CONTRIBUTORS

MIRIAM JOHN, MD Resident, Newark Beth Israel Medical Center Newark, New Jersey MICHAEL D. JONES, MD Brooke Army Medical Center SAUSHEC EM Residency Program Fort Sam Houston,Texas JEFFRY L. KASHUK, MD, FACS Associate Clinical Professor of Surgery Hahnemann University Hospital Philadelphia, Pennsylvania MARK E. KEIM, MD Medical Officer and Team Leader International Emergency and Refugee Health Branch National Center of Environmental Health U.S. Centers for Disease Control and Prevention Atlanta, Georgia Clinical Associate Professor Department of International Health and Development Tulane University School of Public Health and Tropical Medicine New Orleans, Louisiana Honorary Faculty Center for International, Emergency, Disaster and Refugee Studies Johns Hopkins University School of Medicine Baltimore, Maryland KATHARYN E. KENNEDY, MD Assistant Professor of Emergency Medicine Department of Emergency Medicine University of Massachusetts Medical School Director of Emergency Medicine, Marlborough Hospital Worcester, Massachusetts PAUL D. KIM, MD Associate Director, Operations The George Washington University Response to Emergencies and Disasters Institute Ashburn,Virginia SYLVIA H. KIM, MD Harvard Affiliated Emergency Medicine Residency Beth Israel Deaconess Medical Center Boston, Massachusetts LEO KOBAYASHI, MD University Emergency Medicine Foundation Department of Emergency Medicine Brown University Providence, Rhode Island LARA K. KULCHYCKI, MD Harvard Affiliated Emergency Medicine Residency Program Beth Israel Deaconess Medical Center Boston, Massachusetts

RICK G. KULKARNI, MD Assistant Professor of Medicine David Geffen School of Medicine at UCLA Attending Physician, Director of Informatics Department of Emergency Medicine Olive View – UCLA Medical Center Los Angeles, California CHRISTOPHER R. LANG, MD Department of Emergency Medicine George Washington University Washington, DC GREGORY L. LARKIN, MD, MS, MSPH, FACEP Professor, Department of Surgery Division of Emergency Medicine University of Texas Southwestern Medical Center Dallas,Texas THOMAS P. LEBOSQUET III, MD Resident in Emergency Medicine Duke University Medical Center Durham, North Carolina BRUCE Y. LEE, MD, MBA Assistant Professor of Medicine Section of Decision Sciences and Clinical Systems Modeling University of Pittsburgh Pittsburgh, Pennsylvania CATHERINE Y. LEE, MPH Faculty Associate, New York Medical College Valhalla, New York DAVID C. LEE, MD Director of Research Department of Emergency Medicine North Shore University Hospital Manhasset, New York Clinical Assistant Professor Department of Emergency Medicine New York University New York, New York JAY LEMERY, MD Attending Physician, Emergency Medicine Weill Cornell Medical College Attending Physician, Emergency Medicine New York-Presbyterian Hospital New York, New York

DANIEL L. LEMKIN, MD Deputy Medical Director, Baltimore City Fire Department EMS Fellow University of Maryland Baltimore County Clinical Instructor Division of Emergency Medicine University of Maryland School of Medicine Baltimore, Maryland JEANETTE A. LINDER, MD Assistant Professor Radiation Oncology University of Maryland Medical Center Baltimore, Maryland LAWRENCE S. LINDER, MD, FACEP, FAEM Director, Emergency Department Senior Vice President/Chief Medical Officer Baltimore Washington Medical Center Glen Burnie, Maryland SHAN W. LIU, MD Instructor, Surgery Harvard Medical School Faculty, Emergency Medicine Massachusetts General Hospital Boston, Massachusetts CRAIG H. LLEWELLYN, MD Professor of Medicine and Surgery Director, Center for Disaster and Humanitarian Assistance Medicine Uniformed Services University for the Health Sciences Bethesda, Maryland FRANCESCA LOMBARDI, MD Resident in Anaestesiology and ICU University of Eastern Piedmont Maggiore della Carità Hospital Novara, Italy HEATHER LONG, MD Attending Physician Department of Emergency Medicine North Shore University Hospital Manhasset, New York EDWARD B. LUCCI, MD, FACEPLTC Chief, Emergency and Operational Medicine Walter Reed Army Medical Center Washington, DC DONALD MACMILLAN, MA, PA, EMT-P Yale University School of Medicine Division of EMS New Haven, Connecticut

CONTRIBUTORS xvii

LAURA MACNOW, MD Instructor, Emergency Medicine Harvard Medical School Attending Physician Emergency Department Beth Israel Deaconess Medical Center Boston, Massachusetts JAMES M. MADSEN, MD, MPH Colonel, Medical Corps, Flight Surgeon, U.S.Army Scientific Advisor, Chemical Casualty Care Division U.S.Army Medical Research Institute of Chemical Defense (USAMRICD) APG-EA, Maryland Associate Professor of Preventive Medicine and Biometrics, Uniformed Services University (USU) Assistant Professor of Pathology, of Military and Emergency Medicine, and of Emerging Infectious Diseases, USU Bethesda Maryland BRIAN J. MAGUIRE, DR.PH, MSA, EMT-P Associate Director Department of Emergency Health Services University of Maryland, Baltimore County Baltimore, Maryland JOHN D. MALONE, MD, FACP, FIDSA Professor of Medicine Uniformed Services University of the Health Sciences F. Edward Hebert School of Medicine Department of Preventive Medicine and Biometrics Bethesda, Maryland PAUL M. MANISCALCO, MPA, EMT/P Deputy Executive Director Former President, National Association of Emergency Medical Technicians The George Washington University Response to Emergencies and Disasters Institute Ashburn,Virginia DAVID MARCOZZI, MD Emergency Division, Department of Surgery Duke University Medical Center Durham, North Carolina PIETRO D. MARGHELLA, CFAAMA, FACCP Commander, Medical Service Corps, U.S. Navy Adjunct Assistant Professor Uniformed Services University of the Health Sciences Washington, DC JAMES F. MARTIN, MDCPT San Antonio Uniformed Services Health Education Consortium Emergency Medicine Residency Program Brooke Army Medical Center Fort Sam Houston,Texas xviii CONTRIBUTORS

JAMES MCKINNELL, MD Resident Physician, Department of Medicine Los Angeles County Harbor-UCLA Medical Center Torrance, California MICHELLE MCMAHON-DOWNER, MD Department of Emergency Medicine Rhode Island Hospital Brown University School of Medicine Providence, Rhode Island C. CRAWFORD MECHEM, MD, FACEP Associate Professor Department of Emergency Medicine University of Pennsylvania Medical Center EMS Medical Director City of Philadelphia Fire Department Philadelphia, Pennsylvania SUMERU MEHTA, MD, MPH Staff Physician and Director of Emergency Ultrasound Department of Emergency Medicine Brooke Army Medical Center San Antonio Uniformed Services Health Education Consortium San Antonia,Texas PATRICIA L. MEINHARDT, MD, MPH, MA Executive Medical Director Center for Occupational and Environmental Medicine Arnot Ogden Medical Center Elmira, New York LAURA DIANE MELVILLE, MD New York Methodist Hospital Brooklyn, New York JEFFERY C. METZGER, MD Emergency Medicine Resident Duke University Medical Center Durham Police Department Selective Enforcement Team Durham, North Carolina ANGELA M. MILLS, MD Assistant Professor Department of Emergency Medicine University of Pennsylvania Medical Center Philadelphia, Pennsylvania ANDREW M. MILSTEN, MD, MS, FACEP Clinical Assistant Professor Division of Emergency Medicine University of Maryland College Park, Maryland Assistant Medical Director Anne Arundel County Fire Department Medical Director Expresscare Critical Care Transport and Mass Gathering Events Newsletter Editor, Disaster Medical Section, ACEP

CLIFFORD S. MITCHELL, MS, MD, MPH Associate Professor of Environmental Health Sciences Johns Hopkins Bloomberg School of Public Health Baltimore, Maryland ELIZABETH L. MITCHELL, MD Assistant Professor of Emergency Medicine Boston University School of Medicine Department of Emergency Medicine Boston, Massachusetts DALE M. MOLÉ, DO, FACEP Captain, Medical Corps, U.S. Navy Executive Officer, U.S. Naval Hospital Okinawa, Japan Assistant Professor of Military and Emergency Medicine Uniformed Services University of Health Sciences Bethesda, Maryland LOUIS N. MOLINO, SR., CET, FF/NREMT-B/FSI/EMSI WMD EMS Instructor, WMD EMS Program The Texas A&M University System Texas Engineering Extension Service Emergency Services Training Institute National Emergency Response and Rescue Training Center College Station, Texas JOHN MOLONEY, MBBS FANZCA MAIES Area Medical Coordinator, Medical Displan Victoria Head,Trauma Anaesthesia The Alfred Australia SEAN MONTGOMERY, MD Harvard Affiliated Emergency Medicine Residency Beth Israel Deaconess Medical Center Boston, Massachusetts JERRY L. MOTHERSHEAD, MD, FACEP Assistant Professor Uniformed Services of the Health Sciences Bethesda, Maryland Physician Advisor, Medical Readiness and Response Group Battelle Memorial Institute Columbus, Ohio LEWIS S. NELSON, MD Assistant Professor Department of Emergency Medicine New York University School of Medicine New York, New York Fellowship Director, Medical Toxicology New York City Poison Control Center New York, New York CONSTANCE G. NICHOLS, MD Assistant Professor of Emergency Medicine Department of Emergency Medicine University of Massachusetts Medical School Worcester, Massachusetts

PATRICIA A. NOLAN, MD, MPH Director of Health Rhode Island Department of Health Clinical Assistant Professor of Community Health Brown University Providence, Rhode Island DANIEL F. NOLTKAMPER, MD, FACEP Commander, Medical Corps, U.S. Navy Emergency Physician, Naval Hospital Camp Lejeune Jacksonville, North Carolina DZIWE W. NTABA, MD, MPH Resident in Emergency Medicine Department of Emergency Medicine

JAMES PFAFF, MD, FACEP, FAAEM Staff Physician, Brooke Army Medical Center SAUSHEC EM Residency Program Fort Sam Houston,Texas WILLIAM PORCARO, MD Harvard Affiliated Emergency Medicine Residency Program Beth Israel Deaconess Medical Center Boston, Massachusetts LAWRENCE PROANO, MD, FACEP Attending Physician Brown University Program in Emergency Medicine Rhode Island Hospital Providence, Rhode Island NAJMA RAHMAN-KAHN, MD Attending, Lutheran Hospital Brooklyn, New York VITTORIO J. RAHO, MD Resident, Harvard Affiliated Emergency Medicine Residency Program Beth Israel Deaconess Medical Center Boston, Massachusetts PRASANTHI RAMANUJAM, MBBS Department of Emergency Medicine Boston Medical Center Boston University School of Medicine Boston, Massachusetts WENDE R. REENSTRA, MD, PHD Department of Emergency Medicine Beth Israel Deaconess Medical Center Boston, Massachusetts ANDREW REISNER, MD Instructor, Harvard Medical School Massachusetts General Hospital Emergency Medicine Boston, Massachusetts MARK C. RESTUCCIA, MD, FACEP, FAAEM Assistant Professor of Emergency Medicine University of Massachusetts Medical School UMass Memorial Health Care Worcester, Massachusetts JAMES MICHAEL RILEY, REMT-P Senior Security Analyst Office of Security and Investigations US Citizenship and Immigration Services Washington, DC

xx CONTRIBUTORS

ALBERT J. ROMANOSKY, MD, PhD Medical Director Office of Public Health Preparedness and Response Maryland Department of Health and Mental Hygiene Baltimore, Maryland PETER ROSEN, MD Senior Lecturer, Department of Medicine Harvard University School of Medicine, Attending Physician Department of Emergency Medicine Beth Israel/Deaconess Medical Center Boston, Massachusetts MARC S. ROSENTHAL, PHD, DO Assistant Professor of Emergency Medicine Attending Physician Research Director/Assistant Residency Director Wayne State University Sinai-Grace Hospital Emergency Medicine Residency Program Department of Emergency Medicine Sinai-Grace Hospital Detroit, Michigan JONATHAN M. RUBIN, MD Associate Professor of Emergency Medicine Medical College of Wisconsin Associate Director of Medical Services Milwaukee County EMS Milwaukee,Wisconsin LEON D. SANCHEZ, MD, MPH Attending, Emergency Medicine Clinical Instructor Emergency Medicine Harvard Medical School Beth Israel Deaconess Medical Center Boston, Massachusetts DEBRA D. SCHNELLE, MS Project Staff Associate/Assistant Program Manager The Research Foundation The State University of New York Buffalo, New York JEREMIAH D. SCHUUR, MD Chief Resident Brown University Emergency Medicine Residency Providence, Rhode Island ERIC M. SERGIENKO, MD Lieutenant Commander Bureau of Medicine and Surgery U.S. Navy Shoreline,Washington

KINJAL SETHURAMAN, MD, MPH Albert Einstein University Emergency Department Long Island Jewish Medical Center International Emergency Medicine Fellow New York MARC J. SHAPIRO, MD University Emergency Medicine Foundation Department of Emergency Medicine Brown University Providence, Rhode Island SAM SHEN, MD, MBA Attending Physician St. Luke’s Hospital Southcoast Health System New Bedford, Massachusetts SUZANNE M. SHEPHERD, MD, FACEP, DTM&H Associate Professor Director, Education and Research PENN Travel Medicine Hospital of the University of Pennsylvania Philadelphia, Pennsylvania WILLIAM H. SHOFF, MD, DTM&H Department of Emergency Medicine PENN Travel Medicine Hospital of the University of Pennsylvania Philadelphia, Pennsylvania SEAN MICHAEL SILER, DO Captain, U.S.Army, Medical Corps Senior Resident, San Antonio Uniformed Services Health Sciences Consortium Emergency Medicine Residency Brooke Army Medical Center Department of Emergency Medicine Fort Sam Houston,Texas ALISON SISITSKY, MD Harvard Affiliated Emergency Medicine Residency Program Beth Israel Deaconess Medical Center Boston, Massachusetts CRAIG SISSON, MD Rhode Island Hospital Brown University Emergency Medicine Program Providence, Rhode Island PETER B. SMULOWITZ, MD Harvard Affiliated Emergency Medicine Residency Beth Israel Deaconess Medical Center Boston, Massachusetts

JOHN H. SORENSON, PhD Distinguished Research and Development Staff Oak Ridge National Laboratory Oak Ridge,Tennessee CHARLES STEWART, MD, FACEP, FAAEM Colorado Springs, Colorado M. KATHLEEN STEWART, MS Colorado Springs, Colorado KENT J. STOCK, DO, MBA, FACP, FAAP Lowcountry Infectious Diseases, P.A. Charleston, South Carolina CAROL SULIS, MD Associate Professor of Medicine Boston University School of Medicine Hospital Epidemiologist Boston Medical Center Boston, Massachusetts NICHOLAS SUTINGCO, MD Department of Emergency Medicine Brigham and Women’s Hospital Harvard Medical School Boston, Massachusetts NELSON TANG, MD, FACEP Director, Division of Special Operations Department of Emergency Medicine The Johns Hopkins University School of Medicine Baltimore, Maryland ELIZABETH TEMIN, MD Instructor, Emergency Medicine Boston University School of Medicine Physician, Emergency Medicine Boston Medical Center Boston, Massachusetts RICHARD A. TEMPEL, MD Division of Emergency Medicine Duke University Medical Center Durham, North Carolina CRAIG D. THORNE, MD, MPH, FACP, FACOEM Assistant Professor of Medicine University of Maryland Medical Director, Safety and Employee Health University of Maryland Medical Center Baltimore, Maryland JASON A. TRACY, MD Assistant Residency Director Beth Israel Deaconess Medical Center Harvard Affiliated Emergency Medicine Residency Harvard Medical School Boston, Massachusetts CONTRIBUTORS xxi

STEPHEN J. TRAUB, MD Co-Director, Division of Toxicology Department of Emergency Medicine Beth Israel Deaconess Medical Center Instructor in Medicine Harvard Medical School Boston, Massachusetts JONATHAN HARRIS VALENTE, MD Assistant Professor, Brown Medical School Department of Emergency Medicine Rhode Island Hospital and Hasbro Children’s Hospital Providence, Rhode Island VICTORIA M. VANDERKAM, RN, MBA UCI Regional Burn Center University of California Irvine Medical Center Orange, California

ROY KARL WERNER, MD, MS Assistant Professor of Emergency Medicine University of Iowa Carver College of Medicine Iowa City, Iowa SAGE W. WIENER, MD Assistant Professor Department of Emergency Medicine SUNY Downstate Medical Center Assistant Director of Medical Toxicology Department of Emergency Medicine Kings County Hospital/SUNY Downstate Medical Center Brooklyn, New York ABIGAIL WILLIAMS, RN, JD, MPH Abigail Williams & Associates, PC Worcester, Massachusetts

CAROL L. VENABLE, MD Department of Emergency Medicine Boston Medical Center Boston, Massachusetts

KENNETH A. WILLIAMS, MD University Emergency Medicine Foundation Department of Emergency Medicine Brown University Providence, Rhode Island

FAITH VILAS, PhD, LP Planetary Astronomy Group NASA Johnson Space Center Dallas,Texas

TRACY E. WIMBUSH, MD Massachusetts General Hospital Harvard Medical School Boston, Massachusetts

GARY M. VILKE, MD, FACEP, FAAEM Associate Professor of Clinical Medicine Department of Emergency Medicine University of California, San Diego Medical Center Medical Director, San Diego County Emergency Medical Services San Diego, California

ROBERT H. WOOLARD, MD Interim Chairman of the Department of Emergency Medicine Brown Medical School Rhode Island Hospital Providence, Rhode Island

BARBARA VOGT SORENSON, PhD Senior Research Staff Oak Ridge National Laboratory Oak Ridge,Tennessee SCOTT G. WEINER, MD, MPH Assistant Professor of Emergency Medicine Tufts University School of Medicine Attending Physician Tufts New England Medical Center Boston, Massachusetts ERIC S. WEINSTEIN, MD, FACEP Medical Director of Emergency Services Colleton Medical Center Walterboro, South Carolina Medical University of South Carolina Charleston, South Carolina Chair,ACEP Disaster Medicine Section SC-1 DMAT Emergency Physician

xxii

CONTRIBUTORS

KEVIN YESKEY, MD, FACEP Deputy Director and Associate Professor Center for Disaster and Humanitarian Assistance Medicine Uniformed Services University of the Health Sciences Bethesda, Maryland SANDRA S. YOON, MD Harvard Affiliated Emergency Medicine Residency Program Beth Israel Deaconess Medical Center Boston, Massachusetts PATRICK ZELLEY, MD, MS Department of Emergency Medicine Rhode Island Hospital Brown University School of Medicine Providence, Rhode Island

F O R E W O R D

Throughout recorded history, disasters have caused immeasurable amounts of pain and suffering to affected populations. By far, the most common disasters have been natural ones with cataclysmic storms and seismic and volcanic events reeking havoc on the unsuspecting. Recently, however, the news of disaster has also included pre-meditated attacks by the various terror factions around the world. Prior to Sept. 11, 2001, it is not unreasonable to presume that most of us in the United States didn’t think long nor hard about terror attacks. We of course were aware of the bad things that were occurring around the world,shook our heads with bafflement at the Sarin attacks in Tokyo, and managed to underestimate and ignore the bombings and terror attacks in our own country, since so few of us were involved. It always seems like an act far out on the bell-shaped curve of sanity. We couldn’t figure out how James Jones could convince a group of people to submit to suicide and murder; we were appalled at the cyanide attacks in the grocery stores; and we came closer to understanding a potential for terror after the bombing in Oklahoma City. There were of course small numbers of people who were well aware of the potential; tried to prepare themselves and their country, and did attempt to increase education, preparation and awareness for that special kind of disaster. Although I was personally almost totally ignorant about bioterror, I was asked to chair a committee on Bioterror for the Institute of Medicine. I still don’t know why I was invited, but it was a challenging and highly educational experience. I learned at the very least to think about terror in terms of possible responses and needs for education as opposed to putting it aside as a very improbable event that I would never encounter as a citizen, never mind as a physician.1 What became increasingly obvious after Sept. 11 was the inability to predict the consequences of the attack, and a need to be able to respond with great flexibility and creativity. In this regard, acts of terrorism, other than the psychological wounding fact that it is deliberate, manmade, and therefore quite unnecessary, is no different than a large unplanned disaster. We have seen many such incidents around the world and learned a certain amount at how to prepare and how to respond, but we are always struck by the fact that we can’t exactly know when or where the next “tragedy” will occur, or just how much damage it will inflict. Many of the ingredients for both accidental and terrorist events are present in our daily lives, and it doesn’t 1

IOM report on Bioterror.

require much to unleash them. Fortune sometimes plays in our favor, as the time when I was at the University of Chicago. We received a phone call that there had been some kind of industrial accident on the South Side of the city, and that a large cloud of chlorine gas had been released.We had no idea how many victims there would be, or where the victims would be, and we were somewhat frustrated in trying to notify all possible Emergency Departments to enable their response—this despite several years of intensive planning and practice that had followed a train crash of a commuter train on the Illinois Central Railroad. Fortunately, the prevailing winds that day blew the cloud out over Lake Michigan, and there was not a single victim. It was estimated at the time, however, that if the wind had not been present,or had changed direction from typical, there would have been over 1 million victims. Similarly, when I was in Denver, there was a cloud of nitric acid released from a train derailment. Again, fortunately, this occurred very early on a Sunday morning. Only 24 hours later, it would have spewed into the traffic rush of early morning workers. This again prevented a horrible disaster, and we had only three victims who were seriously exposed, and about 20 others with very minor exposure. Thus it doesn’t really matter if the disaster is natural or manmade in terms of unpredictability or horrible consequences. It is clear that the best preparation is going to be that of an already developed, practiced, and efficient disaster program. That, of course, doesn’t mean that we have such a program in place, nor does it mean that there are not rare diseases, chemicals, or unprecedented event scenarios that we will have to learn about and prepare for. The following book is a serious attempt to do just that. When I read it, my initial reaction was that perhaps we needed to eliminate some of the terrorism chapters because they were going to suggest methods of attack. I realized then that this is one of the unique characteristics of terror attacks.It is so unthinkable that we begin to think illogically about how to prepare and how to respond. A later thought, more cynical, was that we are spending too much time and money to prepare for events that will not recur, even if they ever occur in the first place. Finally, some sanity resumed and I realized that the only way to prepare for rare, uncommon, and unrepetitive events is to think about them, to attempt to generalize the problems they cause, and to try to develop a system that can respond to the known but can improvise and also respond to the unknown and not previously experienced as well. This book is a very good start in doing just that. It may frighten you, as it did me, and perhaps horrify you, especially when you are stimulated into thinking about how xxiii

many problems you are personally, as well as your system, not publicly prepared to respond and react to, not only from ignorance, but because an efficient system just isn’t there. Whether or not you have a personal role in disaster management in your community, your hospital, or your state, it will be educational and stimulating to be involved in the thinking about, and planning for, how to respond to the unthinkable. Within these pages I believe you will find the descriptions, facts, and creative solutions to many problems you are aware of, as well as many problems you may not have thought about. All the planning in the world will not prevent tragedy from occurring, whether it is by natural causes or manmade. There is no question, however, that the right system will alleviate the tragedy; will salvage lives and psyches, and will help us to feel less despondent about the world we have forced upon us. I think you will find this book a good read. Not only is it well written by a series of authors who are very accomplished and experienced in disaster management,

xxiv FOREWORD

but I believe you will find it one of the most thought-provoking books that you have read. I certainly did, and while I still am horrified at the variety and depths of tragedy that we may still have to endure, it left me feeling much less helpless, and finally much less angry about the whole situation. To plan is to take control; it may be imperfect, but it is significantly better than being a passive victim. Just think how many lives were saved because an alert Emergency Physician was able to think about and diagnose an anthrax victim. Would he have thought about this without Sept. 11, I suspect not, but if only one life is saved by improved education and awareness, this book will have been worth the tremendous amount of work and diligence that went into its preparation. Peter Rosen, MD Senior Lecturer Medicine Harvard University School of Medicine Attending Physician Emergency Medicine Beth Israel/Deaconess Medical Center

P R E F A C E

Walking slowly toward Ground Zero as Commander of one of the first Federal Disaster Medical Assistance Teams into the World Trade Center disaster, I was initially struck by a sense of helplessness at the sight of the devastation. As the plumes of smoke rose from the undulating piles of destruction, we had a sense that the disaster before us was so vast and our task so enormous that we would never be able to mount an effective response. This feeling of helplessness did not abate until we resorted to our training and took up our role in the overall disaster response.We were a cog in a very large machine, placed precisely where we would be supported by the other parts, and function in such a specialized way as to keep the machine running. At that moment of realization, this book was born. The philosophy behind the writing of this textbook is to bring resources together necessary for the development of a comprehensive understanding of Disaster Medicine and its role in Disaster Management. The release of the book comes soon after Hurricane Katrina has devastated the Gulf Coast of America and approximately 1 year after the horror of the Southeast Asia tsunami. After witnessing the devastation of vast areas around the Indian Ocean, and the destruction of a major U.S. city, it is impossible not to be struck by the destructive powers of such natural events. There is, however, another striking feature about both of these events. Whereas the tsunami struck some of the poorest areas, Katrina struck the most developed and richest country in the world. Regardless of these stark socio-economic contrasts, the destruction to the affected areas was remarkably similar: it was nearly total. Disaster strikes without warning, is indiscriminate in its choice of victims, and has the potential of overcoming even the most prepared of systems. If there is no other justification for a book such as this, it must be said that these recent events demand that we, as healthcare professionals, develop an understanding of the basics of Disaster Medicine and stand ready to integrate into the response system if and when disaster should strike close to home. This book is designed to serve as both a comprehensive text and a quick resource. Part 1 introduces the many topics of disaster medicine and management with an emphasis on the multiple disciplines that come together in the preparation for and response to such catastrophic events. It is the integration of these various response and preparedness modalities that makes Disaster Medicine such a unique field. This section is meant to be a comprehensive approach to the study of the discipline of Disaster Medicine and should be used by healthcare professionals to develop and expand their knowledge base. The chapters may introduce topics that

are unfamiliar to the reader, as most practitioners will not be versed in some of the non-medical subjects discussed. Although much of the information may be very new, it may also be crucial in the unexpected event a disaster strikes nearby. Part 2 of the book, or the “Event” chapters, introduces the reader to every conceivable disaster scenario, and the management issues surrounding each. This part of the text can be used as both a reference and a real-time consult for each topic. The reader will find very detailed and specific events described in these chapters. Some disaster scenarios discussed have historical precedence whereas others are considered to be at risk for future occurrence. Many describe natural and accidental events while some are dedicated to very specific terrorist attacks. There is no easy way to discuss these topics. In particular, terrorist events may cause a sense of unease as one reads the chapter. The chapters related to terrorism in this section attempt to account for every possible modality terrorist operatives are thought to currently possess or may acquire in the future. In some cases the scenarios may prove true, and in many they may not. It is imperative, however, that all possible modalities of attack be discussed so that if needed, proper preparedness and response can be mounted. The term “attack” has been deliberately used in many of these chapters to emphasize the point that, if these agents and scenarios are purposefully unleashed, it will, in fact, be in the form of an attack. The need for inclusion of such terminology in an academic medical textbook underscores the climate in which this text has been written. After such events as the Sept. 11, 2001 attacks, the elementary school tragedy in Beslan, Russia, and the London bombings of 2005, the clear need for thorough discussion is apparent. Part 2 of this text discusses these scenarios in as complete a way as possible, while respecting the dignity of those afflicted by past events. In a way it is the pain and suffering of both victims and survivors of such events that has contributed most to this text, and it is in celebration of their spirit that it has been written. Finally, I must mention the outstanding group of editors and contributors you will find within these pages. I went to great lengths to find individuals who are expert in their field, not only because they have studied it, but because they have done it. These are the doers as well as the thinkers. These are the men and women who leave their families when disaster strikes and integrate into the response systems. They are the experts called upon on a regional, national, and international level to prepare for disasters, always learning from the past and planning for the future. This book is more than 2 years in the making, partly because during that time the editors and authors xxv

were all too often deployed for lengthy periods into disaster zones around the world. In the study of Disaster Medicine, perhaps like none other, knowledge borne from experience makes for a very robust textbook. You will feel that experience jump from these pages and you will be rewarded by having learned from the best.

xxvi PREFACE

Because of the ubiquitous nature of disaster, society is indebted to those who choose to learn and practice this field. As a member of that society, I would like to personally thank you for doing so. Gregory R. Ciottone, MD, FACEP

c h a p t e r

1

Introduction to Disaster Medicine Gregory R. Ciottone

Throughout history, emergency medical responders have cared for the victims of disaster. As in other areas of disease and injury, medical personnel assume the responsibility of providing care to patients with illness or injury resulting from the catastrophe. Unlike other areas of medicine, however, the care of casualties from a disaster requires the healthcare provider to integrate into the larger, predominately non-medical multidisciplinary response. This demands a knowledge base far greater than medicine alone. To operate safely and efficiently as part of a coordinated disaster response, either in a hospital or in the field, an understanding of disaster management principles is necessary. In the mid-1980s, disaster medicine began to evolve from the union of disaster management and emergency medicine. Although Disaster Medicine is not yet an accredited medical subspecialty, those who practice it have been involved in some of the most catastrophic events in human history. Practitioners of present day disaster medicine have responded to the aftermaths of the tsunami in southeast Asia,1 hurricane Andrew,2 the Indian earthquake,3 the Madrid train bombings,4 and the World Trade Center attack,5 to name a few. During the past several decades, the first applications of basic disaster medicine principles in real-time events have been carried out, and as demonstrated recently by the 2004 tsunami in southeast Asia, there is sure to be continued need for such applications. The impetus for this text grew from a realization that, as the specialty of emergency medicine grows, emergency physicians must take ownership of this new field of disaster medicine and ensure it meets the rigorous demands put upon it by the very nature of human disaster. If we are to call ourselves disaster medicine specialists and are to be entrusted by society to respond to the most catastrophic human events, it is imperative that we pursue the highest level of scholarly knowledge in this very dynamic area. Until there is oversight from a certifying board, it is our responsibility to the public we serve to maintain this high level of excellence.

THE DISASTER CYCLE Because disasters strike without warning in areas often unprepared for such events, it is essential for all emergency services personnel to have a foundation in the

practical aspects of disaster preparedness and response. As is discussed in other chapters throughout this text, emergency responders have an integrated role in disaster management. All disasters follow a cyclical pattern known as the disaster cycle (Fig. 1-1), which describes four reactionary stages: preparedness, response, recovery, and mitigation/prevention. Emergency medicine specialists have a role in each part of this cycle. As active members of their community, emergency specialists should take part in mitigation and preparedness on the hospital, local, and regional levels. Once disaster strikes, their role continues into the response and recovery phases. By participating in the varied areas of disaster preparation and response, including hazard vulnerability analyses, resource allocation, and creation of disaster legislation, the emergency medicine specialist integrates into the disaster cycle as an active participant. A thorough understanding of the disaster medicine needs of a community allows one to contribute to the overall preparedness and response mission.

NATURAL AND MANMADE DISASTER Over the course of recorded history, natural disasters have predominated in frequency and magnitude over manmade ones. Some of the earliest disasters have caused enormous numbers of casualties, with resultant disruption of the underlying community infrastructure. Yersinia pestis caused the death of countless millions in several epidemics over hundreds of years. The etiological agent of bubonic plague, Y. pestis devastated Europe by killing large numbers of people and leaving societal ruin in its wake.6 As of this writing, there is fear of an impending avian influenza pandemic that may be worldwide in scale.7 Influenza and severe acute respiratory syndrome (SARS) have proven in recent years that, despite the passage of time and the great advances in medicine, the world continues to be affected by the outbreak of disease. Further, diseases that have been eradicated, such as smallpox, now have the potential of being reintroduced into society, either accidentally from the few remaining research sources in existence or by intentional release. Such an event could be devastating, as the baseline intrinsic immunity 3

THE DISASTER CYCLE Mitigation/prevention

Recovery

Preparedness

Response

DISASTER

FIGURE 1–1. The disaster cycle.

the world population had developed during the natural presence of the disease has faded over time, putting much larger numbers of people at risk. Finally, with the advent of the airliner allowing rapid travel to any part of the world, the bloom effect of an outbreak is much harder to predict and control. Disease outbreaks that were previously controlled by natural borders, such as oceans, no longer have those barriers, making the likelihood of worldwide outbreak much greater now than it was hundreds of years ago. In addition to epidemics, with each passing year natural disasters in the form of earthquakes, floods, and deadly storms batter populations. One need only to remember the destruction in terms of both human life and community resources caused by the Indian Ocean earthquake and subsequent tsunami of 2004 to understand the need for preparedness and response to such natural events. Considering the earthquake that caused the tsunami occurred hours before the devastation, it is difficult to understand how today’s advanced society, able to travel far into space among other great achievements, was unable to detect one of the most deadly natural events in recent history. The realization that disaster can strike without warning and inflict casualties on the order of the 2004 tsunami, despite our many technological advances, serves as a warning that mitigation, preparedness, and response to natural disaster must continue to be studied and practiced vigorously. Today, the possibility of terrorist attack threatens populations across the globe. Both industrialized and developing countries have witnessed some of the most callous and senseless taking of life, for reasons not easily fathomed by civilized people. It is unusual to read a newspaper, listen to radio, or watch television news reports without learning of a terrorist attack in some part of the world. These attacks are so frequent that society has become almost numb to them. Today, an event such as a car bombing may be relegated to a side report on a daily newscast. The commonplace nature of a terrorist attack in modern society ensures it is unquestionably something that will continue long into the 4 INTRODUCTION TO DISASTER MEDICINE

future and will very likely escalate in scale and frequency. The multilayered foundation on which ideological belief evolves into violent attack is beyond the scope of analysis this book ventures to undertake. These ongoing events do demonstrate, however, that the principles studied in the field of disaster medicine must include those that are designed to prepare for and respond to a terrorist attack. Because there are very intelligent minds at work designing systems to bring disaster on others, equally there must be as robust an effort to prepare for and respond to those disasters. Such response involves the deployment of law enforcement, evidence collection, and military personnel and equipment, which are typically not seen in the response to a natural disaster. The integration of these unique assets into the overall response is essential for the success of the mission. The disaster medicine specialist must have a thorough understanding of the role of each.

DEFINING DISASTER A thorough discussion of disaster preparedness and response must be predicated on a clear definition of what, in fact, constitutes a disaster. Used commonly to describe many different events, disaster is not easily defined. One of the earliest documented testaments to such an event is that of the great flood, reported in several writings, including the Bible. This flood is described as covering vast areas of land in the most populated part of the ancient world. Such a flood would have killed millions of people and destroyed vast areas of inhabited land. This surely would fit the definition of a disaster. Similarly, the Indian Ocean tsunami in 2004, killing well over 200,000 people, would also meet the criteria for disaster. However, a 2005 bus crash in the Baharampur district of India that killed 48 people has also been called a disaster. Likewise, the 2003 explosion of the space shuttle Columbia on re-entry into Earth’s atmosphere that killed the crew of seven astronauts onboard has often been referred to as the Columbia Disaster in the lay press. How can an event resulting in the loss of seven people be placed in the same category as one that kills hundreds of thousands? Herein lies the paradox of disaster. What is it? Who defines it and by what criteria? It is difficult to dispute that an event causing thousands of casualties should be considered a disaster, but let’s analyze why that is the case. What is it about the sheer number of dead and injured that allows the event to be called a disaster? In terms of medical needs, it is simply because there is no healthcare system on Earth that can handle that number of casualties. Therefore, an event of such magnitude is a disaster because it has overwhelmed the infrastructure of the community in which it occurred. Following this logic, we can then also make the statement that any event that overwhelms existing societal systems is a disaster. This definition is close to the United Nations Disaster Management Training Programme’s (UNDMTP) definition of disaster8:

A disaster is a serious disruption of the functioning of a society, causing widespread human, material or environmental losses which exceed the ability of the affected society to cope using only its own resources.

A similar definition is used by the World Health Organization (WHO). By applying these definitions, one can understand how an event in a rural area with 10 to 20 casualties may also be considered a disaster because the limited resources in that area may prevent an adequate response without outside assistance. The widely accepted UNDMTP and WHO definitions of disaster justify describing both the 2004 tsunami and the 2005 bus accident as disasters. But what about the space shuttle Columbia destruction on re-entry? Clearly this definition does not allow one to justify the use of disaster in describing that horrific accident. This brings to light a discrepancy in how disaster specialists and the lay public term events. The Columbia accident, as an example, does not meet any accepted criteria of disaster. It was, however, an exceedingly tragic event, seen by millions on television as it was unfolding. It was tragic by the word’s very definition in the Cambridge Dictionary: “A very sad event, especially one involving death or suffering.” Public perception of such events may cause this misnomer, with a tragic incident being termed a disaster. Much like disaster, tragedy can also have a profound and lasting effect on society, especially a tragedy that is widely viewed through modern media outlets. This text, however, will follow the UNDMTP and WHO definitions when discussing disaster.

DISASTER MEDICINE Disaster medicine is a discipline resulting from the marriage of emergency medicine and disaster management. The role of medicine, in particular emergency medicine, in disaster response has been clearly defined throughout history. Responsibility for the care of the injured from a disaster has been borne by the emergency specialist. Therefore, disaster medical response, in its many forms, has been around for thousands of years. Whenever a disaster has struck, there has been some degree of a medical response to care for the casualties. In the United States, much of the disaster medical response has followed a military model, with lessons learned through battlefield scenarios during the last two centuries.9 The military experience has demonstrated how to orchestrate efficient care to mass casualties in austere environments. It does not, however, translate directly into civilian practice. For instance, scenarios encountered on the battlefield with young, fit soldiers injured by trauma are vastly different from those encountered in a rural setting, where an earthquake may inflict casualties on a population with baseline malnutrition or advanced age. With this realization came the need to create disaster medicine as an evolution from the military practice. This recent organization of the medical role in disasters into a more formalized specialty of disaster medicine has enabled practitioners to further define their role in the overall disaster preparedness and response system.

Disaster medicine is truly a systems-oriented specialty. There is no “disaster clinic.” There are no practitioners who leave home in the morning intent on seeing disaster patients. Disaster medical care is often thrust upon the practitioner and is not necessarily something that is sought out. The exception to this is the medical specialist who becomes part of organized (usually federal) disaster team, such as a Disaster Medical Assistance team (DMAT). In this case, one may be transported to a disaster site with the intention of treating the victims of a catastrophic event. In all other circumstances, however, the disaster falls on an unsuspecting emergency responder who is forced to abandon his or her normal duties and adopt a role in the overall disaster response. Unlike the organized disaster team member, if an emergency provider treats casualties from disaster, it will most likely be as a result of a disaster event that has occurred in his or her immediate area. Because of the random nature of disaster, it is not possible to predict who will be put into that role next. Therefore, it is imperative for all who practice in emergency health services to have a working knowledge of the basics of disaster medicine and disaster management. In addition, especially with the recent escalation in perceived and real terrorist threats, there are a host of possible attack scenarios, which may involve exotic chemical, biological, or nuclear agents and modalities. Most clinicians will have a very limited knowledge of many of these agents, so it is therefore important to educate our potential disaster responders on their specifics. The field of disaster medicine involves the study of subject matter from multiple medical disciplines. Disasters may result in varying injury and disease patterns, depending on the type of event that has occurred. Earthquakes can cause entrapment and resultant crush syndrome; tornadoes may cause penetrating trauma from flying debris; and disease outbreak, either natural or intentional, can result from many different bacteria, viruses, and fungi. Because of the potential variability in casuality scenarios, the disaster medicine specialist must have training in the many injury and illness patterns seen in disaster victims. Even though the expanse of knowledge required is vast, the focus on areas specifically related to disaster medicine allows the science to be manageable. The study of disaster medicine should not be undertaken without prerequisite medical training. A disaster medicine specialist is always a practicing clinician from another field of medicine first and a disaster specialist second. By integrating these many disciplines, one is prepared for the variety of injury and illness patterns that may be faced. Finally, disaster medicine presents unique ethical situations not seen in other areas of medicine. Disaster medicine is predicated on the principle of providing care to the most victims possible as dictated by the resources available and by patient condition and likelihood of survival. Disaster triage involves assigning patients into treatment categories based on their predicted survivability. This triage process may dictate that the most severely injured patient not be given medical care but rather it be provided to a less critically injured patient. INTRODUCTION TO DISASTER MEDICINE 5

To the best of his or her ability, the triage officer must make a determination as to whether, in the environment of the specific disaster and the availability of resources, a given patient has a significant probability of survival or does not. If it is the latter, disaster triage principles mandate that care be given to the patient with a higher likelihood of survival. This basic disaster triage principle can have a profound psychological impact on the care provider. As a physician, one is trained to render care to the sick and to not leave the side of a needy patient. To deny care to a critically ill or injured patient can be one of the most anxiety-provoking tasks a disaster medicine specialist performs. The unique and ever-changing circumstances under which disaster medicine specialists operate mandate the continued evolution and vigorous pursuit of academic excellence in this new specialty. A comprehensive approach that unifies medical principles with a sound understanding of disaster management procedures will yield a well-rounded and better-prepared disaster responder. If emergency medicine providers around the world can develop a basic understanding of the fundamental principles of this specialty, great advances in the systems included in the disaster cycle will surely follow. The more widely dispersed this knowledge becomes, the better prepared we are as a society to respond to the next catastrophic event.

6 INTRODUCTION TO DISASTER MEDICINE

REFERENCES 1. Wattanawaitunechai C, Peacock SJ, Jitpratoom P. Tsunami in Thailand—disaster management in a district hospital. N Engl J Med. March 2005;352(10):962-4. 2. Nufer KE, Wilson-Ramirez G. A comparison of patient needs following two hurricanes. Prehospital Disaster Med. April-June 2004;19(2):146-9. 3. Jain V, Noponen R, Smith BM. Pediatric surgical emergencies in the setting of a natural disaster: experiences from the 2001 earthquake in Gujarat, India. J Pediatr Surg. May 2003;38(5):663-7. 4. Gutierrez de Ceballos JP, Turegano Fuentes F. Casualties treated at the closest hospital in the Madrid, March 11, terrorist bombings. Crit Care Med. January 2005;33(1 suppl):S107-12. 5. Simon R, Teperman S. The World Trade Center attack. Lessons for disaster management. Crit Care. December 2001;5(6):318-20. 6. Lowell JL, Wagner DM, et al. Identifying sources of human exposure to plague. J Clin Microbiol. February 2005;43(2):650-6. 7. Larkin M. Avian flu: sites seek to respond and reassure. Lancet Infect Dis. March 2005;5(3):141-2. 8. Disaster Management Training Programme. Disaster Preparedness Guide. 2nd ed. Available at: http://www.undmtp.org/english/disaster_preparedness/disaster_preparedness.pdf#xml=http://undmtp. org.master.com/texis/master/search/mysite.txt?q=disaster+preparedness&order=r&id=60413a1214953850&cmd=xml. 9. Dara SI, Ashton RW, et al. Worldwide disaster medical response: an historical perspective. Crit Care Med. January 2005;33(1 suppl): S2-6.

S E C T I O N

c h a p t e r

O N E

Introduction

2

Public Health and Disasters Catherine Y. Lee and James Michael Riley

INTRODUCTION TO PUBLIC HEALTH As early as 310 BC, a public health philosophy was exhibited by the Romans. They believed that cleanliness would lead to good health and made links between causes of disease and methods of prevention. For example, during this time an association was made between the increased death rate of persons living near swamps and sewage, and as a result the Roman Empire began working on two major public health projects in sanitation control: the building of aqueducts to supply clean water to the city and a sewage system to eliminate waste from the streets. Today, the benefits of public health infrastructure in the United States and abroad continue to strengthen the well-being of society. The impact of interventions has been great. In the past century (1900–1999), the 10 greatest public health achievements have been documented as the following1: 1. Vaccination programs, meaning the eradication of smallpox; elimination of poliomyelitis in the Americas; and control of measles, rubella, tetanus, diphtheria, and other diseases around the world 2. Motor-vehicle safety 3. Safer workplaces 4. Control of infectious diseases 5. Decline in deaths from coronary heart disease and stroke 6. Safer and healthier foods 7. Healthier mothers and babies 8. Family planning 9. Fluoridation of drinking water 10. Recognition of tobacco use as a health hazard Public health is founded on the efforts of a society to protect, promote, and restore the health of its citizens. Public health programs and services emphasize the prevention of disease and administration of health needs to the population as an entity, versus the study and treatment of a single patient, as is found in the discipline of medicine.Today, public health is defined as “the science and the art of preventing disease, prolonging life, and promoting physical health and mental health and efficiency through organized community efforts . . . and the development of the social machinery to ensure to every individual in the community a standard of living adequate for

the maintenance of health.”2 The mission of public health is to fulfill society’s desire to create conditions so that people can be healthy. Public health is divided into the staple pillars of assessment, policy development, and assurance.3 All three of these pillars are interdependent and cyclical. Two functions address the issues of assessment: (1) monitor health and (2) diagnose and investigate. Under policy development are the functions (1) inform, educate, empower; (2) mobilize community partnerships; and (3) develop policies. The following functions define assurance: (1) link to and/or provide care, (2) ensure a competent workforce, and (3) evaluate.3 Like traditional programs in public health, ranging from maternal and reproductive health to injury control and prevention, the public health response to disasters also fulfills the same basic tenets of assessment, policy development, and assurance. This chapter introduces the reader to how public health integrates into disaster preparedness and response systems by highlighting some specific subjects relevant to those tenets. It will cover topics like the public health disaster response cycle, policies in disaster response, the provision of disaster medical services, as well as worker safety and epidemiological/data issues (Figure 1-1).

PUBLIC HEALTH RESPONSE CYCLE Mitigation is the process of recognizing risks and vulnerabilities and then working to both reduce the vulnerability and strengthen society’s ability to withstand an unstoppable event or to reduce the effects from a disaster. Public health seeks to mitigate hazards such as explosions, chemical exposures, natural disasters like floods and earthquakes, and infectious disease, as well as reducing vulnerabilities of the infrastructure such as weak assets, resources, personnel, and science. One form of mitigation may be hardening structures against blast, but also can be the placement of surveillance systems to increase early detection of infectious diseases in a hospital setting, for example. Today, these systems, as well as reporting parameters, are being put into place across the country to both recognize and protect populations from a bioterrorism event. Early warning offers the benefit of a rapid response and reduction in morbidity and mortality. 7

Preparedness is the process of developing a formal program of response. Preparedness has many components, including: training and staff development; identification and classification of public health resources including personnel, supplies, and facilities; development of standard operating procedures (SOPs), emergency response plans, and communications plans; and preplacement of key supplies and protective equipment. This phase should also include the participation in tabletop and functional exercises. Public health personnel must be integrated and participate with other response agencies during drills and exercises to better familiarize each stakeholder with their respective roles and abilities. In addition, this is the phase in which public health agencies would develop interagency agreements, memoranda of understanding (MOUs), and external support contracts. The Centers for Disease Control and Prevention (CDC) is one reference source where planners can obtain basic guidelines for disaster preparedness.These include: 1. Form mutual-aid agreements and close relationships with local, regional, state, and federal partners. 2. Conduct a hazard and risk assessment. 3. Conduct a capacity assessment, identifying resources in your system. 4. Obtain those identified resources and surge capacity. 5. Develop plans consistent with other response organizations in your community. 6. Develop surveillance, registries, and data archiving systems. 7. Plan for public affairs and risk communication. 8. Ensure personnel are trained and certified to use personal protective equipment and other health practices. 9. Orientation for volunteers and personnel on procedures, guidelines, and command and management systems. 10. Participate in and conduct exercises. 11. Participate in after-action reviews of exercises and incidents.4 Response is the phase in which each agency and section with responsibility to respond activates its emer-

gency response plan to the specific threat or situation and can incorporate local, regional, and federal response. For example, in response to a biologic or chemical terrorist event, public health agencies would respond by conducting site surveys, recommending public safety measures and communicating risk, providing epidemiologic investigations, providing medical treatment of prophylaxis for those exposed, and initiating disease prevention and environmental decontamination measures.5

RECOVERY Public health agencies must identify what resources may be available to assist in restoring the operation as well as address other physically and emotionally affected populations. Public health recovery operations are multidisciplinary and involve multiple sectors of society (law enforcement, military, public policy, public works), and they vary depending on the extent of the disaster’s societal impact. Furthermore, recovery efforts comprise several components, some of which are Search and Rescue (SAR) in the case of an earthquake, bombing, or landslide; reinstitution of medical services if clinics and hospitals are destroyed; and establishment of corrupted lifelines like sanitation, electricity, and water. Those affected by the horrendous Tsunami disaster—that killed hundreds of thousands in Indonesia,Thailand,India,and so many other nations—demonstrated the international public health relief operation: an extreme example of multilateral, global relief spanning commercial and government sectors.The recovery from this disaster is ongoing and likely will last several years.

DISASTER POLICY For weeks after the 2004 tsunami, survivors on makeshift rafts were miraculously saved and brought back to shore. At the same time, the United States faced its own disasters. Thirteen people were trapped and 6 died from

LOCAL PUBLIC HEALTH RESPONSE TO THE WORST TERRORIST ATTACK IN U.S. HISTORY On Sept. 11, 2001, two commercial jets that were hijacked by terrorists crashed into the two towers of the World Trade Center in New York City. Within 90 minutes, both 110-story towers had collapsed. The New York State Department of Health (NYS DOH) had pre-established Emergency Operations Center committees that came together and began working within 30 minutes of the attack. NYS DOH nursing staff assisted in triaging and treating injured persons at an emergency triage center. In collaboration with the American Red Cross, the DOH also provided nursing staff for emergency shelters that housed displaced residents. Within the disaster site and surrounding commu-

8 INTRODUCTION

nity, DOH performed environmental monitoring. With losses in power and water as well as having tons of airborne contaminants in the area, DOH had its hands full with monitoring both the general public and emergency responders in addition to performing its daily activities. The DOH regularly sent faxes, e-mail alerts, and press releases containing urgent public health information and/or concerns to local hospitals and physicians. The DOH designed and implemented a rescue and recovery worker-safety plan. Additionally, the DOH initiated four disease and injury surveillance systems after the disaster, with assistance from the CDC.

mudslides in La Conchita, California; and a train disaster in Graniteville, South Carolina released concentrated chlorine fumes, leading to 9 deaths and 250 hospitalizations. Finally, in the fall of 2005 Hurricane Katrina devastated the Gulf coast of the United States, resulting in the flooding and complete evacuation of New Orleans. Although these disasters are not on the same scale in terms of death, injury, social loss, and destruction as the tsunami, they still maintain criteria that classify them as disasters. What determines whether an event is treated as a federal disaster? Locally, only the governor of a state or his or her appointee can declare a federal disaster through coordination with the Federal Emergency Management Agency (FEMA) regional director through the Federal Response Plan (FRP), under the Stafford Disaster Relief and Emergency Assistance Act.7 The FRP under the Stafford Act is an interagency plan that outlines the delivery of federal resources to state and local governments when a disaster overwhelms the region's ability to respond self-sufficiently. When state or local resources are insufficient to respond to and recover from a disaster, the presidential declaration sets forth long-term federal disaster recovery programs.7 The Stafford Disaster Relief and Emergency Assistant Act’s definition of a major disaster is stated in the following7: Any natural catastrophe (including any hurricane,tornado,storm,high water, wind-driven water, tidal wave, tsunami, earthquake, volcanic eruption, landslide, mudslide, snowstorm, or drought), or, regardless of cause, any fire, flood, or explosion in any part of the United States, which in the determination of the President causes damage of sufficient severity and magnitude to warrant major disaster assistance under this Act to supplement the efforts and available resources of states, local governments, and disaster relief organizations in alleviating the damage, loss, hardship, or suffering caused thereby.

A major disaster declaration makes available all federal disaster relief assistance to affected communities. This can include repair, replacement, and reconstruction of public and nonprofit facilities; cash grants for personal victim needs; temporary housing vouchers or replacement accommodations; and unemployment assistance.8 Following the Sept. 11 attacks in 2001, the President declared the Homeland Security Presidential Directive (HSPD)-5, in which he called for the development of a new National Response Plan (NRP) “to align Federal coordination structures, capabilities, and resources into a unified, all-discipline, and all-hazards approach to domestic incident management.”6 The premise of this robust plan is to standardize and make seamless the manner of operations for all levels of disaster response from local to federal, as well as private and public, agencies. The NRP will establish a national framework, standardizing aspects of coordination, communications, incident management, and information sharing, as well as streamline disaster policy directives and protocols. Upon full implementation of the NRP, it will supersede the Initial National Response Plan (INRP), the Federal Response Plan (FRP), the U.S. Governmental Interagency Domestic Terrorism Concept of Operations Plan (CONPLAN), and Federal Radiological Emergency Response Plan (FRERP).

The NRP also provides for guidance to initiate long-term community recovery and mitigation.6 When the NRP is fully implemented, the Secretary of Homeland Security will declare “incidents of national significance.” The drafted NRP in December 2004 outlined four criteria that constitute an “Incident of National Significance”: 1. A federal department or agency acting under its own authority has requested the assistance of the Secretary of Homeland Security. 2. State and local resources and authorities are overwhelmed and federal assistance has been requested by the state and local authorities. 3. More than one federal department or agency has become substantially involved in responding to an incident. 4. The Secretary of Homeland Security has been directed to assume responsibility for managing a domestic incident by the President.6 One specific support function most applicable to public health is called the Emergency Support Function #8 —Public Health and Medical Services, or ESF-8. ESF-8 provides supplemental assistance to State, local, and tribal governments in identifying and meeting the public health and medical needs of victims of an Incident of National Significance. This support is categorized in the following core functional areas: • Assessment of public health/medical needs (including behavioral health) • Public health surveillance • Medical care personnel, and • Medical equipment and supplies.6 The NRP stipulates that the coordinator and the primary agency is the Department of Health and Human Services.

OPERATING PUBLIC HEALTH The American Public Health Association (APHA) provides principles to guide public health’s response toward terrorism.11 From a list of 12 principles, the following seven are of specific interest to this chapter: 1. Strengthen the public health infrastructure (which includes workforce, laboratory, and information systems) and other components of the public health system (including education, research, and the faith community) to increase the ability to identify, respond to, and prevent problems of public health importance, including the health aspects of terrorist attacks. 2. Ensure the availability of and accessibility to health care, including medications and vaccines, for individuals exposed, infected, made ill, or injured in terrorist attacks. 3. Educate and inform health professionals and the public to better identify, respond to, and prevent the health consequences of terrorism and promote the visibility and availability of health professionals in the communities that they serve. PUBLIC HEALTH AND DISASTERS 9

4. Address mental health needs of populations that are directly or indirectly affected by terrorism. 5. Ensure the protection of the environment, food and water supply, and health and safety of rescue and recovery workers. 6. Ensure clarification of the roles, relationships, and responsibilities among public health agencies, law enforcement, and first responders. 7. Build and sustain the public health capacity to develop systems to collect data about the health and mental health consequences of terrorism and other disasters on victims, responders, and communities and develop uniform definitions and standardized data classifications systems of death and injury resulting from terrorism and other disasters. This chapter introduces basic concepts, discussions, and recommendations regarding the following key issues arising from these selected APHA principles: (1) public health infrastructure; (2) medical services, including the distribution of drugs and supplies; (3) education, training, and communications; (4) environmental health and precautions; (5) mental health; (6) worker safety and first responders; and (7) data collection and analysis.

PUBLIC HEALTH INFRASTRUCTURE Formal public health programs in the United States have existed for well over 200 years. For example, the origins of the U.S. Public Health Service (USPHS) (initially known as the Marine Hospital Service) may be traced to the passage of an act in 1798 that provided for the care and relief of sick and injured merchant seamen. After its inception and over the next 200 years, the Marine Hospital Service was restructured to provide a much wider variety of essential services. Today’s USPHS is recognized worldwide. Working alongside its other federal partners and state agencies, including the DHHS (and its agencies, such as the CDC, the Food and Drug Administration [FDA]), and the U.S. Department of Agriculture (USDA), the USPHS continues to be an active partner in the nationwide system of public health at the federal level and to influence public health on a national scale. The USPHS has, until recently, provided active support and direction to the NDMS (now directly under FEMA). The USPHS continues to respond to and support operations as a partner of NDMS, providing expertise in several areas. The U.S. public health system encompasses a broad integration of commercial, public, government, and nongovernment entities. It is as diverse as the very population it serves. It includes government public health agencies operating on federal, regional, state, and local levels; healthcare delivery infrastructure, such as hospitals and clinics; public health and health science academic institutions; community entities, such as schools, organizations, and religious congregations; commercial businesses; and the media.3 Public health is also augmented by its partnerships and increasing collaboration with expert military health institutions, such as the U.S. Army Medical Research Institute of Infectious Diseases 10 INTRODUCTION

(USAMRIID) and other defense agencies; national institutions such as the National Institute for Allergy and Infectious Disease (NIAID), under the National Institutes of Health (NIH); law enforcement and emergency responder communities on federal (Federal Bureau of Investigation) and local levels; and the medicolegal community, which is composed of national medical examiners offices and forensic scientists. Public health response is not centralized (for better or worse) and incorporates multiple government agencies, ranging from those involved in research and development (e.g., Bioshield at DHHS) to victim assistance (e.g., NDMS at DHS). Bioterrorist response, for example, involves an enormous breadth of players and their respective functions.9 The DHHS alone elicits responses from its agencies: the Agency for Healthcare Research and Quality (AHRQ), CDC, FDA, NIH, and Office of Emergency Preparedness (OEP). Other departments that participate in public health include the USDA, including its Animal and Plant Health Inspection Service (APHIS),Agricultural Research Service (ARS), Food Safety Inspection Service (FSIS), and Office of Crisis Planning and Management (OCPM); agencies under the Department of Commerce (DOC), including the National Institute of Standards and Technology (NIST); agencies under the DOD, including the Defense Advanced Research Projects Agency (DARPA), Joint Task Force for Civil Support (JTFCS), National Guard, and U.S. Army; the Department of Energy (DOE); the Department of Justice (DOJ), including the Federal Bureau of Investigation (FBI) and the Office of Justice Programs (OJP); agencies under the Department of the Transportation (DOT), including the U.S. Coast Guard (USCG); agencies under the Department of Treasury (Treasury), including the U.S. Secret Service (USSS); the VA; the Environmental Protection Agency (EPA); and FEMA.9 Different agencies function to deliver services to varying target audiences. For example, the target audiences of the CDC are state and local health agencies. In terms of activities, the CDC provides grants, technical support, and performance standards to support preparedness and response planning for bioterrorism; chemical and radiological incidents; natural disasters; and terrorist incidents, such as explosions, that may yield significant physical trauma.9 The OEP enhances medical response capabilities, such as early identification of a biologic incident, mass prophylaxis, mass casualty care, and mass fatality management.9 Its target audiences are local jurisdictions, including fire and police departments, emergency medical services (EMS), hospitals, and public health agencies.9 The DOJ helps states develop strategic plans and funds training, the obtaining of equipment, and the planning of drills and exercises for fire, law enforcement, emergency medical and hazardous response (HazMat) teams, hospitals, and public health departments.9 FEMA supports state emergency management agencies by providing grant assistance to sustain local-consequence management planning, training, and exercises for all disasters, including biological incidents.9 For example, FEMA, with the U.S. Army, conducts the Chemical Stockpile Emergency Preparedness Program (CSEPP) and the Radiological Emergency Preparedness (REP)

program.12 The goal of CSEPP is to improve preparedness in the event of an accident involving U.S. stockpiles of obsolete chemical munitions.12 The REP carries out exercises to ensure that residents living around nuclear power plants are safe and prepared in case of a disaster. In the event of a disaster, responders on the front line will be public health officials, health care workers (physicians, nurses, other medical professionals), public works personnel, firefighters, EMS personnel, and law enforcement officers.9 The core public health component will involve local public health departments, which have been described as “. . . the critical components of the public health system that directly deliver public health services to citizens.”13 A public health department is an administrative and/or service unit of local or state government that is staffed with a median of 20 people, varying between 1 and sometimes more than 20,000, with an average of 72 full-time workers.13 Local public health departments provide services ranging from immunizations to food and milk inspections.13 Most departments conduct childhood and adult immunizations, communicable disease control practices, epidemiology and surveillance, community assessment, and sexually transmitted disease counseling.13 Some others have injury control programs, solid waste management, and comprehensive primary care services.13 Health departments will likely not be the lead agency in a disaster and therefore must work closely with other organizations and fall into the incident command during an emergency.9 Health departments and all emergency response agencies should establish, in the planning phase, mutual aid agreements and close working relationships with key partners in their region. Partners include emergency management agencies (EMAs); EMS; medical and behavioral healthcare providers; fire departments; law enforcement; local emergency planning committees; state, regional, and tribal public health response coordinators; neighboring health jurisdictions; humanitarian and volunteer organizations; private businesses; and academic institutions, such as schools of public health and medicine.9 For example, between August and September 2004, four hurricanes (Charley, Frances, Ivan, and Jeanne) ripped through Florida, ravaging hundreds of thousands of homes; displacing huge populations; and prompting the aid of 5000 FEMA workers in 15 states and 3800 National Guard members who provided security, directed traffic, and distributed supplies.14 Additionally, more than 140,000 volunteers spanning state and national volunteer organizations, such as the Red Cross and faith-based groups, arrived in Florida to lend help, ranging from preparing meals to removing trees.15 Further, the U.S. Public Health Services works alongside its other federal partners and state agencies, including the DHHS and its agencies, the CDC, and the FDA, as well as the USDA.They continue to be an active partner in the nationwide system of public health at the federal level in order to influence public health on a national scale. The USPHS has until recently provided active support and direction to the National Disaster Medical System (now directly under FEMA) in the Department of Homeland Security. They continue to respond and sup-

port operations as a partner of NDMS, providing expertise in several areas.

Medical Services A biologic attack could result in the infection thousands of people without any indication in the first few hours of how many people are infected.16 For example, one hypothetical scenario depicted a national and global spread of smallpox, resulting in 15,000 cases and 2000 deaths.17 It is therefore recommended to provide mass prophylaxis to the population—the use of antibiotics being the primary key to survival for most people.16 Some believe that vaccines are not the first line of defense against biological threats but can be used for control of a smallpox epidemic, prophylaxis against anthrax in combination with antibiotics, control of global pandemic infections, and pre-exposure prophylaxis for high-risk workers in laboratory and health care environments.18 Because most public health departments, hospitals, and local institutions lack the amount of drugs needed for a national emergency, federal medical resources are available through the Strategic National Stockpile (SNS), formerly named the National Pharmaceutical Stockpile (NPS). After institution of the Homeland Security Act of 2002, the DHS and CDC began to jointly manage the SNS, with the DHS defining the goals and performance requirements of the program and being responsible for administering the actual deployment of the 12-hour push package.19 The cache of medical supplies includes antibiotics, chemical antidotes, antitoxins, life support medications, intravenous administration and airway maintenance supplies, and medical/surgical items that can be delivered in the event of a national emergency within 12 hours to strategically designated warehouses across the United States and its territories.19 The SNS is not meant to be a first response tool but rather to augment and restock existing state and local health agencies’ medical supplies. The SNS program conducts quarterly quality assurance checks, rotates materials, performs a full annual inventory of all package items, and regularly inspects environmental conditions, security, and overall package maintenance.19 Deployment of the SNS is made when the state governor’s office directly requests assets from the CDC or DHS.19 Once the SNS cache has been delivered, several key steps must be taken to effectively use it: officially receive the supplies and unload them; have adequate personnel for packaging, distributing, dispensing, tracking, and storing the supplies; have the local public health department assign dosages; and provide communication and security.16 There are additional public health issues beyond these logistics that should be taken into account when distributing mass prophylaxis to the public. They include dividing the population into groups who require medication first, a step that is politically sensitive and should be decided before a biologic attack happens.16 Also, public health personnel should be ready to distribute clear agentspecific and drug information, to make available multilingual staff and handouts, to handle the needs of special populations, to provide personal protective equipment PUBLIC HEALTH AND DISASTERS 11

(PPE) for people at staffing and dispensing centers, and to provide security in case of crowd panic.16 Disasters cause various patterns of injury and disease, ranging from blast injuries by a terrorist bombing to ventilatory failure from the chemical release of a nerve agent. As a result, responses significantly vary in terms of how widespread the response is (local to international), which personnel are used to respond, the duration of the response, and what medical management must be used to treat those affected or exposed. For example, some infectious diseases require a larger response, for which the help of national and sometimes international partners and resources is needed to identify the agent, conduct surveillance, report, and treat the range of people who may be infected. Such responses may vary in location and size. However, natural disasters, such as hurricanes, call for a different type of medical response altogether, in which medical problems seem to arise out of environmental hazards resulting from the natural disaster’s aftermath. For instance, injuries and deaths occur because victims fail to evacuate and take shelter, do not take precautions in securing property, and do not follow guidelines for food and water safety or injury prevention during the recovery phase.20 Injuries from a hurricane can result from near-drowning; electrocution; lacerations from flying debris; blunt trauma or bone fractures from falling trees and other heavy objects; stress-related disorders; heart attacks; gastrointestinal, respiratory, vector-borne, and skin diseases; toxic poisoning; fires; bites from displaced wild animals, such as animals and snakes; and even improper use of mechanical equipment, such as chain saws and power tools.20 Chemical and radiological incidents have more specific medical issues, including the recognition of patterns of injury, prophylaxis, and antidotes. Managing a volume of exposed patients in a limited healthcare environment can be challenging and can include issues of decontamination; on-site prehospital management; transportation; the use of PPE; and treatment of patterns of injury specifically associated with chemical and radiological sequelae, such as skin lesions, blisters and burns, nervous system disorders, inhalational injuries, and acute radiation syndrome. Some disasters fall into less specific points for medical management due to the nature of the event. Consider the blackout on Aug. 14, 2003, in the Northeastern United States and Southeastern Canada (Ottawa and Toronto) that affected 50 million people and a total of 240,00 square kilometers in areas including New York, New Jersey, Vermont, Michigan, Ohio, Pennsylvania, Connecticut, and Massachusetts.21 The blackout, suspected to have been caused by a downed 340,000-volt power grid, caused the shutdown of 21 power plants across the nation.22 The blackout affected all electrical functions, shutting down computers, trapping passengers in high-rise elevators, stalling subways, and disrupting airport control and landing procedures, hospital activities, food refrigeration, traffic operations, and most channels of communication. Facilities with backup generators were able to continue operations, but only sparingly. In the United States, three people died as 12 INTRODUCTION

a result of the blackout and one firefighter was injured. In Ottawa, a teenager died from fire-related injuries and another person died after being hit by a car. In New York during the 30-hour period of no electricity, 3000 fires were reported, mainly from people using candles, and EMS personnel responded to 80,000 calls to 911, double the average.22 On the other hand, finite, sudden disasters causing immediate injury and mortality (such as terrorist bombings, transportation disasters, and building collapses) require a more robust response capacity at a local and perhaps regional level.This differs from the national and sometimes international assistance required after largescale natural disasters that affect vast regions of terrain, as was seen in the case of the 2004 tsunami disaster, as well as in several instances of floods, hurricanes, and even complex humanitarian emergencies overseas. In the case of an explosion, trauma systems must be equipped and ready to accept incoming patients, manage the bulk of patients with minor wounds who will flood the nearest hospital, and prepare for possibly unexpected rates of casualty flow. Physicians should be prepared to treat hundreds of trauma patients, which may be complicated by loss of utilities, difficulty in reaching hospitals, or possible damage to hospital facilities.23 The physically injured from high-energy disasters, such as earthquakes, tornadoes, or explosions, will most likely be treated at regional trauma centers for severe injuries. In the United States, there are 600 regional trauma centers.24 They coordinate EMS, including paramedics and air medical transport. A regional trauma center is composed of paramedics and emergency medical technicians (EMTs) who transport injured victims to trauma teams that include a trauma surgeon, emergency physician, several trauma nurses, and specialized personnel. Up to 16 physicians in various specialties, from neurosurgery to obstetrics, comprise a trauma team ready to receive injured patients in the operating room and critical care unit.24 For disease outbreaks, the provision of medical services and public health capabilities is considerably great and involves a large network of local to sometimes international response. When severe acute respiratory syndrome (SARS) made its way onto the global front as a highly threatening disease in November 2002, it crippled the Asian healthcare system and brought to light serious questions about the U.S. public health system’s ability to respond to a similar crisis at home. SARS had the greatest impact on Asian countries, with 7782 cases and 729 deaths, challenging Asian healthcare systems, adversely affecting Asian economies, and testing the effectiveness of international health codes.25 SARS is part of the coronavirus family. Within 2 to 10 days after infection, the affected person can develop symptoms including cough, fever, and body aches that are indiscriminate from other respiratory illnesses, appearing as an atypical pneumonia.25 The fatality rate from SARS is 11% and can be greater than 50% for people older than 65.25 SARS is a person-to-person transmitted disease that is acquired primarily through direct and indirect contact with respiratory secretions and/or contaminated objects.

An international outbreak of SARS took place from February through deep into the spring of 2003. When an infected physician who treated SARS patients in China stayed at a hotel in Hong Kong on travel, those who resided at the hotel acquired the disease and subsequently departed to Vietnam, Singapore, and Toronto, Canada, seeding secondary outbreaks.25 Cases spread from Asia to 26 countries, and at is peak in May 2003, hundreds of cases of SARS were being reported each week. To prevent and control the spread of SARS, public health efforts of case identification and contact tracing, transmission control, and exposure management were utilized. Case identification and contact tracing is “defining what symptoms, laboratory results, and medical histories constitute a positive case in a patient and tracing and tracking individuals who may have been exposed to these patients.”25 Transmission control is “controlling the transmission of disease-producing microorganisms through use of proper hand hygiene and personal protective equipment, such as masks, gowns, and gloves.”25 Exposure management separates those infected from noninfected individuals through the use of quarantine, which restricts movement of those who are not ill but were exposed to the disease agent and are potentially infectious.25

EDUCATION, TRAINING, AND COMMUNICATIONS Tabletop exercises are one form of disaster planning education. Participants of a tabletop exercise are broad and may include government officials (mayors, city council members, risk manager), public works/utilities personnel (water superintendent, gas company representative), law enforcement (police chief, sheriff), community services (Red Cross representative), emergency management (emergency program manager, National Guard representative), fire department representatives (fire chief, dispatcher), emergency medical/health personnel (emergency medical coordinator, public health official), and public information officers. 12 The tabletop exercise, which commonly includes senior-level officials, prompts participants to discuss how their respective agencies or units might react to a specific set of scenarios, emphasizing higherlevel policy and procedural issues.12 Unlike full-scale exercises or field exercise drills, such as a hospital disaster simulation in which operations are evaluated on scene and equipment is deployed, tabletop exercises do not involve management of equipment or personnel, but are rather classroom-type exercises held in a classroom setting.12 Full-scale exercises engage tactics, techniques, and procedures that could be used in an actual incident and are designed to be realistic.12 In May 2000, May 2003, and most recently May 2005, FEMA led three exercises called the Top Officials (TOPOFF1, TOPOFF2, and TOPOFF3), which were large-scale,“no-notice” field drills involving federal, state, and local agencies. TOPOFF1 in

2000 was jointly led by FEMA and DOJ and was conducted in three cities: a biological weapons incident in Denver, Colo., a chemical incident in Portsmouth, N.H., and a mass casualty radiological incident in the Washington, D.C. region.12 In 2003, the TOPOFF2 4-day drill involved a Radiological Dispersal Device (RDD), or “dirty bomb,” release in Seattle, Washington, and a biologic incident involving Yersinia pestis, or Pneumonic Plague, in Chicago.26 TOPOFF3 was the largest U.S. counter-terrorism exercise to date. It exceeded 10,000 players, and involved 275 federal, state, local, and private organizations, as well as international partners Canada and the United Kingdom, with 13 countries sending representative observers. The exercise simulated a chemical release attack in New London, Connecticut, and a biologic attack in New Jersey. Physicians and other healthcare providers are oftentimes on the front line when detecting a disease outbreak and play a primary role in early detection of the disease: “Health-care providers should be alert to illness patterns and diagnostic clues that might indicate an unusual infectious disease outbreak associated with intentional release of a biologic agent and should report any clusters or findings to their local or state health department. . . .”23,27

Physicians and other healthcare providers are recommended to maintain a high level of suspicion for rare disease, ascertain thorough patient histories, and evaluate occupational and environmental exposures.28 The CDC indicates the following three signs of a possible intentional biological release, emphasizing physicians should stay alert for the following27: 1. An unusual temporal or geographic clustering of illness (e.g., persons who attended the same public event or gathering) or patients presenting with clinical signs and symptoms that suggest an infectious disease outbreak 2. An unusual age distribution for common diseases 3. A large number of cases of acute flaccid paralysis with prominent bulbar palsies, suggestive of a release of botulinum toxin Most of the knowledge base and skills needed to treat patients after a terrorist or nonterrorist disaster involves an extension of everyday tools that physicians already possess.23 What is necessary is to “fill in the blanks,” as proposed by the American Medical Association.23 This may include symptoms to become familiar with for early recognition of an unusual infection, guidelines to manage chemical- and radiation-contaminated patients, and protocols to triage and treat acute trauma patients after an explosion. To this extent, professional organizations and societies have become involved in the development of education on disasters and terrorism, and a great degree of seminars, distance learning programs, books, periodicals, web sites, and self-study material have been organized to educate healthcare providers.23 Such steps have been taken not only in physician communities but also in nursing, physician assistant, and technician communities through the same routes of education and PUBLIC HEALTH AND DISASTERS 13

training. Notable experts have commented that public health Internet sites, such as the CDC’s bioterrorism web page, have kept the public informed and have helped keep physicians aware of the latest developments and recommendations in bioterrorism.28 In times of disaster, there is an essential need to communicate certain health matters to the public. Public health officials often gain and transmit information from a range of various sectors20: • • • • • • • •

The public (most importantly) Hospitals and their emergency departments Community providers Social service agencies First responders, such as fire, police, and EMS National Guard representatives Local and regional laboratories Policy makers, such as public officials, mayors, and governors • Traditional partners, including the American Red Cross and the public works system Through communication with the media, public health agencies can set up a network, delivering health reports regularly so that the general public can receive important updates and educational messages.20 These messages must be factual and credible to the public and delivered through advance protocols, in which a single public information officer has been appointed to deliver the information.20 Some likely public health information might include food and water safety, injury prevention measures, and warnings that, for example, increase timely evacuation from hurricanes and shelter against tornadoes.20 Also, information should contain facts about the expected hazards (natural, man-made, or technological disaster), safety precautions, and requirements for evacuation or shelter-in-place.20 All messages should be clear (messages in writing should be understood and bilingual, if needed) and concise; technical information should be translated into simple language for a general audience. Importantly, the sender of information should verify that the transmitted message has been received and understood by the intended audience. When the public heeds the actions and recommendations made by public health officials, those messages have been adequately delivered to the audiences.20 Experts emphasize that warning messages should not be withheld until the last minute. This has been documented to happen out of fear that panic will overwhelm the public and lead to more deaths and injuries than the actual disaster.20 Internally among public health systems and partners, secure and redundant lines of communication should be set up during a disaster. These include computers with a CD drive, e-mail capability, continuous online Internet access, and security software to protect sensitive data from intruders.20 Fixed facilities such as hospitals and health departments should have a standby source of power to operate electrical and communication systems in case a disaster strikes the main source.20 Communication equipment that has been used for public health response includes radio equipment, such as twoway radios, pagers, broadcast radios, televisions, and satellites; wire lines, such as telephones, facsimile machines, 14 INTRODUCTION

and computer modems; and a combination of both radio and wire lines, including cellular and satellite telephones.20 However, it is important to realize that in times of disaster, routine communications like these may not be readily available, especially to the public and private sectors. Such was the case in the London Bombings on July 7, 2005, when private businesses found it nearly impossible to access e-mails or make mobile phone calls, as cellular networks were congested from a surge in traffic.

ENVIRONMENTAL HEALTH AND PRECAUTIONS Environmental health precautions after a disaster will decrease illness, injury, and death. The risks of infection increase in the days after a disaster due to disrupted water supplies and the problem of sanitation control. These include maintaining water and food safety, proper sanitation and waste disposal, and the control of vector populations.20 The environmental health priorities of most heath departments include the following29: 1. 2. 3. 4. 5.

Ensuring an adequate supply of safe drinking water Providing food protection measures Ensuring basic sanitation services Promoting personal hygiene Assisting the efforts of first responders by providing health risk consultations or advising on exposure pathways 6. Providing information to emergency managers to help assess the scale of the emergency to ensure an effective response Landesman20 recommends a three-tiered approach to reduce exposure to environmental hazards: 1. Measures of control that involve preventing the hazard in question from being released or occurring; controlling its transport; and keeping people from being exposed, such as cleaning, treating, and collecting clean water 2. Establishing multiple barriers, meaning setting up redundant obstacles to separate unsanitary conditions from human contact that can sometimes be a matter of public works engineering 3. Distance between hazards and populations Quantitative analyses must be used in a survey fashion to identify existing disposal facilities and procedures in a community; to determine how to deliver sanitation coverage; and to distribute safe drinking water and establish water consumption rates. Consumption of and contact with contaminated water supplies from run-off sewage and disrupted sewage systems can lead to fecal-oral diseases such as cholera, typhoid fever, hepatitis A, and shigella.20 Public health notices to boil water, avoid certain foods that may have spoiled, and that provide locations of potable water are key to environmental safety. Improper food storage, for example, is often associated with Bacillus cereus, Clostridium perfringens, Salmonella, Staphylococcus

aureus, and group A Streptococcus.20 Sufficient shelter must take into account weather conditions during the disaster, such as warm or cool climates. Insufficient housing can expose people to environmental conditions that make them susceptible to frostbite, hypothermia, heat stroke, and dehydration.20 Especially important to take into account are educational messages and warnings about carbon monoxide poisoning and untrained use of mechanical power generators. Pest control to reduce infestation of rat and mosquito populations is also important.

MENTAL HEALTH Several studies describe, characterize, and propose interventions for mental health issues encountered after a disaster. Experts note the wide range of questionnaires, surveys, interviews, and psychiatric classification systems used to document postdisaster psychological sequelae and note the difficulty in cross-comparison and generalization of these findings toward many disasters.29 Although the disaster community agrees that effects of mental health require more investigation, they also agree that “the worst scars in disasters are psychological and social scars.”30 Mental health issues stemming from disasters are becoming increasingly integrated into postdisaster assessment, with more emphasis on mental health being an urgent aspect of public health relief. The mental health community stresses that providers and disaster relief personnel need to have a meaningful understanding of the psychological and social needs of victims in a disaster.30 Disasters can provoke specific emotional reactions that take on a variety of different psychological responses, affecting primary victims (those directly involved in the disaster) and secondary victims (such as relatives, co-workers, and schoolmates). Other people who can experience mental health issues include onlookers, rescuers, body handlers, health personnel, evacuees, and refugees.30 It is important to realize that most adults and children will experience normal stress reactions for several days after a disaster (Box 2-1).31 One should note that normal stress reactions can also spawn personal introspection, growth, and resilience. The three forms of mental health problems that may follow a disaster are acute stress reactions, posttraumatic stress disorders (PTSDs), and adjustment disorders or enduring personality change.30 Acute reactions are characterized by absence of emotion; lack of response to external stimuli; total inhibition or outward activity and random movements; persons being stunned or shocked; and psychosomatic symptoms such as tremor, palpitations, hyperventilation, nausea, and vomiting.30 PTSD is defined as32: An anxiety disorder (and diagnostic construct used in the Diagnostic and Statistical Manual of Mental Disorders-IV ) that can develop after exposure to a terrifying event, or ordeal in which grave physical harm occurred or was threatened. The criteria for PTSD require:

BOX 2-1 NORMAL STRESS REACTIONS AFTER A DISASTER Temporary emotional reactions Shock Fear Grief Anger Hopelessness Emotional numbness Cognitive reactions Confusion Disorientation Worry Memory loss Unwanted memories Physical reactions Tension Fatigue Difficulty with sleeping Change in appetite and sex drive Interpersonal reactions to relationships at work and school or within a marriage or family (these may be characterized by distrust, irritability, isolation, judgmental attitude, and being distant)

A. Exposure to a traumatic event B. Reexperiencing of the event C. Persistent avoidance of stimuli associated with the trauma D. Persistent increased arousal E. Duration of B, C, D of more than one month F. Clinically significant distress or impairment

One of three survivors experiences severe stress that can lead to PTSD, anxiety disorders, or depression. Severe reactions possibly leading to PTSD include dissociation, intrusive reexperiencing (nightmares), extreme attempts to avoid disturbing memories (substance use), extreme emotional numbing, hyperarousal (panic attacks, rage), severe anxiety (extreme helplessness, compulsions, or obsessions), and severe depression. The mental health ramifications are possibly greater for those who witness or are involved with certain experiences from a disaster. Some examples include loss of loved ones; life-threatening danger or physical harm (especially to children); exposure to gruesome death, bodily injury, or dead and maimed bodies; extreme environmental or human violence and destruction; and loss of home.31 Inherently, specific individuals might have a typically higher risk of severe stress and lasting PTSD, such as those with a history of exposure to other traumas, chronic medical illness and psychological disorders, chronic poverty, and recent emotional strain.31 On the other hand, the National Center for PTSD states that some factors might be protective, including social support, higher income and education, successful mastery of past disasters and traumatic events, reduction of exposure to trauma, and provision of regular and factual information about the emergency. At a recent national workshop on mental health and disasters, experts recommended some early intervention actions.32 Early intervention is defined as32: PUBLIC HEALTH AND DISASTERS 15

The provision of psychological help to victims and survivors within the first month after a critical incident, traumatic event, emergency, or disaster aimed at reducing the severity or duration of eventrelated distress. For mental health service providers, this may involve psychological first aid, needs assessment, consultation, fostering resilience and natural supports, and triage, as well as psychological and medical treatment.

Interventions include provision of the following: 1. 2. 3. 4. 5. 6. 7. 8. 9.

Basic needs Psychological first aid Needs assessment Rescue and recovery environment observation Outreach and information dissemination Technical assistance, consultation, and training Fostering resilience and recovery Triage Treatment

In regard to training, there are specific issues to consider when conducting mental health studies in foreign nations. International authors agree that a definite level of cultural social awareness, support for indigenous and local authorities, multi-integration into capacity and infrastructure rebuilding, understanding of the political dynamic (especially in regions where there is conflict), and assessment of mental health based on scientific and clinical knowledge are imperative from an ethical standpoint and will increase the success of the program.33

WORKER SAFETY AND FIRST RESPONDERS In the United States, there are more than 1 million firefighters, with about 75% of those on a volunteer-basis; 556,000 full-time law enforcement personnel at police departments; 291,000 full-time sheriff’s personnel; and more than 155,000 nationally registered EMTs.34 These first responders are faced with dual functions: report the first observations about the environment and its risks and simultaneously carry out prehospital tasks. Because the disaster scene is dynamic, with active primary and secondary hazards, emergency responders must characterize the site, where oftentimes the evidence of the causative agent is not yet determined and therefore situational awareness is imperative. This poses emotional, mental, and physical challenges where dangers are likely to arise. Disasters present emergency responders with primary hazards stemming from the actual causative agent. For example, the release or spillage of a chemical can cause toxic injury, whether it is by a physical asphyxiant (e.g., hypoxemia from inert gas in an enclosed space such as a silo), respiratory irritant (e.g., pulmonary damage and inflammatory response from chlorine or phosgene), or systemic toxicants (e.g., upper airway or alveolar injury or skin or neurological damage from organophosphates, volatile hydrocarbons, or hydrogen cyanide). 16 INTRODUCTION

Emergency first responders are also jeopardized by secondary risks on site. These hazards can take the shape of several types of environmental risks. For example, rescue personnel can be in danger of confronting hazards from disasters such as riots, explosions and fires, road accidents, farm accidents, factory accidents, and railroad disasters.35 Consider a scenario in which an overturned tanker truck has caused a major road accident; emergency personnel are likely to confront vehicle fires, fuel explosions, the instability of overturned vehicles and truck loads and cargo, the dangers of traffic control and safety, and exposure to release of toxic and dangerous chemicals. Explosions present the first responder with the potential of building collapse, secondary explosions, and toxic smoke release hazards. First responders are trained to use PPE for a chemical, biological, or radiological event, either intentional or unintentional (as is the case with an industrial accident). Toxic agents can be “invisible” to the senses, and the quantity, type, and time of exposure are not easily known. The National Institute of Justice (NIJ) states:“The purpose of personal protective clothing and equipment is to shield or isolate individuals from the chemical, physical, and biological hazards that may be encountered during hazardous materials operations.”36 PPE consists of a wardrobe of clothing and gear that allows the responder to confront and thwart exposure and to function normally. NIJ categorizes PPE into the three following basic categories36: • Respiratory equipment (e.g., air purifying respirators and supplied air respirators) • Protective garments (e.g., encapsulated suits, coveralls, and overgarments) • Other protective apparel (e.g., protective hoods, boots, and gloves) The NIJ Guide for the Selection of Personal Protective Equipment for Emergency First Responders is a good resource for more thorough and detailed information on PPE.36 As the National Institute for Safety and Health points out, large incidents (such as the terrorist attack on the World Trade Center), unlike smaller-scale disasters (such as localized traffic accidents and explosions), pose serious challenges that make it more difficult to protect the responder from injury, illness, and death. Large-scale disasters can do the following37: • • • • •

Affect, injure, or kill large numbers of people Cover large geographical areas Require prolonged response operations Involve multiple, highly varied hazards Require a wide range of capabilities and resources not routinely maintained by local response organizations • Attract a sizable influx of independent (“convergent”) volunteers and supplies • Damage vital transportation, communications, and public works infrastructures • Directly affect the operational capacity of responder organizations

Therefore, responder safety also requires human resource management, in which thoughtful planning can help one to operate in a chaotic, multiagency environment. This includes charting out the chronology of the response (short-term and extended); setting reasonable and efficient work shifts to prevent the exhaustion of personnel; controlling the perimeter and scene to manage convergent volunteers; inventorying and providing access to PPE and resources; and developing highly skilled “disaster safety managers” who possess experience, knowledge, and tactical skills to respond to hazards on site.37 Importantly, and not often considered to be a life-saving function, is the need to manage health and disaster information flooding the scene. This includes the delivery and sharing of critical information among multiple agencies of all types and levels in addition to making sense of overabundant information. This information can include reports of the changing conditions of the disaster scene; data on the number of available workers and their respective health conditions; and standard data on the number, type, and availability of PPE and important resources.38

DATA COLLECTION AND ANALYSIS Public health detection and analysis follow key functional areas that involve the development and use of surveillance systems, analysis via algorithms and statistical methods, and investigation of disease and injury with great emphasis on critical agents.5 Biological agents of highest concern, as categorized by the CDC, are B. anthracis (anthrax), Y. pestis (plague), variola major (smallpox), C. botulinum toxin (botulism), Francisella tularensis (tularemia), filoviruses (Ebola hemorrhagic fever, Marburg hemorrhagic fever), and arenaviruses (Lassa [Lassa fever], Junin [Argentine hemorrhagic fever], and related viruses).27 Epidemiology in bioterrorist incidents is not too different from standard epidemiological investigations.39 First, laboratory and clinical findings are used to confirm that an outbreak has occurred, using case definitions to determine the number of cases and attack rate. To characterize unusual levels of activity, the attack rate for the disease in question is compared against that of previous years to measure deviation from the norm. The outbreak can then be characterized in terms of time, place, and person, lending crucial data to determine the origin of the disease.39 By analyzing data of cases over time, an epidemic curve can be calculated that will allow for differentiation between an outbreak and normal pattern of disease.39 However, if an intentional release of a biological agent is suspected, time is of the essence, and as previously emphasized, early detection is key. Therefore, the development of surveillance systems, including syndromic surveillance systems and real-time computer models, are being developed. Surveillance “concentrates on the incidence, prevalence, and severity of illness or injury due to ecological changes, changes in endemic levels of

disease, population displacement, loss of usual source of health care, overcrowding, breakdowns in sanitation, disruption of public utilities, monitors increases in communicable diseases, including vector-borne, waterborne, and person-to-person transmission” and ultimately helps one to determine an association between exposure and outcome, whether that outcome includes specific injuries, illnesses, or death.20 In setting up a surveillance system, managers should consider using existing systems, such as those used to track reportable diseases, or developing temporary systems to track specific injuries and illnesses before, during, or after the disaster.20 Primary and secondary sources of data need to be identified and can vary from patient medical records (primary) to victim surveys and interviews (secondary). Primary data collection methods are direct observations or surveys, and secondary methods are interviews with key informants or review of existing records.20 Data sets can be obtained from numerous places, including state hospitalization data, hospitals and clinics, private providers, insurance companies, temporary shelters, first responders, and mobile health clinics.20 Increasingly, nontraditional data sources such as worker sick days from employer records are being used to screen for disease outbreaks. Next, case definitions need to be developed for uniformity of reporting outcomes. Finally, appropriate analytical methods should be used and can include descriptive measures, geographical analysis of spread, rates of disease or death, or an analysis over time measuring total numbers of cases and rates of appearance.20 It is also important to remember that in a disaster situation, rigorous epidemiological approaches may not be time-conducive and that there will be an immediate need to quickly collect key, important data that may be perishable as time goes on and populations change in exposure and impact to the hazard. As a result, disaster situations invoke the use of “quick and dirty” data collection, “quick” being simple and flexible and “dirty” being that some quantitative data are rough estimates gathered to answer immediate questions.18 Increasingly, for bioterrorism purposes, health departments are developing and testing syndromic surveillance systems. Syndromic surveillance is “an investigational approach where health department staff, assisted by automated data acquisition and generation of statistical alarms, monitor disease indicators continually (real-time) or at least daily (near real-time) to detect outbreaks of diseases earlier and more completely than would otherwise be possible with traditional public health methods (e.g., by reportable disease surveillance or telephone consultation).” Syndromic surveillance uses nontraditional data sources, or those other than laboratory data.These data reflect events “that precede clinical diagnosis, such as emergency department chief complaints, clinical impressions on ambulance run sheets, prescriptions filled, retail drug and product purchases, school or work absenteeism, and constellations of medical signs and symptoms in persons seen in various clinical settings.”40 PUBLIC HEALTH AND DISASTERS 17

PUBLIC HEALTH ASSESSMENT CDC deployed field teams to New York City emergency departments on Sept. 14, 2001, to conduct surveillance for possible covert biological releases. For the first two weeks, epidemic intelligence service officers (EISOs) staffed 15 hospitals for 24 hours and then provided 18-hour coverage at 12 hospitals for the remaining 30-day surveillance period. The teams entered data on-site and reported data to the New York City departments of Health and Mental Health each morning and followed up on significant cases. Between Sept. 13 and Oct. 12, 68,546 emergency department visits were recorded, with trauma as the highest syndrome-to-none-ratio (SNR) found (18.6%), followed by exacerbation of a chronic respiratory condition (7.6%). Diarrhea/gastroenteritis (4.4%) and upper and lower respiratory infections (4.2%) were also reported. Children younger than 15 years presented most often with respiratory syndrome complaints (67%) and rash syndromes (59%). Those between 25 and 64 years old made up 80% of inhalational visits and 75% of anxiety visits. Analyses were also specifically conducted for home postal codes within a two-mile radius of the World Trade Center and revealed that persons in the two-mile radius were no more likely to have a syndrome of bioterrorism interest than those who were outside of that proximity. However, the study found that people in close proximity to the towers on Sept. 11 were 61.5 times more likely to visit the emergency department for smoke/dust inhalation complaints than people from other areas. Overall, no health data to support a bioterrorist release were found.41

CONCLUSION Historically, promoting and managing the health of a society have shown to increase the welfare of the community. This discipline, called public health, is a broad one, encompassing multiple sectors of the community and professional fields; government and nongovernment agencies; and local, regional, federal, and sometimes international institutions. Collectively, these groups respond to disasters to study, reduce, and develop ways to mitigate adverse health effects in the future. This chapter has summarized phases of the disaster cycle, the players involved, and the basic policy of disaster declaration and response. Additionally, we have reviewed components of public health infrastructure, provision of medical services, education and communications in disasters, mental health issues, worker safety, and finally the value and techniques of data collection and analysis. It is recommended that the newcomer to public health and disaster medicine review the many references in this chapter and refer to resources on the Internet. Importantly, responders should be proactive and become trained, well-informed, experienced providers and openly disseminate factual knowledge to the community and their peers. This is the beginning to a more efficient, life-saving public health response to disasters. 18 INTRODUCTION

REFERENCES 1. Ten Great Public Health Achievements—United States, 1900–1999. MMWR. April 1999;48(12):241-3.Available at: http://www.cdc.gov/ mmwr/preview/mmwrhtml/00056796.htm. 2. Gostin LO. Public health law, ethics, and human rights: mapping the issues. Available at: http://www.publichealthlaw.net/Reader/ ch1/ch1.htm. 3. Institute of Medicine, Committee on the Future of Public Health. The Future of Public Health. Washington, DC: National Academy Press; 1988. 4. Centers for Disease Control and Prevention. Public health emergency response guide for state, local, and tribal public health directors.Version 1.0. Available at: http://www.bt.cdc.gov. 5. Biological and chemical terrorism: strategic plan for preparedness and response: recommendations of the CDC Strategic Planning Workgroup. MMWR. April 2000;49(RR-04):1-14. 6. National Emergency Management Association. National response plan—initial draft. Available at: http://www.nemaweb.org/docs/ national_response_plan.pdf. 7. National Governors Association. A Governor’s Guide to Emergency Management. Volume One: Natural Disasters. Washington, DC: National Governors Association; 2001. 8. Bea K. Federal Disaster Policies After Terrorists Strike: Issues and Options for Congress. American National Government and Finance Division; 2002. 9. US General Accounting Office. Bioterrorism: Public Health and Medical Preparedness. Testimony Before the Subcommittee on Public Health, Committee on Health, Education, Labor, and Pensions. Washington, DC: US General Accounting Office; 2001. Available at: http://www.gao.gov/new.items/d02141t.pdf. 10. US Department of Homeland Security. Initial national response plan fact sheet. Available at: http://www.dhs.gov/dhspublic/display?content=1936. 11. American Public Health Association. One year after the terrorist attacks: is public health prepared? A report card from the American Public Health Association. Available at: http://www.apha.org/ united/reportcardfile.htm#back1. 12. US General Accounting Office. Combating Terrorism: FEMA Continues to Make Progress in Coordinating Preparedness and Response. Washington, DC: US General Accounting Office; 2001. Available at: http://www.gao.gov/new.items/d0115.pdf. 13. National Association of County and City Health Officials. Preliminary Results from the 1997 Profile of U.S. Local Health Departments. Washington, DC: National Association of County and City Health Officials; 1998. Available at: http://www.edgewood.army.mil/downloads/reports/comp_mass_casualty_care.pdf. 14. Landesman LY. Public Health Management of Disasters, the Practice Guide. Washington, DC: American Public Health Association; 2001. 15. CBS News. Floridians seek relief. Available at: http://www. cbsnews.com/stories/2004/09/28/national/main646024.shtml. 16. Community Outreach, Mass Prophylaxis: a mass casualty care strategy for biological terrorism incidents, June 2001. 17. O’Toole T. Smallpox: an attack scenario. Emerg Infect Dis. 1999;5:540-6. 18. Russell PK. Vaccines in civilian defense against bioterrorism. Emerg Infect Dis. July-August 1999;5(4):531-3. 19. Centers for Disease Control and Prevention. Strategic National Stockpile. Available at http://www.bt.cdc.gov/stockpile. 20. Federal Emergency Management Agency. Thousands of volunteers help Floridians recover. Available at: http://www.fema.gov/news/ newsrelease.fema?id=15437. 21. GlobalSecurity.org. Great Northeast power blackout of 2003. Available at: http://www.globalsecurity.org/eye/blackout_2003.htm. 22. CNN.com. Power returns to most areas hit by blackout, U.S.Canadian task force charged with investigating outage. Available at: http://www.cnn.com/2003/US/08/15/power.outage. 23. American Medical Association. Featured CSA report: Medical preparedness for terrorism and other disasters. Available at: http://www.ama-assn.org/ama/pub/category/print/14313.html. 24. National Foundation for Trauma Care. U.S. trauma center crisis: lost in the scramble for terror resources. Available at: http://www.traumacare.com/NFTC_CrisisReport_May04.pdf.

25. US General Accounting Office. SARS Outbreak: Improvements to Public Health Capacity Are Needed for Responding to Bioterrorism and Emerging Infectious Diseases. Washington, DC: US General Accounting Office; 2003. Available at: http:// www.gao.gov/new.items/d03769t.pdf. 26. US Department of Homeland Security. Top Officials (TOPOFF) Exercise Series:TOPOFF2. After action summary report for public release. Available at: http://www.dhs.gov/interweb/assetlibrary/ T2_Report_Final_Public.doc. 27. Recognition of illness associated with the intentional release of a biologic agent. MMWR. Oct 2001;50(41):893-7. 28. Lane HC, Fauci AS. Bioterrorism on the home front: a new challenge for American medicine. JAMA. 2001;286:2595-7. 29. North CS, Kawasaki A, Spitznagel EL, Hong BA. The course of PTSD, major depression, substance abuse, and somatization after a natural disaster. J Nerv Ment Dis. December 2004;192(12): 823-9. 30. Dubouloz M. Mental health. In: de Boer J, Dubouloz M, eds. Handbook of Disaster Medicine. Netherlands: Van der Wees Publishers; 2000. 31. US Department of Veteran Affairs, National Center for PTSD. Available at: http://www.ncptsd.va.gov. 32. National Institute of Mental Health. Mental Health and Mass Violence: Evidence-Based Early Psychological Intervention for Victims/Survivors of Mass Violence. A Workshop to Reach Consensus on Best Practices. Washington, DC: US Government Printing Office; 2002. NIH Publication No. 02-5138. Available at: http://www.nimh.nih.gov/healthinformation/massviolence_intervention.cfm.

33. Weine S, Danieli Y, Silove D, Van Ommeren M, et al. Guidelines for international training in mental health and psychosocial interventions for trauma exposed populations in clinical and community settings. Psychiatry. Summer 2002;65(2):156-64. 34. US Department of Homeland Security. About first responders. Available at: http://www.dhs.gov/dhspublic/display?theme=63& content=237. 35. Badiali S. Pre-hospital care. In: de Boer J, Dubouloz M, eds. Handbook of Disaster Medicine. Netherlands: Van der Wees Publishers; 2000. 36. National Institute of Justice. Guide for the selection of personal protective equipment for emergency first responders. NIJ Guide 102-00 (Volumes I, IIa, IIb, and IIc.) Available at: http://www.ojp.usdoj. gov/nij/pubs-sum/191518.htm. 37. Centers for Disease Control and Prevention. Protecting emergency responders, volume 3. Available at: http://www.cdc.gov/niosh/ docs/2004-144. 38. RAND. Protecting emergency responders: lessons learned from terrorist attacks. Available at: http://www.rand.org/publications/ CF/CF176. 39. Pavlin J. Epidemiology of bioterrorism. Emerg Infect Dis. JulyAugust 1999;5(4):528-30. 40. Centers for Disease Col and Prevention. Draft framework for eval- AU: ? uating syndromic surveillance systems for bioterrorism preparedness. Available at: 41. Syndromic surveillance for bioterrorism following the attacks on the World Trade Center—New York City, 2001. MMWR. September 2002;51(special issue): 13-15. Available at: http://www.cdc.gov/ mmwr/preview/mmwrhtml/mm51SPa5.htm.

PUBLIC HEALTH AND DISASTERS 19

c h a p t e r

3

The Role of Emergency Medical Services (EMS) in Disaster Robert D. Furberg and David E. Marcozzi

The role of emergency medical services (EMS) systems in disaster management is to provide effective, responsible prehospital care; however, multiple considerations must be made long before the first EMS unit arrives on scene. Disaster management may be examined in the following four phases1: 1. 2. 3. 4.

Prevention and planning Preparedness Response Recovery/analysis

The process of prevention and planning uses an effective application of the hazard vulnerability analysis (HVA) concepts discussed briefly later in this chapter and in more detail in Chapter 17. The HVA establishes the probability of risk and identifies key components of an operative response plan. Measures to reduce potential loss of life and property may be achieved through the combined effort among members of the jurisdiction’s local emergency planning committee (LEPC) and other participants in incident response. Preparatory functions of management personnel must occur to ensure that responders, emergency managers, and citizens are adequately informed of and trained on appropriate operational expectations. During the response phase, public safety personnel must implement the Incident Command System early and effectively. Once operating within the paradigm, responders assume the specific tasks required to mitigate the incident. Triage, treatment, and transport are the highest priorities for most paramedics and emergency medical personnel. Specialized medical units with the necessary training and equipment may assume additional duties as directed by the incident commander. Initial and long-term recovery efforts are directed toward the reconstruction and rehabilitation of infrastructure and the community. EMS systems usually do not serve a primary role in recovery, but this final phase of management is critical for system reassessment and improvement. Analysis of specific methodologies used during incident management, including the efficacy of triage and predictive outcome assessments, are useful to the global community.2 20

After their inception on the battlefield, modern civilian EMS systems have found themselves using many of the same techniques, under similar conditions, as the pioneers of the field when managing disasters domestically. Modern EMS systems are capable of moderating the daily burden of emergencies; however, disaster operations often require emergency services to assume a different perspective to ensure effective resolution of significant incidents. This chapter details the operational adjustments that have been designed to optimize the role of EMS in disaster management.3

HISTORICAL PERSPECTIVE EMS is a product of war. From the first organized use of ambulances on the battlefields of Crimea to the birth of the modern field medic in the jungles of Vietnam, the history of EMS is undeniably blood-tinged with rich militaristic tradition. Baron Dominique-Jean Larrey, Napoleon’s surgeon-inchief, is largely credited with placing the first ambulance in service more than 150 years ago during the Crimean War. Larry, well-versed in the critical nature of traumatic injuries, initiated the use of covered, horse-drawn carts to expedite the movement of injured soldiers to treatment areas. This improvement drastically reduced the number of ineffective combat troops recovered from battle. During the Civil War, Clara Barton coordinated and rendered emergency care to wounded infantry. After serving as the superintendent of Union nurses, she crusaded tirelessly for medical relief of sick and wounded soldiers. Barton established the Red Cross within the United States, serving as the organization’s first president. During her tenure, she directed relief work for disasters such as famines, floods, pestilence, and earthquakes in the United States and throughout the world. With the improvement of military technology, casualties increased. As a consequence, soldiers received greater training in the management and transport of injured infantry during World War I. Aeromedical transport systems were established during World War II and refined during the Korean conflict.4

The corpsman of Vietnam most closely resembles the paramedic of today. Personnel were well trained in a variety of increasingly advanced interventions. Care was often rendered in extreme environments to multiple patients at once. The military demonstrated a profound effect on battlefield mortality rates with the aggressive application of early advanced intervention and expeditious transport via helicopter from the front lines of engagement to definitive care installations. The evolution of trauma care in military medicine proved to be the major factor in a progressive decrease in casualties among compromised soldiers. Casualty rates were reduced from 8% in World War I to 4.5% in WWII to 2.5% in the Korean War to less than 2% during the Vietnam conflict.5 Despite aggressive engineering feats that mechanized warfare and drastically increased the power of ordnance, the medical experience gained from the two World Wars and multiple international conflicts resulted in fewer soldiers killed in combat. The shift from empiricism to the practice of evidence-based medicine and the provision of acute care in the field made armed conflict much more survivable. The immense benefits of rapid, advanced field stabilization and swift transport to definitive care facilities realized by the armed services would soon become the expectation of politicians and civilians alike in the United States. After the advances made in trauma care on the battlefield, researchers in the United States during the early 1960s found that an infantry soldier in Vietnam had a statistically greater chance of survival than the average citizen involved in a motor vehicle collision on any of the nation’s highways. This disparity prompted two significant legislative acts in 1966. First, the National Academy of SciencesNational Research Council (NAS-NRC) published Accidental Death and Disability:The Neglected Disease of Modern Society. This white paper put forth 11 recommendations to improve care for injured persons. Recommendations included the creation of various standards within EMS, including training, public safety infrastructure, and the creation of “. . . a single nationwide number to summon an ambulance.” The second bill prepared by Congress was the Highway Safety Act of 1966. This act mandated the creation of the U.S. Department of Transportation (USDOT) and the National Highway Traffic Safety Administration (NHTSA). Both entities provided legislative authority and financial assistance to EMS systems in the United States. Between 1968 and 1972, approximately $142 million was distributed among states to develop and assess the first advanced life support programs. Initial training centered on the kinematics of trauma, stabilization, and provision of appropriate transport to definitive care facilities. Over the last three decades, EMS systems in the United States have established their own niche within the public safety sector. Paramedics have become increasingly autonomous as a result of the steadily expanding complexity of medical conditions and treatment options.In addition to these advancements,EMS systems have remained a reliable resource on the “domestic battleground,” where individuals in need of assistance may exceed available resources. To ensure that an EMS system is used most effectively in large-scale incidents, a specific, highly organized structure was developed.

However, before that structure was established, major incidents in the civilian sector routinely required the response of several agencies. Effective management was often confounded by multiple entities performing independently of one another without adequate interaction or communication. A significant example of how impaired communications can poorly affect the outcome of event mitigation can be demonstrated by what occurred after the attack on the World Trade Center on Sept. 11, 2001. New York City’s Office of Emergency Management (OEM) assumed its current form in 1996 and was headquartered at 7 World Trade Center.6,7 Communications from OEM were based off an antenna atop 1 World Trade Center. Less than nine hours after the first strike, 7 World Trade Center collapsed, significantly impairing coordinative abilities among EMS, the New York Police Department, and the Fire Department of New York. Responders lacked the common resource to communicate reliably among these agencies due to the lack of radio frequency interoperability. Additionally, triage and transport of patients were adversely affected by the lack of coordinated communications with local and regional hospitals in the New York City metropolitan area.8-9 During the early 1970s, fire administrators in California developed the Incident Command System (ICS) to manage rapidly moving wildfires and operational deficits that were previously encountered. Specific complications cited before the creation of the ICS included “too many people reporting to one supervisor; different emergency response organizational structures; lack of reliable incident information; inadequate and incompatible communications; lack of structure for coordinated planning among agencies; unclear lines of authority; terminology differences among agencies; and unclear or unspecified incident objectives.” In 1980, federal officials developed a national program called the National Interagency Incident Management System (NIIMS) based on the original ICS construct. The inherent flexibility of the ICS to accommodate issues of incident size and utilization of available resources has allowed the system to be used to mitigate both minor crises and major disasters exacted by nature and humans alike. As public safety personnel developed familiarity with the ICS, the federal government identified the need for the development of a body of government to establish standards of practice within increasingly complex applications of disaster management. In response to the increasing threat of terror attacks and the need to ensure a more cohesive response to large-scale incidents, federal guidelines were created to establish the role of EMS.10,11 In 1998, Congress issued a report underscoring concern regarding “ . . . the real and potentially catastrophic effects of a chemical or biological act of terrorism.” Legislators indicated that although the federal government is integral in the prevention and secondary response to such incidents, state and local public safety personnel who respond initially require additional assistance. The Appropriations Act (Public Law 105-119) authorized the U.S. attorney general to aid state and local responders in acquiring specialized training and equipment to “ . . . safely respond to and manage terrorist incidents involving weapons of mass destruction (WMD).” THE ROLE OF EMERGENCY MEDICAL SERVICES (EMS) IN DISASTER 21

The U.S. attorney general delegated authority to the Office of Justice Programs (OJP) on April 30, 1998, to develop and administer training and equipment assistance programs for state and local emergency response agencies. To accomplish this mission, the Office for Domestic Preparedness (ODP) was established to develop and administer a national domestic preparedness program. On Oct. 8, 2001, by executive order, the Office of Homeland Security and the Homeland Security Council were established. The functions of the newly created offices included incident management and oversight of preparation, response, and recovery after terrorist incidents. The Homeland Security Act of 2002 formally established the Department of Homeland Security (DHS). In the most significant federal restructuring since the 1960s, the newly anointed DHS has been placed in command of 22 government agencies, including the Federal Emergency Management Agency.12

CURRENT PRACTICE The role of EMS in the disaster management paradigm incorporates the four-phase approach of prevention and planning, preparedness, response, and recovery/analysis. These key phases have defined the mitigation of crises of all sizes since their inception in the early 1970s. After the establishment of the DHS and ODP, both agencies issued guidelines for municipal, state, and federal responders within public safety. These guidelines, in conjunction with the serial reassessment of current practice methodologies, allow responders to ensure that the most appropriate management strategies have been selected for a given situation. Adhering to the use of this construct allows EMS systems to optimize their ability to react to disaster.13,14 The prevention and planning phase includes the identification of specific hazards, threat assessments to life and property, and preemptive steps to minimize potential losses. Measures to reduce potential loss of life and property are commonly referred to as disaster mitigation. Mitigation measures may include public awareness campaigns, LEPC involvement, and legislative action. Preparedness encompasses the training and education of both public safety personnel and members of the community. The DHS has specified the ODP as the lead agency for directing domestic preparedness efforts and creating standards for the implementation of response plans. Under executive order, the National Disaster Medical System (NDMS) was formed in 1983. With cooperation between local communities and the federal government, Disaster Medical Assistance Team (DMAT) and International Medical and Surgical Response Team (IMSuRT) resources have developed throughout the nation. These deployable teams are designed to be a rapid-response element to supplement local medical care until contract resources or federal assistance can be mobilized. The responsibility of DMATs may include triaging patients, providing high-quality medical care despite the challenging environment found within disaster scenes, and assisting with patient evacuation. EMS 22 INTRODUCTION

personnel who participate in operations involving a DMAT deployment often are used in more of a primary care role rather than their typical emergency response capacity. The development of a strong relationship among primary care facilities, providers, and EMS systems regionally during the planning phase of action may significantly improve the transition of EMS personnel into this role. The NDMS also ensures that teams are equipped to sustain operations for 72 hours without additional resources. This dramatic difference underscores the disparity between routine and extended operations. Typically, EMS systems and personnel may be equipped or prepared to function for 24 to 48 hours; however, major disaster scenes are rarely mitigated completely without a more significant time commitment.15–17 On Aug. 1, 2002, the ODP released its Emergency Responder Guidelines to assist agencies in establishing a baseline understanding of the training necessary to safely and effectively respond to incidents involving the use of WMD. Designed and compiled as a resource, the guidelines present advice of experts from the private and public sectors. The guidelines were prepared with assistance from key federal agencies involved with firstresponder training and incorporated existing codes and standards established by the National Fire Protection Agency and the U.S. Occupational Safety and Health Administration. The guidelines provide an integrated compilation of baseline knowledge, skills, and responder capabilities for use as a reference by providers as well as course developers and trainers to underscore the importance of interoperable response strategies. The Emergency Responder Guidelines specify training objectives and establish the baseline level of operational knowledge of three distinct levels of responsibility— awareness, performance, and management—required of specific response disciplines (Table 3-1). Training is based on a provider’s level of experience and operational accountability with the three levels of responsibility. Commonalities among specific response disciplines (e.g., law enforcement, fire, EMS) illustrate areas in which common training and understanding can be established to ensure a more cohesive operational response.18,19 Awareness-level guidelines pertain to law enforcement officers, firefighters, and basic level emergency medical technicians. At a minimum, response personnel within this category are expected to be among the first to encounter an incident. Once management operations are under way, awareness-level personnel assume a more supportive role. These providers are responsible for recognition and referral after encountering a hazardous environment. The training objectives establish a basic understanding of operational actions, including notification of need for additional specialized resources, maintenance of scene control, and demonstrated competence of self-protection measures. Performance-level guidelines apply primarily to advanced level providers on scene, including paramedics and firefighters involved in rescue or fire suppression operations or a hazardous materials event. Depending on the various ICS assignments in use during a given incident, the performance-level providers must efficiently multitask their primary responsibilities with additional

TABLE 3-1

LEVELS OF RESPONSIBILITY

AWARENESS

PERFORMANCE

MANAGEMENT

Recognize hazardous materials (HazMat) incidents.

Have successfully completed proper training at awareness and performance levels. Know ICS and UCS, and assist with implementation as needed. Know and follow self-protection measures and rescue and evacuation procedures. Know and follow procedures for working at the scene of a potential WMD event.

Have successfully completed proper training in awareness, performance, and management levels.

Know protocols used to detect WMD agents or materials. Know and follow self-protection measures for WMD and HazMat events. Know procedures for protecting a potential crime scene. Know and follow agency’s or organization’s scene security and control procedures for WMD and HAZMAT events. Possess and know how to properly use equipment to contact higher authorities to request additional assistance or emergency response personnel.

Know and follow ICS and UCS procedures. Understand how the systems are implemented and integrated. Know and follow protocols to provide emergency medical treatment to persons involved in the event. Know and follow self-protection measures. Know plans and assets available for transporting the victims of events to primary care facilities. Know and follow procedures for protecting a potential crime scene.

Know and follow department procedures for medical monitoring of response personnel involved. Adapted from Office for Domestic Preparedness. Emergency Response Guidelines.August 1, 2003.

assignments from their commander. As a consequence, performance-level personnel require a strong working knowledge of the ICS and the ability to follow the Unified Command System (UCS). The provider must be able to follow procedures for the integration and implementation of each system and know how the two structures can be used to manage the incident. Procedures include establishing adequate communication capabilities to manage the incident; securing triage, treatment, and transport areas; and coordinating multiple responding agencies. The performance-level responder must also demonstrate competence in self-protection measures, rescue and decontamination operations, and evacuation procedures for managing victims. Planning-level and management-level providers are typically service administrators, supervisors, and emergency management officials. Those who operate within these guidelines must first complete both awarenesslevel and performance-level objectives. Individuals responsible for training at this level will be a part of the leadership and management of subordinate emergency medical personnel during the response operation. Objectives include planning before the incident as well as managing resources used to conduct the event. Leadership personnel must also be capable of overseeing medical surveillance of subordinates. In accordance with the preparatory phase, the ODP offers multiple training opportunities for responders at all levels. To enhance the capacity of local and state agencies, the ODP’s Equipment Grant Program provides funds to 50 states, the District of Columbia, the Commonwealth of Puerto Rico, American Samoa, the Common wealth of Northern Mariana Islands (CNMI), Guam, and the U.S. Virgin Islands.20

The priority among EMS responders must be rendering responsible prehospital care. To enable this goal, responders must first integrate an ICS into their response plan to allow for effective management of an incident. During the response phase, multiple responders and agencies must be coordinated to operate effectively. Civilian responses routinely incorporate the responsibility of several different specialties, such as fire and rescue, EMS, and law enforcement, beneath a single commander. As the scale of an incident grows, the command structure must expand to meet the increasingly diverse needs to provide effective management. With large-scale incidents, the underlying organizational construct becomes even more critical as coordination extends to incorporate local, state, and federal resource allocation. All responders on scene must be familiar with the structure and function of the ICS and UCS. The ICS enables integrated communication by establishing a manageable span of control. Beneath a single incident commander (IC), subordinate commanders exercise their own span of control among context-specific divisions. The overall structure of the system describes four divisions beneath the IC, including operations, planning, logistics, and finance. With each application of the ICS, commanders may elect how to delegate these various designations among responders. The benefits of operating within the ICS structure are apparent. First, the role of every responder on scene is clearly defined by the commander. Leadership responsibilities are delegated, optimizing the ability of each officer to complete very specific tasks. Ability to ensure the fulfillment of every critical intervention is simplified. THE ROLE OF EMERGENCY MEDICAL SERVICES (EMS) IN DISASTER 23

As local responders arrive, an initial ICS system is established to manage resources. Upon the arrival of additional local, state, federal, and private-party personnel, the ICS structure may be modified to accommodate the expanding operation. The purpose and function of the UCS is to allow for expansion of the initial ICS structure. When operating within a large-scale incident, the UCS allows for the unification of multiple ICs. The IC is responsible for overall management of the incident and directs incident activities, including development and implementation of overall objectives and strategies as well as the ordering and releasing of resources. Members of the UCS work together to develop a common set of incident objectives,produce strategies,share information, maximize the use of available resources, and enhance the efficiency of the individual response organizations. The final phase of disaster management is the process of recovery/analysis. Initial recovery is the method by which an affected community is assisted in regaining a proper level of functioning after an incident. Long-term recovery addresses community-specific deficits of reconstruction and rehabilitation. The roles of EMS systems in these direct recovery processes are usually limited; however, systems must address their own logistical and psychological recovery so that they can return to a proper level of functioning after an incident. Specifically, equipment must be accounted for and repaired if necessary and disposable supplies must be replaced and organized. A critical function of recovery within an EMS system must also account for responder well-being. Critical incident stress debriefing (CISD) or jurisdictional peer-moderated counseling may accommodate the personal recovery necessary to resume normal operations. Alternatively, this phase affords the EMS system the opportunity to engage in critical analysis of its own performance during the incident. The opportunity to engage in self-assessment is critical in identifying system weaknesses that may be targeted in future improvements as well as create the forum for commending personal actions that had a positive influence on the outcome of an incident. On completion, this analysis offers evidence that may be used to support the use of specific methodologies.20–23 Although also considered an element of preparation, exercise planning and evaluation programs provide valuable data for review. The ODP’s Homeland Security Exercise and Evaluation Program provides state and national opportunities for evaluating response methodologies. For example, the ODP conducted the Top Officials (TOPOFF 2) exercise May 12-16, 2003. The event was the largest of its kind, involving 25 federal, state, and local agencies and departments and the Canadian government to test domestic incident management. The exercise simulated the detonation of a radiological dispersal device in Seattle,Wash., and the release of the pneumonic plague in several Chicago metropolitan areas. There was also significant pre-exercise intelligence play, a simulated cyber-attack, and credible mock terrorism threats against other locations. After the completion of the exercise, significant discussion was initiated to critique the response. After extensive review, DHS provided a detailed after-incident report for public release on Dec. 19, 2003. 24 INTRODUCTION

The “T2 After Action Summary Report” cited multiple topics of interest following analysis. Critical shortcomings were noted within the Homeland Security Advisory System. Participating jurisdictions failed to agree on reaction to the elevation of the nation’s threat condition to “red/severe” for the first time; declarations of “disaster” and “emergency” by officials revealed confusion among interagency responders. During the exercise, DHS used the newly developed role of principal federal official (PFO) in an effort to create a single position of accountability to bridge federal and local governments. Evaluators observed integration of the PFO within ICS/UCS paradigms. In addition, logistically complex prophylaxis distribution from the Strategic National Stockpile was evaluated. Challenges associated with resource allocation, communications, and information-sharing during the mock public health emergency illustrated the need for improvements within the participating municipal systems. Operationally, balancing the safety of first responders and the rescue of victims by conducting a detailed risk-benefit analysis was deficient among participants functioning at the planning/management level. Analysis of significant incidents worldwide may also offer some compelling data. Modeling triage methods based on the predictive value of anatomical scoring systems has revealed evidence-based, outcome-driven improvements in field triage and resource allocation. Significant analysis of the outcome among blunt and penetrating trauma patients provided the framework for the Sacco Triage Method. Support for improvements in the management of disaster result only from effective analysis. Due to the globalization of healthcare and mitigation, the resulting data from events worldwide must be delivered in a useful format. Application of the Utstein template may be useful to ensure international value of data by standardizing terminology and significance. Originally created to classify data used to determine cardiac arrest survival rates and allow for international comparison of statistically similar events, the Utstein method has been applied to disaster outcome in recent years. Applying sound epidemiological methods to postincident management is critical to the reduction of empiricism within disaster medicine methodology.24

PITFALLS The role of EMS systems in a disaster is to provide responsible prehospital care to victims. To facilitate this objective effectively, EMS personnel must use the ICS/ UCS and effective triage methodology. Multiple, universal shortcomings must be addressed even before responders find themselves on the scene of a major incident. Systems easily succumb to inadequacies in the prevention/preparation phase despite the widespread availability of federal training resources and funding. Specifically, failure to provide appropriate HVA, inexperience among responders in the application of ICS, and shortsighted planning on the part of management-level personnel allow for massive deficits in domestic response. HVA describes the process by which potential events are scrutinized using three categories: probability, risk,

and preparedness. Probability is determined by analyzing the known direct risk, relevant historical data, and any additional pertinent statistics. The risk assessment defines potential totals among lives, property, financial, and legal stature. Finally, preparedness integrates the overall value of probability and risk into a cohesive plan that dictates training requirements, contingency plans, and resource allocation. On completion, the HVA allows managers to consider common elements within preparedness procedures. These priorities are then used to direct a coordinated and integrated effort among all necessary participants within incident management, affording an ease of transition into the ICS/USC paradigm. Widespread failure to adequately address HVA has direct implications on the effective establishment of ICS/USC during the initial response phase of an incident. Improper or inadequate training in the use of the approved ICS structure may further complicate an incident during the initial response phase. Failure to acknowledge the importance of a properly functioning leadership model can quickly overwhelm the entire operation.It is critical for responders to understand that implementation of a dynamic command structure, which can expand as needed and easily integrate multiple responding agencies,may precede actual patient care. As a part of the initial assessment by the IC, a detailed risk-benefit analysis must be confirmed to ensure environmental suitability for rescue efforts to even begin. Providers are easily overwhelmed when inadequate resources impair their ability to provide emergency care to those in need. The greater critical failure in this example becomes clear as direct threats to rescuers greatly impede the success of an entire incident. Fortunately, all EMS personnel are taught the basic concepts of ICS in every initial certification course in the United States. It is imperative that agencies recognize the importance of establishing an ICS, whenever reasonable, to maximize exposure and operational familiarity among all responders. As a matter of practical familiarity, services should mandate the use of an ICS at every opportunity. The benefit to personnel at the awareness and performance levels becomes clear. As these providers gain real-time experience with the implementation of the ICS structure, delegation among divisions, and transition of command, they become more reliable with the application of the ICS concept. With repeated use, the responders use the techniques with more certainty, regardless of incident size. Planning and preparation phase failure is extremely common and evident more so in stationary healthcare facilities. Although EMS systems have used proactive measures to ensure preparedness, many are wholly unprepared for significant events within their jurisdiction. Probability is a significant factor within the HVA process previously detailed. Minimal preparation in light of minimal risk is appropriate; however, systems must ensure that all potential incidents are adequately addressed. Despite a decreased risk within a single response area, managers must consider all aspects of mutual aid agreements, neighboring HVA results,preparation phase actions,and cohesive integration of multiple adjacent agencies. Recognizing the

failure to address critical aspects of local and regional planning/preparation efforts and effective program integration, while costly,is better managed during a jurisdiction’s preincident phase rather than after the event. REFERENCES 1. de Boer J. Order in chaos: modeling medical management in disasters. Eur J Emerg Med. 1999;6(2):141-8. 2. Abrahams J. Disaster management in Australia:the national emergency management system. Emerg Med (Fremantle). 2001;13(2): 165-73. 3. Pozner CN, Zane R, Nelson SL, Levine M. International EMS systems: the United States: past, present, and future. Resuscitation. 2004;60(3):239-44. 4. Sanders MJ. Mosby’s Paramedic Textbook. Revised 2nd ed. St. Louis: Mosby; 2001:2-13. 5. Committee on Trauma and Committee on Shock, Division of Medical Sciences, National Academy of Sciences, National Research Council. Accidental Death and Disability: The Neglected Disease of Modern Society. Washington DC: National Academy of Sciences; 1966. 6. New York City Office of Emergency Management. Available at: http://www.ci.nyc.ny.us/html/oem/. 7. New York State Emergency Management Office. Available at: http://www.nysemo.state.ny.us/. 8. Simon R, Teperman S. The World Trade Center attack: lessons for disaster management. Critical Care. 2001;5:318-20. 8a. Asaeda G. The day that the START triage system came to a STOP: observations from the World Trade Center disaster. Acad Emerg Med. 2002;9(3):255-6. 9. US Department of Labor, Occupational Safety and Health Administration. Incident Command System eTool.Available at: http://www.osha.gov/SLTC/etools/ics/nrs.html. 10. National Interagency Management System. Available at: http://www.niims.net/. 11. US Department of Homeland Security. Available at: http:// www.dhs.gov/dhspublic/. 12. Cuny FC. Principles of disaster management lesson 1: introduction. Prehospital Disaster Med. 1998;13(1):88-92. 13. Becker B. Disaster management: problems and solutions. RI Med J. 1991;74(8):383-9. 14. Alson RA, Alexander D, Leonard RD, Stringer LW. Analysis of medical treatment at a field hospital following hurricane Andrew. Ann Emerg Med. 1994;22(11):726-30. 15. Roth PB, Gaffney JK. The Federal Response Plan and Disaster Medical Assistance Teams in domestic disasters. Emerg Med Clin North Am. 1996;14:371-82. 16. US Department of Homeland Security, National Disaster Medical System. Available at: http://www.ndms.dhhs.gov/. 17. US Department of Homeland Security. Initial National Response Plan. Available at: http://www.dhs.gov/interweb/assetlibrary/ Initial_NRP_100903.pdf. 18. Office of Domestic Preparedness. Emergency Responder Guidelines. Washington DC; 2002. 19. US Department of Homeland Security, Federal Emergency Management Agency. Available at: http://www.fema.gov/. 20. Weddle M, Prado-Monje H. Utilization of military support in the response to hurricane Marilyn: implications for future militarycivilian cooperation. Prehospital Disaster Med. 1999;14(2):81-6. 21. Holsenbeck LS. Joint Task Force Andrew: the 44th Medical Brigade mental health staff officer’s after action review. Mil Med. 1994;159(3):186-91. 22. Johnson WP, Lanza CV. After hurricane Andrew. An EMS perspective. Prehospital Disaster Med. 1993;8(2):169-71. 23. Branas CC, Sing RD, Perron AD. A case series analysis of mass casualty incidents. Prehospital Emerg Care. 2000;4(4):299-304. 24. Task Force on Quality Control of Disaster Management. Health disaster management: guidelines for evaluation and research in the Utstein style. Volume 1. Prehospital Disaster Med. 2003;1(suppl 3)17:1-177.

THE ROLE OF EMERGENCY MEDICAL SERVICES (EMS) IN DISASTER 25

c h a p t e r

4

Role of Emergency Medicine in Disaster Management Andrew I. Bern

To understand the role of emergency medicine in disaster management, one needs to understand the development and evolution of the specialty of emergency medicine, disaster medicine and disaster medical services, emergency medical services (EMS), emergency management, public health, and legislative interventions by government and nongovernment entities during the last 50 years (Table 4-1). This chapter highlights historical events that helped mold the current practice of disaster management and shines light on areas that need improvement. Although disasters have global importance, there are differences in the approach to disaster management in the United States when compared with the rest of the world. This may,in part,be due to the nature of historical disasters in the United States. In the area of lives lost in the United States before 1987,for example,Quarantelli1 identified only six disasters with deaths exceeding 1000 individuals. These disasters occurred between 1865 and 1928 and included two hurricanes, two fires (one on board a steamship), a flood, and an explosion on board a steamship.1 The loss of life in the United States is contrasted by disaster events that have occurred in the rest of the world. The 1917 influenza pandemic resulted in 20 million deaths worldwide. The Soviet Union famine in 1932 left 5 million dead. A 1931 flood in the Republic of China resulted in the death of 3.7 million. A Nov. 13, 1985, volcanic eruption in Colombia resulted in the death of 21,800.2 Flash floods killed approximately 2000 people in Mapou, Haiti.3 More recently, more than 200,000 were killed in the tsunami of southeast Asia in December 2004. Death tolls alone do not tell the whole story. Hurricane Andrew, which battered the United States from Aug. 14 to 27, 1992, was the costliest natural disaster in U.S. history. Total costs for both Florida and Louisiana equaled $26 billion. The cost was also felt in the homes and businesses destroyed and the population left homeless in south Florida (between “150,000 to 250,000 people were left homeless with approximately 600,000 homes and businesses destroyed or severely impaired” by the effects of Andrew).4 Hurricane Andrew was a category four storm on the Saffir-Simpson Hurricane Scale, with sustained winds of 145 mph and gusts of up to 175 mph.4 These numbers may be dwarfed by the 26

total cost from damage caused by Hurricane Katrina striking the Gulf Coast of the United States in 2005. Frequently, in nondeveloped or developing countries or those in the midst of conflicts and wars, the civilian population faces complex humanitarian emergencies. These events are multifaceted, of long duration, often involve large geographical areas, and are associated with famine and difficulty in providing or finding shelter. Many of these complex humanitarian emergencies include public health emergencies, with infectious disease outbreaks and loss of infrastructure. They often involve social, psychological, and political problems that have required the assistance of the world community— most often the United Nations, the International Committee of the Red Cross, and the interventions of multiple countries and other nongovernment groups.5–11 Although there is a significant amount of social science and engineering research reported by the Disaster Research Center (Newark, Del.) and the Natural Hazards Center (Boulder, Colo.), there are few centers in pursuit of clinical, bench, or even “evidence based” research that supports how disaster medicine and emergency management are practiced.

HISTORICAL PERSPECTIVE Those who cannot remember the past are condemned to repeat it. George Santayana

The history of mankind’s fears and struggles with disasters and their aftermaths are as old as recorded history and man’s fear of death. In ancient times, pagan belief was that sacrifice, including human sacrifice, would appease their deities and avert their disasters, such as an erupting volcano, climatic catastrophes, and war. Recurrent fires and floods gave rise to systematic attempts to cope with these events. After a fire destroyed almost one quarter of Rome in 6 AD, Roman Emperor Augustus created the Corps of Vigiles. This was the first recorded professionally trained and equipped fire service.12 Early fire mitigation and recovery programs, as

TABLE 4-1

TIMELINE OF DEVELOPMENTAL/SENTINEL EVENTS

YEAR

EVENT

6 AD 13th century 1666 1798 1917 1931 1932 1953 1954 1966 1968 1973 1979

The Corps of Vigiles—first professional fire service established England: Fire protection insurance becomes available Great Fire of 1666 in London—changes that took place after this disaster resulted in the model of today’s fire service Marine Hospital Service created (later to become the Public Health Service) Influenza pandemic Flood in China Famine in Soviet Union U.S. Department of Health, Education, and Welfare (cabinet level) Volcanic eruption in Colombia Accidental Death and Disability report by the National Academy of Sciences/National Research Council Foundation of American College of Emergency Physicians (ACEP) established Emergency medical services created Federal Emergency Management Agency formed FIRESCOPE and Incident Command started Public Health Service is moved to Department of Health and Human Services Critical incident stress debriefing begins ACEP forms Section of Disaster Medicine National Fire Protection Association begins standard development Hurricane Andrew World Trade Center attack Oklahoma City bombing Federal Response Plan Disaster Mitigation Act of 2000 Joint Commission on Accreditation of Healthcare Organizations standards for preparedness change Sept. 11 attacks at the World Trade Center, Pentagon, and in Pennsylvania Anthrax attacks Passage of the Homeland Security Act Homeland Security Presidential Directive/HSPD-5 calls for a National Incident Management System (NIMS) and a National Response Plan (NRP) Department of Homeland Security established States must file to qualify for predisaster hazard mitigation funds—threat assessments completed

1983 1988 1991 1992 1993 1995 1999 2000 2001 2002 2003 2004 (November)

well as building regulations and fire protection insurance, began to appear in England in the 13th century.12 Today’s fire service is modeled after changes that were implemented after the “Great Fire of 1666 in London, which left 200,000 homeless and burned out the heart of the city.”12 As evidenced in the Bible, mitigation principles were practiced by Noah when he constructed the ark. The first recorded mitigation project to prevent flooding occurred when Amenemhet II (pharaoh, 12th dynasty) created an “irrigation canal and a dam with sluice gates.”12 The Exodus story, in the Old Testament, refers to the 10 plagues (disasters) brought down on Egypt to persuade the pharaoh to let the Israelites leave. As man’s weapons have evolved from stones, to knives, to spears, to the use of explosives, guns, chemical, biological, and nuclear agents, so has the ability to medically cope with these consequences and minimize the impact of these events. We can trace and credit the modern approaches of today’s triage to concepts first introduced during the Napoleonic wars by Baron Dominique-Jean Larrey in the 18th century. The triage concept was simple— sort the patients by the severity of their injury and treat and stabilize the most critically injured first. In following this practice, the greatest good could be delivered to the greatest number of casualties. Surgical techniques and rapid frontline interventions were used during the Civil War. The concept of rapid evacuation after initial treatment to an advanced treatment facility demon-

strated a significant reduction in mortality during the Korean and Vietnam wars when compared with World War II. In 1966, a report was released by the National Academy of Sciences/National Research Council, Accidental Death and Disability: The Neglected Disease of Modern Society. The report called for applying these military lessons learned to civilian society. Ultimately, it gave rise to what is currently thought of as EMS in 1973.

Emergency Medicine In the early 1960s, a patient’s personal physician or a physician from the hospital medical staff, who was on rotation for the day, provided medical care for patients who showed up in the “emergency room.” The first fulltime providers of care exclusively in the “emergency room” began appearing in 1965. In 1968, the American College of Emergency Physicians (ACEP) was established in Lansing, Mich. Its mission was to educate physicians in this new practice environment (i.e., emergency medicine) and to improve the quality of care to these patients. ACEP did this by developing and periodically revising a “core content of Emergency Medicine”13 and by creating the American Board of Emergency Medicine in 1976, resulting in approval from the American Board of Medical Specialties for a modified conjoint board in 1979 and primary specialty board in 1989 (with emergency medicine becoming the 23rd medical specialty). ACEP also developed training through residencies in emerROLE OF EMERGENCY MEDICINE IN DISASTER MANAGEMENT 27

gency medicine (with the first graduate in 1970), educational conferences, and a research agenda to further define and develop the specialty.

Disaster Medicine and Disaster Medical Services By 1976, the ACEP published The Role of Emergency Physicians in Mass Casualty/Disaster Management.14 This policy was later approved (1985), reaffirmed (1997), and revised and expanded (2000).15 (See Box 4-1 for the full policy statement.) In this policy,“ACEP believes that emergency physicians should assume a primary role in the medical aspects of disaster planning, management, and patient care.” It also calls for emergency physicians to participate in “local, regional, and national disaster networks.” The University Association of Emergency Medicine echoed the calls for training in disaster medicine and further called for the development of fellowship training in disaster medicine.16 The ACEP also was an advocate for emergency physician participation in the “development of comprehensive plans developed by communities” to cope with disasters and of the National Disaster Medical System through disaster medical assistance team (DMAT) participation (1985, revised 1999).15 The ACEP Section of Disaster Medicine was formed in 1988. Through continued involvement and advocacy of disaster medicine, section members are participating on many levels: participation in DMATs, research and writing, educational conferences, and hospital and community disaster and emergency management.

Emergency Medical Services Today, EMS and disaster medical services are linked through the first responder (emergency medical technician EMT, paramedic, firefighter, law enforcement representative, nurse, and emergency physician).17 Whether it is a fire, transportation, or hazardous materials incident, it is the first responders from the local EMS unit who determine whether adequate resources are available to address the incident. These first responders also are in a position to determine whether there are any injured people who need to be triaged, stabilized, and transported to a definitive medical facility. This unity of purpose was not always so. Disaster management developed from a civil defense model after World War II, with a focus on mitigation and preparedness. EMS developed from an applied military model, with a focus on response. EMS (as an outgrowth of its relationship with fire services) was the first to adopt the Incident Command System.18

Emergency Management The Federal Emergency Management Agency (FEMA) can trace its beginnings to the Congressional Act of 1803. In this first federal disaster legislation,“assistance was provided to a New Hampshire town after an extensive fire.”19 Emergency management concepts developed from a civil defense model (“duck and cover”) to “protect” against a nuclear attack in the 1950s. 28 INTRODUCTION

BOX 4-1 ACEP POLICY STATEMENT— DISASTER MEDICAL SERVICES “The American College of Emergency Physicians (ACEP) believes that emergency physicians should assume a primary role in the medical aspects of disaster planning, management, and patient care. Because the provision of effective disaster medical services requires prior training or experience, emergency physicians should pursue training that will enable them to fulfill this responsibility. A medical disaster occurs when the destructive effects of natural or man-made forces overwhelm the ability of a given area or community to meet the demand for health care. Disaster planning, testing, and response are multidisciplinary activities that require cooperative interaction. Each agency or individual contributes unique capabilities, perspectives, and experiences. Within this context, emergency physicians share the responsibility for ensuring an effective and well-integrated disaster response. Emergency medical services and disaster medical services share the goal of optimal acute health care; however, in achieving that goal, the two systems use different approaches. Emergency medical services routinely direct maximal resources to a small number of individuals, while disaster medical services are designed to direct limited resources to the greatest number of individuals. Disasters involving the intentional or accidental release of biological, chemical, radiological, or nuclear agents present an extremely difficult community planning and response challenge. In addition, they may produce a far greater number of secondary casualties and deaths than conventional disasters. Because the medical control of emergency medical services is within the domain of emergency medicine, it remains the responsibility of emergency physicians to provide both direct patient care and medical control of out-of-hospital emergency medical services during disasters. Improvement of established disaster management methods requires the integration of data from research and experience. Emergency physicians must use their skills in organization, education, and research to incorporate these improvements as new concepts and technologies emerge. Where local, regional, and national disaster networks exist, emergency physicians should participate in strengthening them.Where they are not yet functional, emergency physicians should assist in planning and implementing them. This policy statement was prepared by the Emergency Medical Services Committee. It was approved by the ACEP Board of Directors June 2000. It replaces one with the same title originally approved by the ACEP Board of Directors June 1985 and reaffirmed by the ACEP Board of Directors March 1997.” Reproduced with permission from American College of Emergency Physicians. Disaster medical services. Ann Emerg Med.August 2001;38:198-9.

Four significant hurricanes and two earthquakes in the 1960s and 1970s illustrated the need for national coordination and financial resources, which were beyond the capability of the local communities affected.

These disasters also moved the national mindset from civil defense to natural disasters. The National Emergency Management Association was established in 1974, consisting of state directors of emergency services and emergency management. In 1979, President Carter created FEMA by executive order (Executive Order 12148).To more effectively perform its function as an allhazards emergency management program, multiple existing agencies were consolidated into FEMA. They included the Federal Insurance Administration, the National Fire Prevention and Control Administration, the National Weather Service Community Preparedness Program, the Federal Preparedness Agency of the General Services Administration, and the Federal Disaster Assistance Administration activities from Housing and Urban Development. In addition, civil defense responsibilities were transferred from the Department of Defense’s Defense Civil Preparedness Agency.19 FEMA, like many in the field of emergency management, began to think in terms of the following four unique phases of a disaster incident: • • • •

Mitigation Preparedness Response Recovery

Mitigation involves actions that could prevent a disaster or minimize its consequences. Lessons learned from the 1994 Northridge, Calif., earthquake affected building codes, engineering standards, and where structures were built.20 In a similar way, mitigation actions for a hurricane would include preplanned evacuation routes, building codes, warning systems, and recommendations for family hurricane supplies. Preparedness and planning include taking steps to avoid or minimize the consequences of a threat through probability assessment, currently described as a “hazard vulnerability assessment (HVA).”21 An example would include a community or hospital disaster response plan based on threat assessments.26,27 Response includes all activities involved in bringing resources (supplies, personnel, and coordination) to an incident to minimize health consequences of the affected population and, where appropriate, providing security, rescue, triage, stabilization, and transportation to safety and definitive care. The involvement of government and private organizations to provide interventions is not only associated with response, but also with the fourth phase, recovery. Recovery includes actions needed to return the community to normal operations. Recovery may take weeks and months, or in the case of hurricane Andrew, more than a decade. In some cases, the community may never recover from a disaster incident. In 1982, the International City Management Association conducted a national survey. Its finding was that “20% of local governments did not have a formal disaster plan.”12,22 Almost a decade later, hospitals were not any better prepared. “According to the Joint Commission on Accreditation of Healthcare Organizations (JCAHO, 1990), only 21% of surveyed hospitals meet their requirements for disaster preparedness.”23 In 2002, the Homeland Security Act was passed, and in 2003 the Department of Homeland Security was created. FEMA

was transferred to the Department of Homeland Security, and the National Disaster Medical System was placed under FEMA’s operational control.24 Homeland Security Presidential Directive/HSPD-5 established a “single, comprehensive National Incident Management System.”25 The primary focus was to establish a national standard and improve interoperability between all involved agencies and organizations. This new standard replaces the National Fire Incident Command System.

CURRENT PRACTICE Disaster management is a multidisciplinary practice that involves many professional disciplines. The complexities of this interdependent approach can be appreciated by reviewing the Federal Response Plan (1999). In this plan, Emergency Support Functions (ESFs) are categorized into the following 12 areas: • • • • • • • • • • • •

Transportation Communications Public works and engineering Firefighting Information and planning Mass care Resource support Health and medical services Urban search and rescue Food Energy Emergency medicine (which functions within health and medical services in this plan)

The role of emergency medicine in disaster management can be viewed as one of three: a traditional role, an activist leadership role, or the role of a system integrator. Figure 4-1 identifies nine potential interactions within the system. At the core is the emergency physician-patient relationship (Fig. 4-1, 1). When a disaster strikes locally, every emergency physician will find the need to assume roles identified as 2 through 5 in Fig. 4-1, even if he has no experience in disaster medicine. The on-duty emergency physician will need to provide leadership to his department, hospital, EMS, and community. The emergency physician’s duties will depend on specific “job actions” defined through the hospital’s Incident Command System (a standard required by JCAHO)30 and the disaster plan implemented by the hospital. One model is the Hospital Emergency Incident Command System.31 The roles identified as 1 through 5 in Fig. 4-1 are part of the local hospital response to any given all-hazards event. This is known as a level one local response. Level two and three responses (see Fig. 4-1) refer to the involvement of state and federal resources for incidents that are beyond the capability of the local or regional disaster response. The state and federal resources brought into play and the timeline involved define levels. A central theme in the mitigation, planning, response, and recovery preparations will be the self-reliance of the community for the initial 2 to 3 days, at minimum, after an event. Current practice is also influenced by JCAHO standards that are used in hospital disaster management; ROLE OF EMERGENCY MEDICINE IN DISASTER MANAGEMENT 29

Emergency Physician and Patient Emergency Physician and the Federal Government

9

1 Emergency Physician and the Emergency Department

2 Emergency Physician and the Federal Response including US&R and DMAT

8

Emergency Physician and the State +(EMAC)

3

7

6

Emergency Physician and the Hospital; HEICS (ICS)-Triage

4

Emergency Physician and the Region (the Emergency Operations Center)

Emergency Physician and Emergency Medical Services (EMS) 5

Event Occurrence: Time Zero

Emergency Physician and the Community including CERTs and MMRS Recovery:

Level One: Local Response Level Two: State Response Level Three: Federal Response Timetable of an Event: (in Days) 0-2 (0-48 hours)

2-3+ (48-72 hours)

3+ (72+ hours)- 6 weeks

days---weeks---years

FIGURE 4–1. Rings of engagement: The different roles of the emergency physician in disaster medicine.

principles common to disaster incidents; and future directions, such as the movement to national standards and training.28–30

General Concepts and Definitions Many of these are covered more extensively in other chapters of this textbook. National Incident Management System The National Incident Management System (NIMS) is a national best practice for incident management required by Homeland Security Presidential Directive/HSPD-5, “Management of Domestic Incidents.”25 The directive is to be implemented by fiscal year 2005 as a precondition for eligibility for federal preparedness assistance to state, local, tribal, or local organizations in their mitigation, preparedness, response, or recovery efforts. NIMS evolved from FIRESCOPE,18 the Incident Command System developed by fire services when battling the California wildfires in the late 1980s and which later grew into the National Fire Incident Command System. National Fire Protection Association 1600 The National Fire Protection Association (NFPA) published NFPA 1600: Standard on Disaster/ Emergency Management and Business Continuity Programs 2004 Edition,32 a national best-practice, terminology, and reference resource developed through a consensus between public and private organizations. It is the culmination of work begun in 1991 by the Disaster Management Committee established by the NFPA 30 INTRODUCTION

Standards Council. It was approved January 2004 as an American National Standard. Convergence Convergence is a behavior associated with the movement of people toward or away from a disaster event. It includes the unplanned arrival of individuals, including healthcare providers, who want to become involved in the rescue process. It also includes individuals from the impact zone of the disaster who find their own way, outside of the EMS system, to healthcare providers. Mutual Aid Mutual aid is used in the context of organized, preplanned coordination and use of resources from adjacent or remote organizations through the use of memoranda of understanding or contracts. An Emergency Management Assistance Compact (EMAC) is an example of shared resources between states. Special Response Teams Special response teams include community emergency response teams (CERTs), DMATs, urban search and rescue (US&R) teams, the Metropolitan Medical Response System, the National Response Team (NRT) for releases of oil and nonradiological hazardous substances, and other specialized teams. These resources are accessed through federal channels (taking up to 72 hours for implementation on-site), with the exception of the Metropolitan Medical Response System that is locally controlled and organized and the EMAC teams that are state controlled.

National Pharmaceutical Stockpile

Principles Common to Disaster Incidents

The National Pharmaceutical Stockpile program is part of a level III federal response to provide pharmaceutical support to a medical disaster event.

It had been said that the best way to combat the fear of the unknown or unexpected is to understand it and anticipate it through study, characterization, and shining the light of preparation. We do not fear what we expect and understand. This is the driving force behind the various systems that are used to describe disaster events. Disaster category, class, and type demonstrate one means of classification. Time course of the event is another. A tornado strikes suddenly with little warning. A hurricane usually can be tracked with warning and preparation times of up to 72 hours. Following the rising tide, historical occurrences, monitoring riverbanks, or tracking precipitation can sometimes be used to predict floods. Multiple areas of destruction that take place over a large geographical area define some disasters. The Haddon matrix plots factors and elements such as the prodrome; impact; and recovery against human, structure, physical environment, and socioeconomic conditions in an attempt to better anticipate needs for preparation, response, recovery, and resource allocation.34 Many of the principles associated with the four phases of disaster management—mitigation, preplanning and preparedness, response, and recovery—have been discussed (Table 4-2). Special treatment considerations and skills are associated with particular events. They include, but are not limited to, decontamination; treatment of blast injuries, crush and compartment syndrome, radiation exposure, shock, infectious disease, and injuries resulting from nuclear, biological, or chemical events; mass care; and humanitarian complex disasters. A seven-step process has been developed and is used in critical incident stress debriefing (a systematic program for psychological support developed by Dr. Mitchell in 1983 for first responders or affected members of the event).35

Joint Commission on Accreditation of Healthcare Organizations Eight months before the Sept. 11, 2001, World Trade Center disaster, JCAHO published a revision to its Environment of Care Standards (Box 4-2).One month after the disaster, on Oct. 10, 2001, JCAHO President Dennis O’Leary, MD, delivered testimony before Congress, stating: “Some people believe that the healthcare delivery system—if faced with a bioterrorism event—will somehow be able to accommodate the thousands of ill, injured, and worried well who will seek healthcare in that situation. The unfortunate truth is that we have much to do before such a belief can be fulfilled.” Current JCAHO standards encourage a comprehensive emergency management and “all-hazards” approach in which both internal and external threats are considered. The example of the Houston floods that caused the evacuation of Memorial Hermann Healthcare and Memorial Hermann Children’s Hospital in the summer of 2001 lead to further changes in JCAHO standards that addressed emergency/disaster hospital privileging. The (ACEP) published a policy statement recommending the steps necessary to comply with these standards.33

BOX 4-2 SUMMARY OF REVISED JCAHO STANDARDS January 2001—Significant Changes 1. Shifting attitudes and practices from Emergency Preparedness to Emergency Management (mitigation, preparedness and planning, response, and recovery). 2. “All Hazards” assessment of threat using a Hazards Vulnerability Analysis (HVA) approach to include consideration of NBCEI (Nuclear, Biologic, Chemical, Explosive, and Incendiary) as well as natural and manmade events. 3. Healthcare organization Command and Control—an example, HEICS (Hospital Incident Command System). The purpose of which is to improve interoperability between organizations using a common system. This will include defining criteria for plan activation. 4. Community-wide practice drill with all departments within the hospital organization participating in a live simulation.The prime goal of the drill is evaluate all elements of the written plan and test the interoperability of the response structure, communication capabilities, coordination, and command and control. 5. Off site capacity/treatment is to be developed to include capability for decontamination and potential isolation and treatment of contagious patients and delivery of healthcare in home and at alternative sites. 6. Healthcare organization’s integration with public health to include bi-directional surveillance communication, reporting, vaccination and treatment programs.

Future Directions The implementation of standard terminology and processes,32 education and training,36–39 coordination of the federal response through the Department of Homeland Security,24 establishment of the National Response Plan,40 adoption of the NIMS,25 standardization of a pharmaceutical stockpile, standardization of training and equipment for specialty response teams such as DMATs, focused research through dedicated centers, and increased coordination and communication between interdisciplinary public and private organizations32 will lead to improved and enhanced capabilities in the area of emergency management.

PITFALLS Today, our communities face increasing threats while after-action reports continue to recognize problems in 10 major areas (Box 4-3). These problems were evidenced in the results of the report from the National Commission on Terrorist Attacks upon the United States (also known as the 9-11 Commission), as documented by the New York Times. The lives of many of the first responders were lost due to problems identified in the report, including ROLE OF EMERGENCY MEDICINE IN DISASTER MANAGEMENT 31

TABLE 4-2 DISASTER PRINCIPLES ASSOCIATED WITH THE FOUR PHASES OF EMERGENCY MANAGEMENT Mitigation

Preparedness Response

Recovery

Threat assessments should include: ■ Hazard vulnerability assessment (HVA) ■ Historical events of high probability ■ Findings of agencies such as the National Oceanic and Atmospheric Administration Take corrective and protective actions based on information learned during mitigation. Execute mutual-aid plans and memorandum of understanding. Out of hospital: ■ Impact-notification-verification-first responder actions, including establishing command and control—an Incident Command System (ICS). ■ Identification of hot, warm, and cold zones and a security perimeter. ■ Begin triage, stabilization, and documentation. ■ Transport to secondary assessment areas or definitive care within the healthcare organization with adequate communication. In hospital: ■ Implement the Hospital Emergency Incident Command System ■ Continue triage, stabilization, and treatment or discharge within the healthcare organization ■ Conduct appropriate documentation and communication with patients, family, media, and the community Other: ■ Activate and involve community organizations and public health. Interdisciplinary response that involves multiple organizations returning to normal operations Critical incident stress debriefing of first responders and community members

inadequate communication, inadequate coordination between police and fire rescue units with a history of jurisdictional battles (turf wars), and a lack of a functional, unified command.41 Air traffic controllers suffered “maddening miscommunications, mangled coordination, and broken chains of command. They (were) improvising a defense for a disaster for which they had never trained . . . .”42 Another problem area, as described Auf der Heide in 19891 based on the study by Quarantelli of 29 disasters in the 1970s, is maldistribution of patients among potential receiving hospitals.Auf der Heide reported that “in 75% of cases studied, a majority of the casualties were sent to the closest hospital. In 46% of the cases, more than threefourths of the casualties were sent to the nearest hospital. Only in about half of the disasters did a simple majority of the hospitals in the area receive even one casualty.”1 Causalty distribution during the Sept. 11 events underwent

BOX 4-3 CHRONIC PROBLEMS: THE 10 C’S 1. Charge: who is in charge (operational control)? a. Who has the authority to activate and deactivate the plan? 2. Command and control: the Incident Command System—lack of implementation (chain of command) 3. Communication 4. Coordination 5. Convergence (either the movement of unsolicited volunteers toward the disaster scene or the movement of event individuals outside of the EMS system toward a healthcare organization [hospital]) 6. Contamination and decontamination 7. Capacity and surge capacity issues 8. Cooperation (between community and healthcare organizations) 9. Chaos and confusion with the failure or compromise of a system 10. Critical incident stress debriefing (providing necessary psychological support to first responders and individuals affected by the event) 32 INTRODUCTION

these same problems. Most hospitals in a wide area had activated their disaster plans and were waiting for an influx of patients that never came. At the same time, the closest hospital to the World Trade Center site received more than 600 patients in the first day. The Greater New York Hospital Association, however, reported that “after the attacks, 7300 patients were seen at more than 100 hospitals scattered throughout the metropolitan region.”43 This continues to point out both the lack of adequate plans for patient distribution on a regional basis and the challenge of appropriately capturing disaster epidemiology directly related to the disaster event as opposed to routine patient flow. Preparation through the drilling requirements outlined by JCAHO is quite minimal when compared with the drilling practices elsewhere, such as Israel, where, as often as monthly, hospitals are tested without prior notification at up to 20% of their licensed bed capacity. In the United States, realistic drills and exercises have been cost-prohibitive as hospitals and communities have attempted to fulfill an underfunded mandate from organizations such as JCAHO.43–45 There are multiple triage systems currently in use without uniform standards or agreement as to a single tool that provides accurate triage and identification of critical injury for all patients in all situations.36,37,39 Advancement of disaster medicine as a multidisciplinary professional specialty will require well-funded and organized research and the development of core content and competencies for its practitioners.46 The United States after Sept. 11, 2001, has been in a crisis mode, catching up and plugging the holes.24,47 More than 20 pieces of significant legislation have been passed.48 Recognition that national standards,training,exercising,and equipment have not been adequately funded in the past is supported by a report by the Council on Foreign Relations, chaired by Sen. Warren B. Rudman. The report, Emergency Responders: Drastically Underfunded, Dangerously Unprepared, details how bad the underfunding is. The monetary needs just for emergency responders in all jurisdictions (local, state, and federal) could equal $201.4 billion over 5 years.49

This is the current situation, which provides an opportunity for emergency physicians as they seek to define their role and the role of emergency medicine in disaster management. REFERENCES 1. Auf der Heide E. Disaster Response:The Principles of Preparation and Coordination. St. Louis: Mosby; 1989. 2. The Disaster Center. The most deadly 100 natural disasters of the 20th century. Available at: http://www.disastercenter.com/disaster/ TOP100K.html. 3. Weiner T. Floods bring more suffering to a battered Haitian town. The New York Times. May 29, 2004. 4. Hurricaneville. The story of hurricane Andrew. Available at: http:// www.hurricaneville.com/andrew.html. 5. Burkle FMJ. Complex humanitarian emergencies. In: Hogan DE, Burstein JL, eds. Disaster Medicine. Philadelphia: Lippincott Williams & Wilkins; 2002:431. 6. Sharp TW, Burkle FM Jr, Vaughn AF, Chotani R, Brennan RJ. Challenges and opportunities for humanitarian relief in Afghanistan. Clin Infect Dis. 2002;34(suppl 5):S215-28. 7. Spiegel PB, Burkle FM Jr, Dey CC, Salama P. Developing public health indicators in complex emergency response. Prehospital Disaster Med. 2001;16(4):281-5. 8. Sharp TW, Wightman JM, Davis MJ, Sherman SS, Burkle FM Jr. Military assistance in complex emergencies: what have we learned since the Kurdish relief effort? Prehospital Disaster Med. 2001;16(4):197-208. 9. Burkle FM Jr. Complex emergencies: an introduction. Prehospital Disaster Med. 2001;16(4):182-3. 10. VanRooyen MJ, Eliades MJ, Grabowski JG, et al. Medical relief personnel in complex emergencies: perceptions of effectiveness in the former Yugoslavia. Prehospital Disaster Med. 2001;16(3):145-9. 11. Burkle FM Jr, Hayden R. The concept of assisted management of large-scale disasters by horizontal organizations. Prehospital Disaster Med. 2001;16(3):128-37. 12. Quarantelli EL. Disaster Planning, Emergency Management, and Civil Protection: The Historical Development and Current Characteristics of Organized Efforts to Prevent and To Respond To Disasters. [Preliminary report.] Newark, DE: Disaster Research Center; 1995. Available at: http://www.udel.edu/DRC/preliminary/ 227.pdf. 13. Allison EJ, Aghababian RV, Barsan WG, et al. Core content for emergency medicine. Ann Emerg Med. 1997;29(6):791-811. 14. The role of the emergency physician in mass casualty/disaster management. ACEP position paper. JACEP. 1976;5(11):901-2. 15. Skiendzielewski JJ. American College of Emergency Physicians Policy Compendium 2003. 2003:21-2. 16. Disaster medicine: current assessment and blueprint for the future. SAEM Disaster Medicine White Paper Subcommittee. Acad Emerg Med. 1995;2(12):1068-76. 17. Bern AI. Disaster medical services. In: Roush WR, Aranosian R, Blair T, et al, eds. Principles of EMS System: A Comprehensive Text for Physicians. Dallas:American College of Emergency Physicians; 1989:77-93. 18. Irwin RL. The Incident Command System. In:Auf der Heide E, ed. Disaster Response: Principles of Preparation and Coordination. St. Louis: Mosby; 1989. 19. Federal Emergency Management Agency. FEMA history. Available at: http://www.fema.gov/about/history.shtm. 20. Berman MA, Lazar EJ. Hospital emergency preparedness—lessons learned since Northridge. New Engl J Med. 2003;348(14):1307-8. 21. Joint Commission on Accreditation of Healthcare Organizations. Guide to Emergency Management Planning in Health Care. Oakbrook Terrace, IL: Joint Commission Resources, Inc; 2002. 22. International City Management Association. Emergency Management, Baseline Data Reports V. Vol.15.Washington,DC:International City Management Association; 1983. 23. Community Medical Disaster Planning and Evaluation Guide. 1st ed. Dallas: American College of Emergency Physicians; 1995. Community Medical Disaster Planning and Evaluation Guide. 24. Noji EK. Creating a health care agenda for the Department of Homeland Security. Manag Care. 2003;12(suppl 11):7-12.

25. The White House. Homeland Security Presidential Directive/HSPD-5. Management of Domestic Incidents. Available at: http://www.whitehouse.gov/news/releases/2003/02/20030228-9.html. 26. Terrorism preparedness in state health departments—United States, 2001-2003. Morb Mortal Wkly Rep. 2003;52(43):1051-3. 27. Barbera JA, Macintyre AG. The reality of the modern bioterrorism response. Lancet. December 2002;360 Suppl:s33-4. 28. General Accounting Office. Bioterrorism: Public Health Response to Anthrax Incidents of 2001. October 15, 2003. GAO-04-152. Available at: http://www.gao.gov/new.items/d04152.pdf. 29. Mothershead JL,Tonat K, Koenig KL. Bioterrorism preparedness. III: state and federal programs and response. Emerg Med Clin North Am. 2002;20(2):477-500. 30. Joint Commission on Accreditation of Healthcare Organizations. 2003 Hospital Accreditation Standards. Accreditation Policies, Standards, Intent Statements. Oakbrook Terrace, IL: Joint Commission Resources, Inc; 2003. 31. California Emergency Medical Services Authority. Hospital Emergency Incident Command System (HEICS III) Update Project. Available at: http://www.emsa.ca.gov/Dms2/download.htm. 32. National Fire Protection Association. NFPA 1600: Standard on Disaster/Emergency Management and Business Continuity Programs 2004 Edition. Available at: http://www.nfpa.org/PDF/ nfpa1600.pdf?src=nfpa. 33. Hospital disaster privileging. Ann Emerg Med. 2003;42(4):607-8. 34. Noji E, Siverston K. Injury prevention in natural disasters. A theoretical framework. Disasters. 1987;11:290-6. 35. Mitchell JT. When disaster strikes . . . the critical incident stress debriefing process. JEMS. 1983;8(1):36-9. 36. Kennedy K, Aghababian RV, Gans L, Lewis CP. Triage: techniques and applications in decision making. Ann Emerg Med. 1996;28(2): 136-44. 37. National Disaster Life Support Education Consortium. Basic Disaster Life Support. 2nd draft ed. National Disaster Life Support Education Consortium; 2003. 38. Waeckerle JF, Seamans S, Whiteside M, et al. Executive summary: developing objectives, content, and competencies for the training of emergency medical technicians, emergency physicians, and emergency nurses to care for casualties resulting from nuclear, biological, or chemical (NBC) incidents. Ann Emerg Med. 2001;37(6):587-601. 39. Garner A, Lee A, Harrison K, Schultz CH. Comparative analysis of multiple-casualty incident triage algorithms. Ann Emerg Med. 2001; 38(5):541-8. 40. US Department of Homeland Security. Initial National Response Plan fact sheet. Available at: http://www.dhs.gov/dhspublic/display?content=1936. 41. Smith D. Save the rescuers from one another. The New York Times. May 18, 2004. 42. Schmitt E, Lichtblau E. To the minute, panel paints a grim portrait of day’s terror. The New York Times. June 18, 2004. 43. Greater New York Hospital Association. Hospital expenditures for emergency preparedness. February 2003. Available at:http://www. gnyha.org/pubinfo/200302_Emergency_Prep_Exp.pdf. 44. Bern AI. Question arises as to who pays for disaster drills under DRGs. Emerg Dep News. 1984;6(8):5, 11. 45. Bern AI, Galloway E, Krohmer JR, Gamm SR, Roth RM. Financial implications of disaster preparedness: a cost analysis of an area-wide community-based mass casualty/disaster incident (UAEM, abstract #28). Ann Emerg Med. 1984;13(5):389. 46. Waeckerle JF, Lillibridge SR, Burkle FM Jr, Noji EK. Disaster medicine: challenges for today. Ann Emerg Med. 1994;23(4):715-8. 47. Koenig KL. Homeland security and public health: role of the Department of Veterans Affairs, the U.S. Department of Homeland Security, and implications for the public health community. Prehospital Disaster Med. 2003;18(4):1-7. 48. Rubin CB. Emergency Management in the 21st Century: Dealing with Al Qaeda, Tom Ridge, and Julie Gerberding. [Working paper 108.] Boulder: Natural Hazards Center, University of Colorado; May 5, 2004. 49. Rudman WB, Clarke RA, Metzl JF. Emergency Responders: Drastically Underfunded, Dangerously Unprepared. Report of an Independent Task Force Sponsored by the Council on Foreign Relations. 2003. 50. American College of Emergency Physicians. Disaster medical services. Ann Emerg Med. August 2001; 38;198-9. ROLE OF EMERGENCY MEDICINE IN DISASTER MANAGEMENT 33

c h a p t e r

5

The Role of Hospitals in Disaster Mary W. Chaffee and Neill S. Oster

INTRODUCTION When the first rain began to fall in Houston,Texas, in June 2001, did hospital staff know they would soon be providing care for hundreds of patients without electrical power or running water in flooded hospital buildings? On April 19, 1995, did the emergency department staff arriving for the day shift at 13 Oklahoma City hospitals know that a former soldier was driving a rented van filled with 4000 pounds of ammonium nitrate toward the Murrah Federal Building and that they would soon be faced with 324 bombing victims? In 1984, did restaurant patrons in Wasco County, Ore., have any idea, as they selected food from salad bars, that they would soon be evaluated in hospitals for profuse, watery diarrhea from intentional food contamination by a religious cult? In March 2003, did the 11 Toronto healthcare workers who were caring for patients with respiratory symptoms know they would soon become infected with severe acute respiratory syndrome (SARS)? We can be quite certain that none of them knew. The capricious nature of disaster implies victims and responders are generally caught unaware. But we do know some things. We know there will be hurricanes, typhoons, tornadoes, earthquakes, mudslides, fires, and blizzards this year. We know people will pick up firearms, make bombs, and inflict pain and suffering on others. We know there will be casualties from train accidents, cars crumpled in chain reactions, building collapses, and explosions.We know infectious diseases will do what they do best: spread, sicken, and kill. We know terrorists have not given up their violent assaults. We know there will be mental health symptoms in accident survivors and the caregivers who respond to their needs. It is the hospital, at the heart of the health system, that will receive the injured, infected, bleeding, broken, and terrified from these events. We know the victims will seek life-saving care, comfort, and relief at hospitals, but many U.S. hospitals continue to prepare for disaster as though it will not happen to them.

Hospital Capacity in the United States There are more than 5700 hospitals in the United States that form a diverse patchwork of healthcare services. 34

U.S. hospitals vary greatly by geographic location (urban, suburban, and rural); financial and management structure (for profit, not-for-profit, private, public); type of care (general medical services or specialty care, such as psychiatric or pediatric); and government affiliation (Department of Defense,Veterans Health Administration, or Public Health Service). Any of these hospitals may be called on to respond to the next disaster or may be the victim of a disaster. Many experts believe that these hospitals are not adequately prepared to respond effectively (Table 5-1).

HISTORICAL PERSPECTIVE The Role of the Hospital in Society The hospital was of little significance in American healthcare before the Civil War. Only 178 hospitals existed in 1873 when the first survey was conducted—a time when no proper gentleman or lady would venture into a hospital by choice.1 The murky medical practices of the 1800s offered little that couldn’t be found in homes, and physicians had little in their armamentarium to change the course of disease and injury. However, discovery and scientific advance changed that. Effective anesthesia, surgical antisepsis, antibiotics, the x-ray, and other advances turned the hospital into a place of comfort, hope, and healing. The 20th-century hospital became a sophisticated financial institution, the core of medical education, and the site of dazzling technological display. Medical advances offered aid not only to the chronically ill but offered hope to those who suffered acute trauma or medical or psychiatric emergency.

The Effect of Disaster on Hospitals Past events illuminate the variety and complexity of demands placed on a hospital in a disaster: • Hurricane Katrina. The flooding in the wake of Hurricane Katrina in 2005 left hospitals in greater New Orleans, Louisiana, and Mississippi in crisis. Patients and staff were trapped in facilities without essential services, resulting in the largest mass hospital evacuation in U.S. history.

TABLE 5-1 SNAPSHOT OF 2005 U.S. HOSPITAL CAPACITY* Total U.S. Hospitals

5764

U.S. community hospitals U.S. federal government hospitals Institutional hospitals (e.g., prisons, colleges) Nonfederal psychiatric hospitals Nonfederal long-term–care hospitals

4845 239 23 477 180

Total staffed U.S. hospital beds Staffed community hospital beds

965,256 813,307

* Source: American Hospital Association. Hospital statistics, 2005 edition. Available at: www.hospitalconnect.com/aha/resource_center/fastfacts/fast_facts_us_hospitals.html.

• Floods caused by tropical storm Allison in Houston, Texas. In June 2001, 3 feet of rain from tropical storm Allison fell in the Houston area, causing the flooding and complete disruption of services at the University of Texas Health Science Center and its clinical affiliate hospitals. One of the hospitals, Memorial Hermann Hospital, experienced failure of every hospital system.The main and emergency power generators and communications system failed and personnel could not come, go, or be reached. The water supply failed, and the sewer system stopped functioning. The vertical evacuation of 570 patients was conducted, and the hospital was closed for 38 days. The storm flooded an area not considered to be at risk.2 • The Northridge, Calif., earthquake. An earthquake struck Northridge on Jan. 17, 1994, damaging a number of area hospitals. Six hospitals evacuated patients immediately: four of these evacuated all inpatients, and two evacuated some. Five of the facilities evacuated the most severely ill first, but the sixth, fearing imminent structural collapse, evacuated the healthiest patients first to permit the evacuation of the largest number of patients in the shortest period. That facility moved 334 patients from buildings to open areas in two hours. All hospitals used improvised transport devices, including backboards, blankets, and mattresses.3 • The 2001 World Trade Center bombing. Bellevue Hospital, a level-1 trauma center in New York City, is approximately three miles from the World Trade Center. Ninety patients presented within the first five hours after the incident; a total of 194 were triaged and treated within the first 24 hours. Despite best efforts, the hospital lost track of patients, ran out of supplies, and struggled with coordination of physicians to ensure rest and safety.4 New York University Downtown Hospital, a few blocks from the disaster, received 350 patients within the first two hours of the World Trade Center attacks. Many patients arrived on foot. 5 St. Vincent’s Catholic Medical Center executed its disaster plan within minutes of the bombing, as they had done during the 1993 World Trade Center bombing. On Sept. 11, 2001, St. Vincent’s Hospital

treated nearly 800 victims. Because St. Vincent’s shared water lines with the World Trade Center and telecommunications lines were routed through the World Trade Center, function of these systems was affected. Crisis counseling, pastoral care, and mental health services were immediately made available for victims, families, rescue workers, and staff.6 • The Oklahoma City Bombing. After the explosion of a bomb at the Murrah Federal Building, 168 were killed and 700 were injured—388 with acute injuries. The first patients arrived in emergency departments within 15 minutes, and the hospitals within 1.5 miles of the blast site received the greatest number of victims.7 • The Rhode Island nightclub fire. On Feb. 20, 2003, fire erupted in a crowded nightclub in West Warwick, R.I. Almost 100 were killed immediately, and nearly 200 were injured. Kent County Hospital, a 350-bed community hospital 2 miles from the site of the fire, received 40 victims within an hour; 25 were rapidly intubated. The hospital ran out of critical supplies and ventilators and struggled with supporting family members, poor communications from the scene, and pain management.8 Ultimately, 16 hospitals in Rhode Island and Massachusetts received 196 burn victims; this included the Shriners Hospital for Children, which received and treated 16 adult victims.9 The potential impact of disaster is staggering. The release of 40 tons of methyl isocyanate from the Union Carbide factory in Bhopal, India, in December 1984 exposed more than 500,000 to the deadly gas and killed about 6000 in the first week after the release. In September 1987, workers scavenging a dismantled cancer clinic in Goiania, Brazil, took home a source containing cesium-137. They sold it to a junkman who showed the glowing item to friends and neighbors. Once radiation exposure victims presented to hospitals, and the release became well known, hospitals were overwhelmed. Although 250 were actually exposed and 28 showed signs of radiation sickness, 112,800 people were evaluated. When the Aum Shinri Kyo cult placed sarin on five trains in the Tokyo subway system on March 20, 1995, 4000 people made their own way to hospitals, 641 were transported by authorities, and 245 hospital staff and rescue personnel were contaminated due to poor or nonexistent decontamination procedures.10

Evolving Perspective on the Health System Role in Disasters On Sept. 11, 2001, when U.S. hospitals and healthcare professionals were confronted with the worst attack on American soil, and again during the anthrax attacks along the Eastern Seaboard, individuals and organizations responded heroically. A powerful change in thinking, also called a paradigm shift, occurred after the terror attacks: the health system came to be viewed as a foundation of national security. Another perspective has changed as well. In the event of a disaster, Emergency Medical Services (EMS), police, and fire have long been recognized as first responders. However, THE ROLE OF HOSPITALS IN DISASTER 35

just recently, hospitals also have been designated as first responders—and first receivers. The value of the hospital in national security has been increased, and hospitals are recognized as safe havens in communities, the public expects hospitals to be prepared to care for their needs, and the hospital is now recognized as a first responder in emergencies. However, hospitals remain significantly underprepared to respond as effectively as the public expects. Most importantly, preparedness is at direct odds with productivity. Daily operating requirements stretch most hospitals’ resources. Allocating funds to improve emergency response capabilities that may never be used could be viewed as foolhardy. Community integration is now seen as necessary, but hospitals (other than those in networks or that are government facilities) have had few reasons to build healthy relationships with other hospitals in their communities. To meet the needs of communities in a disaster, business competitors must work as partners.

Public Expectations Hospitals play a vital role in the health,social structure,and economic life of a community. Patients expect hospitals, and health system workers, to be available to provide care for them in all circumstances. A level of preparedness that was viewed as adequate in the past is no longer seen as acceptable. To be more highly prepared and to be able to respond effectively, hospitals must make substantial investment in equipment, training, facilities improvements, and supplies.11 Hospitals depend on public trust; poor performance during a disaster could be financially crippling to a facility. Rubin12 writes that hospitals are expected to handle whatever they receive and do it right the first time.

CURRENT PRACTICE Sources of Hospital Vulnerability Hospitals are vulnerable to the stresses of disaster responses due to a number of inherent characteristics: • Complexity of services: Hospitals are facilities that provide healthcare but must also function as laundromats, hotels, office buildings, laboratories, restaurants, and warehouses. • Dependence on lifelines: Hospitals are completely dependent on basic public services: water, sewer, power, medical gases, communications, fuel, and waste collection. • Hazardous materials: The hospital environment contains toxic agents and poisonous liquids and gases. • Dangerous objects: Heavy medical equipment, storage shelves, and supplies can fall or shift during an event such as an earthquake.13

Forces Influencing Preparedness Multiple forces have placed hospitals in a precarious preparedness posture. The capacity of the health system 36 INTRODUCTION

has been scaled down to a bare minimum to cut operating costs. Emergency departments are crowded with the uninsured and the underinsured who have no other access to care. The nursing workforce has withered, and physicians have left practice due to uncontrolled liability insurance costs.

Surge Capacity Many hospitals determine their surge capacity by the number of patients they could comfortably care for using standard spaces, quality care standards, and additional teams of personnel to help. In reality, a disaster is not going to comply with the limits of hospital capacity. If 300 bombing victims arrive at a 50-bed community hospital, spaces will need to be converted and used that planners may have never imagined, such as chapels, hallways, and offices. Nurses accustomed to a certain nurseto-patient ratio may find the ratio in a disaster much higher and have to adapt practice accordingly. Surge capacity must not be viewed only as the number of beds or spaces that can be allotted to care for patients, but it must include all supporting hospital services that are involved in patient care.

Critical Elements in Hospital Preparedness If hospital services fail during a disaster, the hospital fails the population depending on it. The population includes not just the victims of the disaster, but the others presenting for needed care—women preparing to give birth, patients with chronic disease exacerbation, and children with lacerations that need sutures. A vital hospital emergency management program acts as an insurance policy that increases the chances of continued operations under difficult circumstances. An effective hospital emergency management program guides the development and execution of activities that mitigate, prepare for, respond to, and recover from incidents that disrupt the normal provision of care.14 The program should include the following components: • Emergency manager: The emergency manager is the primary point of leadership in the development, improvement, exercise, and execution of the hospital’s emergency management plan. • Emergency management plan: The plan identifies the hospital’s response to internal and external emergencies. Deliberate (advance) planning permits the development of strategies while the organization is not under pressure to react. • Executive leadership: Hospital executive leadership charts the course for an organization. A hospital that lacks executive leadership committed to emergency preparedness will be significantly hampered in its efforts. • Strategic planning: The hospital’s strategic plan is the blueprint that guides all efforts to achieve its mission. It is critical that emergency management and preparedness efforts are woven into strategic planning. • Emergency management committee: Extremely broad membership is desired to ensure all hospital

operations that will be stressed in a disaster are integrated and well prepared. • Hazard vulnerability analysis (HVA): The HVA is a tool used to assess the risks in a specific environment. The emergency management plan can be tailored to address the hazards most likely to affect hospital operations. • Vulnerability analysis: Every aspect of hospital operations that will be depended on in a disaster should be assessed to determine whether there are weaknesses present that fail when stressed. Hospitals in the U.S. Navy Medical Department and a number of civilian hospitals in New York have had their level of preparedness assessed using the Hospital Emergency Analysis Tool (HEAT). The HEAT examines more than 230 factors that contribute to effective emergency preparedness and response. After the systematic analysis by a team of experts, the hospital receives an after-action report that documents strengths and weaknesses and permits the development of a strategic plan to improve preparedness.15 • Staff training, exercise, and continuous improvement: The Joint Commission on Accreditation of Healthcare Organizations requires hospital staff members involved in the execution of the emergency management plan to receive orientation and education relative to their role in an emergency. Exercise of the emergency plan is also required. Lessons learned should be integrated into plans to continuously revise them.

Hospital Preparedness Philosophy A commitment to the following philosophies will enhance hospital emergency preparedness: • Imagine the unimaginable: When flood waters rise in a community, when a tornado touches down and demolishes an elementary school, when a disgruntled hospital employee opens fire with an automatic weapon in the emergency department, when a passing train derails and spills toxic chemicals, or when a wildfire closes in, it is too late to update an old plan, train staff to respond effectively, check phone numbers, and stock disaster supplies. Disaster complacency— believing a problem won’t happen to you or your hospital—is a significant threat to effective planning and response. • Protect the staff: Only a true obsession with self-protection will ensure that staff members are not injured or become ill during disaster response. Adequate stockpiles of gloves, masks, and other equipment must be available, along with training and leadership commitment to self-protection policies. • Build in redundancy: Expect the primary plan to fail and build in alternatives to every emergency measure. • Rely on standard procedures whenever possible: People perform best in unusual situations when they perform activities that closely mirror what they do under normal conditions. • Maintain records: Patient care records are critical to obtaining reimbursement for disaster care provided.

• Plan to degrade services: Normal levels of services cannot be maintained during disaster response. Identify services, such as elective surgery, that can be temporarily curtailed or minimized so that personnel and resources can be reassigned.

The Federal Role in Hospital Emergency Preparedness and Response The federal government has implemented programs to augment local and state capabilities when they are overwhelmed. The National Disaster Medical System The United States has a well-established emergency medical safety net: the National Disaster Medical System (NDMS). The NDMS has two primary capabilities designed to enhance disaster medical response. The first is specialized disaster response teams who augment the medical emergency response at the site of disaster. The second NDMS capability is a plan to share the inpatient bed capacity of the civilian and federal health systems in the event either system is overwhelmed with patients requiring inpatient care. NDMS federal coordinating centers (FCCs) play a regional role in maintaining a supply of NDMS hospital members and providing training and exercises. When the NDMS is activated, FCCs coordinate patient reception and distribution of patients being evacuated. Hospitals enter into a voluntary agreement to participate in the NDMS. They must be accredited and generally have more than 100 beds. The agreement commits a hospital to provide a certain number of acute care beds to NDMS patients; however, it is recognized that hospitals may or may not be able to provide the agreedupon number of beds. Hospitals that receive NDMS patients are reimbursed for care by the federal government.16 The Strategic National Stockpile The Strategic National Stockpile (SNS) was established in 1999 as the National Pharmaceutical Stockpile. It is now managed by the U.S. Department of Homeland Security and serves as a national repository of antibiotics, chemical antidotes, antitoxins, intravenous therapy, airway management equipment, and medical/surgical items. The stockpile is designed to supplement local agencies that are overwhelmed by a health emergency. The Noble Training Center The Noble Training Center in Anniston,Ala., (on the site of the former Fort McClellan army base) is the only hospital facility in the United States that trains healthcare professionals in disaster preparedness and response. The Department of Homeland Security operates the Noble Training Center, which offers a variety of training programs, including one for hospital leadership. More THE ROLE OF HOSPITALS IN DISASTER 37

information is available online at: http://training.fema. gov/emiweb/ntc/. Even though the federal government has many emergency response assets that can help in the response to an emergency, experience has shown that hospitals must be prepared to be self-sufficient for 24 to 72 hours after an event.14

Critical Elements in Hospital Disaster Preparedness A comprehensive hospital emergency management program must address a number of critical elements to adequately protect patients and staff and permit the facility to continue to operate. These are discussed in the following. Incident Command Just as one team leader is necessary for a controlled response to a cardiac arrest, an organized approach is essential to a successful hospital-wide emergency response. The Hospital Emergency Incident Command System (HEICS) is designed to provide that coordination. Developed and tested in Orange County, Calif., in 1992, it provides structure to response. HEICS uses: • A reproducible, predictable chain of command • A flexible organizational design that can be scaled to the scope of the problem • Checklists for each position to simplify response and carefully define each task • A common language that permits communication with outside agencies Emergency Operations Center (EOC) The EOC will serve as the command post for operations during an emergency response. It should be fully operational and integrated into local and county emergency operations (Box 5-1). Exercises, Drills, and Training Hospital disaster drills have often been treated as annoyances and are planned in ways to render them futile. Exercises are generally announced (unlike actual events), planned during regular business hours, and rarely include all hospital operations that will be affected by an actual event. Hospitals are encouraged to drill individual units—frequently and during nights and weekends—and then build up to full, functional exercises involving management of moulaged “casualties.” Community participation is critical to identify elements that work or that need fine-tuning. Only through exercise will the plan be adequately stressed so that failure points are identified. Essential Services and Facilities Engineering The facility’s structural integrity and essential services are an often overlooked part of preparedness. In 2003 a 38 INTRODUCTION

BOX 5-1 RECOMMENDED EQUIPMENT AND SUPPLIES FOR A HOSPITAL EOC Location • Secure interior space; windows not desirable • Alternative, equipped space in distant part of complex or building in the event the primary EOC is damaged or disabled Equipment • Incident command gear to identify EOC staff (vests, ball caps) • Computers with Internet access • Dedicated telephone lines • Communications-on-wheels (COWS) • Two-way communications (400 MHz, 800 MHz) • Fax • Television with cable access • Refrigerator • Radio • Bull horns • Barrier tape • Flashlights and batteries • Back-up power generator • Chalk board, dry-erase board, or other means of communicating to EOC team member Information • Hospital emergency management plan • Reference materials (emergency response, clinical references, hazardous materials) • Emergency reference contact numbers/e-mail addresses/fax numbers for local emergency response agencies (police, fire, emergency medical services, office of emergency management, department of health) • Emergency contact information for national resources, including Centers for Disease Control and Prevention (CDC), Radiation Emergency Assistance Center/Training Site (REAC/TS), Agency for Toxic Substances and Disease Registry (ATSDR), Environmental Protection Agency (EPA), and National Response Center • Staff notification information (phone contact numbers) • Memoranda of understanding/agreement (MOU/ MOA) with agencies and vendors • Local and regional maps that include utility stations, hyperbaric capability, emergency medical services, police departments, fire stations, burn units, and other critical infrastructure

major power blackout in the northeastern United States and Canada demonstrated the impact of the loss electrical services. It is recommended that every hospital: • Possess emergency power generating capacity for 3 to 4 days’ duration • Perform annual load testing on the generator(s) • Maintain the water supply and an alternative water supply in secure areas in sufficient quantity to support all services (sanitation, hygiene, laundry) for 3 to 4 days • Maintain medical gases in a secure location and have a 3- to 4-day supply for the hospital • Configure the heating-ventilation-air conditioning

(HVAC) system so that it can be shut down and, ideally, so that specific zones can be manipulated to control airflow in the building in case of contamination • Maintain a fuel source for full-load demand for 3 to 4 days’ duration • Develop a plan for the management and disposal of increased volumes of contaminated waste Physical Security Maintaining the physical security of the structure is important on a daily basis but becomes more of a challenge during a disaster. To ensure that the environment remains safe, egress must be controlled. Additional elements of the physical security plan should include the following: • A security force with full-time security responsibilities; the force should have undergone criminal background checks and professional law enforcement training. • All entrances and exits should be controlled, monitored, and capable of being locked. • The hospital should be able to perform perimeter security protection (“lockdown”) within minutes of notification. • Hospital staff should be trained and drilled on the performance of lockdown. • Hospital leadership should know what triggers the execution of a lockdown procedure. • A plan should exist for supplementing security staff in a disaster. Situation Report (Rapid Needs Assessment) It is critical that a hospital be able to rapidly assess the impact of a disaster on its operations and communicate the status to leadership in a situation report (often referred to as a “sitrep”), or a rapid needs assessment (RAN). The assessment should, at a minimum, include the following: • The extent and magnitude of the disaster and the scope and nature of casualties • The status of operations and any disrupted critical services • The impact of disruptions on operations and the ability to sustain operations17 Staff Notification Hospital staff must be able to receive timely and accurate notifications in a disaster, including when and where to report and for how long and other essential information. Contact information for all staff members must be continuously updated and tested. Additionally, the facility must be able to receive warnings and notifications from external agencies and be able to send warnings. Triage System Triage is performed daily in emergency departments, where the most critical are treated first. But during a dis-

aster, triage procedures must adapt to become like what is used on the battlefield, where the greatest good is offered to the greatest number. Multiple disaster triage systems exist, including START (simple triage and rapid treatment), ID-ME (immediate, delayed, minimal, expectant), and MASS (move, assess, sort, and send). It is important that a hospital use a system that is consistent with what is being used by services delivering patients to the facility. Whatever system is selected, there must be predisaster training and exercises. Alternative Triage Area When casualties present to an emergency department in numbers that overwhelm the facility, an alternative area must be available to manage overflow. The alternative triage area should be lit so that it can be used at night, weatherproofed, and temperature-controlled. Risk Communications and Media Management Plan A plan for working with the media will be needed. It is not recommended that media personnel be permitted access to a hospital during a disaster, but rather be provided regular, factual updates on activities and the status of the facility at a predetermined meeting place. Risk communications involve using credible experts to deliver carefully worded messages to communicate most effectively in a high-stress, low-trust environment, such as a disaster. Preparing hospital leaders in risk communications principles will ensure that they are able to communicate effectively to the public via the media. Disaster Mental Health Services There is conflicting evidence about the value of certain types of mental health services in the wake of disaster, but it is clear that every disaster creates emotional trauma victims. Primary victims are those who have been directly affected by the disaster. Secondary victims are rescue workers in whom symptoms develop, and tertiary victims are relatives, friends, and others who have been affected. The critical incident disrupts a victim’s sense of control as daily life is abruptly changed.18 Hospitals must plan for providing mental health services to disaster victims but must also consider the needs—acute and long-term—of the hospital staff who attempt to respond to an overwhelming event. It is recommended that hospitals have trained crisis intervention teams that are well integrated into the emergency management plan. Evidence and Crime Scene Management In the event of an intentional act that results in mass casualties, not only must a hospital care for the victims, but it has a critical role in bringing perpetrators to justice. Hospital staff members require training in proper management of potential evidence—in both collection and preservation. Evidence collection containers, including 50-gallon drums for patient decontamination THE ROLE OF HOSPITALS IN DISASTER 39

run-off, should be available as well as bags to preserve other types of evidence. Law enforcement agencies and forensic departments can provide training and guidance. Staff members should be familiar with and follow procedures for maintaining chain of custody for evidence that is collected during patient care activities. Food Services A disaster will place significant demands on the food service system of a hospital. The adequacy of food supplies for patients and staff should be evaluated. Because a hospital may need to be self-sufficient for several days in a disaster, a 3- to 4-day supply of food products is advisable. Food service personnel should be included in disaster exercises. Role of Volunteers Volunteers may or may not be of assistance, depending on their relationship with the hospital and their background. A volunteer pool that consists of individuals who serve regularly at the facility, are familiar with standard procedures, and participate in exercises can add valuable manpower to a disaster response effort. On the other hand,disasters will draw volunteers who wish to assist,a phenomenon known as “convergent volunteerism,” in which unexpected and uninvited healthcare workers arrive and wish to render assistance at a large-scale incident.19 These “freelancers” may cause problems or may even be impostors. Disaster Supplies Despite “just-in-time” supply schedules and empty warehouses, hospitals should maintain dedicated disaster supplies and arrangements for rapid resupply in the event of a disaster. Disaster response will rapidly deplete critical supplies—administrative as well as clinical. Conducting realistic exercises will help with the determination of the adequacy of stock and can be done without opening actual supplies so they can be restocked. Disaster supplies can be rotated into the daily-use stream to ensure stock does not expire.

PITFALLS Experience with disasters has demonstrated a number of predictable pitfalls that occur in hospital disaster response.

Distribution of Casualties Because immediate on-scene control of a disaster is chaotic and communication is often problematic, patients will present to the closest hospital available. This often leaves other nearby facilities with capacity and personnel that go unused.

Personal Protective Equipment Hospital personnel must be experts in protecting themselves, or they will become part of the problem and fur40 INTRODUCTION

ther stress the facility. Some controversy exists over the level of protection needed in certain environments, but it is clear that masks (N95) and gloves (latex or nonlatex) will prevent transmission of biological agents.

Communications Communications failure has often been identified as a predictable failure in disaster response. Hospitals need to examine both internal communications systems (with staff and patients) and with external agencies. Multiple layers of redundancy are essential to deal with expected failures and include the use of 800-mHz radios, dedicated trunk lines in the emergency operations center, two-way communications for hospital units and essential personnel, communications-on-wheels (COWS), and access to amateur radio (Ham) operators. The last resort is using runners who carry messages.

Emergency Patient Decontamination Hospitals must be able to identify and decontaminate patients who have been exposed to radiation or a compound that poses a threat to the patient’s health and the safety of the facility. If the hospital depends on an external agency or has decontamination equipment that requires time to set up, an immediate alternative must be in place, such as a hose and hose bib outside of the emergency department. Consideration should be given to patient privacy, managing patient valuables and clothes, and handling weapons brought into the hospital. A trained, exercised, and well-equipped team will be the foundation of successful efforts.

Child Care Hospitals will benefit from having a plan to care for children and other dependents of staff. In a disaster, staff will be called on to work extended hours, and usual family care arrangements may be unavailable.

Patient Admission, Identification, and Tracking The creation of emergency patient admission packs that are maintained with disaster equipment will facilitate the admission of a large number of patients. If an automated patient tracking system is used, a back-up manual system should be available. All systems should be able to manage unidentified (John and Jane Doe) patients.

Mass Fatalities Many hospitals have wholly inadequate or nonexistent plans to manage mass fatalities. Morgue space is generally limited in most facilities, so additional surge capacity must be identified in advance. Arrangements for refrigerated storage trucks, refrigerator space, and other alternatives, including ice rinks, should be addressed with socially sensitive plans. Complex cultural and religious issues may come into play in the event that there are contaminated remains and should be examined in advance.

Disaster Pharmaceuticals Emergency drugs must be available at the point of care. Often they are secured in pharmacy departments or warehouses, resulting in precious minutes of life-saving time being lost as personnel try to locate and obtain critical medications. In addition to drugs needed to respond quickly to nerve agents and other emergency situations, stockpiles of antibiotics should be maintained to provide prophylaxis to patients and staff.

CONCLUSION In a disaster, patients converge on the place they know they can obtain care—the hospital—and they arrive using any means possible. Furthermore, with the victims of disaster, come their families, loved ones, and the media—all who have very important needs that must be addressed. Hospitals can no longer approach disaster planning with a minimalist attitude that relies heavily on luck and belief that it will be someplace else that gets hit by the disaster. The hospital that received the most patients from the Rhode Island nightclub fire got lucky—the victims began arriving during a change of shift so there were two shifts of nursing staff available. However, the hospital also attributes its effective response to having drilled critical departments and procedures.

Emergency planning is the backbone of preparedness, but events will occur in each disaster that demand creative responses under pressure. This ability to respond flexibly is known as planned innovation. Good plans will use general “all hazards” templates for disaster management but will permit independent initiative and a tailored response to a specific situation.20 The U.S. health system appears to be emerging from the dark ages of emergency planning. A minimalist attitude of preparedness was acceptable in the past despite the regular occurrence of natural disasters. The threat of terrorism and the resulting health system impact have stimulated investment in research, a resurgence of disaster training in nursing and medical schools, and visionary projects such as ER One. ER One is a national prototype for a next-generation emergency department. Located in Washington, D.C., it is developing new approaches to the medical consequences of terrorist attacks, natural disasters, and emerging illnesses. More information is available online at: http://er1.org. The next phase of hospital emergency management will be a renaissance if creative planning prevails over naysayers, if resources are applied to priority preparedness activities, and if healthcare leaders are committed to ensuring that all who depend on hospitals will receive the care they need in a disaster (Box 5-2).

REFERENCES

BOX 5-2 HOSPITAL PREPAREDNESS AND RESPONSE RESOURCES • Auf der Heide E. Principles of hospital disaster planning. In: Hogan DE, Burstein JL, eds. Disaster Medicine. Philadelphia: Lippincott Williams and Wilkins; 2002:57-89. • National Advisory Committee on Children and Terrorism. Recommendations to the Secretary, U.S. Department of Health and Human Services. (Includes recommendations on prehospital and hospital care.) Available at: http://www.bt.cdc.gov/children/word/ working/Recommend.doc. • Preparing for the Psychological Consequences of Terrorism—A Public Health Strategy. This 2003 publication of the National Academies of Science includes an examination of current infrastructure and response strategies. Available at: http://search. nap.edu/books/0309089530/html/. • Joint Commission on Accreditation of Healthcare Organizations. Guide to Emergency Management Planning in Health Care. Oakbrook Terrace, IL: Joint Commission Resources; 2002. • Rocky Mountain Regional Care Model for Bioterrorist Events. Available at: www.ahrq.gov/ research/altsites.htm. • The Hospital Emergency Incident Command System. Available at: http://www.heics.com/. • The American Academy of Experts in Traumatic Stress. Available at: http://www.aaets.org/. • The International Critical Incident Stress Foundation, Inc. Available at: http://www.icisf.org/.

1. Rosenberg CE. The Care of Strangers—The Rise of America’s Hospital System. Baltimore: The Johns Hopkins University Press; 1987:5. 2. Nates JL. Combined external and internal hospital disaster: impact and response in a Houston trauma center intensive care unit. Crit Care Med. 2004;32:686-90. 3. Schultz CH, Koenig KL, Lewis RJ. Implications of hospital evacuation after the Northridge, California, earthquake. N Engl J Med. 2003;348:1349-55. 4. Wolinsky PR,Tejwani NC,Testa NN, et al. Lessons learned from the activation of a disaster plan: 9/11. J Bone Joint Surg Am. 2003; 85:1844-6. 5. Cushman JG, Pachter NL, Beaton HL. Two New York City hospitals’ surgical response to the September 11, 2001 terrorist attack in New York City. J Trauma. 2003;54:147-55. 6. Feeney J, Parekh N, Blumenthal J, et al. September 11, 2001: a test of preparedness and spirit. Bull Am Coll Surg. 2002;87:12-17. 7. Hogan DE, Waeckerle JF, Dire DJ, et al. Emergency department impact of the Oklahoma City terrorist bombing. Ann Emerg Med. 1999;34:160-7. 8. Dacey MJ. Tragedy and response—the Rhode Island nightclub fire. N Engl J Med. 2003;349:1990-2. 9. Gutman D, Biffl WL, Suner S, et al. The Station Nightclub fire and disaster preparedness in Rhode Island. Med Health R I. 2003;86:344-6. 10. Sullivan DK. Mass decontamination: why re-invent the wheel? J Emerg Mgmt. 2001; 2:52-4. 11. Healthcare Association of New York State. Meeting New Challenges and Fulfilling the Public Trust: Resources Needed for Hospital Emergency Preparedness. New York: Healthcare Association of New York State; 2001:1-4. 12. Rubin JN. Recurring pitfalls in hospital preparedness and response. J Homeland Security. January 2004;1-15. Available at: http://www. homelandsecurity.org/journal/articles/rubin.html. 13. Pan American Health Organization. Principles of Disaster Mitigation in Health Facilities. Washington, DC: Pan American Health Organization; 2000:7-25. 14. Joint Commission on Accreditation of Healthcare Organizations. Health Care at the Crossroads—Strategies for Creating and THE ROLE OF HOSPITALS IN DISASTER 41

Sustaining Community-wide Emergency Preparedness Systems. Oakbrook Terrace, IL: Joint Commission on Accreditation of Healthcare Organizations; 2003:11. 15. Chaffee MW, Miranda SM, Padula R, et al. DVATEX: Navy Medicine’s pioneering approach to improving hospital emergency preparedness. J Emerg Mgmt. 2004;2:35-40. 16. US Department of Homeland Security. National Disaster Medical System. Available at: http://oep-ndms.dhhs.gov/dmat_faq.html. 17. Briggs SM, Brinsfield KH. Advanced Disaster Medical Response— Manual for Providers. Boston: Harvard Medical International Trauma and Disaster Institute; 2003:27-33.

42 INTRODUCTION

18. Oster NS, Doyle CJ. Critical incident stress. In: Hogan DE, Burstein JL, eds. Disaster Medicine. Philadelphia: Lippincott Williams and Wilkins; 2002:41-6. 19. Cone DC, Weir SD, Bogucki S. Convergent volunteerism. Ann Emerg Med. 2003;41:457-62. 20. Gabriel EJ. Making room for outside the box thinking in emergency management and preparedness. Jt Com J Qual Saf. 2003;29:319-20.

c h a p t e r

6

Complex Emergencies Frederick M. Burkle, Jr. and P. Gregg Greenough

Since the end of the Cold War, 95% of all major conflicts have been internal nation-state wars. These are commonly referred to as complex emergencies (CEs) because of the myriad political, sociocultural, and economic factors that provoke them. Zwi and Ugalde1 defined CEs as “situations in which the capacity to sustain livelihood and life are threatened primarily by political factors and, in particular, by high levels of violence.” National disruption resulting from conflict and war has occurred this last decade in nationstates such as Liberia, Somalia, Rwanda,Angola, the former Yugoslavia, the province of Kosovo, East Timor, and Iraq. Unfortunately, CEs represent catastrophic public health emergencies that often develop into a continuum of protracted social conflict.

MAJOR CHARACTERISTICS

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The defining characteristics of CEs include the following: • CEs have existed for many years; however, during the last two decades, they have become the most common type of human-generated disasters.2 Currently there are 35 countries at risk of serious conflict, 11 of which are near collapse. Primarily because of unresolved war and conflict, worldwide hunger has climbed 18%, leaving more than 850 million people without food for basic health.3 Conflict has degraded the agricultural and public health infrastructures during the past decade, directly increasing the toll of civilian morbidity and mortality. • CE victims commonly suffer from social, economic, and gender inequities; poverty; injustices; cultural and religious persecutions; ignorance; racism; oppression; religious fundamentalism; and other lethal factors that contribute to internal strife among varied ethnic, tribal, and religious groups. All adversely affect the public health and the access to and availability of healthcare. • The majority of victims are civilians, with mortality and morbidity largely among vulnerable and unprotected children, women, the elderly, and the disabled. During the Cold War, one-half of all conflict-related deaths were among civilians. Civilians in CEs account

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for 90% of all war-related deaths, and more children than soldiers, about 2 million through 1993, have died as a result of internal civil strife.4 Genocide and other wanton violations of the Geneva Conventions have contributed to the high violence rates directed at civilians. There is a linear relationship between mortality of children younger than 5 years (per 1000) and the percentage of nations engaged in armed conflict. The worst conditions and highest mortality rates are recorded among orphaned and unaccompanied children who frequently fall through the cracks of the humanitarian response effort and who require parental or surrogate adults for the distribution of critical aid. In large, rapidly forming refugee camps, the most vulnerable can easily be lost among the masses and go unrecognized by those operating fledgling humanitarian relief efforts. CEs must be understood and managed in the context of politics. Intervention, relief, success, and failure of CEs are dependent on politics and outside military actions to end, or at least contain, the violence. During the 1990s, the world community, with varying success, responded to the more publicized CEs (Iraqi Kurds fleeing the Saddam regime to northern Iraq, severe hunger in rebel-ravaged Somalia, the ethnic and religious cleansing in the Balkans, and the political plight of East Timor). However, outside assistance has been limited or avoided in other conflicts (mass slaughter in Rwanda and the Democratic Republic of the Congo and the unrelenting conflict in Sudan). With minority and ethnic groups at risk of extinction, the customs, skills, and the very foundations of health and public health refinements that have defined their cultures have ceased to exist. Healthcare professionals face major challenges just to decrease the immediate mortality and morbidity resulting from communicable disease, trauma, and the dire health consequences of infrastructure losses in water, sanitation, shelter, and food. The targeting of healthcare providers and medical neutrality is a consistent feature of CEs. Hospitals are predictably the first to be destroyed and the last to be rehabilitated.5 Therapeutic feeding centers for starving infants and primary health centers are commonly 43

destroyed and looted, and female and child patients are slain in their beds. Warring factions have purposely politicized health and with it have summarily executed or detained physicians and nurses to foment fear. As political violence increases, access and availability to healthcare diminishes.1

HISTORICAL PERSPECTIVE A wealth of evidence has accumulated for more than 25 years on the massive effect of war on health. Field epidemiological research has defined the health and public health characteristics of CEs.6 Data have further demonstrated a consistent negative association between violent conflict and health outcome indicators (life expectancy, infant mortality rates, and immunization rates).1,7 Additional studies have confirmed the negative impact of landmines and sanctions on the health of children and that government instability and societal decline are the complex catalysts whereby controls on tuberculosis, malaria, and human immunodeficiency virus (HIV) become unchecked. Between 1990 and 1995, the disease burden of war equaled that of homicide and suicide when measured in disability adjusted life years (DALYs). Further, data analyses now suggest a trend in which the ranking of lives lost from the total consequences of war and conflict would move from the top 20 causes of disability, where it is now, to the top 10 by the year 2010.8 Populations suffer both direct and indirect effects of conflict. Direct effects include injuries, deaths and disabilities, human rights and international humanitarian law abuses, and psychological stress. Indirect effects actually contribute to the majority of mortality and morbidity due to population displacement, disruption of food supplies, and destroyed health facilities and public health infrastructure. At least three epidemiological models exist that may guide the current practice of the humanitarian response effort.

afforded to refugees by the UNHCR (United Nations High Commissioner for Refugees). Internally displaced populations must fend for themselves without benefit of basic healthcare services, food, water, or sanitation. Stripped from their supportive infrastructure, refugees suffer mortality rates that are 7 to 10 times higher than those for the baseline indigenous populations. In the refugee camps at Goma, Congo, the crude mortality rates exceeded 60 times those of the baseline population.9 The health consequences are both directly and indirectly related to the conflict itself.4 Three-fourths of all epidemics of the last decade took place in CEs. Epidemiological indicators show high crude mortality rates and, if disaggregated, demonstrate the vulnerability among the populations as to age (children younger than 5 years and the elderly) and gender (women and femaleheaded households). For instance, high case fatality rates were common among malnourished children in Somalia, with measles contributing to between 50% and 81% of deaths.4,10,11

Developed Country Model Countries such as Iraq, the former Yugoslavia, Macedonia, and Kosovo had relatively healthy populations with demographic profiles similar to those of Western countries before the onset of internal conflict. In these places, the few epidemics and low prevalence of malnutrition among children and infants were superseded by undernutrition and chronic diseases among the elderly who could not flee the conflict or were unable to access healthcare. In these settings, war-related trauma from advanced weaponry contributed to the primary cause of mortality. Children, adolescents, and pregnant women were specific targets in Yugoslavia, with more than 3000 children killed by snipers alone. Rape and traumatic exposures commonly contributed to psychological morbidity.12

Chronic or Smoldering Country Model EPIDEMIOLOGICAL MODELS Developing Country Model The health profile of countries in Africa and Asia during the acute phase of a conflict or war is usually identified by moderate or severe malnutrition, outbreaks of communicable diseases, or often both. The most common CEs of the past two decades have involved famine and forced migration in developing countries. Since the 1980s, few famines have occurred that were not human induced, and many famines catalyzed the onset of CEs.4 The most severe consequences of population displacement have occurred during the acute phase, when relief efforts have not yet begun or are still in the early stages.6 Refugees (populations that cross borders) and internally displaced populations have experienced high mortality rates during the period immediately after their migration. Internally displaced populations do not enjoy the immediate protections against persecution and human rights abuse under international law that are 44 INTRODUCTION

Both Haiti and Sudan have unique problems related to long-standing conflict and unrest that prevent progress in health, healthcare delivery and access, disease prevention, and education. Except for high rates of HIV/AIDS, Haiti’s health profile in disease is representative of one that was last seen in the United States in the early 1900s. Massive deforestation has led to severe environmental collapse that has contributed inextricably to chronic health and infrastructure loss.13,14 Haiti is representative of a smoldering country model that is suffering both an acute emergency situation as well as ongoing severe development problems. It is a dilemma to know where the assistance should be placed to do the most good. Some would rightly argue that without attention first to critical development priorities, acute emergency situations will continue to worsen. Sudan has experienced war since 1955, and as such, its children grow up chronically malnourished and know only a culture of violence with little access to healthcare and education. Reproductive health is an unknown luxury, and most healthcare must be imported.

EVOLUTION OF INTERVENTION Pugh15 describes evolutionary phases of intervention seen during the 1990s. Initially, humanitarian assistance was believed to be all that was needed to meet the demands of what were considered temporary post-Cold War conflicts. By the mid-1990s, it was clear that CEs were more dangerous, longer lasting, and complex than first thought. The humanitarian response was first dominated by international relief organizations, which based their presence on neutrality and impartiality protected under international treaties and covenants such as the Geneva Conventions. If and when military forces became involved, they did so under the rubric of ensuring relief security, which in places such as Somalia had been severely compromised by undisciplined rebel groups who had no knowledge about protections afforded to relief workers under the Geneva Conventions. Intervention, relief, and the successes and failures of CE interventions depend on politics and the political action of many countries, agencies, and organizations. For both the United Nations (UN) and Western powers, political action is translated as “military action.” In the early 1990s, the UN response consisted of deploying peacekeeping forces under Chapter VI of the UN Charter to help quell the conflict and provide some semblance of security for the intervening UN agencies and international relief organizations (IROs). These loosely defined civil-military relationships over time proved problematic. Many in the humanitarian community considered military involvement dangerous and unnecessary because a foreign, primarily Western, military presence threatened the neutral status of all expatriate workers. In these civil-military “interventions” both sides were ambivalent about their roles, cooperation, and under what security criteria the military should leave (the so-called exit strategy or end state that is constantly debated within the humanitarian and military-political communities). It was soon recognized that sustained development and long-term improvements would never occur without a political solution. The “humanitarian imperative” that drove the initial relief assistance was threatened by naysayers and others who strongly believed that assistance without a clear political road map to mitigate the causes of the conflict was self-defeating. By the mid1990s, studies exposed a parallel crisis in humanitarian protection. The humanitarian community was not protecting those that needed protection. The relief agencies, called on to implement assistance programs, were inconsistent and lacked professionalism. In addition, despite growing needs worldwide for intervention, both donors and governments were allocating less and less to fund the needed resources. The frustration during the 1990s was characterized over time by healthcare providers meeting the challenge to save lives, only to find the situation sliding back into crisis.15 By the turn of the century, studies revealed alarming data on mortality from intentional violence and banditry against humanitarian relief agencies and peacekeeping forces. One study16 found that 68%, or 253 deaths, of

375 deaths among staff of certain relief agencies and UN peacekeeping forces between 1985 and 1998 were a result of intentional violence. Of 52 deaths among staff for the International Committee of the Red Cross (ICRC) and the International Federation of Red Cross and Red Crescent societies, 77% were a result of intentional violence.16 These events contributed to the decision to replace UN peacekeeping forces with peace enforcement troops. The peacekeeping forces had been deployed by the Security Council under UN Charter Chapter VI, which lacked the military resources and legal mandate to quell the violence. With the new method, under Chapter VII, peace enforcement troops have the resources to cease the violence required to protect civilians before a peace agreement is in place. This process of moving from peacekeeping to peace enforcement was slow, taking three years and 33 new Security Council resolutions to complete. All UN military interventions have been authorized under Chapter VII since its inception.17 Encouragingly, relief organizations found common ground for collaboration and cooperation in projects, programs, education, training, and decision-making. This common ground catalyzed the relationship between health and human rights and the defining of the “rights discourse,” which declares that victims have the right to humanitarian assistance and that nongovernment organizations (NGOs) and UN agencies have the duty to provide assistance. This common ground process also spurred the argument for a consistent framework of standards of care and benchmarks for professionalism within the ranks of the relief community. In the midst of the chaos of CEs, healthcare professionals have taken on roles, other than that of providers, to negotiate and mediate with and cajole the warring factions to spare the health infrastructure from total annihilation. In doing so, negotiation and mediation with warring factions and rogue regimes have become increasingly necessary to maintain viable health programs threatened by political violence. This increasing presence of healthcare providers in the “political process”as decisionmakers in conflict resolution is not always a comfortable role. Rather, these interventions could be fraught with personal risks and seeming violations of an organization’s impartiality and neutrality strictly defined under existing covenants. In taking on these roles, healthcare providers have been instrumental in developing unique solutions through negotiating “immunization days” with rebel groups and delineating “tranquility zones,” where vulnerable groups are isolated from the surrounding fighting.

CURRENT PRACTICE Multinational Model Response It is not uncommon for NGOs and other relief organizations to be established in a country in conflict long before the violence garners the attention of the international community. The larger multinational humanitarian response begins with a decision by the international community to intervene, usually because of increasing COMPLEX EMERGENCIES 45

violence and the migration of refugees across the borders into neighboring nations. This process comes after weeks and often months of debate within the UN Security Council before a resolution is passed that directs the scope of the humanitarian assistance and defines the actors who will participate. Since the major reason for intervention is to cease the violence that leads to health consequences, a UN resolution will first define the requirements of peace enforcement troops authorized under Chapter VII of the UN Charter. These peaceenforcement troops are needed to end the violence and abuses of international law and human rights, to provide a protective environment that allows for assistance to decrease mortality and morbidity, and to ensure a secure environment in which IROs can function. Diplomatic assets are used to develop peace accords and agreements that must be in place before the peace enforcement troops are redeployed and replaced by UN peacekeeping forces, who function to maintain the peace (under Chapter VI of the UN Charter). Humanitarian assistance usually comes from assets contributed by the UN Office of the Coordinator for Humanitarian Assistance (OCHA) and UN agencies such as the World Food Program (WFP),World Health Organization (WHO), and the UN Children’s Fund (UNICEF); the Red Cross Movement; NGOs; and donor agencies that primarily represent industrialized nations’ governments, such as the U.S. Agency for International Development (USAID), the Canadian International Development Agency (CIDA), and Japan International Cooperation Agency (JICA). The multiagency response to CEs grew rapidly in the decade of the 1990s. NGOs assumed increasingly more responsibilities for governments and international organizations by implementing major relief and assistance programs for vulnerable civilian refugees and displaced populations. In 1991, NGOs numbered 28 in northern Iraq; by 1995 in Haiti, there were more than 710 NGOs.

Health Assessment The humanitarian community (international organizations, NGOs, private government organizations, and peacekeeping militaries) has a professional obligation to base assistance on the best evidence available.18 This supposition is the cornerstone of the concept of evidence-based healthcare. The need and demand for healthcare in CEs increases at a rate determined, in part, by the rate at which public health infrastructure is destroyed and the moral integrity of governance disappears. Initially, healthcare needs may be greater than the rate at which resources are being made available.19 Historically, response activities in CEs have often been ineffective because of the poor quality of information available as well as the manner in which an assessment was conducted. Assessment and assistance are often hampered by organizational problems and lack of personnel, medical records, and financial resources.20 Epidemiological methods established for situations in which there are restricted resources use a simpler method of statistical analysis, which is known as a rapid assessment20 and is sometimes referred to as 46 INTRODUCTION

a “quick and dirty” assessment.21 The initial assessment by an experienced interdisciplinary team must be carried out as soon as it is clear that an emergency exists. During the decade of the 1990s, both health and nutritional assessments, despite being performed rapidly and under difficult situations and restraints, gained a reputation for quality. With critical advances in indicator identification, epidemiological analysis, data retrieval technologies, and education and training of relief personnel, health and nutritional assessments have continued to improve as an art and science. Data collection commences before the field assessment and originates from existing country profiles, maps, census data, previous demographic and health surveys, early warning system tools, and previous or ongoing in-country assessments.22 Additional data may come from overflights and satellite imagery; these are especially useful in tracking refugee migration. Background health information is gleaned from previous reports inherent to organizations such as WHO, the Disaster Epidemiology Research Center in Belgium, the European Expert Group in Practical Epidemiology (EpiCentre), and the Centers for Disease Control and Prevention’s (CDC) Mortality and Morbidity Weekly Report (MMWR) publications. This information includes, but is not restricted to, baseline data on the following4,23–25: • • • • • •

Endemic diseases Mortality rates Morbidity-incidence rates Nutritional status Sources of healthcare Impact of disruption of health services

Assessment documents are available that provide detailed checklists, information on the principles of an assessment, planning techniques, methods, and forms. Use of an evidence-based approach makes it possible for decision-makers (policy, operational, and field level) to differentiate the needs of the population, the resources available, and the costs of any decision. An evidence-based approach helps one to differentiate between what is supported by evidence and that which is made on an unsubstantiated assertion. Health assessments today are expected to be reliable and valid and, as such, are inextricably linked to the analysis of specific performance and outcome indicators, region- and disaster-specific epidemiological studies, and measures of effectiveness.26 Assessment in one form or another never stops.25,27* The assessment tool used can vary depending on the phase of the CE. The rapid health assessment of a CE concentrates on the needs of relief managers and decision-makers to obtain timely and accurate data necessary to rationally allocate available resources according to the emergency situation. Rapid assessment stimulates the development of more organized and focused surveys and the longer-lasting surveillance system, as well as a *A full account of the assessment process can be found in: Burkle FM. Evidencebased health assessment process in complex emergencies. In: Cahill KM, ed. Emergency Relief Operations. New York: Fordham University Press and The Center for International Health and Cooperation; 2003.

health information system (HIS). The HIS facilitates the collection of demographic and vital statistics data, administration of a disease surveillance system, regular monitoring of hospital and clinic discharge diagnoses, and investigation of disease outbreaks.28 How rapidly an HIS can be implemented is often used as a measure of efficiency and effectiveness of the relief effort. During the early 1990s, response initiatives suffered because of poor and inconsistent humanitarian response and lack of assessment standardization. By the late 1990s, WHO rapid assessment protocols23 and the Humanitarian Charter and Minimum Standards (SPHERE Project) provided the needed standardization guidelines to assess and assist in water supply and sanitation, nutrition, food aid, shelter and site planning, and health services.24 The Sphere Project’s Humanitarian Charter describes the core principles that govern humanitarian action and defines the legal responsibilities of states and parties in conflict to guarantee the right to assistance and protection.13 When states are unable to respond to a CE, they are obliged to allow the intervention of humanitarian organizations, which in itself begins with an assessment. The concept of excess deaths is a critical epidemiological tool, especially in areas where there is conflict and where population movements are high. In waraffected areas of the eastern Democratic Republic of Congo (largely inaccessible to aid organizations and assessments because of insecurity),29 the ongoing fighting drove hundreds of thousands of internally displaced people into forests, jungles, and other remote areas where they had no food, medicine, or shelter. Health systems and basic environmental public health infrastructure were destroyed.An epidemiological assessment was conducted, at considerable risk to the assessment team, of 11 mortality surveys in five provinces throughout eastern Congo. Results determined that over a 32-month period, approximately 2.5 million excess deaths (deaths greater than expected during the period studied) had occurred due to the conflict in that country. Previous reports had documented that approximately 100,000 people had died as a result of war.29 The assessment revealed that the war casualties were not limited to victims of violence, but rather that 90% of the deaths were attributed to infectious diseases (e.g., malaria, diarrheal diseases) and other nonviolent causes (e.g., malnutrition) directly or indirectly related to the environmental disruptions. The destruction of the region’s health infrastructure and lack of regional security meant that the vast majority of the population had minimal access to medical and public health services, making them more prone to disease. In addition, this assessment provided the only evidence that a humanitarian crisis of “staggering proportions” existed.29 The assessment demonstrated the critical importance of how an epidemiological approach to an assessment can be used to document the denial of human rights associated with a lack of access to medical care, basic public health, and environmental services. Even though the study lacked the empirical scrutiny guaranteed with exact numbers, the assessment did reveal that a massive international response was indicated.

Health Interventions All health and nonhealth interventions that support public health needs in CEs are determined by rapid assessments, focused surveys, and surveillance. Poor surveillance design, at all three levels (rapid assessment, surveys, and surveillance) will lead to a predictable resurgence of disease and public health disruption. If survey indicators and surveillance methodologies are incomplete or inaccurate, the ability to monitor the sensitive relationships between health, nutrition and environmental indicators, endemic disease, injury prevention (e.g., landmine injuries), and gender- and age-specific vulnerabilities will be lacking. The goal of any health intervention is to minimize mortality and morbidity. Endemic disease control, especially in a developing country model, is always a priority. All children in developing countries in conflict should receive measles vaccine and vitamin A supplementation to mitigate the complication rate of measles and other infectious diseases, such as diarrheal and respiratory diseases. Malaria, HIV, and sexually transmitted diseases (STDs) also take a severe toll. Once humanitarian assistance reaches these populations, during the acute phase (first 4 to 6 weeks), the mortality and morbidity rates should decline. Priorities in camps shift to maintaining the public health protective infrastructures in water and sanitation, food, and shelter; ensuring security and fuel; and rebuilding the basic public health system. Abuses against women and failures in reproductive health have led to high rates of STDs and pregnancy in refugee camps. WHO Emergency Health Kits, which include safe birthing and surgical supplies to care for a population of 10,000 for approximately three months, can provide immediate assistance in CEs.30

Food Programs Food programs must ensure proper nutrition for the general displaced population as well as therapeutic or supplemental feedings for the acutely malnourished. These programs also should address micronutrient deficiencies as well as give special attention to the nutrition needs of those with HIV/AIDS or tuberculosis. Emphasis must be placed on maternal and child health, reproductive health, and the protection of those with disabilities and injuries. Attacks on infant feeding centers occurred with regularity in Sudan, Mozambique, Ethiopia, Somalia, Angola, and Liberia, and the diversion of food by warring factions became commonplace. Protein energy malnutrition (PEM) has three components: malnutrition, micronutrient deficiency diseases (especially those related to a lack of vitamins A, C, B6 and zinc), and secondary infections. The term PEM is often used instead of kwashiorkor or marasmus to define the state of illness. Indeed, many cases are mixed in their presentation (marasmus-kwashiorkor) and difficult to clinically distinguish. Nutritional assessments are performed with population convenience samples, in which new arrivals to the refugee camps are screened, and through cluster sample surveys. The malnutrition rate of children younger than 5 years ranks just below COMPLEX EMERGENCIES 47

crude mortality rates as the most specific indicator of a population’s health.9,18,25,31 The malnutrition rate also determines the urgency for food ration delivery and requirements for supplementary feedings and therapeutic feeding centers. Some interventions are now so routine that they no longer require an assessment before implementation in the acute phase of CEs. Most demonstrable is the provision of vitamin A supplementation and measles vaccine in refugee populations in developing countries. Studies from the early 1990s on CEs have shown that vitamin A reduces mortality and morbidity in malnourished children, especially those with measles (active, susceptible, and exposed) and other respiratory illnesses. Indeed, vitamin A supplementation reduces all-cause mortality in children.32 By the time measles becomes identified in a population-dense camp environment, the mortality and morbidity may already be out of control. Based on this evidence, it has become protocol to provide all children between 1 and 6 years old, at the time of registration into the camp, both measles vaccine and vitamin A supplementation. This being the case, the initial assessment focuses on identifying the population in need of services and in ensuring continuing monitoring through program outcome surveys and surveillance. Relief programs emphasize a primary health care approach, focusing on oral rehydration, feeding centers, immunization, promoting involvement by the refugee community in the provision of health services, and stressing effective coordination of programs and information sharing among the NGOs that deal directly with the recipients of care.33

Medical Personnel Medical and nursing assets that are needed most under the developing country model are personnel from public health, preventive medicine and infectious disease, primary care, obstetrics and gynecology, family practice, and emergency medicine.34 For CEs in developed country, the desired expatriate medical and nursing care includes surgery, anesthesia, and emergency medicine.34 Chronic and smoldering countries with CEs require a public health focus; however, it is critical to provide healthcare personnel based on the assessment of need to restore both the curative as well as the preventive public health core of the society. This assessment usually reflects the objectives of individual projects and programs. Typically, assistance agencies use trained personnel from relief, development, and advocacy groups.

UNILATERAL MODEL RESPONSE In the 2003 war with Iraq, the United States and its coalition partners chose a unilateral approach that did not adhere to Chapter VII of the UN Charter. This approach was based on the assumption that this was first a war that would be short with no major humanitarian crisis occurring. Internal U.S. governmental changes also occurred. Under presidential directive, the Department of Defense (DoD) assumed the lead for humanitarian assistance, a position traditionally played by the U.S. 48 INTRODUCTION

State Department and USAID’s Office of Foreign Disaster Assistance (OFDA). Planning for relief, recovery, and reconstruction was placed under the DoD’s newly formed Office of Reconstruction and Humanitarian Assistance (ORHA), later renamed the Coalition Provisional Authority (CPA). Initially, because it was determind by the DoD that there would be little need for humanitarian assistance, the UN agencies and major NGOs had a minimal role in the planning and received little funding support from the United States. Many, including UNHCR, WHO, and ICRC, had expended their reserve funds in limited preparations. However, international studies published since the end of the Persian Gulf War suggested that civilian health was substantially worse and that specific humanitarian outcomes might occur. Specifically, since 1990 some indicators demonstrated a progressive decline, whereas others reached a nadir in the mid-1990s before the Oil-for-Food and Oil-for-Medicine programs allowed Iraq to import and distribute food,medication,and health supplies and equipment. Infant mortality rates (deaths in children younger than 12 months per 1000 live births) increased from 47.1 to 108 during the period from 1994 to 1999. During the same time, mortality rates for children younger than 5 years increased from 56 to 131 (per 1000 live births). Acute malnutrition increased from 3.6% in 1991 to 11% in 1996.However,the rate of acute malnutrition decreased to 4% in 2002 because of the coordinated work of Iraqis with UNICEF, WHO, the Red Cross Movement, and several major international NGOs. Increases were seen in reported cases of tuberculosis,cholera,typhoid fever,amoebic dysentery, giardiasis, leishmaniasis, and malaria. It was not known whether this represented a true increase or was the result of better surveillance and record keeping.35–39 As a contingency, the main relief resources warehoused by the humanitarian organizations included nationally and regionally prepositioned WHO emergency health, surgical, and safe birthing kits; tents; blankets; water bladders; and high-protein food baskets.30 Many NGOs chose not to work with the military-dominated relief effort. The ICRC was the only humanitarian organization functioning during the war, with specific responsibilities mandated under the Geneva Conventions to mitigate civilian casualties and provide repair to vital infrastructure destroyed during the hostilities. Iraqi national staff previously trained by WHO and UNICEF provided a functional semblance of outbreak control, basic healthcare, and repair of water and sanitation infrastructure. Unfortunately,widespread looting and trashing of public health facilities and hospitals caused a collapse of the health system. The U.S. and coalition militaries, due to flawed planning, were unprepared and undermanned for the security and recovery needs required under international law as an occupying power. In general, health consequences were similar to those found in the developed country model, where trauma and unattended chronic diseases in the elderly predominate. In time,the United States actively requested and supported the return of UN agencies; however, security continued to be the overriding concern that prevented the rapid return of essential services.

Whether this unilateral approach to conflict and war will represent a new model for dealing with CEs has yet to be determined. Even with the paucity of NGOs serving in Iraq and Afghanistan, there were more fatal attacks reported among humanitarian aid workers in both countries in 2003 than in any prior year. Of the 76 humanitarian workers killed in 2003, 43 were victims of “terrorist-style or terrorist affiliated attacks.”The majority of victims in both countries were local staff employed by NGOs.40

PITFALLS Problems persist. The world humanitarian community lacks a concerted approach to meeting the needs that occur during CEs. Reforms are needed in the UN and its agencies. NGOs are nonhomogeneous organizations; their proliferation during the past decade has made coordination in the field of operations difficult. Major inconsistencies of Sphere standards occur: the use of basic indicators such as mortality rates in evaluating and monitoring programs are often improperly interpreted or neglected. Whatever the epidemiological model, the larger humanitarian community has found itself often unprepared and at times overwhelmed with the demands for assistance. Wanton violations of the Geneva Conventions and international humanitarian law make it increasingly difficult for relief workers to maintain security for their programs and projects. The recent trend since the Balkan Wars—to militarize and politicize humanitarian assistance—has made it almost impossible for relief organizations to maintain neutrality and impartiality. Although both the multilateral and unilateral approaches have desperate flaws that need immediate reform, humanitarian assistance will always require an integrated, international approach with lateral integration, communication, and information sharing of multisector and multiagency participants. This cannot be accomplished without coordinating with the leadership of UN agencies and IROs. The urbanization of populations in warfare has caused humanitarian assistance to move from traditional rural to urban settings. Almost two-thirds of African populations are now living in urban settings with tenuous social and physical protections. Ninety-five percent of the Iraqi population lives in cities where public health infrastructure disrepair and lack of security are major impediments to recovery and reconstruction. Currently, the humanitarian community is unprepared to defend the collapse of urban public health, especially when the environment remains insecure. Training for work in a CE is essential before deployment. To be both successful and safe, health providers need to expand their knowledge base to include issues of integrated management, transportation, logistics, communications, negotiations and mediation, security, and international humanitarian law. Despite growing trends toward the professionalization of and educating and training the humanitarian community in the late 1990s,

the career requirements for training and education have not kept up with demands.

REFERENCES 1. Zwi A, Ugalde A. Political violence in the Third World: a public health issue. Health Policy Plan. 1991;6:203-17. 2. Burkle FM. Lessons learnt and future expectations of complex emergencies. BMJ. 1999;319:422-6. 3. International Crisis Group. Crisis Watch. Available at: http://www. crisisgroup.org/home/index.cfm?id=1200&l=1. 4. Toole MJ, Waldman RJ. Refugees and displaced persons: war, hunger and public health. JAMA. 1993;270:600-5. 5. Coupland RM. Epidemiological approach to surgical management of the casualties of war. BMJ.1994;308:1693-7. 6. Burkholder BT, Toole MJ. Evolution of complex emergencies. Lancet. 1995;17(3):187-201. 7. Spiegal P, Burkle FM, Dey CC, Salama P. Developing public health indicators in complex emergency response. Prehospital Disaster Med. 2001;16(4):281-5. 8. Michaud CM, Murray CJL, Bloom BR. Burden of disease: implications for future research. JAMA. 2001;285:535-9. 9. Davis AP. Targeting the vulnerable in emergency situations: who is vulnerable? Lancet. September 1996;348:868-71. 10. Moore PS, Marfin AA, Quenemoen LE, et al. Mortality rates in displaced and resident populations of central Somalia during 1992 famine. Lancet. April 1993;341(8850):935-8. 11. Toole MJ. Mass population displacement. A global public health challenge. Infect Dis Clin North Am. June 1995;9(2):353-66. 12. Spiegel PB, Salama P. War and mortality in Kosovo, 1998-99: an epidemiological testimony. Lancet. 2000;357(9257):2204-9. 13. Deforestation rates for Haiti: forest cover statistics for 2000. Available at: http://rainforests.mongabay.com/deforestation/2000/ Haiti.htm. 14. Bradshaw AL. International Environmental Security: The Regional Dimensions. Carlisle Barracks, PA: Center for Strategic Leadership; 1998. 15. Pugh M. Military intervention and humanitarian actions: trends and issues. Disasters. 1998;22(4):339-51. 16. Sheik M, Guitierrez I, Bolton P, et al. Deaths among humanitarian workers. BMJ. July 2000;321:166-8. 17. Burkle FM. Complex emergencies and military capabilities. In: Maley W, Sampford C, Thakur R, eds. From Civil Strife to Civil Society: Civil and Military Responsibilities in Disrupted States. Tokyo and New York: United Nations University Press; 2002:68-80. 18. Davidoff F. In the teeth of the evidence: the curious case of evidence-based medicine. Mt Sinai J Med. 1999;66:75-83. 19. Desendos JC, Michel D, Tholly F, et al. Mortality trends among refugees in Honduras, 1984-1987. Int J Epidemiol. 1990;19(2): 367-73. 20. Margolis RA, Franklin RR, Bertrand WF, et al. Rapid post-disaster community needs assessment: a case study of Guatemala after the civil strife of 1979-1983. Disasters. 1987;13(4):287-99. 21. Gregg MB. Field Epidemiology. Oxford, UK: Oxford University Press; 1996. 22. United Nations High Commissioner for Refugees. Handbook for Emergencies. 2nd ed. Geneva: United Nations High Commissioner for Refugees; 2002:40-60. 23. World Health Organization. Rapid Health Assessment Protocols for Emergencies. Geneva:World Health Organization; 1999. 24. Sphere Project. Humanitarian Charter and Minimum Standards in Disaster Response. 2nd ed. Oxford, UK: Oxfam Publishing; 2003. 25. Hakewill PA, Moren A. Monitoring and evaluation of relief programs. Tropical Doctor. 1991;21(suppl 1):24-8. 26. Burkle FM, McGrady KAW, Newett SL, et al. Complex emergencies: III. Measures of effectiveness. Prehospital Disaster Med. 1995;10(1):48-56. 27. Burkle FM. Evidence-based health assessment process in complex emergencies. In: Cahill JM, ed. Emergency Relief Operations. New York: Fordham University Press and the Center for International Health and Cooperation; 2003:55-79. COMPLEX EMERGENCIES 49

28. Elias CJ, Alexander BH, Soky T. Infectious disease control in a longterm refugee camp: the role of epidemiologic surveillance and investigation. Am J Public Health. July 1990;80(7):824-8. 29. Roberts L. Mortality in Eastern Democratic Republic of Congo: Results from Eleven Mortality Surveys. Final draft. New York: Health Unit, International Rescue Committee; May 2001. 30. World Health Organization. The new emergency health kit: 1998. Available at: http://www.who.int/medicines/library/par/newemergency-health-kit/nehk98_en.pdf. 31. Anker M. Epidemiological and statistical methods for rapid assessment: introduction. World Health Stat Q. 1991;44(3):94-7. 32. Glaziou PT, Mackerras EM. Vitamin A supplementation in infectious diseases: a meta-analysis. BMJ. 1993;306:366-70. 33. Organization for Economic Cooperation and Development. Evaluation and Aid Effectiveness: Guidance for Evaluating Humanitarian Assistance in Complex Emergencies. London: Development Assistance Committee/Overseas Development Institute; 1999:13-14. 34. Van Rooyen MJ, Eliades MJ, Grabowski JG, Stress ME, Juric J, Burkle FM. Medical relief personnel in complex emergencies: perceptions

50 INTRODUCTION

of effectiveness in the former Yugoslavia. Prehospital Disaster Med. July-September 2001;16(3):145-9. 35. UNICEF, Ministry of Health Iraq. Child and Maternal Mortality Survey 1999: Preliminary Report. New York: UNICEF and Ministry of Health Iraq; 1999. 36. International Study Team. Health and welfare in Iraq after the Gulf Crisis: an in-depth assessment, 1991. Available at: http://www. warchild.ca/docs/ist_1991_iraq_report.pdf. 37. UNICEF, Central Statistical Office, Ministry of Health Iraq. Multiple Indicator Cluster Sample (MICS-1996). Baghdad: UNICEF, Central Statistical Office, and Ministry of Health Iraq; 1996. 38. UNICEF, Ministry of Health Iraq. Integrated Nutritional Status Survey of Under Five Years and Breastfeeding/Complementary Feeding Practices of Under Two Years in S/C Iraq. New York and Baghdad: UNICEF and Ministry of Health Iraq; 2002. 39. World Health Organization. Communicable Disease Profile— Iraq. Geneva:World Health Organization; 2003. 40. King DJ. The year of living dangerously:Attacks on humanitarian aid workers in 2003. [Special posting.] Washington DC: Humanitarian Information Unit, Washington DC: US State Department; March 29, 2004.

c h a p t e r

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Children and Disaster Bruce M. Becker

Children, along with the elderly and pregnant women, are the most vulnerable populations in disasters. Physiologically and psychologically they are less fit than adults are to survive the acute, subacute, and chronic stresses imposed by a disaster. The younger the child, the more vulnerable he or she is. Children depend on their parents or guardians for food, clothing, shelter, hygiene, sanitation, water, medical care, and general personal safety. Regardless of the type of disaster, inevitably a certain percentage of surviving children will be separated from one or both of their parents or guardians, sometimes forever. Without the appropriate stewardship of adults, the hazards imposed on children by the disaster situation are multiplied. Children are more likely than others to suffer from malnutrition in the predisaster period and, therefore, are more sensitive to decreased food availability after a disaster when the incidence of protein energy malnutrition and micronutrient deficiencies increases. Children are also more likely to suffer closed head injury during a disaster due to their body proportions. In addition, they are more vulnerable to the risks of dehydration and respiratory insufficiency from acute infection or hypothermia if rendered homeless in the wake of the vast structural destruction that follows many natural and manmade disasters. Disruption of the social fabric of their lives can lead to long-term depression, posttraumatic stress disorder (PTSD), interruption of normal growth and development, and lifelong disability. Sadly, orphaned children are also potential victims of unscrupulous adults who may seek to exploit them in as slave workers, sex workers, or combatants in civil war and rebellion. Children fare as badly or worse than their adult counterparts during and after a disaster because of their unique physical and psychological vulnerability, with age inversely related to increased morbidity and mortality. Disaster planning modules in the past have given children short shrift, with small and inadequate chapters devoted to their needs. Clearly an entire text could be written about the proper medical and psychological care of children in disasters. This chapter will serve as an introduction and overview. References and additional readings are included at the end of the chapter for the interested reader. Disaster response planners must consider the unique characteristics and needs of children when designing,

preparing, implementing, and assessing any disaster relief intervention. This chapter focuses on and highlights the particular needs of children in disasters. It provides a historical perspective; focuses on current practice; highlights pitfalls; and provides references and additional readings. It is important to note that most medium- to large-scale natural or manmade disasters destroy the homes and social structures of the families of children. The children and their parents or guardians, if they survive, then become displaced populations or refugees. Therefore, it is impossible to discuss the disaster response issues for children without focusing on the medical aspects of children as refugees or displaced populations, as well. This chapter considers both of these issues, which represent a continuum of medical and psychological challenges for children. Acute medical care must be provided in the immediate wake of the disaster (assuming that there is a discrete chronological impact), and then subacute and chronic care must be provided to locally or distantly displaced or refugee populations of children who were forced out of their domestic environment as a result of the disaster itself.

HISTORICAL PERSPECTIVE In the past, the international community’s response to disaster was very disorganized, poorly monitored, and inefficient, focusing on capital investment, structural replacement, and trans-shipment of large amounts of materials such as medical supplies and equipment, clothing, canned food, and tentage. Much of this material was outdated, culturally unacceptable, untranslated, misunderstood, shoddy, and of little use to the affected population, particularly children because almost none of it was pediatric-specific. The cost of transporting, sorting, storing, and distributing these disaster relief materials was quite high, diverting resources that could have been better used in other ways. Moreover, there were unintended negative outcomes resulting from improper use of pharmaceutical agents and equipment by personnel untrained in their use. These historical problems associated with disaster relief were magnified when children were considered. Using the example of 51

the emergency medical services (EMS) system in the United States, it was only in the very recent past that EMS began to treat children differently than adults in the prehospital setting. This change came about because most of the equipment, medications, and training were completely irrelevant to the care of most children and, therefore, children were not receiving an adequate, medically appropriate, evidence-based approach to prehospital medical care. In the same vein, the disorganized and rarely assessed response to disaster relief that existed before the mid-1980s completely disregarded the separate and even more important medical and psychological needs of children affected by disasters. This was especially tragic because almost half of the population of most developing countries is younger than 15 years, and the most medically devastating natural and manmade disasters typically occur in developing countries. The level of human devastation is a direct result of inadequate intrinsic infrastructure, severely compromised vulnerable populations before the disaster, and inadequate local and nationwide resources to provide acute and long-term responses to the disaster. Even though many healthcare practitioners were eager to “do something” before there was a change in focus on children affected by disaster, few had experience and almost none was trained specifically in pediatric disaster medicine. Preliminary need assessments were not performed, planning was haphazard, and outcomes research was nonexistent. Reportage ruled. In the 1980s, primary healthcare, which was just beginning to be applied to healthcare development projects in developing countries, began to be applied to refugee and disaster medicine. Concepts of immunization; nutrition; oral rehydration therapy; cooperation and collaboration with the affected populations; involvement of the local ministry of health; collaboration between local and international nongovernment organizations; appropriate information gathering, including postimpact (but preresponse) assessment; and outcome assessment were becoming more commonplace. This conceptual and process approach to disaster and refugee medical relief has demonstrated increased effectiveness. Despite the increase in the number of articles and texts addressing these concepts and processes, there remains a paucity of information and research in this field, specifically information and research directed toward the treatment of children in disaster, complex emergency, and refugee situations. This is unfortunate because its quite clear that children make up the highest mortality rates in disaster situations, and those rates are highest for children younger than 5 years.1,2 There are many specific examples of the high mortality rates among children in the disaster literature. In Thailand, Sudan, and Somalia in the 1980s, children younger than 5 years were twice as likely as the rest of the population to die during forced transmigration or in the early days of arrival to a refugee camp, with accrued mortality rates exceeding 105/1000 per month.1 To provide some perspective, the rate of 90/1000 per month must be compared with a baseline crude mortality rate in the country before disaster of 1–2/1000 per month, an 52 INTRODUCTION

increase of almost 4500%. Among Ethiopians displaced to Sudan in the mid-1980s, the overall mortality rate was 27/1000 per month, but the mortality rate among children younger than 5 years was 65/1000 per month.3 In the mid-1990s, among Nicaraguan and Honduran children displaced to refugee camps because of the Contra war, babies represented 42% of all deaths and children younger than 5 years represented 54% of all deaths.4 During the famine of 1992 in Somalia, the death rate for displaced children was 74%.5 During the civil unrest in Rwanda in 1996, displaced Tutsi children represented 54% of all deaths among refugees in camps in Goma, Zaire.6 The accrued mortality rate for children younger than 5 years in the Zaire refugee camps averaged 36/1000 per month, 15 to 18 times greater than their baseline mortality rates. It is clear from these examples that the highest mortality rates among populations who are suffering as a result of natural or manmade disasters and who are also generally displaced or become refugees are children and that the youngest children have the highest mortality rates. These mortality rates reflect tremendous suffering and waste of human capital; they represent the most specific indicators available in the acute and chronic situations of the underlying health status of the population but are likely to be underestimated.The rates are underestimated due to recall bias, the failure to report perinatal deaths in many cultures, and the political forces that inflate denominators (baseline population for increased aid) and deflate numerators (decreased deaths, which represents better health and relief service). Why are children dying? The common reported causes of death of children caught up in natural and man-made disasters involving civil unrest or war and transmigration to refugee camps include acute respiratory infection, measles, malaria, severe malnutrition, diarrheal disease, injury (gunshots, mines and shrapnel, contusions), and burns.2 There is little evidence in the current medical literature that improved response to disaster, complex emergency, and refugee crises has changed either the causes of childhood death or, in many situations, the death rates themselves. Clearly, better approaches to the assessment and treatment of children in disaster situations are needed if great improvements are to be made on these distressing mortality rates.

CURRENT PRACTICE Appropriate disaster intervention aimed at decreasing the morbidity and mortality of children requires proper predisaster preparation, training, and equipment; prompt and appropriate assessment of the disaster situation; rapid intervention appropriate to the specific disaster and the particular health and psychological needs of the children affected; and short- and long-term intervention strategies. During a disaster, implementation of sustainable programs that address the acute, subacute, and chronic predictable problems of children associated with different forms of disaster and complex emergencies is also important.

During the last few decades, disaster medical relief activities have been more scrupulously reviewed, and sufficient data have been gathered and analyzed to allow planners to appropriately train and prepare disaster intervention teams to respond to most types of disaster and complex emergencies that may arise in the world. Some of that data have focused on the needs of children. There are six major pillars that support the foundation of disaster response, particularly as it relates to the care of children: water, sanitation, nutrition, shelter, medical response and treatments, and psychological support. If any of these pillars or supporting columns is inadequately addressed, the protective edifice that the disaster response team or organization is trying to build to help the affected populations will collapse. The following sections briefly address these subject areas from the perspective of children and disaster.

Water Water is essential for life. Most manmade or natural disasters and complex emergencies interrupt the clean water supply to a population. Earthquakes may destroy wells, urban water lines, and water treatment systems. Hurricanes and tsunamis introduce fecal material, toxic chemicals, and salt water to standing water sources and wells. Combatants in war and civil unrest often destroy water sources as strategic acts of war. The minimum personal water requirement is 10 L per day. It is not acceptable to assume that children require less. Fifteen to twenty liters per person per day is needed for drinking, cooking, and personal hygiene. Twenty to thirty liters per person per day is required for children being fed in collective feeding centers that address the needs of children who are undernourished or malnourished. Hospitals require 40 to 60 L per person per day. Water must be accessible; wells must be within a reasonable distance. Family members must have containers to transport and store water. In most cultures, women, mothers, or older female children are responsible for collecting and managing water. A mother’s time spent on water is diverted from other aspects of caring for her children. It is also important to note that contamination of water sources by human contact, especially by the small hands of children reaching through large openings into jars and bottles, is a major concern for the spread of fecal-orally transmitted pathogens such as shigellosis, cholera, and typhoid, which are key sources of mortality for those same children. Gastroenteritis followed by dehydration may be the leading causes of death in children younger than 5 years in disaster situations. The so-called dirty hands diseases, which include diarrheal dysentery, cholera, typhoid, hepatitis A, polio, and helminthiasis, are prominently prevalent in baseline pediatric populations in developing countries and are transmitted as a result of poor hygiene and a lack of adequate clean water and soap. Providing soap and educating the population about appropriate handwashing before meals and after defecation can have a profound effect on the incidence and new cases of diarrheal disease. Soap distributed to refugees from Mozambique decreased the incidence of diarrhea in chil-

dren by almost 30%.7 Water containers with covers or small spouts provided to the same population of refugees led to a 30% reduction in diarrheal disease in children younger than 5 years.8 Some members of the disaster response team should have training and experience in the assessment of the water supply and water treatment as well as simple interventions directed at keeping the water supply safe and available to mothers and children. Short-term rapid interventions may involve the provision of a mobile water supply or the installation of temporary filtration systems. Long-term interventions include the drilling of deep or artesian wells that are protected from contamination by fenced wellheads. Soap-and-water carrying devices can decrease the incidence of waterborne and potentially fatal gastrointestinal illness.

Sanitation The lack of sanitation is a very important problem on-site during and after disasters and complex emergencies. Sewage lines and sewage treatment are disrupted by most natural and manmade disasters. Many countries do not have any toilets, underground sewage, or sewage treatment in rural districts. Children are particularly vulnerable to fecal-oral pathogens. In a Kurdish refugee population in 1991, children younger than 5 years had mortality rates of 15/1000 per month, and more than three quarters of those cases were a result of diarrheal disease associated with malnutrition.9 Disaster response teams should be prepared to understand the implications of poor sanitation after a disaster. They should have an ability to assess the sanitation needs of the disaster-struck population and the cultural and sociological parameters of defecation in the affected population. In many developing countries, it is uncommon for children younger than 3 years to wear diapers or other coverings. Defecation takes place randomly throughout populated areas, facilitating the spread of fecal pathogens. It is common for mothers to place children with diarrhea over their legs to defecate, thereby facilitating fecal contamination of the mother and other siblings. Defecation fields, trenches, and pit latrines all provide protection from fecal pathogens; however, responders must consider traditional methods and habits of defecation as well as religious, cultural, and social mores concerning defecation and joint use of facilities across gender and age. These problems are more easily solved in the developed world, where individual toilets are widely accepted but just not functional after disruption by the forces of natural and manmade disasters. Decisions must be made and solutions implemented rapidly because large populations separated from free access to toilets will find other means and sites of relief that are fraught with the potential for spreading epidemics. Cholera is a common and deadly postdisaster disease. Risk factors include poor sanitation and a lack of soap and clean water. There is a direct relationship between the incidence of cholera in a family and the number of children younger than 5 years in that household.10 Mortality as a result of cholera is greatest in children CHILDREN AND DISASTER 53

younger than 4 years, with a relative risk of 4.5 when compared with older children and adults.11 Most deaths among these young children occur within 24 hours of diagnosis and hospital admission.

Nutrition Protein energy malnutrition (PEM) is highly prevalent in children who have suffered a natural or manmade disaster and is a major contributor to death in these children. The case fatality rate (CFR) for most infectious diseases, including measles, malaria, diarrhea, and acute respiratory infection, increases dramatically in children who are also afflicted by PEM. Children who are 0-5 years old are at greatest risk.12 Even mild to moderate undernutrition can be a significant contributor to the death of children in complex emergencies or disasters.13,14 PEM in children after a disaster often is a result of an exacerbation of underlying famine conditions that existed in that population before the disaster. Such postdisaster famine conditions can be predicted based on an understanding of the socioeconomic condition of the population before the event. Pre-existing conditions that will evolve into famine include widespread poverty; intractable death; underemployment; and a high prevalence of malnutrition, with a moderate to large percentage of the pediatric population who were routinely underfed and were experiencing hunger and starvation. Unfortunately, this is not an unusual condition in many developing countries in the world today. The prevalence of PEM is directly proportional to the crude mortality rate in the underlying population of children. PEM in less than 5% of the children’s population is associated with a crude mortality rate of less than 0.9 deaths/1000 per month. Conversely, a prevalence of PEM exceeding 40% in the underlying pediatric population generally is reflected in a crude mortality rate of 30–40/1000 per month, an increase of more than 4000%. A disaster assessment team arriving on-site should be prepared to evaluate the pediatric population’s nutritional status. Nutritional assessments of children in these situations focus on changes in the child’s weight in relation to his or her height (weight for height [WFH]). Weight and height are easily, quickly, and accurately measured in sample populations of children. Weight is more sensitive than height to sudden changes in food availability. WFH measurements are also appropriate for assessing the effectiveness of feeding programs. Heightfor-age (HFA) measurements reflect more chronic nutritional deficiency, and an abnormal HFA is referred to as stunting. Both WFH and HFA measurements are compared with established normal values for the particular population being evaluated (a reference population), and the results are reported as Z scores. Z scores are the number of standard deviations (SD) the patient falls above or below the median when compared with the reference population. In well-nourished populations, less than 3% of children younger than 5 years have WFH Z scores of less than –2, or 2 SD below the median. In countries where children normally experience some degree of undernutrition, up to 5% of those younger than 5 years have WFH Z scores 54 INTRODUCTION

of less than –2. A nutritional emergency exists if more than 8% of the WFH Z scores among these very young children are less than –2. The prevalence of moderate to severe PEM in a random sample of children younger than 5 years is a strong indicator of this condition in the underlying population. Causes of death of children with severe PEM include dehydration, infection, hypothermia, cardiac failure, and severe anemia. Acute respiratory infection, urinary tract infection, measles, diarrhea (either infectious or malabsorbed), malaria, skin infections, and sepsis are more common and more fatal in children with PEM. Clinical symptoms such as fever and pain may be masked. For example, measles in children with PEM can have a CFR of up to 30% (a //chemdef.apgea.army.mil/. 9. University of Delaware, Disaster Research Center. Disaster data. Available at: http://www.udel.edu/DRC/disdat/busbib.html. 10. University of Colorado, Natural Hazards Center. Available at: http://www.colorado.edu/hazards. 11. Emergency Management Institute. FEMA’s EMI Higher Education Project.Available at: http://training.fema.gov/emiweb/edu/. 12. American Society for Testing and Materials. F1288-90(2003) Standard Guide for Planning for and Response to a Multiple Casualty Incident Available at: http://www.astm.org/cgi-bin/ SoftCart.exe/DATABASE.CART/REDLINE_PAGES/F1288.htm?L+my store+qjcg0290+1089149374. 13. American Society for Testing and Materials. Committee E54 on Homeland Security Applications. Available at: http://www. a s t m . o r g / c g i - b i n / S o f t C a r t . ex e / C O M M I T / C O M M I T T E E / E54.htm?L+mystore+qjcg0290+1089168340. 14. National Fire Protection Association. Hospital requirements. In: NFPA 99: Standard for Health Care Facilities, 2002 ed. Quincy, MA: National Fire Protection Association; 2002. 15. Federal Emergency Management Agency. Capability Assessment for Readiness (CAR). Available at: http://www.fema.gov/pdf/rrr/ car.pdf. 16. National Emergency Management Association, Emergency Management Assistance Compact. Available at: http://www. emacweb.org/emac/index.cfm?CFID=5327&CFTOKEN=28115803. 17. National Emergency Management Association, Council of State Governments. Available at: http://www.csg.org/CSG/default.htm. 18. Joint Commission on Accreditation of Healthcare Organizations. Emergency Management Standards—EC.1.4 and EC.2.9.1.Available at: http://www.jcrinc.com/subscribers/perspectives.asp?durki= 2914&site=10&return=2897. 19. Drabek T. Strategies for Coordinating Disaster Responses. Boulder: Institute of Behavioral Studies, University of Colorado; 2003:42. Monograph 61. 20. Dynes RR. Community emergency planning: false assumptions and inappropriate analogies. Int J Mass Emerg Disasters. 1994;12:141-58.

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Community Hazard Vulnerability Assessment James C. Chang

The community hazard vulnerability assessment (HVA) is the systematic examination of the multitude of hazards, their individual probabilities, and consequences that may be encountered in the community. This assessment requires an in-depth knowledge of the community and is typically performed by a multidisciplinary team. The HVA is often used as the basis for the community’s emergency management program. Like the hospital-based HVA presented in Chapter 18, the community HVA helps emergency planners define the universe of potential threats that the community may face. As with the hospital-based example, community leaders face the same challenges of budgeting, limited resources, and selection of hazards on which to focus their resources. Unlike the hospital-based HVA, however, the scope and performance of a community HVA are often beyond the direct control (and sometimes, influence) of hospital-based planners and are conducted by local emergency management officials. For a healthcare facility to develop a successful emergency preparedness program and meet its obligations to provide care to the members of the community, it must engage with community planners and response agencies, since healthcare facilities are integral components of the community.

HISTORICAL PERSPECTIVE To understand where the practice of HVA arose, one must look at the short, fragmented history of emergency management in the United States. After a devastating fire in Portsmouth, N.H., that overwhelmed both local and state resources in 1803, the U.S. Congress established the precedent for federal aid that is in place today by passing legislation allowing federal resources to be used to support state and local governments. Congress passed 128 other similar pieces of ad hoc legislation in support of victims of the 1906 San Francisco earthquake and other major disasters between 1803 and 1950.1 In 1916, civil defense programs were born when Congress enacted the U.S. Army Appropriations Act. 112

This act established the Council of National Defense (CND) with subordinate state and local defense councils in response to a perceived enemy threat. Much of the interest in civil defense ceased with the end of World War I. After a brief hiatus, federal agencies were given the authority to respond to specific disasters. In 1933, the Reconstruction Finance Corporation was given the authority to fund the repair and/or reconstruction of public facilities damaged by earthquakes. In 1934, the Bureau of Public Roads was given the authority to provide grants to repair federal-aid highways and bridges damaged by natural events (i.e., primarily floods). A noteworthy change in the approach from response to proactiveness (preparedness) occurred with the Flood Control Act of 1936. This act allowed the U.S. Army Corps of Engineers to proactively construct dams, dikes, and levees to reduce local vulnerability to floods.1 Continuing in the track of responding to actual or perceived emergencies, in 1941 the CND was dissolved and the Office of Civil Defense was established. As with the CND,the focus of the Office of Civil Defense was the establishment of protective services programs oriented toward a specific (i.e.,enemy) threat. These activities included the establishment of the Civil Defense Corps, which coordinated the activities of approximately 10 million volunteers and 44 state and 1000 local councils. The Office of Civil Defense was abolished with the end of World War II.1 The Federal Civil Defense Administration (FCDA) was established by President Truman in 1949 in response to increasing Cold War concerns. The Federal Civil Defense Act of 1950 was quickly passed to give the FCDA the authority and resources to begin planning and coordination activities. One of the most noteworthy successes of the FCDA and its new director, Val Peterson, was the idea that civil defense activities such as disaster planning had a peacetime value. Meanwhile, Congress continued to reinforce the role of the federal government in responding to (but not preparing for) disasters with the Federal Disaster Act of 1950. This act, intended for “getting assistance to rebuild the streets and farm-tomarket highways and roads,”1 was viewed by many as Congress’s establishing the legal basis for a continuing

federal role in disaster relief.1 Subsequent acts, including the Disaster Relief Acts of 1970 and 1974, reinforced the federal government’s role in disaster relief. In 1972, the Office of Civil Defense, which had been reestablished in 1961, was renamed the Defense Civil Preparedness Agency.Increasing international tensions and growing stockpiles of nuclear weapons gave rise to the concept of Crisis Relocation Planning (CRP). The premise behind CRP was the dispersal of the populace from highrisk areas in times of heightened international tensions; in essence, this was an extension of existing hurricane evacuation programs that many coastal areas had successfully developed. In 1974, Congress passed the Disaster Relief Act of 1974 that specifically authorized the federal government to assist in disaster preparedness activities. Difficulties in implementing CRP and the resulting frustrations experienced by federal, state, and local emergency planners led to a study and report by the National Governor’s Association (NGA) in 1978 calling for a coordinated federal policy and approach to emergency planning. The NGA report introduced the concept of comprehensive emergency management (CEM), which is the cornerstone for emergency management today. In response to the NGA report and pressure from the constituency,President Jimmy Carter established the Federal Emergency Management Agency (FEMA) in 1979 to pull together many fragmented federal programs and implement a CEM program. The new agency, under Director Louis Giuffrida, adopted a position calling for an enhanced civil defense program with an improved ability to deal with natural disasters and other large-scale domestic emergencies. In response to continued skepticism and outright resistance to CRP, the new agency abandoned CRP in favor of CEM. Under CEM, instead of focusing on specific scenarios and their consequences (e.g., nuclear attack, earthquake, or flood), local and state agencies were now encouraged to ask the following: • What hazards confront our community? • What resources are available? What needed resources are not available? Over what period of time could local government reasonably acquire these resources? • What mitigating actions could be taken to reduce future vulnerabilities? These questions are integral to an Integrated Emergency Management System (IEMS) approach; IEMS is the tool under which FEMA implements CEM. Under IEMS, emergency managers perform systematic assessments of both hazards and response capabilities. Gaps are identified, and then multiyear remediation plans, along with hazard mitigation and recovery plans, are created to address these gaps. Implicit in the use of IEMS is the change from a reactionary to a proactive approach to emergency management. This planning approach facilitates the transition from a hazard-specific to an all-hazards approach to emergency management.1

CURRENT PRACTICE To properly plan for emergencies in the community, it is necessary to identify the list of potential hazards, their

probability or relative risk, and their consequences. This HVA helps the planning team decide what hazards merit special attention, what actions must be planned for, and what resources are likely to be needed. To better describe the community HVA process, it will be broken down into the following actions: • HVA team membership • Hazard identification • Hazard profiling (probability and consequences)

HVA Team Membership2 A team approach should be considered for both the HVA and the development of the final Emergency Operations Plan for many reasons, including: • To share (synergistic) expertise • To develop and foster teamwork and working relationships • To ensure that a holistic view of hazards is taken • To create a sense of ownership and buy-in from all parties The constituency of the teams will differ depending on their stated purpose (e.g., HVA versus plans development). Prospective members of the HVA team may include representatives from: • Emergency Management Agency • Community leadership (e.g., city manager, county executive) • Each community public safety agency (law enforcement—police department, sheriff’s office; fire department; emergency medical services [EMS]) • Hospitals and other community healthcare facilities • Public health agencies (local health department) • Planning departments or agencies • Public works • Local Emergency Planning Committee (LEPC) • Professional groups (e.g., Certified Hazardous Materials Managers,American Society of Safety Engineers) • Special hazards occupancies or operations (e.g., military bases, industrial complexes, dams, nuclear power plants) • Major business entities • Other emergency management planners (e.g., from local, county, regional, or state agencies or private industry)

Hazard Identification Hazard identification is the exercise of identifying what kinds of emergencies have occurred or could occur within the jurisdiction. For assessment purposes, it may be helpful to divide emergencies into the following categories: • Naturally derived emergencies: (e.g., floods, hurricanes, tornadoes, winter storms) • Technologically derived emergencies: (e.g., power or utility failures, hazardous materials releases, computing systems failures) • Manmade emergencies: (e.g., attacks involving weapons of mass destruction) COMMUNITY HAZARD VULNERABILITY ASSESSMENT 113

A partial listing of potential emergencies is provided in Box 17-1. This listing is not all inclusive, and care must be taken to ensure that hazards are not inappropriately excluded or omitted when assembling the community’s overall list of potential hazards.2 It is also important to note that hazards may arise from differing sources (e.g., epidemics may be naturally occurring or the result of bioterrorism). Finally, hazards and emergencies may be linked together. For example, a hurricane may generate flooding, mudslides, and loss of utilities. There are many potential sources of information to support the hazard identification effort, including3: • Experiences of planning team members • Experiences of utilities or other major business entities in the community • Local and/or state Emergency Management Agency records • Local emergency response agency records • Newspaper or other historical archives • Experiences of similar or adjacent communities • Hazard information maps compiled by FEMA and state emergency management agencies, the U.S. Geological Survey (USGS) and state geological surveys, the National Weather Service (NWS), and the Federal Insurance Administration (National Flood Insurance Program)

BOX 17-1 LIST OF POTENTIAL EMERGENCIES Naturally Derived Avalanche Drought Earthquake Epidemic Flood Hurricane (cyclone, typhoon) Landslide Mudslide Severe thunderstorm Temperature extremes Subsidence Tornado Tsunami Volcanic eruption Wildfire Windstorm Winter storm (blizzard, ice storm) Technologically Derived Airplane crash Dam failure Hazardous materials release Hog or other animal farm waste containment failure Information technology system failure Power failure Radiological release Train derailment Urban conflagration Utility interruption (natural gas, water, sewer, telephone, data) Water supply contamination Manmade Civil disturbance Mass casualty events Terrorism (chemical, biological, radiological, nuclear, or high-yield explosive [CBRNE]) 114 PRE-EVENT TOPICS

• Maps of 10- and 50-mile emergency planning zones (EPZs) around nuclear power plants • Maps of hazardous materials sites prepared by the LEPC • Risk management plan submittals by users of extremely hazardous substances • Local American Red Cross or other disaster relief agency records • Results of any federal, state, or private hazard analyses • Local or state historical society or area universities (e.g., departments of history, sociology, geography, engineering) • Professional or business associations (e.g., insurers, engineers, and builders) • Engineering assessments (e.g., reliability studies, mean time between failure studies) • Longtime community residents

Hazard Profiling (Probability and Consequences) Once the list of possible hazards has been assembled, the next action is to profile or characterize each hazard for probability and effect or consequence. Probability This is an assessment of the likelihood of the hazard or emergency occurring and is often described as improbable, low, medium, or high. Other related factors that may be helpful in assessing or describing probability include4: • Frequency of occurrence: The more frequent the occurrence, the higher the likelihood. • Location of the hazardous event and the region affected: Events that occur within or proximal to the community are more likely to affect the community, whereas events that occur at some distance may be less likely to affect the community. • Seasonal (or other cyclical) variations: Events that occur with some regularity may be presumed to be more probable. Commonplace examples include the occurrence of “influenza season”each fall through winter and drought and/or floods (location-dependent) associated with El Niño. Some hazards, such as civil disorder and terrorism, are by their nature highly unpredictable and may be difficult to properly assign a probability level. Consequences This is the effect of the hazard on the community and may be categorized into human, property, and business. Examples of each category include, but are not limited to: • Human impact • Injuries • Illnesses • Fatalities • Psychological impact

• Property damage • Damage to or loss of use of buildings, structures, or domiciles • Damage to or loss of use of infrastructure (e.g., roadways, utility distribution systems) • Business loss • Business interruption (including recordkeeping issues arising from loss of records, inability to access, compromise of integrity) • Unanticipated costs • Loss of revenue (from all causes such as loss of tourism, sales tax revenue, and fees for services) • Decline in property values • Adverse publicity • Fines, penalties, and legal costs The degree of impact may be expressed qualitatively as nonexistent, low, medium, high, or catastrophic, or it may be expressed quantitatively as a numerical score. As a consideration, the HVA team may wish to add greater weight to hazards that occur without warning (e.g., tornado strike).

SUMMARY The end goal of a community HVA should be a listing of hazards facing the community. Depending on the needs of the emergency management or lead planning agency, this listing may or may not be prioritized. An example of Durham County’s (N.C.) HVA, excerpted from the county’s 2001 Emergency Operations Plan, is presented in Box 17-2.5 As mentioned earlier in this chapter, the HVA is the foundation for the community’s integrated emergency management activities, such as creation of plans, preparedness activities, hazard mitigation programs, and recovery plan development.

BOX 17-2 EXAMPLE OF DURHAM COUNTY’S HVA PLAN Durham County is exposed to many hazards, all of which have the potential to disrupt the community, cause damage, and create casualties. Potential hazards (natural, technological, and national security) are: a. Major Fires b. Floods/Dam Failure c. Tornadoes/Severe Thunderstorms d. Severe Winter Storms e. Hurricanes f. Power Failure g. Drought h. Earthquake i. Mass Casualty/Fatality j. Hazardous Material k. Fixed Nuclear Facility (Ingestion pathway) l. National Security Emergency m. Civil Disorder n. Sabotage/Terrorism o. Aircraft Crash (Civilian/Military) p. Severe Bridge Damage q. Public Utility Damage (Phone, Electricity, Water, Sewer, etc.)

Threat Assessments A subset of the community HVA that is receiving increased emphasis is the terrorism-specific vulnerability assessment (or threat assessment) tool. Although a threat assessment appears similar to a community HVA in format and process, the threat assessment differs in several ways. For example, the threat assessment focuses only on the effects of malicious activities or persons on the community (versus all hazards). More sophisticated threat assessments actually look at the consequences of these malicious acts on specific targets, such as infrastructure, critical function areas, symbolic targets, or even special events (e.g., concerts). Threat assessments also are typically performed by law enforcement officials (versus a multidisciplinary team). An excellent discussion of the terrorism vulnerability assessment process is provided in Risk Management Series: Reference Manual to Mitigate Potential Terrorist Attacks Against Buildings.6 Other good examples of terrorism threat assessments are the North Carolina Department of Agriculture & Consumer Services’ Terrorism Threat Vulnerability Self Assessment Tool7 and the Pennsylvania Municipal Police Officer’s Education and Training Commission’s Vulnerability Assessment Worksheet.8

CONCLUSION The HVA is a critical step for any community’s emergency management activities. It is the HVA that methodically defines the scope and breadth of hazards that may be encountered in the community. Under CEM, hazards identified (and prioritized) by the HVA team will be addressed through a variety of means, including the development of emergency operations and response plans, hazard mitigation programs, and preparedness efforts such as training and drills. Although it is not possible to plan or prepare for every conceivable emergency, the HVA can ensure that plans are developed to deal with higher probability hazards or those with more significant consequences. A special type of HVA, the threat assessment, focuses on the threat from terrorism or other malicious acts. There are even more specialized versions of these threat assessments that focus on specific utilities, industries, or operations. For example, RAM-W (or Risk Assessment Methodology—Water) is a threat assessment tool developed by Sandia Laboratories that focuses on the terrorism threat to potable water treatment plants.9 Healthcare facilities can both contribute to and benefit from the community HVA effort. Hospital administrators and experts may provide expertise to community emergency managers on issues such as mass casualty management, infectious disease consequences, and surge management. At the same time, the community HVA may be used as a basis for external hazards in the healthcare facility’s own HVA. For example, if the community HVA identifies mass casualties arising from a hazardous materials event as a probability, this should be reflected COMMUNITY HAZARD VULNERABILITY ASSESSMENT 115

in the healthcare facility’s HVA. Ultimately, it should be the goal of both community and healthcare facility emergency planners to have a coordinated response to all likely hazards. REFERENCES 1. Federal Emergency Management Agency. State and Local Guide (SLG) 101: Guide for All-Hazards Emergency Operations Planning. Chapter 2: The Planning Process. Available at: http://www. fema.gov/pdf/rrr/2-ch.pdf. 2. Drabek T. The evolution of emergency management. In: Drabek TE, Hoetmer GJ, eds. Emergency Management: Principles and Practice for Local Government. Washington, DC: International City Management Association; 1991:6-8, 10-13, 17-18. 3. The National Lessons Learned & Best Practices Information Network. Emergency Management Programs for Healthcare Facilities: Hazard Vulnerability Analysis: Comparing and Prioritizing Risks. Available at: https://www.llis.dhs.gov/frontpage.cfm.

116 PRE-EVENT TOPICS

4. Mitigation and hazard management. In: Drabek TE, Hoetmer GJ, eds. Emergency Management: Principles and Practice for Local Government. Washington, DC: International City Management Association; 1991:140-2. 5. Basic Plan. In: Durham/Durham County Emergency Operations Plan. Durham, NC: Durham County Emergency Management Agency; 2001:BP-2. 6. Federal Emergency Management Agency. Risk Management Series: Reference Manual to Mitigate Potential Terrorist Attacks Against Buildings. FEMA publication 426. Washington, DC: Government Printing Office; December 2003. Available at: http://www. fema.gov/pdf/fima/426/fema426.pdf. 7. North Carolina Department of Agriculture & Consumer Services. Terrorism Threat Vulnerability Self Assessment Tool. Available at: http://www.ncagr.com/BioTerror_Assessment.htm. 8. Municipal Police Officers’ Education and Training Commission. Vulnerability Assessment Worksheet. Available at: www.mpoetc. state.pa.us/mpotrs/cwp/view.asp?a-1133&q-441444 9. Sandia National Laboratories Security Risk Assessment Methodologies Overview. Available at: http://www.sandia.gov/ram/RAM%20 Overview%20%20Pres%20 rev1.pdf.

c h a p t e r

1 8

Health Care Facility Hazard and Vulnerability Analysis James C. Chang, William Gluckman, and Eric S. Weinstein

In 1988 Jan deBoer and collegues1 published the first attempt to mathematically score and classify a disaster to be used prospectively during the management of the calamity. A disaster was defined as “a destructive event that caused so many casualties that extraordinary mobilization of medical services was necessary.”1 In the proposed Medical Severity Index of Disasters, the parameters needed to quantify a disaster were the casualty load (number of casualties), the severity of incident (severity of injuries sustained), and the capacity of medical services.1 Seventeen years later, the importance of determining the impact of a disaster on a healthcare facility (HCF) has heightened because HCFs have become industrial leaders in the community and therefore must be able to swiftly return to normal business functioning. Individual healthcare providers are acutely aware of the business side of their practice while at the bedside, but they are not cognizant of the ramifications that a disruption of normal HCF operations would have on the community. Business and industry emergency management principles for HCFs to accommodate the clinical impact of a disaster are discussed in this chapter. Disasters are events that cause significant enough damage to disrupt the normal activities or function of a community and overwhelm the local resources. What may be an easily handled event in a large urban city may be a disaster for a rural town. Although disasters are not predictable with any great accuracy, many consequences of disasters can be anticipated as part of a comprehensive emergency management plan that includes a hazard and vulnerability analysis (HVA). The HVA will help HCFs plan for these events and allow them to continue operating while assessing structural and operational damage, acquiring needed essentials, and protecting staff and patients. Much can be learned from business and industry with respect to preparedness. Although not a new concept in business and industry, an HVA is a component in the development of a hospital disaster plan, as recognized since 2001 by the Joint Commission on Accreditation of Healthcare Organizations (JCAHO). The emergency management standard (EC.4.1) requires hospitals to identify specific procedures in response to a variety of disasters based on an HVA per-

formed by the organization.2 The HVA will assist in the mitigation and preparedness of the HCF to respond to and then recover from a disaster. A hazard can be any threat that could cause injury; fatality; property, infrastructure, or environmental damage; or impair operations. An HVA is a tool used by emergency management to screen for risk and plan for strategic use of potentially limited resources.

HISTORICAL PERSPECTIVE Many events have affected HCFs in the past. The future is certain to exhibit challenges as we move into a more technologically advanced society challenged by geopolitical terrorist threats. Hospitals inherently have to be prepared for emergencies. Preparation traditionally was based on informal HVAs and largely dependent on perceived issues. For example, hospitals in northern climates typically planned for adverse winter weather related issues; hospitals in the South planned for hurricanes; and hospitals in Southern California planned for forest and wild land fires and earthquakes. Failure to consider all hazards when developing the facility emergency response plan was a flaw in the informal approach. Hazard identification relies on the collection of potential emergencies that the HCF or operation could anticipate encountering. This list may be assembled by cause, by location, or by a combination of both criteria. Causes may be divided into the following categories for assessment purposes: naturally derived emergencies, technologically derived emergencies, and manmade emergencies ( Box 18-1). HCFs experience two types of disasters: (1) those internal to the HCF, isolated to the confines of the HCF physical plant,and (2) those occurring external to the HCF that produce direct effects (casualties) and indirect effects (e.g., loss of electricity, supply due to damaged roads). The more common internal disasters are similar to those encountered by business and industry and until recently were not formally considered in an HVA. Milsten’s3 exhaustive review of direct and indirect disasters that hospitals faced from 1977 to March 1997 showed that external and internal disasters are not mutually exclusive. 117

BOX 18-1 HAZARD IDENTIFICATION Natural Events Drought Earthquake Flood Hurricane (cyclone, typhoon) Landslide Severe thunderstorm Temperature extremes Tidal wave Tornado Wildland fires Windstorm Snow/ice storms/blizzard Volcanic ash Meteor crashes Infestation Technological Events Aircraft crash Medical evacuation helicopter Other aviation crash Loss of medical gases Air Oxygen Nitrogen Nitrous oxide Electrical/power shortage or failure Loss of backup generator(s) Fire: chemical, paper, wood, other Computer network disruption or loss Loss of fire alarm, smoke detection Loss of steam Food contamination Pneumatic tube disruption or loss Food supply interruption Loss or leak of potable water Fixed facilities incidents Loss of suction/vacuum Loss of fuel oil supply or delivery Elevator service disruption or loss Hazardous material release Structural failure Natural gas/pipeline disruption Noxious fumes Sewer failure HVAC failure Loss of equipment requiring cooling Patient/staff at risk Loss of instrumentation (thermostat control/regulation) Supply chain interruption Labor dispute Shortage of labor Communication failure Paging: internal, external Emergency medical services or other radio Internal HCF telephone External telephone Cellular phone Satellite Transportation disruption Labor dispute Roadway/highway incident/blockage Human Events: With or Without Political, Terrorist, or Criminal Intent Mass casualty incidents Trauma Civil disturbance CBRNE* Infectious disease Foodborne illness 118 PRE-EVENT TOPICS

BOX 18-1 HAZARD IDENTIFICATION—cont’d Abduction (infant, child, or adult) Armed or threatening intruder Bomb threat Civil disorder Forensic admissions Hostage situation Violent labor action VIP visitor Workplace violence *Chemical, biological, radiological, nuclear, or high-yield explosive.

This chapter focuses on the HVA for events specific for internal disasters or those that directly occur within the confines of the HCF or indirectly affect the HCF due to consequences of the disaster.

CURRENT PRACTICE Successful mitigation efforts and effective response plans are based on the best possible knowledge of the HCF’s vulnerability in terms of deficiencies in its capacity to provide services, physical weaknesses, and organizational shortcomings in responding to emergencies. The HVA should also highlight and identify strengths within personnel, processes, plans, and other attributes. Past successes during disasters should be revisited to learn best practices, even if these occurred spontaneously due to inventiveness, teamwork, and a strong spirit to succeed. All HVAs have some degree of subjectivity in their findings because many assumptions are made with regard to the perceived risk and even the level of preparedness if hard data are not available. Use of a multidisciplinary team should be encouraged to ensure a holistic characterization of each hazard and to help minimize the inherent subjectivity of the analysis and skewed or erroneous results. The team should be led by someone familiar with the HVA process and consist of representatives from at least the following areas within the HCF: • Emergency management • Security/safety • Facilities (e.g., engineering, maintenance, information technology, telecommunications) • Operations (e.g., nursing, medical staff, laboratory, radiology) • Ancillary services (e.g., materials, food, housekeeping or environmental services) • Administration • Finance/business Community representatives, such as the local emergency manager, fire official, police official, and city manager, can also provide valuable input. Additional members, including the hospital administrator-at-large may be beneficial as long as the group size remains manageable and consensus is achievable within a reasonable amount of time.

Regularly scheduled meetings with a defined agenda and other business-related models will assist the completion and maintenance of the assignment of the HVA team. Most HVA tools come preloaded with a listing of likely hazards that the developer believes the average HCF could face. It is important that the HVA team begin by reviewing the listing of hazards in the HVA tool to ensure that it is applicable to the facility(s) and comprehensive. The HVA tool should address all possible events regardless of their likelihood. The first step is to “brainstorm” and determine all possible hazards, which can be accomplished with assistance from the county Local Emergency Planning Committee (LEPC) in conjunction with the Office of Emergency Management for both the county and state. The hazards are then classified into categories, as described in Box 18-1. Risk, or impact, relates to the threat a particular hazard has with respect to the human impact: safety of people (patients and staff); property impact: structure(s) and property; and business impact: the ability to continue operations. Each risk can be assigned a numerical value to allow for a comparison or relative risk. The three types of impacts are averaged, and a score is assigned for each category. This will be important in the overall assessment. Examples of each category include but are not limited to:4 • Human Impact • Potential for injury or death to staff members • Potential for injury or death to visitors • Potential for injury, death, or adverse outcomes to patients • Property Impact • Damage to the facility (up to and including loss of the facility) • Loss of use of the facility • Loss of or damage to equipment and/or supplies • Costs associated with replacement/repair of the facility, equipment, or services • Business Impact • Business interruption • Unanticipated costs • Loss of revenue (from all causes) • Recordkeeping issues (e.g., loss of records, inability to access, compromise of integrity) • Employees unable or unwilling to report for work • Patients unable to reach the facility • Damage to reputation • Fines, penalties, and legal costs • Future insurance premium increases The degree of risk may be expressed as a numerical score or verbally with use of terms such as nonexistent, low, medium, high, and catastrophic. As a consideration, the HVA team may wish to add greater weight to hazards that occur without warning (e.g., tornado strike). Probability relates to how likely an event is to occur at the facility or affect the facility, based on proximity. This, too, can be assigned a numerical value and is best determined from historical data (e.g., a scale of 1 to 5, with 1 representing a low probability of occurrence and 5 a very high probability of occurrence). Looking back

at historical data is critical in making an “educated guess” about the future. This is an assessment of the likelihood of a hazard or emergency occurring and is often described as improbable, low, medium, or high. Other related factors that may be helpful in assessing or describing probability include the following5: Frequency of occurrence: Obviously, the more frequent the occurrence, the higher the likelihood. Location of the hazardous event and the region affected: Events that occur proximal to the healthcare facility are more likely to directly (or indirectly) affect the facility, whereas events that occur at some distance may be less likely to affect the HCF. Seasonal (or other cyclic) variations: Events that occur with some regularity may be presumed to be more probable. Commonplace examples include the occurrence of “influenza season” each fall through the winter and drought and/or floods (locationdependent) associated with El Niño. Where possible, probability should be based on objective data such as historical archives to learn of local disasters. Equipment failure rates or mean time between failure data should be available to the HVA team. Even maintenance records and expected length of service of equipment may lead to objective data that influence an HVA. Often, however, probability assessments are colored by the prior experiences of HVA team members and recent organizational memory. Facility preparedness may be expressed explicitly in a separate category or integrated with another element (probability or risk). Intuitively, if the facility is well prepared to deal with an emergency, the impact of the emergency should be lessened. The presence of a preparedness component aids in tracking the organization’s preparedness efforts and is a means to decrement HVA scores as preparedness levels increase. Preparedness also should be reported to help determine the need for improvement in areas that have high risk and/or probability. Preparedness may be assigned a numerical value, or it simply may be a listing of what, if any, plans currently exist to address that particular event. It may also represent resources and the amount of them available (e.g., a lot, little, or none); resources can be subdivided into internal and external resources. The average of these two is the numerical value for preparedness. Adding the numerical values of these three components (risk, probability, and preparedness) provides a value. Graphically looking at probability versus impact (Fig.18-1), one would expect higher sums for those events that fall in the high probability–high impact areas and lower values for those events in the low probability–low impact areas. For maximum benefit, the HVA should generate a prioritized listing of hazards with sufficient detail to characterize each one. To do this, a means to grade or rank each hazard, vulnerability, risk (consequence), and preparedness level should be considered. This characterization may be qualitative or quantitative; each approach has pros and cons. Qualitative assessments may be simpler and faster to perform; however, these are often more difficult to fully HEALTH CARE FACILITY HAZARD AND VULNERABILITY ANALYSIS 119

Probability

High probability Low impact

High probability High impact

Low probability Low impact

Low probability High impact

Impact FIGURE 18–1. Probability versus impact.

implement in the end. A qualitative analysis may be as simple as having HVA members team rank-order a listing of potential hazards based on their subjective judgment. A slightly more involved approach to qualitative assessment is found in the HVA model provided by the Emergency Management Strategic Healthcare Group (EMSHG) of the Veterans Health Administration. This model uses a scoring system from 0 (not applicable) to 3 (high) for probability and risk (consequence). Any hazard with a score of 2 or greater in either category requires action.6 Qualitative HVA models often generate little differentiation between hazards and tend to group all hazards into one category (such as “high”) or another. These models have little flexibility in implementation and do not help the organization when it is time to determine organizational priorities for emergency planning and/or allocation of resources. Quantitative assessments can be used to provide additional flexibility in implementation by enhancing the differences between each hazard. Depending on the HVA tool chosen, the scores for each hazard may be the sum or product of probability, risk, and preparedness scores or may be derived from more complex weighting schemes. For example, the HVA model used by Duke University Hospital (Durham, N.C.) takes the sum of the products of the probability of a hazard multiplied by the risk to people, property, and business, and then multiplies the resulting product by a facility preparedness score. Σ (Probability of Each Event × Risk of Each Event) × Facility Preparedness Score = Weighted Score of Event See Table 18-1 for an example of the Duke University Hospital HVA. The end result of the Duke University Hospital and similar quantitative HVA models is weighted scores that address the probability, consequences, and preparedness level of each hazard. The weighted score of the event is then used to order its priority for emergency planning purposes. An institution may choose to address potential emergencies beginning with the highest-scoring event and progress down the list until all potential events are addressed. A variation of this theme may be to address the top five (or other number) high-scoring 120 PRE-EVENT TOPICS

events in year one, and presuming completion of planning, preparedness, and/or mitigation activities, address the next five-highest scoring events in year two and so on. A third alternative may be to establish a predefined threshold level; any hazard scenario exceeding this threshold value would require some type of action (i.e., planning, preparedness, mitigation). Some more sophisticated HVA tools, such as the one developed by the Kaiser Permanente healthcare system, take the quantitative approach one step further by generating scores (percentages) and a graphical/visual output product.7 The HVA is the foundation for the organization’s emergency management program. It is therefore advantageous to expend the effort and resources to ensure that the job is done properly. The assessors should begin by developing a list of potential emergencies that the organization may face and then characterize each hazard as to its probability and consequence. An automated HVA tool is a significant time saver both as a means to test different scenarios for each hazard and as a documentation aid. Often a quick review of actual disasters, internal and external, that the HCF faced over the past 5 to 10 years is sufficient to commence action by the HVA team. A systematic and consistent approach is needed. The team leader should ensure that all team members have equal input into the process. The end product of the HVA should be a prioritized, all-encompassing, objective (to the extent possible) assessment of the possible, potential, or historical internal and external indirect events that may affect the HCF. The HVA produced is the foundation of the HCF’s emergency management program. It is used as the basis for planning and budgeting for hazard mitigation, preparedness, and response efforts within the institution. It should be intuitive that emergencies with the highest scores or ranks should be addressed first and lesser items handled as time and funding permit. An annual review and revalidation of the HVA should be performed to ensure that changes to the operating environment of the facility are assessed for their impact on the facility’s emergency management program. Another reason for periodically reassessing the HVA is to reflect the benefit of hazard mitigation and preparedness activities. For example, as hospital preparedness activities reduce the risk (and consequences) of an emergency, such as a power failure, the item may be moved down on the list of priorities and other more pressing items may be moved up. As a final consideration, the HVA work product (including drafts and working papers) should be considered a sensitive document and protected to the same degree as a patient record or a peer review, quality assurance/improvement, or sensitive business document. Remember that the HVA details the organization’s vulnerabilities, and depending on the format used and level of supporting documentation maintained, may describe how the facility will respond to an emergency. In the wrong hands, this information may actually increase a facility’s vulnerability to attack, and for this reason, it should not be freely disseminated (e.g., placed on the Internet). Contact the Interagency OPSEC Support Staff

TABLE 18-1 TYPE OF EMERGENCY

Score

SAMPLE HVA

PROBABILITY RATING

HUMAN IMPACT

High Low

High Impact

5

5

1

PROPERTY IMPACT

BUSINESS IMPACT

IMPACT RATING

Low Impact 1

INTERNAL RESOURCES

EXTERNAL RESOURCES

Few Resources

Many Resources

5

RESOURCE RATING

EMERGENCY PLANS IN TOTAL* PLACE?

1

Technological Events Electrical failure Transportation failure Fuel shortage Natural gas failure Water failure/ contamination Sewer failure Steam failure Fire alarm failure Communications failure Medical gas failure Medical vacuum failure HVAC failure Information systems failure Fire, internal Hazardous materials exposure, internal Unavailability of supplies Structural damage

3

1

3

1

1.7

2

2

2.0

6.7

2

1

1

2

1.3

3

2

2.5

5.8

2 2

1 1

1 1

1 1

1.0 1.0

1 2

1 1

1.0 1.5

4.0 4.5

3

1

1

1

1.0

3

3

3.0

7.0

2 2 3

1 1 1

1 1 1

1 1 1

1.0 1.0 1.0

3 3 3

3 3 1

3.0 3.0 2.0

6.0 6.0 6.0

5

3

3

3

3.0

2

2

2.0

10.0

2

2

1

1

1.3

2

2

2.0

5.3

2

3

1

1

1.7

2

2

2.0

5.7

3 3

2 3

1 3

2 3

1.7 3.0

2 2

2 2

2.0 2.0

6.7 8.0

4 4

4 2

4 1

4 2

4.0 1.7

2 3

1 1

1.5 2.0

9.5 7.7

3

1

1

2

1.3

2

2

2.0

6.3

2

2

2

2

2.0

4

2

3.0

7.0

3 2 4

3 1 2

3 3 2

4 2 2

3.3 2.0 2.0

2 2 2

2 2 2

2.0 2.0 2.0

8.3 6.0 8.0

5 4 2 1 4

2 3 1 1 2

1 2 3 2 1

3 3 1 1 1

2.0 2.7 1.7 1.3 1.3

2 2 2 2 1

2 2 2 2 1

2.0 2.0 2.0 2.0 1.0

9.0 8.7 5.7 4.3 6.3

3 2

2 3

2 2

2 3

2.0 2.7

2 2

2 2

2.0 2.0

7.0 6.7

2 1 1 3

1 1 1 2

1 1 1 1

1 1 1 4

1.0 1.0 1.0 2.3

1 1 1 2

1 1 1 2

1.0 1.0 1.0 2.0

4.0 3.0 3.0 7.3

5

4

1

4

3.0

3

3

3.0

11.0

Natural Events Hurricane Tornado Severe thunderstorms Snow fall Ice storm Earthquake Tidal wave Temperature extremes Drought Flood, external Wild fire Landslide Volcano Epidemic Human Events Mass casualty incident (trauma)

Continued HEALTH CARE FACILITY HAZARD AND VULNERABILITY ANALYSIS 121

TABLE 18-1 TYPE OF EMERGENCY

Mass casualty incident (medical) Mass casualty incident (hazardous materials) Terrorism, chemical Terrorism, biological Terrorism, nuclear Accidental, chemical Accidental, biological Accidental, nuclear VIP situation Infant abduction Hostage situation Civil disturbance Labor action Forensic admission Bomb threat

SAMPLE HVA—cont’d

PROBABILITY RATING

HUMAN IMPACT

PROPERTY IMPACT

BUSINESS IMPACT

IMPACT RATING

INTERNAL RESOURCES

EXTERNAL RESOURCES

RESOURCE RATING

EMERGENCY PLANS IN TOTAL* PLACE?

5

4

1

4

3.0

3

3

3.0

11.0

4

3

1

4

2.7

3

3

3.0

9.7

5

5

1

5

3.7

3

3

3.0

11.7

5

5

1

5

3.7

3

3

3.0

11.7

5

5

3

5

4.3

3

3

3.0

12.3

4

5

1

5

3.7

3

3

3.0

10.7

1

5

1

5

3.7

3

3

3.0

7.7

1

5

3

5

4.3

3

3

3.0

8.3

3 2

1 4

1 1

1 3

1.0 2.7

2 2

2 2

2.0 2.0

6.0 6.7

3

3

1

3

2.3

3

2

2.5

7.8

5

2

2

3

2.3

2

2

2.0

9.3

3 4

1 1

1 1

3 1

1.7 1.0

2 2

2 2

2.0 2.0

6.7 7.0

5

2

1

2

1.7

2

2

2.0

8.7

Total* is the sum of the probability, impact rating, and resource rating.

(IOSS) (www.ioss.gov) for operational security program development guidance, training courses, and consultative support.8

PITFALLS A typical pitfall is underestimating the time required to develop an HVA and not allowing sufficient time to adequately complete the evaluation. In a large facility in a complex urban environment, an HVA may be a multiday process. A related pitfall is the gradual decline in interest as the evaluation progresses; the amount of time spent on each topic is typically directly related to how long the team has been working. Most assessments begin with an extremely thorough discussion of hazards and decline rapidly to more cursory examinations as the day progresses. It is sometimes necessary to reiterate the sole purpose of the HVA—that is, the development of a prioritized listing of hazards to be addressed in the hospital’s emergency planning process. It is not uncommon for representatives of a particular service or group to consider any mention of a hazard in their area as a personal affront. Care should be taken to ensure that this bias does not cause hazards to be arbitrarily dismissed with an “it’ll never happen here” attitude. HVAs are important in a well-designed disaster plan and thus need to be updated on a regular basis. 122 PRE-EVENT TOPICS

Geographic and industrial changes will affect a hospital and need to be considered. The establishment of a new chemical company in town, for instance, may make a significant change in an institution’s assessment of hazardous materials threat. Another problem, sometimes referred to as the “paper plan syndrome,” gives the illusion of true preparedness simply because a written document exists. “Disaster planning is an illusion unless: It is based on valid assumptions about human behavior, incorporates an inter-organizational perspective, is tied to resources, and is known and accepted by the participants.”9

CONCLUSION In today’s resource-constrained healthcare environment, it is not realistic to plan for every conceivable hazard or eventuality that may befall the institution. Healthcare administrators need to allocate their limited resources to ensure that likely scenarios are addressed promptly, whereas the “one-in-a-million” occurrences may be held in abeyance until some later date. The HVA is a tool for HCF administrators to systematically assess and characterize the plethora of hazards that their facility may face. Failure to exercise due diligence when conducting the HVA may have adverse consequences, ranging from professional embarrassment on the part of the emergency

management coordinator to loss of life, business interruption, damage to reputation, and litigation from inadequate emergency planning. Proper use of the HVA helps minimize these risks. REFERENCES 1. deBoer J, Brismar B, Eldar R, et al. The medical severity index of disasters. J Emerg Med. 1989;7:269-73. 2. Joint Commission on Accreditation of Healthcare Organizations. Available at: http://www.jcaho.org/. 3. Milsten A. Hospital responses to acute-onset disasters: a review. Prehospital Disaster Med. 2000;15(1):32-45. 4. The National Lessons Learned & Best Practices Information Network. Emergency Management Programs for Healthcare Facilities: Hazard Vulnerability Analysis: Comparing and Prioritizing Risks. Available at: https://www.llis.dhs.gov/frontpage.cfm.

5. The National Lessons Learned & Best Practices Information Network. Emergency Management Programs for Healthcare Facilities: Hazard Vulnerability Analysis: Identifying Potential Disasters and Probability. Available at: https://www.llis.dhs.gov/ frontpage.cfm. 6. Emergency Management Strategic Healthcare Group,Veterans Health Administration. Section 3.10.3-Hazard Vulnerability Analysis (HVA) Instructions. Available at: http://www1.va.gov/emshg/apps/ emp/emp/hva_instructions.htm. 7. California Emergency Medical Services Authority. Kaiser Permanente Medical Center Hazard and Vulnerability Analysis. Available at: http://www.emsa.ca.gov/dms2/kp_hva.xls. 8. Interagency OPSEC Support Staff. Available at: http://www. ioss.gov/. 9. Auf der Heide E. Disaster Response: Principles of Preparation and Coordination. Chapter 3. Available at: http://orgmail2.coedmha.org/dr/DisasterResponse.nsf/section/03?opendocument.

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c h a p t e r

1 9

Public Information Management Sharon Dilling, William Gluckman, Marc S. Rosenthal, and Eric S. Weinstein

In the chaos and craziness that ensues during or immediately after a disaster, whether it is a suspected contagious disease, an earthquake, or the explosion of a dirty bomb, there will be two constants: (1) the public will demand information about what is happening and (2) the media will be at the scene trying to tell them. Ever since images from Vietnam broadcast live into the living rooms of millions of Americans, the public has come to see breaking news coverage not only as a given, but as their right. The thirst for information grows with every passing minute, fueled by the ever-increasing competition within the media for advertising, sponsorship, and viewers. All of this factors heavily into disaster response. Balancing emergency care for the sick or injured with the need to disseminate accurate public information is always a challenge. Emergency responders would never think of treating a patient without having the proper medical training. Training for disaster communication is also highly important—preparation is the key. Understanding what types of information the public and the media will want and need will help mitigate the effects of the disaster, win the confidence of the media, and reassure the public. Information presented in a clear and truthful manner within a reasonable amount of time will further its effectiveness.

By the late 20th century, new media outlets developed, offering 24-hour-a-day news coverage, as cable television proliferated America. A few years later, as a new millennium approached, the Internet and e-mail revolutionized communication, allowing information to travel rapidly right to the desktop. This, coupled with the competitive news business, created even more demand by both the public and the media for up-to-the-minute communication. This urgency for information has surpassed accuracy and even, in some cases, reason. In 1994, millions tuned in to watch a white Ford Bronco with O.J. Simpson inside drive down a freeway. And then there was Sept. 11, 2001. The television images could not be edited to shelter viewers. They unfolded in real time, with real heartache. The world watched again and again with the hope of somehow hitting the pause button to allow the victims an additional moment or two of peaceful existence. Viewers tuned in for days, hoping to see people emerge alive from the burning rubble. News coverage was 24 hours a day for almost two weeks. Regular programming was preempted, and viewers struggled to come to terms with what had happened. As sad as it was, this horrific tragedy is a good example of what is expected of emergency response and public information.

MEDIA HISTORY

MEDIA AND DISASTERS

The development of the printing press in the 15th century allowed inexpensively produced newspapers and books to spread information to large numbers of people.1 When Marconi sent a wireless message in 1896, radio came alive, allowing electronic communication during World War I.2 The newsreel brought edited pictures of World War II to moviegoers, albeit somewhat delayed. In the 1950s the “American dream”turned out to be a television as the centerpiece of every living room. By the 1960s, nearly all of America tuned in to watch the son of President John Fitzgerald Kennedy salute the flagdraped coffin of his father. Walter Cronkite became “the most trusted man in America.” And, of course, there was the Vietnam War. Television coverage has arguably changed the course of history by providing a window into the harsh realities of war that had never been seen before by most of America.

The medical management of disasters, both small and large, requires a multifaceted response to ensure timely evacuation, assessment, treatment, and recovery. This response, usually based on the Incident Command System (ICS), requires the appointment of an incident commander, a logistics chief, and others. One important and often overlooked component of the ICS and disaster management in general is an area defined as public information management. The ability to provide appropriate, timely information can significantly affect the disaster response. The components of public information management include not only the release of information to prepare rescue workers and volunteers, but the dynamic ongoing release of information to the media and the incorporation of the media within the response mission. Effective interaction with the media can improve the accurate

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distribution of information that ultimately aids the response, while at the same time satisfying the needs of the media to “get the story.” This applies not only to hospitals or other institutions providing support in a disaster, but also to the rapid response elements (e.g., police, fire, and emergency medical services [EMS]) and to intermediate response organizations, such as the National Disaster Medical System’s disaster medical assistance teams, the U.S. Department of Health and Human Services’ Medical Reserve Corps, and the Federal Emergency Management Agency, to name a few. During a disaster, potentially significant amounts of information should be communicated to the region affected to achieve a good response. This information provides the basis for management of the disaster as well as development of the public trust in the responsible agencies. For example, if a government frequently notifies the population of potential storms and their need to evacuate immediately, and subsequently, each storm causes insignificant damage,the population will learn to not trust the local government. If a category 5 hurricane then heads to this same region, the population may not heed requests to evacuate because they have been misled many times before and may not believe the local government or disaster coordinators. However, if the local government warns residents of only potentially dangerous storms and only requests evacuation for events that most likely will cause significant damage and injuries, while providing the details behind its decisions, the population will more likely respond to an evacuation request and, therefore, injuries and loss of life will be reduced. Obviously, the decision to warn or request evacuations is not just dependent on actual risks, but also on potential legal action or bad publicity should the disaster be worse than expected. Further, immediately after an event, those who evacuated or had interests in the area will want to access the affected area to find family members, recover personal items, and assess the damage so that they may start to rebuild or repair. They will depend on information provided by functioning public communications systems. If this recovery action by those affected is not coordinated in a timely manner, people returning to the affected area can hamper appropriate response efforts and hinder response communications. For example, cellular phone towers may become overloaded with users and, therefore, important phone calls are not able to be placed. Providing re-entry instructions contained in the evacuation order and subsequent evacuation instructions is the best strategy. Phone numbers, radio stations,Web sites, and other means to provide timely and accurate information to those returning to an evacuated area will reduce anxiety, potential traffic jams, and the overuse of the limited resources of response agencies that will have to divert their focus to communication to an uninformed population searching for information. Finally, information about sources of food, potable water, medical care, cash, shelters and housing, fuel, and available government assistance needs to be communicated to the residents returning to the affected area. Effective management of information can help minimize property loss and reduce the chance of injuries, even deaths, but also can improve the effectiveness of

response teams. To do this, methods need to be developed to communicate information to the population from one reliable, consistent source. Disasters do not just include the typical natural occurrence (e.g., flooding, hurricane, tornado) or manmade acts (e.g., industrial accident or terrorism) but also include loss of infrastructure (e.g., computer information systems, power grids, potable water, sewers, job action). Even though a disaster may not result in any injuries or fatalities, the fact that “something” went wrong brings the problem into the public eye. In such cases, the news media become interested and so do the government and public. The handling of the incident by the “offending” corporation or entity (1) can provide for a good public relations (PR) review and minimize the PR effect of the disaster, or (2) if poor PR ensues, can make the disaster more significant and potentially harm the corporation.

CURRENT PRACTICES When a disaster strikes, media flood into the area. Be prepared to share your space. As word of the planes crashing into the two World Trade Center towers and the Pentagon spread, firefighters, police, and rescuers rushed to the scene. Not far behind were reporters, photographers, and camera crews. Tune into the local television station near where a hurricane is headed and undoubtedly reporters donning bright yellow rain slickers will be broadcasting from an evacuated beachfront while waves crash around them and lightning lights up the seas. Turn on the radio to hear broadcasters coughing out their report as the smoke of a nearby wildfire burns brush just steps away. Pick up a newspaper to learn how a reporter interviewed a family as they crouched in a storm cellar with a tornado blowing overhead. Accepting media presence at events is important. Reporters will not go away, so it is best to help them find their way to a place that is close enough to the action to satisfy their needs, yet far enough away to prevent them from broadening the crisis by becoming a victim, or worse, placing emergency personnel at risk. When the media shift into crisis mode, they will broadcast whatever information they have in the order in which they receive it.3 Providing factual information to the media will allow one to effectively control the information instead of the information being in control. Reporters may or may not have time to verify the information, but they would rather report something than have nothing to report. If they have nothing to report, they probably will speculate. When the New York Post went to press with its July 6, 2004, headline, “Kerry’s Choice,” they declared Dick Gephardt as presidential candidate John Kerry’s running mate. Kerry announced his choice of John Edwards for vice president that same morning. The debacle mirrored the infamous 1948 Chicago Daily Tribune headline, “Dewey Defeats Truman.” In the Gephardt case, the already tarnished reputation of the Post took a hit, and the Kerry campaign benefited from the exposure.4 Although a mistake by the media can hardly be deemed a crisis, it clearly illustrates the pressure that time and competition weigh on the media. In PUBLIC INFORMATION MANAGEMENT 125

most instances, it is best to offer some information, even a small amount, to the media as long as it is correct. Provide the media with factual information as soon as possible; even small or minor details or known truths can be helpful. The first source often becomes the most credible. Also, remember to demonstrate empathy when providing information.5 In the immediate aftermath of the destruction of the World Trade Center towers, New York City Mayor Rudy Giuliani spoke to the people of New York and the nation. He provided very little new information, but he told what he knew and demonstrated empathy—that he was grieving, too. “The number of casualties,”he said,“will be more than any of us can bear.”6 This was not an unknown fact, and it most certainly was not a new piece of information. Giuliani had never been known for his compassion, and his behavior after the World Trade Center disaster was a turning point in his career, making him arguably the most popular mayor in the city’s history. Be honest. The truth almost always comes out anyway. There are numerous instances throughout history in which an initially dishonest action was forgiven by the public after the truth was told. If one shares inaccurate information and later the information is determined to be false, all credibility will be lost. Time and space in the media are money.When a newspaper is put together, the first pieces to go in are the advertisements. Articles fill in the spaces around them. Space is at a premium. Select words wisely. Studies have shown that the average level of reading comprehension is at grade 6. If the message is targeted to a sixthgrader, the majority of the population will understand it; however, keep the audience in mind and adjust accordingly. For television, the rule of 27/9/3 is extremely helpful. Developed by Dr. Vincent Covello of the Center for Risk Communication, this rule suggests keeping messages to 27 words, 9 seconds, and 3 ideas or concepts for maximum comprehension.7 Media may not always be a friend, but they do not have to be an enemy.3 The media have a job to do, just like those who respond to a disaster. The media may play an essential role in communicating to the public during a disaster situation by offering evacuation routes, safety tips, or other important advice. Keeping the media upto-date in an emergency is essential and should not be overlooked. Failure to provide frequent updates may result in the media using any means to get closer to the scene to get the information firsthand or going to possibly less-reliable sources. Make the media a friend, and let them relay the information you provide, as opposed to what someone else provides. “Hope for the best but prepare for the worst” is a very applicable cliché concerning the need to have prepared public information systems in place before a disaster. Current practice for emergency preparation is to plan and drill response. This should always include testing the public information component.8

Medical/EMS/Fire Models Disasters occur frequently, ranging from bus accidents with 10 to 20 injured persons, to hazardous material 126 PRE-EVENT TOPICS

events requiring local evacuation, to regional incidents such as hurricanes. In all of these cases, the local community or larger region enters a disaster mode as the resources needed are greater than one segment can provide. EMS must redirect ambulances and rescue vehicles, hospital emergency departments must prepare for casualties, and government provides resources for scene control and forensic investigation, with preservation of evidence balanced with response and recovery. All of this must occur while the daily standard delivery of healthcare and maintenance of law and order are maintained and the community infrastructure is preserved. The totality of the response is dependent on the size of the disaster and the numbers affected with the dynamic match of available resources, supplies, and the specific demands. Many events happen simultaneously during the early stages of a disaster response:EMS/fire/police personnel are dispatched to the event and use an incident management system. Bystanders render aid, or as the word spreads, people arrive who may be able to help, but more than likely, they are not suitable responders. Plans should be made for this convergent volunteerism because it cannot be avoided (this is explored in other chapters of this text).9 Local emergency management representatives should work with local media to prevent a situation in which the media take it upon themselves to call emergency responders for help before the responders get direction from their office. If the media are asked to communicate a call for help, specific emergency personnel, upon arrival to the disaster scene, can then be directed to a gathering place and then directed to their duty station. Management of volunteers can consume precious resources away from critical aspects of a timely response. By reporting certain types of information, the media can fulfill an important role in assisting healthcare providers travel to their workplace, ensuring that any response teams are directed to their prearranged muster stations, and helping in prevention of injuries to unnecessary volunteers. The media responding to an event must also be directed to a location that enables them to accurately report while being kept safe. In addition, it must be recognized that each response unit from various government and nongovernment agencies will have differing perspectives based on their interpretation of the dynamics of the event guiding their management or role. Unfortunately, all these views can diverge and provide a confusing and inconsistent picture of events,simply due to each unit’s perspective and underlying knowledge base. Caution must follow because each unit or members of each unit may be approached separately by members of the media and innocently provide inconsistent information. This can lead to misperception and loss of public trust. Further, if such misperception is acted upon by members of the command and control system, this may lead to disruption of the disaster response. Such misinformation may be a direct consequence of the real-time reporting that often occurs around disaster scenes. With media at the scene reporting in real time but missing vital elements or reporting unsubstantiated information, decisions can be rendered that can interfere with the dynamic response and recovery or divert resources, triggered by political expediency or a microphone held in someone’s face under bright lights.

Effect of Media Reports A new area of media interaction related to disaster medicine is how the public responds to news reports and images that have the potential to induce posttraumatic stress disorder (PTSD).10 It has been reported that there is increased incidence of PTSD with intense coverage of an event, especially one associated with many images. This was reported to be especially true with the pediatric population.11 The authors believe that intense exposure to significant events, such as the World Trade Center disaster, is associated with psychopathology.12

Media Communication Several studies have looked at the public’s response to uncertainty. These results can have implications on how the public will respond to media communications. One study found that a majority of respondents prefer ranges of risk estimates because they believe that these ranges makes the government look more honest. However, about half just want to know whether an area is safe or unsafe. Finally, disagreement among scientists about risk, even if a majority has one opinion, tends to result in the public assuming the worst. The implications of this reinforce the need for one spokesperson for a disaster response.13 Other studies looking at risk communication have provided goals for risk communication that could also apply to disaster communication, especially before the event. These are building trust,raising awareness,education,agreement,and motivating action. Before a hurricane or another major disaster, the development of these goals will help foster action by the community. The media become the vehicle for the communication of these goals and needs to work with the public information officer (PIO) and responsible organization to develop them.14

Detroit Free Press Example The media are also concerned with safety and minimizing interference with the relief effort. The Detroit Free Press requests that their reporters and photographers work as teams. These teams are allowed to do whatever is needed to get a story as long as they feel comfortable or safe, obviously a very large leeway for the reporter. The teams are expected to be as inconspicuous as possible and to identify themselves to responsible agencies, including the police, to reduce potential problems. Reporters and their editors want to publish information that they believe is accurate, timely, and has been verified with multiple sources, if possible. They prefer to verify information with at least two, but preferably three, sources. In addition, they have deadlines that must be met. Finally, these teams are willing to help responsible agencies to disseminate information as long as they have access (T. Fladung, managing editor, Detroit Free Press, private communication, 2004).

Lessons from Recent Disasters Multiple disasters have occurred within the last 10 to 15 years that provide a glimpse into the do’s and don’ts of

public information management. These events have stemmed from airplane and train disasters, earthquakes, and terrorist actions. In each case, lessons learned have improved disaster response and have shown the importance of public information management. Tokyo Sarin Attack, 1995 On March 20, 1995,Tokyo experienced a nerve gas poisoning attack with sarin. The first patient from this attack arrived at the hospital before ambulances began delivering patients. Approximately 2.5 hours after the event, the first press conference was held at one hospital, and the first televised news announcement was made 3 hours after the attack. At this point, most patients had reported to a local medical facility. In addition, there was no initial report to the population from an official source until after all patients had left the scene. In this case, the media notification and distribution of information from an official were late, but the information after the initial conference was consistent.15 Oklahoma City Bombing, 1995 On April 19, 1995, a terrorist action caused an explosion that destroyed the Murrah Federal Building in Oklahoma City. The blast was felt by many in the local area and was reported by news networks very quickly. The local emergency departments (EDs) immediately became fully staffed; many medical personnel immediately offered their services to local EDs, and as the departments became staffed, personnel decided to go directly to the explosion site and provide freelance medical care and rescue efforts. In addition to the local response, the local media, without notification or request, directed those with medical training to go to the federal building to provide care. This resulted in more than 300 volunteers at the site. Even though volunteers provided evacuation assistance, the site was unsafe and the responders did not have protective gear; as a result, one volunteer died from falling debris.16 Some of the lessons learned from this disaster included how to request that additional healthcare providers go to their respective facilities and how to prevent untrained and superfluous volunteers from converging on the scene. If the need for additional support arises at the incident location, the incident management commander can request this through emergency management channels. The media can then receive a specific request for specific volunteers to be directed to a gathering, muster, or staging area for credentialing, briefing, equipping, and transportation assignments. The receiving medical facilities can then, either by direct communication or preexisting disaster protocols, have their requests met through proper channels and be prepared for the additional healthcare professionals, limiting resources dedicated to incorporate them into the existing staff. The media should be informed early in a disaster of set expectations of their role, any boundaries placed on them, and how they could potentially hinder the response and recovery. This partnership should be communicated to the public to build public trust. In PUBLIC INFORMATION MANAGEMENT 127

addition, if the incident management team does not want bystanders because of safety concerns, this should also be conveyed to the media so that they might communicate this information to the public.

response for best results, and stay on your message.8 Repeat your main idea as many times as necessary. Do not deviate from your main message or key points.

Do Not Predict PITFALLS OF MANAGING PUBLIC INFORMATION Managing the flow of information in a crisis or disaster is no small task. There are, however, 10 common pitfalls to be avoided.

Failing to Bring in Experts Emergency responders are supposed to respond to emergencies: physicians are supposed to take care of sick or injured patients, search and rescue teams are called in to look for trapped individuals, and firefighters battle fires. When a disaster occurs, be it large or small, an expert who can speak about it effectively should be summoned. This is not to say that a firefighter is not the best spokesperson at the scene; it means that anyone speaking to the media, or formally to the public, should have some basic public information officer training.3 In a large-scale disaster, it is strongly recommend to have a designated key spokesperson. There are training programs available through the Centers for Disease Control and Prevention, the Federal Emergency Management Agency, and a number of private companies that specialize in crisis and risk communication.

Avoid Using Complex Language or Jargon17 In a crisis situation, the listening skills of people involved are highly challenged. They often do not hear correctly, are overcome with emotion, and are experiencing high anxiety. Additionally, audiences in a crisis may vary in their level of education and comprehension. A best practice guideline is to target communications to the reading level of a sixth-grader.17 Try to keep information clear, succinct, and to the point. Do not use acronyms or abbreviations because they may confuse the public.

Avoid Arguing, Fighting, or Losing Your Temper Disasters by nature are stressful. It is difficult to remain calm when dealing with situations that involve extensive loss of life or property. Often,disaster workers go without proper rest for long periods, and it is easy for tempers to flare. When speaking to the public or a reporter, remaining calm is the key. Do not be afraid to politely end a conversation if it becomes heated or uncomfortable. Reporters almost always win an argument; they have the editor on their side. Offer a succinct and truthful 128 PRE-EVENT TOPICS

Often, questions about what will happen next will be asked after a crisis. Unless one arrives on-scene with a working crystal ball, these kinds of questions should not be answered. No one can predict the future. Reassure the public that every effort is being made to mitigate the crisis or that the best possible care is being offered.18

It Is OK to Say, “I Don’t Know” Do not answer a question that you are not qualified to answer. In fact, when offering information to the public, be prepared to repeat the information you do know several times in several different ways. Admitting you are not qualified to answer a specific question and suggesting someone who can may even add to your credibility.7

Failing to Show Empathy Empathy or sensitivity is essential in disaster communication. Whereas many first responders or healthcare providers often emotionally detach themselves from a crisis situation, public information officers cannot. The most effective communicator is one who cares.7

Lying, Clouding the Truth, or Covering Up History has shown us, from Watergate to the Monica Lewinsky scandal to the legal woes of Martha Stewart, that it is often not the initial incident that is the problem, but rather the cover-up. Never cover up or hide information. In this day and age of e-mail, cellular phones, and up-to-the-minute communication, the information is almost always going to get out. Of course, discretion and good judgment are factors, but avoid lying or blatant cover-ups.

Not Responding Quickly Slow and steady do not win the race in a disaster response, be it rescuing the injured or communicating the issues.18 Respond quickly and thoughtfully. Also, be sure to be accurate and truthful.

Not Responding at All The infamous words “no comment” bring chills to experienced PIOs everywhere. There is almost always something better to say than “no comment.” Some suggestions include, “I don’t know,” or “I’ll get back to you with an answer to that question.” The main thing to remember when tempted to respond with “no comment” is that this refrain instantly makes the speaker sound as if something is being hidden or there is something dishonest about what is happening. Always remember what can be commented on and offer that instead, even if it does not answer what the reporter asked.

Failing to Practice Emergency Communications Schools practice fire drills. Communities practice evacuations. Hospitals drill for emergency response. Communications should be an essential part of any drill. Practice is the key to success when a real disaster hits. Allow the information officer to participate in scheduled exercises, and ask local media to attend. Work with them in advance so that they may provide a more realistic scenario with the stresses that come along with the reporting of a major event.8 The key to managing public information is to be prepared, respond quickly with accurate information, and show empathy.

3. 4. 5. 6. 7. 8. 9.

CONCLUSION Good disaster management provides for a mass communication system with appropriate information. The goal of this system is to establish relationships between the response agencies, the media, and the public. A major underpinning for success is accurate and timely information to the public.19 The media can be a friend or foe. Mutual respect for each other will generally result in better cooperation and a smoother interaction. The provision of timely and accurate information will help keep reporters from searching for unreliable facts. The media most likely will not be the cause of any panic. Any panic by the population will be based on the incident, not the reporting of it.20 It is recommended for organizations that may have to deal with the media to have a media policy in place before an event. In addition, a representative or PIO is needed on-site. The media also do not just want facts, but human interest stories. Establish procedures to allow responders to tell their story: highlight outstanding efforts or acts of heroism and then notify the media.21 PIOs should consider predeveloped news release forms and develop a contact list for the area and a list of “experts” to call on to explain the situation to the public and reporters.22 Even though the media can be intrusive, they also can disseminate accurate information as well as advice or warnings.23 Recommend that the media assist in providing accurate information to the public. Before events, have the media participate in disaster drills and network with organization leaders for disaster events.24

REFERENCES 1. McLuhan M. The Gutenberg Galaxy. Toronto: University of Toronto Press; 1962. 2. Weightman G. Signor Marconi’s Magic Box: The Most Remarkable Invention of the 19th Century and the Amateur

10. 11. 12. 13. 14. 15. 16. 17. 18. 19. 20. 21. 22. 23. 24.

Inventor Whose Genius Sparked a Revolution. New York: DeCapo Press; 2003. Society for Healthcare Strategy and Market Development. Crisis Communications in Healthcare: Managing Difficult Times Effectively. Chicago: 2002. Colford P. Another Post Exclusive. New York Daily News. July 7, 2004. Emergency Management Laboratory of the Oak Ridge Institute for Science and Education. Emergency Public Information Pocket Guide. Oak Ridge,TN; May, 2001. Pooley E. Time Magazine Person of the Year 2001: Mayor of the World. Time Magazine. Dec. 31, 2001. Covello VT. Risk Communication. New York: Center for Risk Communication/Consortium for Risk and Crisis Communication Slides; 2004. Reynolds B, Hunter-Galdo J, Sokler L. Crisis and Emergency Risk Communication. Atlanta: Centers for Disease Control and Prevention; 2002. Cone DC, Weir SD, Bogucki S. Convergent volunteerism. Ann Emerg Med. 2003;41:457-62. Njenga FD, Nyamai C, Kigamwa P. Terrorist bombing at the USA embassy in Nairobi: the media response. East African Med. 2003;80(3):159-64. Pfefferbaum B, Seale TW, Brandt EN Jr, et al. Media exposure in children one hundred miles from a terrorist bombing. Ann Clin Psychiatry. 2003;15(1):1-8. J Ahern, Galea S, Resnick H, et al. Television images and psychological symptoms after the September 11 terrorist attacks. Psychiatry. 2002;65(4):289-300. Johnson BB. Further notes on public response to uncertainty in risks and science. Risk Analysis. 2003;23(4):781-9. Bier VM. On the state of the art: risk communication to the public. Reliability Engineering System Safety. 2001;71:139-50. Okumura T, Suzuki K, Fukuda A, et al. The Tokyo subway sarin attack: disaster management, part 2: hospital response. Acad Emerg Med. 1998;5:618-24. Maningas PA, Robison M, Mallonee S. The EMS response to the Oklahoma City Bombing. Prehospital Disaster Med. 1997;12(2): 9-14. Covello VT. Best practices in public health risk and crisis communication. J Health Communication. 2003;8:5-8. Sandman PM. Anthrax, Bioterrorism, and Risk Communication: Guidelines for Action. Presented at: Centers for Disease Control and Prevention; November 20, 2001;Atlanta. Quarantelli EL. Ten criteria for evaluating the management of community disasters. Disasters. 1997;21(1):39-56. Garrett L. Understanding media’s response to epidemics. Public Health Reports. 2001;116(suppl 2):87-91. Anzur T. How to talk to the media: televised coverage of public health issues in a disaster. Prehospital Disaster Med. 2000;15(4)196-8. Allison EJ. Media relations at major response situations. JEMS. December 1984; 39-42. Auf der Heide E, Lafond R, et al. Theme 1. Disaster coordination and management: summary and action plans. Prehospital Disaster Med. 2001;16(1)22-5. Schultz CH, Mothershead JL, Field M. Bioterrorism preparedness I: the emergency department and hospital. Emerg Med Clin North Am. 2002;20:437-55.

SUGGESTED READING 1. Covello VT. Message Mapping, Risk Communication, and Bio-terrorism. Presented at: World Health Organization Workshop on Bio-terrorism and Risk Communication; October 1, 2002; Geneva, Switzerland.

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Informatics and Telecommunications in Disaster Churton Budd

The United States and many other countries are facing the threat of a number of new crises as the result of terrorist activities. Behind them looms the ever-present danger of a natural disaster, such as an earthquake, fire, or hurricane, and manmade or technological disasters, such as a transportation accident or loss of an electrical grid. All of these incidents generate strong demands on the collection, analysis, coordination, distribution, and interpretation of many types of health and preparedness information. Along with the increasing risk of bioterrorism, there is a greater requirement and stronger emphasis on the use of sophisticated information-gathering tools and information technologies to accomplish. These tools are necessary to manage the complex surveillance needs and the data analysis necessary to spot trends and make early identification of outbreaks, as well as allow for rapid communication of health information, mitigation strategies, and treatment modalities to healthcare workers in the field. Fortunately, many of those involved in emergency management have begun to embrace technology, and consequently, many vendors have recognized the need to produce hardware and software to meet the needs of disaster responders. Various tools have been used to help mitigate, prepare for, and respond to disasters. One of the more difficult issues during a response to a disaster is the inability to communicate. The breakdown of communications has been a recognized effect of almost every major response to a disaster. Communications issues occur at some level in almost every disaster response, no matter how large or small. As the disaster community has experienced these failing communications systems, it has found strategies to improve the systems or replace them with methods that work. Over time, the ability to accumulate, analyze, and disseminate disaster preparedness and response information has improved. Largely, this is due to advances in information technology that have taken place during the past half century.

HISTORICAL PERSPECTIVE1 The disaster response community got off to a slow start with embracing information technology; however, this 130

technology is rapidly gaining momentum. In the past, before the 1980s, computer systems were primarily used in the business, banking, and scientific communities. For the most part, anything close to emergency or disaster planning use of these systems was limited to the Department of Defense and large commercial research firms who did operation planning and simulation, or occasionally, epidemiological or sociological studies. During the 1980s, the desktop, or personal computer (PC), was introduced. Data could be stored on a disk that was easily carried in a briefcase. By the mid-1980s, disaster responders could enter data into a computer so that documents could be produced, spreadsheets updated, and commodities and resources tracked, sometimes even in the field. During the late 1980s, the Internet began to gain popularity and became more in the reach of the average person. The precursors to the Internet—BITNET and ARPANET—transformed into the World Wide Web, and at that time the average citizen began getting a dial-up Internet connection via CompuServe or America Online. Online resources at major centers of learning began to accumulate databases related to disaster management and planning. People could exchange files and documents via e-mail or by way of a number of sites that acted as file repositories, called FTP sites (for file transfer protocol—the methodology of transferring binary and text files from one computer to another). Special software programs called “gophers” (short for “go for this and that”) cataloged these file repositories and allowed a person to search for them by keyword. These programs were the precursor to the big search engines such as Yahoo and Google. Applications such as CAMEO (computer-aided management of emergency operations) were developed in 1988 by the National Oceanic and Atmospheric Administration. CAMEO is used to assist first responders with easy access to response information. It provides a tool to enter local information and develop incident scenarios. It contains mapping, an air dispersal model, chemical databases, and other tools to help display to the emergency responder critical information in a timely fashion. Hazardous materials information and material safety data sheets (MSDS) became available on CD-ROM.

Other databases also became available on CD-ROM to allow the responder access to a library of information while at the disaster site. About this time, the Centers for Disease Control and Prevention (CDC) released Epi Info (www.cdc.gov/epiinfo). Using this software, an epidemiologist or public health professional could develop a questionnaire or form, customize the data entry process, and enter and analyze data. Epi Info can be used to produce epidemiological statistics, tables, graphs, and maps. Specialized computer mapping software called geospatial information systems (GIS) integrates data with map information. Because disasters are usually spatial events, GIS can assist in all phases of disaster management. It is often easier for disaster planners to see a map of the disaster to assist in plan development. A map will show the scope of the disaster, where damage is greatest or has the greatest impact, what property or lives are at risk, and what resources are available and where are they needed. Disaster managers, using GIS to graphically display critical information that is location-based, can quickly map the disaster scene, establish priorities, and develop action plans. In the 1990s, information exchange improved exponentially. List servers on the Internet allowed emergency managers, disaster responders, and medical providers the ability to discuss disaster response in an informal setting. It was not uncommon to see a post to a list server from a responder actually at the site of the disaster. Lessons learned could be immediately disseminated throughout the disaster response community. Agencies such as the Federal Emergency Management Agency, the Natural Hazards Center at the University of Colorado, and the CDC all began to publish large amounts of public information about disasters on their Web sites. The use of satellite telephone systems and cellular phone–based data networks allowed those with a laptop to stay connected in the field and collect and transmit a large amount of information to other responders and to their response agencies. Today, it is hard to find someone in the disaster response field that has not used e-mail or some type of computer resource to do his or her job. It appears that the use of information technology is reducing operational costs and increasing productivity, although this is difficult to quantify because information technology is still growing so rapidly. Portable computers have now decreased in size to as small as a handheld personal digital assistant (PDA). The cellular phone and PDA have merged into a communications/information device. Although still falling behind that of the corporate sector, information technology training for disaster response and management personnel is beginning to be a job requirement. Electronic commerce is allowing disaster responders to achieve real-time procurement and payment for relief supplies. Broadband and wireless networks can be set up rapidly and cheaply to allow for access to vast informational resources. The public has become far better educated, and they seek information on their own healthcare; manage their finances online; and now are able to research, mitigate, and prepare for disasters using the many publicly available resources on the Internet.

What does the future hold for informatics in disaster management? It is hard to tell because information technology in general continues to develop so quickly. It is more than likely that the disaster responder will one day use a wearable computer with a small flexible screen. It is also probable that voice and data technologies will continue to merge so that interaction with digital devices can be accomplished by voice command. Storage devices will continue to become smaller so that victims of a disaster may have their entire financial records, health records, and other personal information archived on a chip they carry in their pocket, which will allow them to save this important personal information from being destroyed by a disaster. Real-time monitoring and surveillance will assist the disaster responder to become aware of an impending disaster sooner. The ability to monitor patient flow, track resources, and perform real-time mapping and visualization of the disaster scene will allow planners and managers to “roll with the punches” during a disaster and modify the response effectively. It is likely that information technology will continue to be a stronger and stronger tool for disaster response personnel.

CURRENT PRACTICE To help understand how informatics and telecommunications can assist during disasters, various tools and elements of informatics and communications that are currently being used by disaster managers and responders are discussed. Some of these tools are used in the preparation and mitigation stage, and some are used during the response phase. Some tools can be used in all phases of the disaster cycle.

Computer Devices One can quickly realize that the computer has revolutionized many aspects of our lives. Some people are so dependent on e-mail for doing their daily work that when the corporate e-mail system goes down, they find it hard to conduct business. The same is true for researchers using the Internet and the vast amount of knowledge on the World Wide Web to do their research—when it is inaccessible, they almost feel withdrawal symptoms. There are many types of computer devices available to a disaster manager or responder—everything from corporate mainframes to wearable personal computers. The Laptop Probably the most commonly used device other than the desktop PC is the laptop. As technology improves, the speed and power of laptops are becoming close to that of a desktop. Because memory and storage are cheap, the average laptop has a larger hard drive than it did just a few years ago. Many of the applications written for the desktop are also used on the laptop, so many laptops have memory equivalent to that of the desktop. New chipsets and microprocessors use lower power and run cooler, allowing for longer running time on INFORMATICS AND TELECOMMUNICATIONS IN DISASTER 131

batteries. Some laptops are even fanless, greatly improving battery life. Laptops are getting thinner, and many of them are bundled with all the accoutrements such as wide theater-like screens, DVD players, CD burners, and high-speed connections for peripheral devices such as fire wire and universal serial bus (USB) connectors. Most new laptops also include wireless access technologies, such as Bluetooth and WiFi. With a docking station and external keyboard, mouse, and monitor, many people are finding that they can use their laptop docked at their desk and then pop it out and take it when they travel. This takes the place of a desktop computer and provides the user all the amenities of the office or home while out in the field. See Box 20-1 for tips on traveling with a laptop. The Tablet PC Similar to a laptop is a specialized portable computer called a tablet PC. Only recently on the market but finding rapid popularity, these devices use primarily a pen input for data entry. Tablet PCs are finding a niche in vertical markets such as healthcare and on the warehouse floor. They can be extremely useful for filling out forms such as a medical record or a field survey at a disaster site that can be plugged into a GIS for mapping. Tablet PCs usually have equivalent performance to that of a laptop, with the added convenience of usually a

BOX 20-1 CHECKLIST FOR TRAVELING WITH A LAPTOP ●

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Update the antivirus and spyware protection software to the latest virus definitions because one cannot be sure that a network used on the road is fully protected. Use a program, such as Norton Ghost, that can make a drive image, which creates an image of the laptop’s hard drive, so that if the hard drive crashes, it can be recovered from the image. Check the batteries and if time permits, cycle them all the way down and back to full charge again. If possible, take an extra battery that is charged to extend your PC time if you are isolated without power. Consider alternative power sources, such as solar panel chargers, disposable battery replacements and power cells, and a 12-volt adapter for converting power from a car battery to use your laptop. Preparations for traveling with a laptop include placing the computer in a hard-shell padded case. It also helps to have an assortment of plugs and adapters and an extra network cable, just in case. Don’t forget a power/recharge cable. Put everything in plastic baggies, even when the equipment is in its case. If you can find a large enough baggie for your laptop, you can protect it from moisture should your case be exposed to the elements and leak. Temperature changes can cause condensation, so if you do pack your equipment in baggies, throw a couple of silica gel desiccator packs into the baggie, too. If you know you will be in an area operating on generator power, take a surge protector to prevent power spikes from damaging your devices. At all costs, avoid having your laptop or computer device go through a baggage check—make sure it can be stowed as a carry-on. Try to keep it away from metal detectors because they might erase magnetic media. Take a cable lock so that you can secure your laptop somewhat. Although it won’t prevent a thief who really wants it, it may deter someone walking by and snatching it while you have your back turned.

132 PRE-EVENT TOPICS

longer battery life, a slightly smaller form, and the penbased input. When selecting a laptop or tablet PC to take to the field, one will be deluged with hundreds of choices. In selecting a device, it is important to consider the conditions under which the device will be used. There are many “hardened” devices, specifically designed to military standards for shock and vibration resistance, water resistance, and dust impingement. These hardened PCs can be twice the price of the regular off-the-shelf laptop. If a hardened PC is affordable, one can rest assured that it will more than likely survive being taken into the field and be able to keep data safe. An alternative, however, is to purchase an off-the-shelf laptop from a local computer/electronics store and an insurance policy for it. Oftentimes, a $50-per-year policy with a deductible of only a few hundred dollars is available. This would easily cover a catastrophic loss of the device (e.g., major drop, crush, or immersion), but it probably would not cover minor damage such as the disk drive door breaking off. When buying a hardened PC, one should ask the vendor specific questions about drop and immersion tests and whether the device meets Mil standards (Box 20-2). If at all possible, test a device in various types of weather, from direct sun to night time. Make sure the screen is readable in direct sunlight, can be dimmed for use during night operations, and is ergonomic when held and does not cause undue strain due to weight or bulkiness. Try the doors, accessory ports, and plugs to make sure that by simply plugging a peripheral into the PC, it is not rendered immobile or unwieldy or that its water resistance or another hardened standard is not rendered ineffective. The Personal Digital Assistant Another handheld device that is usually smaller than the tablet PC is the palm-sized personal digital assistant (PDA). The PDA has become the peripheral brain for many in the healthcare setting. Rather than wear or carry a laboratory coat full of plastic cards with scores and scales, quick guide books, and other reference texts, a healthcare provider can store all of this information in a PDA. The information can be indexed and referenced quickly. PDAs come in two types: the Palm Operating System and the Microsoft Pocket PC Operating System. Most of the major vendors are authoring software for both platforms, but the Palm platform has been around longer and has more shareware and freeware medical titles. A PDA can be an invaluable resource for the disaster responder. Often in the field, the disaster responder does not have the luxury of ducking into the

BOX 20-2 MIL-STD 810 MIL-STD is a series of specifications set by the U.S. Department of Defense. When purchasing a hardened device for field use, look for vendor affirmatiom that their device meets military standards to ensure that it will survive use in a post-disaster field environment.

emergency department library to look up something in the Physicians Desk Reference or another medical text. With a PDA, however, one can “take” those texts to the field (Box 20-3). In many cases, searches can be done with a keyword to rapidly find the needed information. The address book, calendar, contacts, tasks, and notes are probably the more commonly used built-in applications on a PDA. Other uses of the PDA for disaster response include keeping track of contact information for other disaster responders and agencies. There are also a number of programs that allow for rapid form filling and database applications for recording data and creating quick ad-hoc reports. Some PDAs have built-in cameras, allowing one to rapidly document a disaster scene for later use. With accessories such as an external keyboard, one can even type full documents on the PDA and can print the documents with an infrared-capable printer. Although PDAs may seem to be stand-alone devices, they require periodic visits to the laptop or desktop for synchronization. During this synchronization process, vendors provide updates to software over the Internet; calendars, address books, tasks, and notes are synchronized with desktop software; and new software can be installed from the desktop to the PDA. If you are recording data on forms on the PDA, this synchronization may also be required to pass the data from the forms tool on the PDA to an application running on the desktop as a full-featured database. As with the laptop, there are a number of accessories that are useful to have when traveling. An attachable keyboard is helpful to type reports on the PDA for printing later. The PDA should have a hard-shell case, and it is advisable to pack the PDA in a plastic baggie for protection against the elements. With the PDA, hundreds of free medical texts and references available on the Internet can be accessed and would be quite useful if a disaster responder becomes isolated from reference resources. These can be found by searching the Internet for texts and software related to healthcare and disaster and response; some will be free, some will be for sale. A solar battery charger is ideal for a PDA because its batteries do not require much energy to charge. Lastly, make sure that data on the PDA are uploaded to a desktop or laptop computer, and try to store critical files and infor-

BOX 20-3 USEFUL PDA PROGRAMS FOR DISASTER RESPONDERS 1. ●

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Epocrates (www.epocrates.com): Enhanced drug and formulary reference with integrated ID treatment guides and tools. WISER (http://wiser.nlm.nih.gov/): WISER provides a wide range of information on hazardous substances, including substance identification support, physical characteristics, human health information, and containment and suppression advice. Skyscape Books (http://www.skyscape.com): This is a portfolio of medical references for use on handheld devices. PEPID (http://www.pepid.com/): PEPID is a physician, critical care, and nursing reference suite. Sites that have PDA medical software: ● http://www.medspda.com ● http://www.collectivemed.com ● http://www.medicalsoftwareforpdas.com

mation on the removable memory media. In the event that power is unavailable and the PDA loses its charge, all the data may be lost without that backup.2 Like the laptop or tablet PCA, a PDA comes with many choices. For those not familiar with a PDA, it is advisable to borrow one for a day, if possible, to get a feel for the work flow and how it would be used during a typical day. Pay attention to whether the device can fit into your pocket or whether you will have to carry it around in a case that you might put down and forget or not have on hand when you need it. The ideal device is small and unobtrusive; however, the device should have enough computing power, storage, and functionality to meet the user’s needs. One should also consider purchasing a hardened PDA. Although not expensive in comparison with a hardened laptop, a PDA that has been designed to take into the elements will still be twice the price of an off-the-shelf model. The small size and highly portable nature of the PDA may make it a better investment because the user may be more likely to take it into the field than a laptop. Local Area Network/Wide Area Network/Wireless Network As emergency managers are getting more sophisticated in their use of information technology, it is not uncommon to see disaster responders establish a local area network (LAN) where their incident command is set up (e.g., in the Emergency Operations Center or in the disaster field office). This network links a group of computers together and allows instant messaging between computers; the sharing of files and documents between computers; and, better yet, the centralization of file storage to one large networked hard drive that each workstation has rights to access. Thus, a backup can be taken of just that centralized hard drive periodically rather than each individual workstation. In many cases, a wide area network can be established, which is the linking of more than one LAN. For example, the disaster field office may be linked over a public network through a virtual private network (VPN) to the main office or headquarters. This VPN connection provides a secure tunnel through the Internet from point to point so that sites in between cannot access passing traffic. This creates a wide area network that is not limited by geography or distance, just connectivity. Wireless networks are fairly new and take advantage of a network access point, which is a transceiver that communicates with a wireless transceiver card on the workstation or laptop. Essentially, this topography creates a wireless network similar to a wired one, but with the convenience of rapid setup without the need to string network cable all over the site. Wireless networks could even be deployed in a tent city, linking treatment areas in the tents to a command tent. Unfortunately, wireless networks, like voice radio frequencies, can be fairly easily received and decrypted by an eavesdropper, thus making them fairly insecure. Sophisticated encryption methods must be put into place to protect sensitive operational security and patient information that may be transferred across a wireless network. INFORMATICS AND TELECOMMUNICATIONS IN DISASTER 133

Communications Devices Geographical Positioning System The Geographical Positioning System (GPS) began as a military system in 1985 and is based on a 24-satellite configuration of transmitters. By measuring the distance to four satellites from the user location, it is possible to establish three coordinates of the user location (latitude, longitude, and altitude). Although originally developed for the Department of Defense, the not-quite-complete system was offered to the civilian community in 1983 by President Reagan after Korean Airlines flight 007 was shot down when it accidentally strayed into Soviet Union airspace. The satellite configuration was complete in the early 1990s, and the Gulf War prompted the sale of thousands of commercial GPS receivers; at that time the military had not manufactured many GPS receivers. Since then,GPS has found its way into the travel,surveying,mapping, and delivery industries. In addition, many casual users take a GPS when they are recreating in remote areas or to locate their favorite fishing spot. For the disaster responder, a GPS unit can be helpful in giving an exact location of a shelter or the location of a landing zone for helicopter evacuation and can assist in the location and mapping of resources to be used to respond to the disaster. There are a number of accessories that will convert a PC or PDA into a sophisticated GPS mapping unit.3

Cellular Phones A cellular phone is probably the most common tool that people use to communicate. Many disaster response agencies consider the cellular phone to be their primary communications tool and issue them to their disaster responders. Consequently, cellular sites after a disaster may experience a high demand as the civilian population makes calls to friends and family to check on their welfare, as responders arrive and begin to arrange resources, as the media arrive and make arrangements to cover the story, and as people shift to cellular as their primary phone if their land line phone is inoperable because of a power outage or other disruption. It is reasonable to assume that a cellular phone may have difficulty in making a connection during a postdisaster response due to the cellular site being overwhelmed. Normally, cellular providers scale their cellular sites to handle only 20% to 30% of their customer base at a time. This is fine for normal traffic, but when a disaster strikes and customers all need to make a contact in a compressed time frame or when outside people come into the area with their cellular phones, the cellular sites may be congested into uselessness. Fortunately, a few initiatives are in place that might reduce this congestion on the cellular systems, especially for disaster responders. Cellular phone providers can deploy a trailer with a cellular antenna, repeater, and generator power, as well as a cell site on wheels (COW) that can be strategically placed in the disaster area and connected to the public telephone network to increase the availability of cellular connections. Also, a few cellular providers have enabled a capability in their systems in which an emergency worker can receive 134 PRE-EVENT TOPICS

priority on the cellular phone system and get a connection sooner. Unfortunately, there is no legal requirement for them to do so, and as a result of the expense of purchasing additional hardware to make this happen, only a few providers have adopted this technology. Most have not; therefore, this is not a reliable option. After the 2003 summer blackout, only one cellular phone provider in New York City provided priority access.4 Satellite Phone Systems There are a number of satellite phone system providers that use a number of different technologies. IMARSAT is probably the oldest vendor of satellite phone service; it started its service in the early 1990s. The early phone systems consisted of a fold-out, umbrella-like antenna and a briefcase-sized box with a handset. They were portable, although bulky, and the transmission of data over the phone system, if possible, was done at very slow speeds of 300-4800 bits per second (compared with 700-1500 Kbits per second on a broadband cable modem). Satellite phone costs originally were as high as $3 a minute, but most of the current vendors charge about $1 per minute. Phone size also has shrunk to more the size of a laptop. The flip-up lid of the phone, similar to opening the screen of a laptop, acts as the antenna and should be pointed at an angle toward one of the satellites. Because many of these phone systems use a geostationary orbiting satellite constellation, one must be geographically aware and point the antenna in the correct direction and at the correct inclination to get a good signal on the satellite. There are automatic antenna systems on a number of vendors’ satellite phones, which can be mounted to a vehicle so that the phone can maintain a line of sight link to the satellite and be used during travel to the disaster site. Dense leaves or vegetation as well as very dense rain can reduce the signal strength. Some newer phone systems, such as Iridium and Globalstar, have a handset that is not much bigger than a cordless phone for home use. These systems use a constellation of low earth-orbiting satellites and incorporate the group special mobile (GSM) protocol for cellular phone technology, allowing the handset to connect to terrestrial GSM cellular networks while in signal range to a cellular site and then automatically switch to an orbiting satellite when out of the terrestrial GSM range. Unfortunately, satellite phone systems are very expensive to bring into service and maintain. A number of vendors have been close to bankruptcy and been saved by investors.5 Mobile Communications Vehicles Many response agencies have built and deployed vehicles that are outfitted with communications and computer equipment that is capable of performing a variety of functions. These vehicles usually are equipped with their own generators for power and contain a number of different radio systems that can be programmed to communicate on many different radiofrequencies. A radio operator in the vehicle can pass information between disparate radio systems and agencies and may be able to help with some of the lack of interoperability issues. These vehicles also

have the ability to patch into a telephone network and the Internet. Depending on their sophistication, they may have satellite phone systems, high frequency radio, and facsimile capability computers with scanners and printers. Specially trained teams of radio operators, both amateur and public safety dispatchers, and information technology personnel usually staff one of these vehicles. Oftentimes, the incident command staff makes use of these vehicles as part of their command post, or the vehicle can support a disaster response team or disaster field office until more permanent communications can be set up. In events such as mass gatherings or disasters of limited duration,a communication vehicle such as this can be used to provide rapidly deployed communications support in a small footprint and then be completely disassembled at the end of the event.

TABLE 20-1 TYPICAL RADIOFREQUENCIES USED IN DISASTER RESPONSE BAND

FREQUENCY

DESCRIPTION

HF

3-30 MHz

High frequency

VHF

30-300 MHz

UHF

300-3000 MHz

SHF

3-30 GHz

Radio Systems Whole books have been written on radio communications, even specifically on disaster communications. Professional communications specialists and many amateur radio operators have spent hundreds of hours training themselves on these systems,so this chapter only gives a mile-high view of the communications systems and frequencies that may be used during a disaster response. It is a good idea for the disaster responder to be aware of what systems are in use, when they should and should not be used, and how to best take advantage of these tools. Radiofrequency (RF) is the part of the electromagnetic spectrum in which electromagnetic waves can be generated and fed through an antenna. There are a number of different modes of the RF spectrum that are most often used for voice and data transmission during a disaster response (Table 20-1). High frequency (HF) is the frequency range from 3-30 MHz and is classically termed “shortwave.” HF radio waves are often reflected off the ionosphere, thus frequencies in this range are often used for medium- to long-range terrestrial communications. Sunspot and other solar activity, polar aurora, sunlight/ darkness at the transmitting and receiving station, and even the choice of frequency within the spectrum can diminish the relative difference between the signal strength over the background noise (signal-to-noise ratio) and make communication on HF radio unusable at times. In other words, if interference increases the static (noise), a transmitter must be more and more powerful to have the transmitted signal hearable above that noise. HF radio is used in some widely dispersed populations for domestic broadcasting. HF radio is often used for HF networks of radio operators who can, in short term, pass information from one radio station to another, essentially allowing, by a number of “hops,” worldwide communications. Amateur radio operators oftentimes provide the first information to the outside world when a disaster site is cut off after a hurricane or a major geological event. For more local communications, very high frequency (VHF) may be used and ranges from 30-300 MHz. FM radio (88-108 MHz) and various television signals are included in this range. VHF is not usually reflected off the ionosphere so it is limited to local communications. VHF is not as affected as lower frequencies by atmos-

USES/LIMITATIONS

Good for long distance because the radio waves bounce off the ionosphere back to earth. Subject to environmental noise and interference. Very high Line of sight, less affected frequency by environmental noise. More easily blocked than HF by land features. Ultra high Line of sight, better frequency penetration of land and manmade features. Smaller wave size allows for smaller antennas. Super high Passes more easily frequency through the (microwaves) atmosphere and terrestrial features than VHF and UHF. More radio spectrum available in this band.

pheric noise and interference from electromagnetic sources; it does, however, penetrate buildings and other substantial objects more than higher frequencies. Ultra high frequency (UHF) includes frequencies from 300 MHz to 3 GHz. UHF also includes some frequencies dedicated for television signals (in the United States, above channel 13). UHF frequencies penetrate some densely built buildings a little better than VHF frequencies do. UHF wavelengths are very small, allowing for more compact antennas, which some people feel are more convenient and more attractive than the longer VHF antennas. In more sophisticated communications systems, there may occasionally be a super high frequency (SHF) signal, which includes microwaves transmitted from one antenna in line of sight to another. These SHF microwave signals can carry voice and data. Satellite radio bands are contained within this range of frequencies. With a two-way radio, there are two types of uses of the frequencies. Simplex use of a frequency means that the same frequency is being used to transmit and receive; while one person is talking, nobody else can talk. Duplex use of the frequencies allows duplex conversations, like on a telephone. Additionally, duplex frequency use can allow for a repeater to be placed centrally in the disaster area. The repeater receives on one frequency and rebroadcasts out at higher power on the other frequency. The repeater is usually put in a high location or has a high antenna. Repeater antennas have a high gain, meaning they can pull in weak signals and strong transmitters that can transmit signals farther. A repeater allows the transmission of handheld radios to be extended from just a few miles to tens of miles. Frequencies that do not penetrate buildings well, such as UHFs, have better transmission.6 INFORMATICS AND TELECOMMUNICATIONS IN DISASTER 135

Specialized Informatics Systems and Decision Support Tools In recent years, the need for specialized information systems composed of databases, surveillance tools, personnel and patient tracking, and evidence-based medicine to support disaster response and management have been recognized. Health departments, which in many cases did not operate 24-hours a day, seven days a week and in some situations did not even have fax capability 10 years ago, now are developing and putting into place sophisticated systems to monitor for bioterrorism, emerging diseases, and ecological impact on a population. The television cable network CNN is often at the disaster scene rapidly passing on information. This was the case Sept.11,2001,when millions of people witnessed the second plane hitting the World Trade Center as broadcasters were on the air covering the event in minutes. Field personnel can send hundreds of e-mails a day from the disaster site back to their agency. Resources come into play faster as response plans gear up and agencies and their personnel begin reporting back their status. There are many ways to communicate, and the amount of information available to decision makers has increased and is dispersed more rapidly. Information can come into the local response center and at agency headquarters oftentimes directly from the source. Each piece of information must be interpreted and requires a familiarity with the source. Assessments, requirements, and needs from the field may come in from many different sources, each with possibly contradictory information. Oftentimes, this can only be correctly interpreted by the local incident commander. In a wide-area disaster, this may be very difficult to consolidate and evaluate at a higher level. The analysis of the information coming in from field responders is as important as the information flow itself. Consolidation in a meaningful manner and then appropriate communication to the headquarters should be done by someone knowledgeable enough at the local level to pass only that consolidated information gathered by their support personnel. Many examples exist of these types of decision support systems. The CDC makes its decisions based on information consolidated from state health departments. State health departments make their reports to the CDC based on information passed on by local health departments, who, in turn, received their information from the emergency department physician who, for example, may have noticed six patients with the same abnormal symptoms in the last hour. If that emergency physician were to call the CDC directly, the information would be documented but may not account for much until the physician had passed the information through the correct channel for consolidation and communication to a higher level.7

Humanitarian Information Systems Humanitarian information systems (HIS) are specialized systems linking many sources of information and consolidating and reporting them. HIS consists of an early warning and reporting system, which includes the monitoring of specific trends of values, such as rainfall 136 PRE-EVENT TOPICS

amounts, vegetation mapping, crop production, and market prices, and measures of human factors, such as nutritional status, unemployment, and poverty level. In a smaller-scale disaster, this could include a severity score tabulated from a door-by-door outreach effort to rate the occupants of a dwelling on a number of health, psychosocial, and life safety scores and then map those using a GPS location and a GIS to plot the overall postdisaster health and safety of the community. Thus, a needs assessment is conducted to estimate the needs of the affected population. An HIS should track the resources on hand and the delivery of those resources and then gauge whether the resources are meeting their goals and being delivered to the victims in an efficient manner.8

Surveillance and Bioterrorism Detection Systems Whereas an HIS is a mix of various pieces of software integrated into a single system,bioterrorism detection systems are being developed with federal funds and by private corporations that include continuous surveillance of hospital data from a number of sources. This allows for normalizing and analysis of that data for statistically significant patterns and less specific indicators and rapidly alerting health officials of a developing trend. In the recent past, public health surveillance did not occur in real time, but that has changed and data must begin to be collected often before cases are confirmed and cultures are reported positive. Often there is a narrow window of opportunity after an exposure in which treatment is most effective, such as for anthrax, and rapid identification of similar symptoms from multiple sources can be facilitated if a surveillance system is in place, where real-time reporting can take place. As technology improves, environmental biosensors can be linked to the system to provide even earlier detection before widespread infection and symptoms occur. As most hospital information systems register every patient, de-identification can be done on patient data and the reason for visits can be easily transferred to a local database and even to a national database such as the National Electronic Disease Surveillance System advocated by the CDC. It is more likely that the initial detection of a covert biological or chemical attack will occur at a local level. More and more local and state health agencies are developing ways to detect unusual patterns of disease and injury. Early response to such patterns is essential for ensuring a prompt response to a biological or chemical attack. Unfortunately,many of these projects are at a regional or state level. Local and even some state health agencies budgets are still meager, and the cost of research and development of these systems is still out of reach for many smaller municipalities. If a system is developed, it usually lacks integration with other information systems and often relies on a person to do the daily initial data load or complex schemes of transmitting the data between systems. The Department of Defense system, ESSENCE, which downloads outpatient data from almost 300 Army, Navy, Air Force, and Coast Guard installations around the world each day currently receives the data in one to three days of patient visits, longer than ideal for an optimal reaction to a potential outbreak. Systems that rely

on a person interpreting patient visits for key indicators and inputting them into a central database are prone to variations and interpretation of how the data should be tabulated and entered, creating room for error and inconsistency. Furthermore, it has been demonstrated that early detection of just hours can make an enormous difference in a covert attack. Unfortunately, prototype automated surveillance systems have never been able to prove that they can detect a pathogen that quickly and may render a false sense of security. There are very few vendors of bioterrorism surveillance software. Currently the most promising endeavors are those funded by grants from the Department of Defense, CDC, and other federal agencies.3

SUMMARY Disaster informatics and telecommunications have become indispensable tools for disaster managers and responders. As pervasive as these tools are in our daily lives, they are finding their way more and more into the field. E-mail, instant messaging, LANs and intranets, cellular phones, two-way radios, teleconferencing, and many other sophisticated tools are becoming common in handheld devices and in the pockets of disaster responders. Information is a commodity, and the ability to analyze and distribute it to aid in the reduction of human suffering is probably the best money spent. Device selection will probably be the disaster responder’s most difficult task because there are thousands of brands on the market for desktops, laptops, tablet PCs, and PDAs. Vendors may be of help in selecting a product that meets the user’s needs, but many vendors are not familiar with the disaster responder’s role and may not understand what “punishment” the device may endure. Generally, vendors who sell hardware that is being used in the public safety and field service fields will have a better idea of the harsh environments in which the equipment will have to operate. These vendors are a good first choice to talk with about the different devices. Protecting the device and data is the next important task for the technologically armed disaster responder. Making sure that the device is stored in a padded, hard shell case for shipping and travel and ensuring that there are redundant backups of the data at multiple points in the preparation, deployment, and demobilization phases are important. This includes taking backup copies of software on a CD in the event that the hardware is damaged in the field. GPS receivers, cellular phones, radio systems, and the Internet are all tools that a disaster responder may use during a response to help establish and maintain communications with the home agency and other responders. These tools will be a lifeline for ongoing support and the reporting of events. Again, the user will be faced with trying to determine the best radiofrequencies to use for any given circumstance. The disaster responder will need to locate the best vendor for cellular service near the disaster area—one that’s large enough or has a large enough customer base that it is in the vendor’s best financial interest to supplement local or damaged cellu-

lar stations to ensure better usability of the system after the event. Having multiple options for Internet access, such as dial-up, wireless, and fixed LAN ability, will ensure the user flexibility in plugging into whatever is available after a disaster. As the disaster responder becomes more reliant on electronic equipment for postdisaster duties, he or she will need to consider alternative power sources and methods of recharging batteries, such as solar chargers, hand generators, and disposable power packs. He or she will need to consider taking any number of wall chargers, cords, dongles, adapters, and plugs to the disaster site. The electronic and communications demands for rapid information and assessment in the response and recovery efforts of a disaster mission will prompt the disaster responder to become more computer savvy, more electronically aware, and more technically knowledgeable, and as a result, the disaster responder will be more productive. Reports and assessments must be rapidly tabulated and disseminated through the chain of command. Assessment efforts may rely on computerized surveillance techniques, information gathering and database development for resource tracking, and statistical analysis—all with the ability to rapidly communicate this information to various players and agencies at the disaster site in an organized and succinct manner. As pervasive as each of these technologies is getting in our daily lives, it is obvious that they are becoming equally so in our role in disaster response.

REFERENCES 1. Gantz J. 40 years of IT—An Executive White Paper from IDC. International Data Corp; 2004. Availlable at: http://edn.idc.com/ prodserv/downloads/40_years_of_IT.pdf. 2. Bucklen KR. Earthquake in Iran: using the pocket PC for disaster medical relief. Pocket PC. June/July 2004;69-72. 3. Zubieta JC, Skinner R, Dean AG. Initiating informatics and GIS support for a field investigation of bioterrorism: the New Jersey anthrax experience. Int J Health Geogr. November 2003;2(1):8. 4. Schumer C. Schumer reveals:When cell phones failed during blackout, only one NY cell phone company had emergency plan in place [press release]. Available at: http://schumer.senate.gov/Schumer Website/ pressroom/press_releases/PR01953.html. 5. Requirements on Telecommunications for Disaster Relief from the International Federation of the Red Cross and Red Crescent Societies. Presented at: ITU-T Workshop on Telecommunications for Disaster Relief; 2003; Geneva. 6. Coile RC. The role of amateur radio in providing electronic communications for disaster management. Disaster Prev Manage. 1997;6(3):176-85. 7. Henry W, Fisher I. The role of information technologies in emergency mitigation, planning, response and recovery. Disaster Prev Manage. 1998;7(1):28-37. 8. Maxwell D, Watkins B. Humanitarian information systems and emergencies in the Greater Horn of Africa: logical components and logical linkages. Disasters. March 2003;27(1):72-90. 9. Farrel B. The National Communications System. Available at: http://www.naseo.org/committees/energysecurity/energy assurance/farrell.pdf. 10. Fazio S. The need for bandwith management and QoS control when using public or shared networks for disaster relief work. Presented at: ITU-T Workshop on Telecommunications for Disaster Relief; 2003; Geneva. 11. Garshneck V. Telemedicine Applied to Disaster Medicine and Humanitarian Response: History and Future. Presented at: 32nd Hawaii International Conference on System Science; 1999; Hawaii. INFORMATICS AND TELECOMMUNICATIONS IN DISASTER 137

Available at: http://esd12.computer.org/comp/proceedings/hicss/ 1999/0001/04/00014029.PDF. 12. Teich JM,Wagner MM, Mackenzie CF, Schafer KO. The informatics response in disaster, terrorism and war. J Am Med Inform Assoc. March-April 2002;9(2):97-104. 13. Brennan PF, Yasnoff WA. Medical informatics and preparedness. J Am Med Inform Assoc. March-April 2002;9(2):202-3. 14. Sessa AB. Humanitarian Telecommunications. Presented at: ITU-T Workshop on Telecommunications for Disaster Relief; 2003; Geneva.

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15. Garshnek V, Burkle FM Jr. Applications of telemedicine and telecommunications to disaster medicine: historical and future perspectives. J Am Med Inform Assoc. January-February 1999;6(1):26-37. 16. Zimmerman H. Communications for Decision-making in Disaster Management. Presented at: ITU-T Workshop on Telecommunications for Disaster Relief; 2003; Geneva.

c h a p t e r

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Disaster Mitigation Robert M. Gougelet

The definition of mitigation includes a wide variety of measures taken before an event occurs that will prevent illness, injury, and death and limit the loss of property. Mitigation planning commonly includes the following areas: • The ability to maintain function • Building design • Locating buildings outside of hazard zones (e.g., flood plains) • Essential building utilities • Protection of building contents • Insurance • Public education • Surveillance • Warning • Evacuation It is of critical importance that emergency planners incorporate the basic elements of mitigation and have the authority and resources to incorporate these changes into their organization/facility/community. Emergency planners should have a basic idea of the concepts of mitigation through their use in natural disasters over the years. The recent federally mandated transition to the all-hazards approach in disaster emergency response has also given a new perspective on mitigation. Although it is not necessary to redefine mitigation, it is essential to understand how the scope and complexity of mitigation and risk reduction strategies have evolved as the United States adapts to new threats. For example, what measures can be taken in advance to protect the population and infrastructure from an earthquake, flood, ice storm, or terrorist attack? As with each mass casualty event, the answers to this question are location-specific and heavily dependent on the circumstances surrounding the event. However, a common understanding of the goals and concepts of mitigation along with knowledge of its policy history and current practices will help a community develop mitigation plans that are both locally effective and economically sustainable. This chapter illustrates how mitigation strategies have evolved, outlines key historical elements of U.S. mitigation policy, highlights critical current mitigation practices, and describes common pitfalls that can hamper mitigation efforts. The realm of mitigation planning is

far reaching and complex, and, therefore, the emphasis of this chapter is on the continuity of medical care during a mass casualty event within a community.

GOALS AND CONCEPTS OF MITIGATION In the simplest of terms, mitigation means to lessen the possibility that a mass casualty event can cause harm to people or property. However, this simple definition covers a broad range of possible activities. For example, an effort to ensure that essential utilities, such as electricity and phone service, continue to be available throughout a natural disaster is very different from efforts to minimize the economic damage of postdisaster recovery from a major flood or attempts to educate the public on how to reduce their risk of exposure during a dirtybomb incident. Mitigation strategies can range from focusing exclusively on “hardening” to focusing more on resiliency. Hardening of targets is best described as measures that are taken to physically protect a facility, such as bolting down equipment, securing power and communications lines, installing backup generators, placing blast walls, or physically locking down and securing a facility. Mitigation through hardening has only limited use in systems or facilities such as hospitals where open access to the surrounding community is the hallmark of their operations. In these circumstances, a resilient system capable of flexing to accommodate damage and the ability to maintain or even expand current operations will make that system ultimately more secure. Mitigation through resiliency also has limitations. In many cases, hardening structures is most appropriate, particularly when many citizens may be quickly affected without prior notice or warning. This may include hardening structures in earthquake zones, physically protecting and monitoring the food chain and drinking water systems, and physically securing and protecting nuclear power plants. In these cases, resiliency may come too late to prevent illness and death in large numbers of patients, and planners should target hardening to whatever degree is practically and financially feasible. The threats of nuclear, radiological, chemical, and biological attacks present new challenges for emergency planners. The potentially covert nature of 139

the attack, the wide variety of possible agents (including contagious agents), and soft civilian targets make planning efforts exponentially more difficult than in the past. This complexity has also eroded the distinction between mitigation and response activities. Although it is never possible to mitigate or to plan responses for all contingencies, we do know, however, that there is a basic common response framework. This framework includes coordination, communication to enable inter-agency information sharing,1 and flexibility to rapidly adapt emergency plans to different sitvations.

RECENT HISTORICAL PERSPECTIVE Traditionally, mitigation in the United States has focused on natural disasters; however, early mitigation planning against manmade disasters included civilian fallout shelters and the evacuation of target cities if a nuclear attack was eminent. The Federal Emergency Management Agency (FEMA) states2: Mitigation is the cornerstone of emergency management. It’s the ongoing effort to lessen the impact disasters have on people’s lives and property through damage prevention and flood insurance. Through measures such as; zoning restrictions to prevent building in hazard zones (e.g. Flood plains, earthquake fault lines), engineering buildings and infrastructures to withstand earthquakes: and creating and enforcing effective building codes to protect property from floods, hurricanes and other natural hazards, the impact on lives and communities is lessened.

Mitigation begins with local communities assessing their risks from recurring problems and making a plan for creating solutions to these problems and reducing the vulnerability of their citizens and property to risk.3 However, since the mid-1990s, mitigation planning has become increasingly more complex. Terrorist attacks, industrial accidents, and new or reemerging infectious diseases are just a few of the threats that have started to consume more planning time and resources. The growing scope of threats that must be addressed in mitigation strategies challenges all aspects of planning and response at all levels of government.4–6 The importance of sharing intelligence information at the earliest possible stage of a terrorist attack, especially a bioterrorism event, is now recognized in national policy as a critical mitigation asset. Theoretically, if there were the slightest indication of a contagious biological attack occurring within the United States, then early recognition triggered by intelligence alerts followed by appropriate local responses could allow for isolation, treatment, and containment of a potentially widespread event. This intelligence sharing must become a large part of mitigation efforts aimed at limiting the effectiveness of manmade disasters. A similar analogy can be made with the early warning given to the medical community when a surveillance system picks up an unusual cluster of illnesses, long before the initial diagnosis may be made at a physician’s office or healthcare facility. The new National Incident Management System (NIMS) states that intelligence must be shared within the incident management structure and states that a sixth functional area, or 140 PRE-EVENT TOPICS

Incident Command System Section, covering intelligence functions may be established during the time of an emergency. The elevated status of intelligence within NIMS establishes the importance of early and effective intelligence sharing. The challenge is to establish these sharing relationships before the disaster by incorporating them into an ongoing hazard monitoring process and by integrating them into drills, exercises, and day-to-day activities to ensure that this critical resource is operational when needed to mitigate the consequences of a disaster.7 The Disaster Mitigation Act of 2000 (DMA-2000) elevated the importance of mitigation planning within communities by authorizing the funding of certain mitigation programs and by involving the Office of the President. Under DMA-2000, the president may authorize funds to communities or states that have identified natural disasters within their borders and have demonstrated public-private natural disaster mitigation partnerships. DMA-2000 provides economic incentives through promoting awareness and education to prioritize the following objectives for federal assistance to states, local communities, and Indian tribes: • Forming effective community-based partnerships for hazard mitigation purposes • Implementing effective hazard mitigation measures that reduce the potential damage from natural disasters • Ensuring continued functionality of critical services • Leveraging additional nonfederal resources in meeting natural disaster resistance goals • Making commitments to long-term hazard mitigation efforts to be applied to new and existing structures This important legislation sought to identify and assess the risks to states and local governments (including Indian tribes) from natural disasters. The funding would be used to implement adequate measures to reduce losses from natural disasters and to ensure that the critical services and facilities of communities would continue to function after a natural disaster.8 Further evidence of the expanding complexity of mitigation efforts can be found in the Terrorism Insurance Risk Act of 2002. This act fills a gap within the insurance industry, which typically does not provide insurance coverage for large-scale terrorist events. The federal government, in the wake of the Sept. 11, 2001, attacks, promptly passed this act, addressing concerns about the potential widespread impact on the economy. The act provides a transparent shared public-private program that compensates insured losses as a result of acts of terrorism. The purpose is to “protect consumers by addressing market disruptions and ensure the continued widespread availability and affordability of property and casualty insurance for terrorism risk; and to allow for a transitional period for the private markets to stabilize, resume pricing of such insurance, and build capacity to absorb any future losses, while preserving State insurance regulation and consumer protections.”9,10 Effective mitigation planning now is expected to include many different aspects of private industry. Private industry is a critical partner; its involvement may range from being a potential risk to the community, such as a chemical plant, to providing assistance in responding to an event. This is especially

true in the area of healthcare; most healthcare in the United States is provided by the private sector. It is important to note that the National Fire Protection Association (NFPA) recently released NFPA 1600,Standard on Disaster/Emergency Management and Business Continuity Programs, 2004 edition. This standard establishes a common set of criteria for disaster management, emergency management, and business continuity. Planners may use these criteria to assess or develop programs or to respond to and recover from a disaster.11 Although mitigation planning has become an essential feature of nearly every industry and institution in the wake of Sept. 11, 2001, healthcare settings are disproportionately affected by new challenges and complexities in mitigation. The severe acute respiratory syndrome (SARS) outbreak shook the foundation of mitigation and prevention in healthcare when healthcare workers and first responders in China and Canada died in 2003 after caring for patients with the SARS virus. Access to several Toronto area hospitals was significantly limited for several months because of illness, quarantined staff, and concerns about contamination. The economic costs to the city of Toronto were in the billions of dollars. Hospitals and their communities were thrown into a complex mitigation and prevention crisis. The Association of State and Health Officials (ASTHO) has come out with specific guidelines and checklists to help prepare states and communities prepare for a possible outbreak.12 Pan-influenza planning closely parallels SARS planning, with considerable effort toward preventive vaccination of the population and emphasis on protecting healthcare workers.13 Effective strategies were learned during the Toronto SARS outbreak, although it was definitely a “learn-as-you-go-along” situation. The most effective mitigation strategies to prepare for the consequences of an outbreak would be to plan for the home quarantine of patients, establish public information strategies to reduce public concern, to close affected facilities until the knowledge base permitted their safe reopening, plan for a coordinated information and command and control center, and have preestablished protocols and procedures in place to protect the health of healthcare workers and first responders.14 Vaccination is an essential component of hospital and community mitigation planning. During the fall of 2002, the U.S. government requested that all states prepare for a smallpox attack. The preparations called for each state to present a plan within 10 days to vaccinate all persons within the state, starting with healthcare workers.15 Each facility and community needs to look at the risk of a disease, the effect of vaccination on healthcare workers, and the ability to maintain continuity of care. If properly informed, healthcare workers could respond and treat patients without risk to themselves or their families. The availability of a vaccination and the ability to mass vaccinate the majority of the population should be considered in all community response plans. The plans for both SARS and paninfluenza now need to address the availability and possible stockpiling of antiviral agents as well as procedures for mass vaccination of the population, if a vaccine were to become available.

We have learned much from the many earthquakes, tornadoes, hurricanes, fires, and floods that the United States has experienced, but it is extremely difficult to plan for terrorist and natural events that can quickly overwhelm communities, states, or even the whole nation. These historical events, policy developments, and shifts in public attention have created a very complex planning and operating environment. The next section of this chapter addresses some of the key current practices that mitigation strategists should consider.

CURRENT PRACTICE Current mitigation strategies are as varied as the circumstances in which they are formed. This section illustrates the impact of mitigation through a comparison of responses to two earthquakes that were broadly separated in geography and community preparedness. These examples are followed by a discussion of critical elements of mitigation and risk reduction practice in three broad categories: coordination with other organizations and jurisdictions, hospital concerns, and mitigation strategies based in community health promotion and surveillance. The first step for protecting communities and their critical facilities against earthquakes is a comprehensive risk assessment based on current seismic hazard mapping. This determination of location should also include the assessment of underlying soil conditions, the potential for landslide, and other potential hazards.15 Communities located on seismic fault lines must also develop and enforce strict building codes. After the Bam, Iran, earthquake, a large section of the city, at first glance, looked like a burned forest with only the bare trees left standing. It soon became clear that these were steel vertical beams standing upright in mounds of concrete rubble. In comparison, after the Northridge, Calif., earthquake many of the buildings were structurally compromised but did not collapse on their occupants. Undoubtedly, this was the result of the strict building codes and enforcement throughout the state of California. To the victims of the Bam earthquake, the most important lifesaving measures may have been the development and enforcement of strict building codes.16 Building codes are minimum standards that protect people from injury and loss of life from structural collapse. They do not ensure that normal community functioning might continue after a significant event.17 Structural protection of facilities requires the active role of qualified and experienced structural engineers during planning, construction, remodeling, and retrofitting. The immediate response of a structural engineer after a disaster is to assess building damage and to assist in determining the need for evacuation and the measures needed to ensure continuity of function. Extensive analysis of seismic data taken during an earthquake that are compared with subsequent building damage has given structural engineers valuable information on structural failures of buildings. This information allows communities to rebuild with better and stronger facilities.18 DISASTER MITIGATION 141

The following measures to protect the structural integrity of a facility should be in place before an incident19: • A contract with a structural engineering firm to participate in planning, construction, retrofitting, and remodeling • A contractual agreement guaranteeing the response, after an event, of a structural engineer (with appropriate redundancy) to ensure structural stability, to assess the need for evacuation, and to take additional measures to ensure the continuity of essential functions • Inventory and classify all buildings • Conduct a vulnerability assessment • Ensure code compliance • Determine public safety risks • Determine structural reinforcement needs, and prioritize them • Prepare lists of vulnerable structures for use in evacuation and damage assessment Extensive resources and technical assistance for structural earthquake protection are available on the Internet. FEMA’s Web site itemizes these resources into three major categories: earthquake engineering research centers and National Earthquake Hazards Reduction Program-funded centers, earthquake engineering and architectural organizations, and codes and standards organizations.20 FEMA has released the Risk Management Series publications, which provide very specific guidance to architects and engineers about protecting buildings against terrorist attacks.21 The Institute for Business and Home Safety is also an excellent source of incident-specific information for both businesses and homes.22 The protection of facilities from earthquake damage also involves protecting the facility’s nonstructural elements. These nonstructural elements do not comprise the fundamental structure of the building (Box 21-1). Primary damage to nonstructural elements may be the result of overturning, swaying, sliding, falling, deforming, and internal vibration of sensitive instruments. Relatively simple measures, which do not require a structural engineer, may be taken to prevent damage to or from nonstructural elements. These measures may include fastening loose items and structures, anchoring top-heavy

BOX 21-1 NONSTRUCTURAL ELEMENTS Cabinets Compressed gas tanks Fuel tanks Generators Equipment and supplies Signs and pictures Electrical lines Communication and information technology lines Bookshelves Windows Electrical fixtures Storage containers Hazardous materials Lockers Building parapets and facings Computer hard drives 142 PRE-EVENT TOPICS

items, tethering large equipment, or using spring mounts. Other elements, such as stabilizing a generator from vibration damage by placing it on spring mounts or from sliding damage by having slack in attached fuel and power lines, may require the assistance of an engineer. Hospitals and other medical care facilities are especially vulnerable to damage from nonstructural elements. Consider the placement of routine medical care items such as intravenous poles, monitors/defibrillators, and pharmaceutical agents and medical supplies on shelves. Loss of emergency power to key services, such as computed tomography scanners, laboratory equipment, and dialysis units, may also significantly affect the continuity of medical care (E. Aur der Heide, personal communication, February 2005).23 Loss of generator power may be due to failure of crossover switches, loss of cooling, or loss of connection of power and fuels lines. A process for the continual review of the power needs of new and critical equipment should be a part of a hospital’s emergency planning process. Cooperating with the federal government and understanding the resources, structure, and timeframe in which the federal resources are available are critical to appropriate mitigation planning.24 NIMS and the National Response Plan are described elsewhere in this book. Each document describes in detail the organizational structure and response authority of the federal government in the time of a disaster.25,26 Healthcare organizations, communities, and states are mandated to ensure that their strategies for mitigation, response, and recovery are developed in coordination with these national models. Presidential Decision Directive Homeland Security Presidential Directive (HSPD) #5 mandates that by fiscal year 2005,“the Secretary shall develop standards and guidelines for determining whether a State or Local entity has adopted the NIMS,”27 and all mitigation and risk reductions strategies should be designed accordingly. In addition to efforts to coordinate with federal plans, mitigation strategists must also build functional partnerships within communities and across jurisdictional lines. This point has been emphasized in several recently published planning guides.17,28–30 These guides help hospitals and their communities plan for mass casualty events by incorporating key features of planning, risk assessment, exercises, communications, and command and control issues into functional and operational programs. Hospitals also present special challenges. Presidential Decision Directive HSPD #8 specifies that hospitals qualify as first responders.31 As such, they have important mitigation activities to consider. What does mitigation mean for a hospital? In the current threat environment, it means minimizing the impact of an event on the institution and ensuring continuity of care. Accessibility to the public 24-hours a day, seven days a week has been a hallmark of hospital emergency care. However, one of the most important mitigation strategies a hospital can adopt is the ability to limit and control access to patients and families during the time of a mass casualty or a hazardous materials event. Additionally, facilities must have plans and the ability to decontaminate patients, protect essential staff and their families, handle a surge of patients with complimentary plans for

the forward movement of patients to surrounding areas, set up alternative treatment facilities within the community, to train staff in early recognition and treatment of illness or injury related to weapons of mass destruction, and ensure continuity of care and financial stability during and after an event. Although hospitals will always form the cornerstone for medical treatment of patients during mass casualty events, best practices for hospitals must now also incorporate healthcare resources within the community.32 Hospitals will have to work with other first responders within the community to conduct drills and exercises that realistically test the whole hospital’s ability to respond to a mass casualty event.33 Hospitals also will have to ensure that staff members have the proper training to complete hazard vulnerability assessments34 and to set up and staff outpatient treatment facilities to ensure continuity of care.35,36 Even with very careful planning, most communities will be overwhelmed for the first minutes to hours or possibly days after a massive event, until an effective and prolonged response can occur. Communities must also look at the continuity of medical care as a communitywide issue and not just emphasize the hospital or emergency medical services aspects of medical care. The loss of community-based clinics, private medical offices, nursing homes, dialysis units, pharmacies, and visiting nurse services can significantly increase the number of patients seeking care at hospitals during a mass casualty event. Risk communication and education, specifically aimed at protecting the affected population, can help prevent surges of medical patients.1 Hospitals now have enormous community responsibilities in terms of preparing for and mitigating mass casualty events. Hospitals in hurricane, flood, earthquake, and tornado zones have prepared for many years against these threats. However, a pattern of repeated systems failures within hospitals continues and includes communications and power loss, with additional physical damage to the facility.37 To prevent such failures, hospitals need to recognize that mitigation and risk reduction planning must approach the level of detail and logistical support that parallels military planning. Surveillance is another key mitigation strategy for health emergencies. Early recognition of sentinel cases in biological events can significantly affect the outcome, particularly in contagious events. States are funded and required to participate in the surveillance programs mandated in CDC and Health Resources and Services Administration guidelines.38,39 The earlier an event is recognized, especially if it involves a contagious disease, the earlier treatment can begin and preventive measures can be taken to prevent the spread of illness to healthcare workers and responders, as well as the rest of the community. Public health departments are critical to establishing relationships between local providers and their communities. Local, state, and federal public health agencies must ensure that effective surveillance at the community level occurs. These agencies can also assist in awareness-level and personal protection training for hospital staff, emergency medical service employees, and law enforcement first responders.

PITFALLS Motivating healthcare facilities to take part in mitigation is one of the largest challenges in disaster medicine. It is always best to take measures beforehand to minimize property damage and prevent injury and death. In the case of hospitals, some preliminary research indicates that four factors affect an institution’s motivation to mitigate: influence of legislation and regulation, economic considerations, the role of “champions” within the institution, and the impact of disasters and imminent threats on agenda-setting and policy making. It was discovered during this research that “mitigation measures were found to be most common when proactive mitigation measures were mandated by regulatory agencies and legislation.”40 Tax incentives, government assistance grants, and building code and insurance requirements may also serve to motivate administrators and decision makers to put the necessary time and effort into mitigation planning.17

CONCLUSION Extensive mitigation activities are a necessary prerequisite for the response and recovery activities that must follow a large-scale mass casualty event. We have never seen the number of casualties in the United States we are preparing for today. We do have the threat of an enemy who will strike within the United States with the purpose of inflicting mass numbers of casualties on the civilian population. We must maintain the perspective that even the smallest chance of such an incredibly devastating event, whether manmade or natural, warrants our full attention. If there is no other motivating factor, the possibly such an event must suffice.

REFERENCES 1. Aur der Heide E. Principles of hospital disaster planning. In Hogan DE, Burstein JL, eds. Disaster Medicine. Philadelphia: Lippincott,Williams & Wilkins; 2002. 2. Federal Emergency Management Agency. Mitigation Division. Available at: http://www.fema.gov/fima/. 3. State of Vermont Emergency Management Agency. Mitigation. Available at: http://www.dps.state.vt.us/vem/mitigation.htm. 4. Centers for Disease Control and Prevention. Smallpox Response Plan and Guidelines (Version 3.0). Available at: http://www.bt. cdc.gov/agent/smallpox/response-plan/index.asp. 5. Centers for Disease Control and Prevention.Severe acute respiratory syndrome (SARS). Available at: http://www.cdc.gov/ncidod/sars/. 6. Centers for Disease Control and Prevention. Biological and chemical terrorism: strategic plan for preparedness and response. Recommendations of the CDC Strategic Planning Workgroup. Morb Mortal Wkly Rep. April 2000;49:RR-4. 7. Federal Emergency Management Agency. NIMS compliance. Available at: http://www.fema.gov/nims/nims_compliance.shtm# nimsdocument. 8. Federal Emergency Management Agency. The Disaster Mitigation Act of 2000. Available at: http://www.fema.gov/fima/dma2k.shtm. 9. U.S. Department of the Treasury. H.R. 3210. Terrorism Risk Insurance Act of 2002. Available at: http://www.treasury.gov/ offices/domestic-finance/financial-institution/terrorism-insurance/ pdf/hr3210.pdf. 10. Manns J. Insuring against terror? Yale Law Journal. June 2003;112(8):2509-51. DISASTER MITIGATION 143

11. National Fire Protection Association. NFPA Standard on Disaster/ Emergency Management and Business Continuity Programs. 2004 ed. Available at: http://www.nfpa.org/PDF/nfpa1600.pdf?src=nfpa. 12. Association of State and Territorial Health Officials and National Association of County and City Health Officials. State and Local Health Official Epidemic SARS Checklist. Available at: http://www.astho. org/pubs/SARSChecklist.pdf. 13. Association of State and Territorial Health Officials. Preparedness Planning for State Health Officials. Available at: http://www.astho. org/pubs/Pandemic%20Influenza.pdf. 14. Gopalakrishna G, Choo P, Leo YS, et al. SARS transmission and hospital containment. Emerg Infect Dis. March 2004;10(3):395-400. 15. Federal Management Emergency Agency. Mitigation ideas: possible mitigation measures by hazard type, a mitigation planning tool for communities. Available at: www.fema.gov. 16. Personal observations during deployment: DMAT NM#-1 Northridge Earthquake 1994, IMSURT-East Bam, Iran 2004. 17. Auf der Heide E. Community medical disaster planning and evaluation guide: an interrogatory format. Am Coll Emerg Physicians. 1995. 18. Hays W. Data acquisition for earthquake hazard mitigation— abstract. Presented at: International Workshop on Earthquake Injury Epidemiology for Mitigation and Response; July 10-12, 1989; John Hopkins University, Baltimore. 19. State of California, Governor’s Office of Emergency Services. Hospital and Earthquake Preparedness Guidelines. Available at: http://www.oes.ca.gov/Operational/OESHome.nsf/978596171691 962788256b350061870e/C38723C529A5CA5188256BBF005E375 F?OpenDocument. 20. Federal Emergency Management Agency, National Earthquake Hazards Reduction Program. Publications and resources. Available at:http://www.fema.gov/hazards/earthquakes/nehrp//eq_links.shtm. 21. Federal Emergency Management Agency, Mitigation Division. Risk Management Series publications. Available at: http://www.fema. gov/fima/rmsp.shtm. 22. Institute for Business and Home Safety. Available at: http://www. ibhs.org/. 23. Technical Guidelines for Earthquake Protection of Nonstructural Items in Communication Facilities. Bay Area Regional Earthquake Preparedness Project (BAREPP). 24. Federal Emergency Management Agency, Response and Recovery. A guide to the disaster declaration process and federal disaster assistance. Available at: http://www.fema.gov/rrr/dec_guid.shtm. 25. U.S. Department of Homeland Security. National Incident Management System. Available at: http://www.dhs.gov/interweb/ assetlibrary/ NIMS-90-web.pdf. 26. U.S. Department of Homeland Security. National Response Plan. Available at: http://www.dhs.gov/dhspublic/interapp/editorial/editorial_0566.xml. 27. U.S. Department of Homeland Security. Homeland Security Presidential Directive/HSPD-5: Management of Domestic Incidents. Available at: http://www.dhs.gov/dhspublic/display?content=4331. 28. Gougelet R,Athher Mughal M. It takes a community: the Army’s integrated bioterrorism response model. Frontline First Responder. September 2003. Available at: http://www.emsmagazine.com/ffr/ ffrsep0003.html.

144 PRE-EVENT TOPICS

29. Rosen J, Gougelet R, Mughal M, Hutchinson R. Medical Disaster Conference. Coordination draft: conference report. June 13-15, 2001; Dartmouth College, Hanover, NH. Available at: http://www. dartmouth.edu/~engs05/readings/md/summary/DartMedDisRepv 1.2.pdf. 30. Improving Local and State Agency Response to Terrorist Incidents Involving Biological Weapons. Available at: http://www.edgewood.army.mil/downloads/bwirp/bwirp_planning_guide.pdf. 31. The White House. 2003 Homeland Security Presidential Directive/ HSPD-8: National Preparedness. Available at: http://www.whitehouse.gov/news/releases/2003/12/20031217-6.html. 32. Joint Commission on Accreditation of Healthcare Organizations. Health Care at the Crossroads: Strategies for Creating and Sustaining Community-wide Emergency Preparedness Systems. Available at: http://www.jcaho.org/about+us/public+policy+initiatives/emergency_preparedness.pdf. 33. Joint Commission on Accreditation of Healthcare Organizations. Revised Environment of Care Standards for the comprehensive accreditation manual of hospitals. Joint Commission Perspectives. December 2001;21(12). Available at: http://www.jcrinc.com/sub scribers/perspectives.asp?durki=1018. 34. Joint Commission on Accreditation of Healthcare Organizations. Analyzing your vulnerability to hazards. Joint Commission Perspectives. December 2001;21(12). Available at: http://www. jcrinc.com/subscribers/perspectives.asp?durki=1007. 35. Acute Care Center: A Mass Casualty Care Strategy for Biological Terrorism Incidents. Available at: http://www.edgewood.army. mil/downloads/bwirp/acc_blue_book.pdf. 36. Neighborhood Emergency Help Center Pamphlet: A Mass Casualty Care Strategy for Biological Terrorism Incidents. Available at: http:// www.edgewood.army.mil/downloads/bwirp/nehc_green_book.pdf. 37. Milsten A. Hospital responses to acute-onset disasters: a review. Prehospital Disaster Med. January 2000;15(1):32-45. 38. U.S.Department of Health and Human Services,Health Resources and Services Administration. National Bioterrorism Hospital Preparedness Program. Available at: http://www.hrsa.gov/bioterrorism/. 39. Centers for Disease Control and Prevention. Continuation Guidance for Cooperative Agreement on Public Health Preparedness and Response for Bioterrorism—Budget Year Five. Available at: http://www.bt.cdc.gov/planning/continuationguidance/index.asp. 40. RP Connell. Disaster Mitigation in Hospitals: Factors Influencing Decision-making on Hazard Loss Reduction [thesis]. University of Delaware; 2003. Available at: http://www.udel.edu/DRC/thesis/ connell_thesis.DOC.

SUGGESTED READING 1. Guidelines for Vulnerability Reduction in the Design of New Health Care Facilities. Available at: www.paho.org/english/dd/ped/vulnerabilidad.htm. 2. Principles of Disaster Mitigation in Health Facilities. Available at: http://www.paho.org/English/PED/fundaeng.htm. 3. Protecting New Health Care Facilities from Disasters. Available at: http://www.paho.org/english/dd/ped/proteccion.htm.

c h a p t e r

2 2

Vaccines Kent J. Stock

HISTORICAL BACKGROUND The Biological and Toxin Weapons Convention was established in 1972. Members of the convention produced a treaty that prohibited the development, production, stockpiling, and acquisition of biologic weapons. This was the first comprehensive, international effort to ban biologic and chemical weapons since the Geneva Protocol in 1925, and it was the first international treaty to ban an entire class of weapons. The treaty was opened for signature on April 10,1972,and entered into force on March 26, 1975. The treaty has been signed by 144 nations, including the United States and the Soviet Union. On Oct. 4, 2001, a case of inhalational anthrax was reported in Florida.1 Epidemiologists at the Centers for Disease Control and Prevention (CDC) later identified and confirmed 22 cases—11 cases of inhalational anthrax and 11 cases of cutaneous anthrax.2 The dissemination of these anthrax spores via letters through the U.S. mail appeared to be an intentional act of bioterrorism. In the aftermath of the Al-Qaida attacks on the World Trade Center and Pentagon buildings, this pernicious act illustrated our country’s vulnerability to terrorist attacks, particularly those involving the use of biologic weapons. In response to the terrorist attacks the United States, the federal government passed the USA Patriot Act in October 2001 and the Public Health Security and Bioterrorism Preparedness and Response Act in June 2002. These acts created the Department of Homeland Security and empowered the Department of Health and Human Services (DHHS) to begin efforts to protect the civilian population against future attacks with biologic weapons by enhancing surveillance and promoting preparedness. DHHS, in conjunction with the CDC and National Institutes of Health, convened members of the research community to discuss the development of a research agenda and strategic plan for biodefense research. These efforts to counter bioterrorism focused on a group of microbes that included Yersinia pestis, Francisella tularemia, Bacillus anthracis, variola major virus, Clostridium botulinum, and the hemorrhagic fever viruses.3 Variola major virus (smallpox) was particularly feared because of its high mortality rate, the absence of specific therapy, and the highly susceptible general population.4 The CDC published its Interim

Smallpox Response Plan and Guidelines in November 2001.5 These guidelines were later updated in 2002.6 This was the first time a U.S. government agency sponsored and implemented a large-scale civilian vaccination strategy in anticipation of a potential threat with a biologic weapon. The initial debate focused on whether the entire population should be vaccinated to eliminate the threat of a future attack or whether to institute a targeted vaccination program only after an attack occurs or if the likelihood of an attack is deemed high by government officials. CDC officials decided to support a “ring vaccination” approach after a case of smallpox was identified.5 The vaccination approach focuses on a surveillance and containment strategy. It involves the identification of smallpox cases, isolating those individuals, and vaccinating contacts and household contacts of those contacts.5 The plan did not recommend mass vaccination in response to a documented case. Additional measures were instituted to voluntarily vaccinate first responders and healthcare and emergency personnel who would be responsible for caring for smallpox victims. Unfortunately the response on behalf of healthcare and emergency personnel was subdued due to concerns regarding vaccine safety and the low likelihood of a smallpox threat. Large-scale vaccination programs in noncivilian populations have been conducted in the past. In 1998, the U.S. Department of Defense recommended vaccinating military recruits against anthrax. Opposition by some recruits was voiced because of a fear of unwanted side effects. Recent efforts to vaccinate military personnel in Iraq against anthrax have been conducted with substantial compliance and success.7 Implementation strategies for mass vaccination programs against anthrax in the military are continuing to be studied closely so that the lessons learned can be applied to civilian vaccination programs.

IMMUNITY Immunization is the method of artificially inducing immunity to prevent the development of disease. The artificial induction of immunity was first demonstrated by Edward Jenner in 1796.8 He observed that milkmaids 145

who had contracted cowpox were immune to smallpox. He developed the practice of vaccination, inoculating fluid from cowpox lesions into the skin of susceptible individuals. Inoculated individuals typically developed mild illness; however, some did develop disseminated infection with secondary complications. Immunization can be induced via active or passive methods. Active immunization typically involves the administration of a vaccine to induce the host to produce an immune response against a particular microorganism. Passive immunization refers to the practice of providing temporary protection by passively transferring exogenously produced antibody, such as immune globulin, to a susceptible host. Immunizing agents include vaccines, toxoids, antitoxins, and antibody-containing solutions. Immunizing agents are derived from either animal or human sources. The initial response of the immune system to the introduction of an antigen occurs after the primary exposure. After a period, one witnesses the development of humoraland cell-mediated immunity. Circulating antibodies do not typically develop for 7 to 10 days. If an antigen is presented for a second time, an exaggerated humoral- or cellmediated response occurs, called an “amnestic response.” These amnestic responses usually result in antibody formation within 4 to 5 days. There are multiple determinants of immunogenicity. Immunogenicity is determined by the physiological state (e.g., nutrition, immune status, age) and the genetic characteristics (e.g., major histocompatibility complex polymorphism) of the host, the manner in which the immunizing agent is presented (e.g., route, timing of doses, use of adjuvants), and the composition and degree of purity of the antigen.

VACCINES The ideal vaccine should possess the following characteristics9: • The agent should be easy to produce in well-standardized preparations that are readily quantifiable and stable in immunobiological potency. • It should be easy to administer. • It should not produce disease in the recipient or susceptible contacts. • It should induce long-lasting (ideally permanent) immunity that is measurable by available and inexpensive techniques. • It should be free of contaminating and potentially toxic substances. • Adverse reactions should be minimal and minor in consequences. Current vaccines do not typically meet all of these criteria. Most possess limited efficacy or have unwanted side effects. Vaccines typically consist of live-attenuated or killedinactivated microbiological agents. Many viral vaccines contain live-attenuated virus (e.g., measles, mumps, rubella, oral polio). The vaccines for some viruses and most bacteria are killed-inactivated, subunit preparations 146 PRE-EVENT TOPICS

or are conjugated to immunobiologically active proteins (e.g., tetanus toxoids). Live-attenuated vaccines tend to elicit a broader immunological response on behalf of the recipient. Live-attenuated vaccines also tend to elicit a more durable immunological response. Killed-inactivated vaccines, which typically have a lesser antigenic mass, require booster vaccinations. Currently licensed vaccines are both effective and safe; however, adverse events are associated with vaccine administration. Adverse events can be both trivial and life-threatening. Examples include injection site reactions, fever, irritability, and hypersensitivity reactions. Administration of live viruses can sometimes lead to disseminated infection and therefore is contraindicated in certain populations (e.g., immunocompromised). The National Childhood Vaccine Injury Act was passed by Congress in 1986. This act required the reporting of certain vaccine adverse events to the secretary of the DHHS. It also led to the creation of the Vaccine Adverse Events Reporting System.10 The system’s primary function is to investigate and study new vaccine adverse events or changes in the frequency of known vaccine adverse events. The reporting system has helped identify rare adverse events, including intussusceptions associated with rotavirus vaccine,11,12 myopericarditis and ischemic cardiac events among smallpox vaccine recipients, 13 and viscerotropic and neurotropic disease after yellow fever virus administration.14 The development of vaccines and the implementation of vaccination strategies have had a profound impact on childhood morbidity and mortality.15 From 1951 to 1954, approximately 16,000 cases of polio occurred each year in the United States, four years before vaccine licensure.16 The impact on the health of schoolchildren was tremendous. In response to the health hazards posed by polio, the United States began a field trial in 1954, in which thousands of susceptible schoolchildren were administered an unlicensed, live polio vaccine developed by Dr. Jonas Salk. Life magazine referred to the study as “the biggest experiment in U.S. medical history.”Twenty-five years after this historic experiment, the last recorded case of wild-type poliovirus in the United States occurred.17 In 1988, the World Health Organization launched the global polio eradication effort. Polio is now eradicated from the Western hemisphere, and in 2003 there were only 677 cases recorded worldwide in six different countries.

BIOLOGIC AGENTS The CDC has designated three categories of biologic agents according to their potential as weapons of terrorism.18 Category A agents were given the highest priority because they are easily disseminated or transmitted, associated with high mortality rates, can cause panic and social disruption, and require special action for public preparedness. Category B agents are moderately easy to disseminate, cause moderate morbidity and low mortality, and require enhanced diagnostic capacity and disease surveillance. Category C agents include emerging pathogens

that have the potential for becoming biologic weapons in the future. Immunizing agents are available against several bioterrorist agents.

largely due to the concern for hypersensitivity reactions. There are no licensed botulism toxoid vaccines currently available.

Category A

Smallpox (Variola Major)

Anthrax (B. Anthracis) BioPort Corp. in Lansing, Mich., manufactures the only human vaccine for the prevention of anthrax in the United States. Licensed in 1970, the vaccine was formerly known as Anthrax Vaccine Adsorbed (AVA). Its current name is BioThrax. The vaccine is prepared from a cell-free culture filtrate of a nonencapsulated, attenuated strain of B. anthracis.19 The antigen primarily responsible for inducing protective immunity is the protective antigen.20 The immunization schedule involves six immunizations. The vaccine is administered subcutaneously in a 0.5-mL dose at 0, 2, and 4 weeks and 6, 12, and 18 months.21 Annual boosters are recommended thereafter. The available vaccine is recommended for select laboratory workers and military personnel.22 The vaccine is effective for the prevention of cutaneous disease in adults. Studies in nonhuman primates suggest protection from inhalational disease as well.23 Adverse events include injection site reactions, fever, chills, myalgia, and hypersensitivity reactions. The vaccine is not licensed for use in children or pregnant women. The vaccine is not currently licensed for postexposure prophylaxis; however, vaccination with antibiotic administration would be recommended in the event of a biologic attack.4 Botulism (C. botulinum) Therapy for botulism includes passive immunization with antitoxin. Human-derived botulinum antitoxin (formerly known as Botulism Immune Globulin Intravenous [BIG-IV]) is only indicated for use in cases of infant botulism.24 Efficacy was demonstrated in a randomized trial.25 In the United States, the California Department of Health can be contacted for procurement of BIG-IV. Trivalent equine botulinum antitoxin (types A, B, and E) and bivalent antitoxin (types A and B) are available for the treatment of foodborne or wound botulism. Equine antitoxin can be obtained from the CDC through state health departments. Intravenous administration of equine antitoxin neutralizes toxin molecules that have not yet bound to nerve endings. One vial (10 mL) of trivalent antitoxin (7500 IU of type A, 5500 IU of type B, and 8500 IU of type E) is administered per patient.26 No additional doses are recommended. The half-life is estimated to be 5 to 8 days.27 A hypersensitivity reaction has been reported in 9% of individuals.27,28 A retrospective study demonstrated that the early administration of antitoxin (within 24 hours of onset of symptoms) was associated with an overall mortality rate of 10%, compared with 15% in patients in whom antitoxin was administered after 24 hours of symptoms and 46% in patients who did not receive antitoxin at all.29 Equine antitoxin is not currently recommended for use in cases of infant botulism. This is

Vaccination against smallpox was first performed by Edward Jenner in 1796.8 The currently available smallpox vaccine was first licensed in 1903.30 The last case of smallpox in the United States occurred in 1949. Routine vaccination against smallpox was discontinued in the United States in 1972. Eradication of smallpox was officially declared in 1980 by the World Health Organization. Wyeth Laboratories, Inc., the only licensed producer of smallpox vaccine in the United States, discontinued distribution to the civilian population in May 1983.31 By 1984, only the CDC in Atlanta, Ga., and the Research Institute of Viral Preparations in Moscow, Russia, possessed variola virus isolates. Because of the threat of bioterrorism, the United States produced 15 million doses of smallpox vaccine derived from the New York Board of Health vaccinia strain.32 An additional 280 million doses of vaccine were to be available by late 2002. Sanofi-aventis has also identified 70 to 90 million doses of vaccinia vaccine from storage that will be added to the nation’s stockpile.32 The only licensed smallpox vaccine in the United States is a lyophilized, live preparation of vaccinia virus.24 The vaccine preparation contains vaccinia virus, distinct from the variola virus, which causes smallpox and cowpox virus that was initially used by Jenner. The vaccine is highly effective in preventing smallpox. Protection typically wanes 5 to 10 years after a single dose.24 The federal government has recently contracted for the production and purchase of a new vaccine preparation. It is derived from tissue cell culture and may become available for use in the next 1 to 2 years. Modified vaccinia virus Ankara (MVA) may be suitable as a new smallpox vaccine.33 It is an attenuated strain and may be safer than unattenuated products. Smallpox vaccine is currently approved by the U.S. Food and Drug Administration for use in persons in special risk categories, including laboratory workers. The CDC recommended and implemented a voluntary vaccination plan for public safety and public health personnel because of the threat of bioterrorism. The vaccine is administered with the use of a bifurcated needle. A droplet of vaccine is held by capillarity action between the two tines. The needle is introduced into the epidermis. Fifteen perpendicular strokes are rapidly made in a 5-mm area. The site should be covered with a loose, nonocclusive dressing. One should avoid touching the area to avoid transferring the virus to other body sites. An evolution of skin lesions will occur at the site of inoculation 3 to 21 days after inoculation.24 The lesion will eventually scab and leave a scar. Smallpox vaccine is considered safe, but adverse events are described. Approximately 70% of children experience fever.24 Injection site pain and myalgia are other minor side effects. Complications include postvaccinial encephalitis (12.3/1 million primary vaccinations), progressive vaccinia (1.5/1 million primary vaccinations), eczema vaccinatum (38.5/1 million primary vaccinations), generalized vaccinia (241.5/1 VACCINES 147

million primary vaccinations), inadvertent inoculation (529.2/1 million primary vaccinations), rashes (1/3700 vaccinated; erythema multiforme is the most common), Stevens-Johnson syndrome (rare), and myopericarditis (300,000 1 billion

MORTALITY PER ANNUM 3.3 million >125,000 >3000

liters of urine/day. One can easily see how quickly proper disposal and management of waste can become a problem. When considering a sanitation system, one needs to be culturally sensitive to the population that is being served. It is a futile effort to set up a sanitation system if no one is going to use it. Therefore, it is a good idea to involve local residents in setting up a system. Environmental implications should be considered as well: what impact may it have, how long is it going to be used, and is there any potential to contaminate the water supply? Sanitation systems come in two forms, which are listed in Table 48-2.7

TABLE 48-3 DISEASE STATES ASSOCIATED WITH MALNUTRITION DISEASE

DEFICIENCY

Anemia Goiter/cretinism Scurvy Rickets/osteomalacia Beriberi Pellagra Ariboflavinosis Night blindness/xerophthalmia Kwashiorkor

Iron/vitamin B12 Iodine Vitamin C Vitamin D Vitamin B1 (thiamine) Niacin Vitamin B2 (riboflavin) Vitamin A Protein

Food and Nutrition The demand for food may lead to displacement. This may occur from a natural disaster or from the effects of conflict and war. Malnutrition is a significant cause of morbidity and mortality in many disasters. It is important to not only remember the direct complications of malnutrition and disease states (Table 48-3), but to understand that many diseases are accelerated or severe secondary to malnutrition—particularly in the pediatric population, where the main causes of death go hand and hand with malnutrition. The following are strongly tied to malnutrition: diarrhea, pneumonia, HIV, tuberculosis, malaria, measles, hypoglycemia, and hypothermia. The daily minimum nutritional requirement should be 2100 kilocalories/person/day. At least 10% of the calories in the general ration should be in the form of fats, and at least 12% should be derived from proteins.8 The caloric demand may be higher based on shelter, environment, burden of disease, and underlying nutritional status of the population.Distributing food equitably is an important aspect of feeding large populations. Ideally, this should be done in a community-based setting in an organized and secure manner.Otherwise,food stores will not be distributed equally. Feeding centers should be established for the severely malnutritioned. A food basket for distribution may include wheat flour, rice, sugar, vegetable oil, salt, and possibly local fish or meat. Other supplements may be included for additional nutritional benefit. It is preferable to use local food when available and to encourage the planting of vegetables. Seeds and other equipment can be distributed to the population. Cultural practices and diet also need to be considered. Utensils and fuel for cooking need to be supplied, depending on the food being distributed. Breast-feeding should be encouraged and bottle feeding avoided.

TABLE 48-2 SANITATION SYSTEMS WET

DRY

Water seal latrines Aquaprives

Trench Pit latrines VIP latrine Bore holed Composting

OXFAM Sanitation Unit

Nutritional screening of the population should be performed to assess particular needs. In general, the incidence of malnutrition in children younger than 5 years of age is used as the general indicator of malnutrition for the population. The weight-to-height index (ideally used), evidence of edema, and the mid-upper arm circumference are means to do a nutritional survey.9

Shelter Depending on the size of the displaced population, several different options may be considered for shelter. With small populations, an attempt may be made to house them with the local population in their homes. As the size grows, this is not possible. Another shelter option is to use existing structures that are already available (e.g., schools, factories, warehouses, and public buildings). Finally, camps can be established for the population to live in. When a camp is being established, considerations on shelter and the site will be based on a number of factors, including type of disaster, size and demographics of the population, anticipated time of displacement (although this is often underappreciated), environmental health risks, terrain, accessibility, available existent structures and infrastructure, climate, security (ideally away from borders), local building materials, and cultural considerations. Table 48-4 lists some general guidelines that are used for site planning.10

TABLE 48-4 RECOMMENDATIONS FOR SHELTER CONSIDERATION

SPACE

Area available per person Shelter space per person Number of people per water point Number of people per latrine Distance to water point Distance to latrine Distance between water point and latrine

30 m2 3.5 m2 250 20 150 m, maximum 30 m 100 m 75 m every 300 m 2 m, minimum

Firebreaks Distance between two shelters

DISPLACED POPULATIONS 315

Medical Care Medical needs may be anticipated based on the circumstances of the event leading to the displaced population. There are some general principles in responding to the acute medical needs of a displaced population. The goals of the healthcare system should be to treat the common communicable diseases (i.e., diarrhea, respiratory tract infections, measles, and malaria), reduce the suffering from debilitating diseases, afford easy access to the necessary care for the population, deal with the majority of diseases at the basic level, and carry out public health surveillance. Whenever possible, local healthcare facilities and professionals should be used. A large population can quickly overburden the local system, and often a parallel system needs to be developed. A four-tier model for the levels of healthcare managing the initial acute phase has been repeatedly used with success in reducing excess mortality. The levels include a referral hospital (preferably an already functioning local hospital), a central health facility, a peripheral health facility, and home visits/assessments. A referral hospital is used for more specialized care such as major surgery, obstetric emergencies, and more elaborate laboratory and diagnostic facilities. Patients should be referred to this facility only by one of the other tiers, preferably from the central health facility. Depending on the situation, one central health facility should be present for every 10,000 to 30,000 persons in a camp. This facility should include triage, an outpatient clinic (including minor surgical procedures), simple inpatient services (including uncomplicated deliveries), a pharmacy, and simple laboratory facilities. A peripheral health facility should be established for every 3000 to 5000 persons. Here a simple outpatient clinic or department can treat basic health needs (e.g., dehydration, dressing changes) and refer patients to a higher level of care. At all levels, public health surveillance should be conducted.11

316 POST - EVENT TOPICS

Based on disease prevalence in the population or region, certain medications may be required. In general, “essential” medical kits have been developed and are available from a number of government and nongovernmental organizations. Ideally, healthcare treatment protocols should be established for the more common illnesses. This affords easier management and better treatment when dealing with large populations. It also allows for the anticipation of necessary supplies and medications.

REFERENCES 1. United Nations High Commission of Refugees. Convention and Protocol Relating to the Status of Refugees. Geneva: UNHCR; 1951:16. 2. United Nations High Commission of Refugees. The Scope and Content of the Principle of Non Refoulement. Geneva: UNHCR; 2001:5. 3. Norwegian Refugee Project. Internal Displacement: A Global Overview of Trends and Development in 2003. 4. Médicins Sans Frontières. The emergency phase: the ten top priorities. In Hanquet G, ed: Refugee Health: An Approach to Emergency Situations. London: Macmillan; 1997:39. 5. Cutaneous viral diseases. In: Cook GC, Zumla A, eds. Manson’s Tropical Disease. 21st ed. Philadelphia:WB Saunders; 2003:842. 6. International emergency medicine. In: Cahill J, ed. Updates in Emergency Medicine. New York: Kluwer Academic Publishing; 2003a, 131-3. 7. Eade D. The OXFAM Handbook of Development and Relief. Oxford, UK: OXFAM; March 1994:22-23. 8. Famine-affected, refugee, and displaced populations: recommendations for public health issues. MMWR. 1992;41(RR-13). 9. Médicins Sans Frontières. Clinical Guidelines. Paris: Médicins Sans Frontières; 2003. 10. United Nations High Commission of Refugees. Handbook for Emergencies. Geneva: UNHCR; 1982. 11. Médicins Sans Frontières. Health care in the emergency phase. In Hanquet G, ed: Refugee Health an Approach to Emergency Situations. London: Macmillan; 1997:125-32.

c h a p t e r

4 9

Rehabilitation and Reconstruction Elizabeth Temin

There are four phases of emergency management: 1. Preparedness: Planning a response to a disaster. 2. Response: Activities that occur immediately after a disaster. These actions are designed to provide emergency assistance to victims. This phase usually lasts a few days to a few weeks. 3. Recovery: Returning the community to normal or near normal. This phase may last for many years. 4. Mitigation: Preventing or reducing the effects of a disaster. This phase should be integrated into the other three.1 This chapter discusses the third and least understood2 phase of emergency management: recovery. There are many factors that go into recovery, for example, the physical reconstruction of homes and public buildings, transportation, and basic services infrastructure, as well as psychological mending of the community and economic recovery of lost time and resources. This stage cannot be considered in isolation because mitigation, the fourth phase, must be integrated into recovery for it to be sustainable. In 1977, Haas et al3 became the first group to identify and describe the recovery process. They listed recovery as a sequential four-stage model of emergency, restoration, replacement, and development. Current models describe a more fluid recovery process with these stages overlapping and potentially occurring simultaneously.4 For example, replacement reconstruction may occur in some locations while at the same time debris clearance occurs elsewhere. Recovery currently focuses on the idea of sustainable development,4 a concept created by a United Nations Commission in 1986, which refers to recovery as a way to improve the quality of lives and durability of communities.5 This has been defined in the World Commission on Environment and Development as “meeting the needs of the present without compromising the ability of future generations to meet their own needs.”6 In the short run, it may cost more; better materials may be used, houses and businesses may be relocated, and more stringent building codes and zones laws may be implemented. In the long run, its goal is to protect and strengthen key social and economic infrastructure before disasters strike so as to reduce the likelihood of loss of life and assets7 and ultimately improve the community and save money.5

There is a vast spectrum of disasters, and the process of disaster recovery can adapt the available tools to fit the specific situation. It is useful to apply a framework in thinking about the similarities and differences in disasters. They can be categorized as natural or manmade, sudden onset or slow onset. Examples of natural disasters that are slow onset are droughts or epidemics such as severe acute respiratory syndrome (SARS); sudden onset examples are floods, hurricanes, and earthquakes. Examples of manmade disasters that are slow onset are wars such as the war in Iraq, and sudden onset examples are bombings or terrorist activities such as the Sept. 11, 2001, attacks and the Exxon Valdez oil tanker spill in 1989. In general, the important differences are the duration of the impact and the severity of direct and indirect effects. Direct effects are defined as the physical destruction and lives lost as a result of the disaster. Indirect effects are the work time lost, jobs lost, and the change in spending in the community involved. There is also a framework in which to categorize recovery; it can be designated as vertically or horizontally mediated. Vertical mediation recovery refers to the hierarchy of local communities, the state government, and the federal government. Horizontal mediation refers to the network of groups within a community. Every recovery and management process needs a balance of both vertical and horizontal mediation. The next three sections of this chapter discuss how certain communities and countries have handled disaster recovery historically, how the United States currently handles disaster recovery, and finally, pitfalls that are common in recovery efforts.

HISTORICAL PERSPECTIVE The literature on disaster recovery discusses both manmade and natural disasters but has primarily been only descriptive. When the Tsarist regime in Russia was overthrown in 1917, there was an almost complete nullification of all property rights, and the black market became the form of informal barter. Industrial production fell to 20% of pre-war levels by 1920.8 Hyperinflation occurred, impeding the ability to rebuild the country. In Hamburg, a series of raids over a period of 10 days in 1943 destroyed almost half the buildings in the city. 317

In the aftermath, there were as many injured as fatalities, and over two thirds of the city’s hospital beds had been destroyed. Over a period of months, 300,000 refugees were rehoused and 500,000 permanently evacuated. Adequate water supply was a problem even though wells had been dug prior to the event. Yet within 5 months, Hamburg had recovered up to 80% of its former productivity.8 In 1945, the atomic bomb was dropped on Hiroshima. Deaths were estimated at 80,000, and almost 70% of buildings were destroyed. In this case, recovery took much longer. It was only by 1949, 4 years later, that the population had recovered to its former numbers and 70% of the destroyed buildings had been reconstructed.8 In 1982, Marin County experienced continued floods and mudslides until finally a presidential disaster was declared. Federal teams had trouble appropriately identifying local public priorities from the myriad of recovery issues. As an example, the Intelligence Hazard Mitigation Team identified two sites for priority attention. County officials indicated that those were not the priorities they would have selected.1 Damage survey reports were begun in over 300 sites, and many were held up by disagreements over the definition of a mudslide versus a landslide and how to define repair versus permanent restoration. Each of these occurrences receive different levels of funding.1 On the positive side, Marin County actively included mitigation into recovery efforts. They created landslide-protection zones and required that prospective home buyers receive mandatory notification of stability problems.1 In 1988, Jamaica was hit with Hurricane Gilbert. This was the first direct hit with a hurricane in more than 35 years. As a result, Jamaica had been in a period of complacency with a low sense of preparedness and concern for mitigation. Nineteen of the 33 watershed areas had been eroded by deforestation and the expansion of agriculture onto high-slope areas. When Hurricane Gilbert struck, there occurred not only the destruction from the hurricane but also subsequent significant flooding and landslides. Many Jamaicans lived in highly vulnerable locations. The low-income housing in the area that was not built up to the housing codes,and those in floodplains and gullies suffered predominantly.9 It was estimated that 20% of all housing was damaged and 2% destroyed.9 In 1989 when the Loma Prieta earthquake hit Santa Cruz County, the local community was strong. When the Federal Emergency Management Agency (FEMA) came and set up a disaster assistance center (DAC) in the city of Santa Cruz, the citizen leaders requested a satellite DAC to support the rural population. FEMA accepted the request after determining that a significant number of families had been overlooked in their initial assessment. By working together,the community and the federal government were able to adequately support the victims of this disaster.2

CURRENT PRACTICE In the United States, recovery planning started in 1803 when local resources were overwhelmed during a fire in Portsmouth, New Hampshire. The local government 318 POST-EVENT TOPICS

asked Congress for help, creating the first legislative act for federal resources. In 1950 the first permanent and general legislation, the Federal Disaster Act, came into existence. This was revolutionary because it was the first Act to create a general response to all disasters. Before this, each disaster resulted in Congress passing a new localized piece of legislation. In 1979, President Carter pulled all the distinct response groups together along with the military resources to create FEMA. In 1988 Congress passed the Stafford Act,which focused FEMA toward hazard mitigation and coordination of disaster recovery programs. The Disaster Mitigation Act of 2000 established specific requirements for hazard mitigation planning, and grants became available to allow local and state governments to use mitigation funds for predisaster planning.6 In 2001 the actions of Sept. 11 pushed Congress to create the Department of Homeland Security, which was the largest reorganization of federal agencies since the Great Depression.6 The magnitude of disaster recovery depends on the magnitude of the destruction. In a small local disaster, volunteer organizations such as the Red Cross and private insurers may be enough to aid victims. When a disaster overwhelms the recovery forces of a community, that community can turn to the state government, and ultimately to FEMA, for resources. Within the first 48 hours of a disaster, an assessment team should provide an initial assessment of the damage. This includes identifying immediate needs such as food, shelter, and infrastructure. A preliminary damage assessment by the local government will determine whether federal aid may be needed and should be requested. Once the immediate needs are identified, and if federal aid is requested, a second, more in-depth survey should be done by FEMA. This second survey should include asking the plans of the displaced citizens: Do they plan to move, or rebuild in the same spot? Public infrastructure, sewers, and storm drains should be examined. What about the town? What was there before the disaster? What currently exists? Were there any existing plans for expansion of the area that could be used for rebuilding? What are opportunities looking at the long term?10 Every U.S. state maintains an Emergency Management Agency (EMA) and an Emergency Operations Plan. Their role is to establish and maintain an emergency program concerned with preparedness, response, mitigation, and recovery; to coordinate and train state and local governments; to recommend whether federal aid is needed in the case of a disaster; and to coordinate state and federal resources and act as an intermediary between local and federal groups.6 In the past, the majority of these plans have been concerned primarily with the short-term response.2 Recently many states have been trying to adapt to a more long-term response. When a disaster, whether natural or manmade, strikes a community in any part of the United States, including the Virgin Islands, Guam, U.S. Samoa, and the commonwealth of the Northern Mariana Islands,11 if that state is overwhelmed and state resources are not enough to provide aid, the federal government may declare a disaster under the Robert T. Stafford Disaster Relief and Emergency Assistance Act.11 In 2000 there were 45 major

disaster declarations made in 31 states and the District of Columbia.12 These disasters ranged from tornadoes to wildfires to winter storms. Initial response resources include food, water, emergency generators, and the mobilization of specialized teams (e.g., search and rescue, medical assistance, damage assessment, and communications). For more long-term relief, there are loans and grants to repair or replace housing and personal property, roads, and public buildings. There is also assistance for mitigation opportunities, counseling, and legal services. These services are outlined in the Federal Response Plan (FRP), which describes the policies and plans of 25 federal departments and the U.S. Red Cross.11 The FRP can be implemented in conjunction with other specialized groups including plans for telecommunications support, the National Oil and Hazardous Substances Pollution Contingency Plan, the Federal Radiological Emergency Response Plan, and the Terrorism Incident Annex.11 In addition to the FRP, some federal agencies have the authority to provide disaster aid even when the magnitude is not sufficient for the president to declare a federal disaster, including the Department of Agriculture, Department of Commerce, Department of Housing and Urban Development, and the Small Business Association (SBA). The FRP employs a multiagency operations structure based on the Incident Command System (ICS). (See Chapter 30, The Incident Command System.) Disaster Field Offices under the Department of Homeland Security may be created along with a national emergency response team. Recovery efforts are the responsibility of logistics and administration teams within the disaster field offices. The first source of insurance for all homeowners, businesses, and towns is private insurance. If that is not adequate or not available, the next action should be to register with FEMA by the stated deadline, usually within 2 months of the disaster. After individual private insurance carriers, the SBA provides the next largest portion of aid. All those above a minimum income are referred to SBA and should apply for SBA loans.10 The loans must be repaid, but they carry low interest rates. These loans include: 1. Home disaster loans to homeowners or renters to repair personal property; 2. Business physical disaster loans to businesses to repair or replace property including real estate, equipment, and inventory (not-for-profit organizations are also eligible); 3. Economic injury disaster loans to small businesses and agricultural cooperatives to replace working capital.10 FEMA also offers three types of assistance: 1. Individual and family grants: These loans are granted to persons with needs not met by private insurances, SBA, or volunteer organizations. These grants are for basic needs only, not to return life to normal. Costs can include medical and counseling assistance, housing repair, funeral expenses, and insurance premiums. 2. Public assistance:This program gives aid to local governments for emergency services and the repair or

replacement of public facilities, for example, the removal of debris, repair of infrastructure, or emergency protective measures. It is often the most costly element of recovery, and typically the cost is shared with the state in a 75%/25% split.6 3. Hazard mitigation grant program10: These grants are used by the federal, state, and local governments to incorporate mitigation into the recovery process. Actions may include acquisition of homes, public education, and retrofitting structures to better resist subsequent disasters such as floods and hurricanes. Cost will be shared between federal and state resources.6 Businesses have special considerations in light of a disaster. The primary objective of recovery planning is to enable an organization to survive a disaster and to continue normal business operations. To survive, the organization must ensure that critical operations can resume/continue normal processing and minimize the duration of a serious disruption to operations and resources (both information processing and other resources); a premade contingency plan is the best method of accomplishing this.13 Specific measures may include having an alternate site of operations if the current facility is damaged, storing vital documents off-site, and having an alternative energy source such as a generator. Larger businesses may be better able to withstand a disaster because assets and the workforce may be dispersed across a wider geographical area.6 A disaster is a life-altering event. Survivors share an enormous experience and come to view the world around them in new and different ways. Seeking help from the government, voluntary agencies, and insurance companies can be long and frustrating, which may only compound the feelings of helplessness. Anger and further despair are common. Mental health staff may assist persons by reassuring them that this “second disaster” is a common phenomenon14 and that they are not alone in their frustration. Many people may not want to seek formal counseling, either because of the stigma some still associate with psychiatric help or because they are unwilling to take time away from putting their lives back together or helping others. Very effective mental health assistance can be provided while the worker is helping survivors with concrete tasks. The “over a cup of coffee” method of informal intervention may be the best method to help. For example, a mental health worker can use skilled but unobtrusive interviewing techniques to help a survivor sort out demands and set priorities while they are jointly sifting through disaster rubble.14 Although having community involvement is beneficial to the process of recovery, it is also very important for the mental well-being of the community. Failing to involve the community can lead to resentment and fragmentation. The inhabitants may be unhappy when aid is not appropriate to the community’s perceived needs, and this insult may be compounded if they are then labeled unappreciative of the federal help. When people have a hand in their own recovery, they feel empowered and will increase their involvement. This leads to a stronger community network that in turn increases the ability to provide self-help. REHABILITATION AND RECONSTRUCTION 319

PITFALLS In general, there are two broad problems with disaster recovery: too little horizontal planning or too much dependence on vertical aid. The pitfalls occur when the horizontal and vertical planning are not balanced. In the case of too much dependence on vertical planning, the community does not contribute anything to the recovery process and the government organizations and nongovernmental organizations dictate the recovery plans. In the past, these groups have come in with the intention of “fixing” the situation. This is referred to as “top down” theory.9 In addition to not providing the optimal care, this may impede the self-sufficiency of these disaster-struck areas. Assumptions may be made, including the following: (1) the victims are a burden; (2) the host government is weak and cannot manage alone; (3) foreign aid organizations don’t require accountability; (4) aid for the victims reflect the defined needs of the victims (when, in fact, the aid reflects the projected need by the donor).9 An example of this last point was when Hurricane Hugo struck Montserrat in 1989. Ninety-eight percent of all homes were affected, 50% severely and 20% completely destroyed.9 The Peace Corps brought in large numbers of prefabricated housing to replace all the destroyed homes. Although they were able to help a lot of people numerically, the homes they provided had two-sided pitched roofs instead of the typical Caribbean four-sided roofs that were better able to withstand tropical winds. They also did not have an interior design to allow for cross ventilation. The early recipients of the homes reported this finding to the Peace Corps, but the Peace Corps was unable to change the design. Though well intentioned, the Peace Corps was predominantly meeting the need projected by the donors instead of the actual needs of the victims.9 Overdependence on vertical planning can also result in a lack of accountability and thus uneven recovery results. In Jamaica, after Hurricane Gilbert, the primary housing aid program was the Building Stamp Programme, which was set up by the Jamaican government, the World Bank, Canada, Germany, Japan, OPEC, and the United States. Homeowners were issued building stamps based on the extent of damages and financial need. These stamps would then be redeemed only at building supply stores who were members of the Jamaican Hardware Merchants Association for building materials, including zinc sheets, nails, and lumber. Squatters and renters were not eligible for stamps and were left without any recourse for finding aid. People who were not at home during the time of the survey were not listed as needing aid.9 Additionally, it was found that the stamps were distributed unequally. As a result, many needy people were left without any support. There is always the risk of creating a “dependency syndrome” by not thinking of sustainable development when investing money and effort into the recovery process.9 This occurs by the replacement of homes and infrastructure that are likely to be destroyed by subsequent disasters or that do not benefit the town, resulting in the need for continued care for each disaster. Instead of being able to learn from prior occurrences and create a more resilient 320 POST-EVENT TOPICS

town/infrastructure, the same mistakes are repeated over and over again. For example, Jamaicans used the stamps to fulfill daily needs such as mattresses and utensils and did not spend time reinforcing their homes against further hurricanes or floods. When the next hurricane hits, these people will have the same destruction to their homes as occurred with Hurricane Gilbert.9 In the case of too little horizontal planning, the results may be a chaotic lack of cooperation between groups and potential leaders. Studies have shown that many community plans focus primarily on the emergency period and do not give adequate attention to recovery and reconstruction. If there is a plan, it often exists on paper only and in the case of an actual disaster it is not used. In fact, many officials are not aware that a plan exists.4 These flaws lead to chaotic implementation of an ad hoc recovery. The community lacks the ability to work together and thus fragments and cannot unify to control its own affairs. As a result, the redevelopment is likely to be inadequate to fulfill the needs of the community. If there is aid from government and nongovernmental groups, they are sometimes uncoordinated, either duplicating actions, leaving areas without any aid,4 or giving aid that is inadequate for the needs of the area. In Saragossa, Texas, a small isolated community that was devastated by a tornado in 1987, there was no local government in place at all. When a disaster advisory board was created, it was done without any input from the local inhabitants. The outcome was that the Saragossans considered themselves worse off 2 years after the tornado than they had been beforehand, both because of the quality of the rebuilt neighborhoods and because they felt they were looked on as helpless and ungrateful.2 Studies in the Caribbean have shown that the different power levels in an uncoordinated community may lead to powerful interest groups pressuring public authorities to rebuild first in areas in which they have the greatest interest. Poorer neighbors with weaker ties to public authorities will get delayed care.2 In the United States, vertical planning predominates because few communities have detailed plans in place and because they may not have the financial reserve to pay for the recovery. When a plan is in place before a disaster, it allows for a strong horizontal network. Then, when a useful vertical element is added, the results can work wonders. By 1975 recurrent floods had repeatedly decimated the town of Soldiers Grove, Wisconsin. Each time they rebuilt. At one point they added a dam, and they planned for a levee but were unable because of financial restrictions. They decided they would take the funds allocated for the levee and use it to plan for town relocation. Although federal funds were slow in coming, they did create a plan. In 1978, when the largest flood in the history of the area occurred, they were ready with a fully written strategy. When they were granted funds for reconstruction, they put their plan into effect. Not only did they relocate out of the flood plain to prevent reoccurrence of this destruction, but they decided to create a town that was 75% solar powered.5 Because they had had the luxury of time in the planning stage, they had asked each business owner where they wanted to be located and how they wanted their business to be built.

As a result, the town became not only exactly what the community wanted, but its creation instilled a great sense of pride and satisfaction in its citizens, thus creating a happier community as well. REFERENCES 1. Drabek T, Hoetmer G. Emergency Management: Principles and Practice of Local Government. International City Management Association:Washington DC; 1991. 2. Berke P, Kartez J, Wenger D. Recovery after disaster: achieving sustainable development,mitigation and equity.Disasters.17(2):93-109. 3. Haas E, Kates R, Bowden M. Reconstruction Following Disaster. Cambridge, Mass: MIT Press, 1977. 4. Petterson J. A Review of the Literature and Programs on Local Recovery from Disaster. Natural Hazards Research and Applications Information Center, Institute of Behavioral Science, University of Colorado; 1999. 5. Smart Communities Network. Rebuilding for the future: a guide to sustainable redevelopment of disaster-affected communities, September 1994. Available at: http://www.sustainable.doe.gov/ articles/RFTF1.shtml.

6. Emergency Management Institute. Holistic disaster recovery: creating a more sustainable future [online course]. Available at: http://www.training.fema.gov/emiweb/edu/sdr.asp. 7. World Bank Finances Emergency Recovery and Disaster Management Program for the Caribbean. News release no:99/2035/LAC. 8. Hirshleifer J. Economic Behavior in Adversity. Brighton: Wheatsheaf Books Ltd; 1987. 9. Berke P, Beatley T. After the Hurricane. Baltimore: The Johns Hopkins University Press; 1997. 10. Minnesota Homeland Security and Emergency Management. Recovery from Disaster Handbook. Available at: http://www.dps. state.mn.us/dhsem/Hsem_ view_Article.asp?docid=313&catid=4. 11. Department of Homeland Security. National Response Plan 2004. Available at: http://www.dhs.gov/interweb/assetlibrary/NRPbase plan.pdf. 12. FEMA News. FEMA hails 2000 as year of major gains in disaster prevention, December 22, 2000. Available at: http://www.fema.gov/ news/newsrelease. fema?id=9993. 13. Disaster Recovery Journal. DRJ’s Sample DR Plans and Outlines. St. Louis, Mo. Available at: http://www.drj.com/new2dr/samples.htm. 14. Myers D. Psychological recovery from disaster: key concepts for delivery of mental health services. NCP Clinical Q 1994;4(2). National Center for Post-Traumatic Stress Disorder, US Department of Veterans Affairs. Available at: http://www.ncptsd.org//publications/cq/v4/n2/myers.html.

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Disaster Education and Research Kenneth A. Williams, Leo Kobayashi, and Marc J. Shapiro

Disaster education, regardless of the audience, has two goals: (1) prevention of disasters, and (2) mitigation of disaster effects, including improved outcome for victims and safety for responders. Disaster education should be based on principles of adult education and valid research. Education competencies and design should go hand in hand with the design and implementation of disaster research. Unfortunately, most current disaster research is descriptive and not relevant for education planning. For the general public, disaster preparedness once consisted of personal knowledge. People tended to know their limitations and had familiarity with the risks inherent in local activities and trades. Technological advances have both protected the population in developed countries and increased the risk of extraordinary catastrophe. Disaster research and education must address these changes in order to remain relevant.

HISTORICAL PERSPECTIVE Various public health triumphs mitigated epidemics and disasters through the years. Dr. John Snow,1 after brilliant but straightforward epidemiologic investigation,mitigated a cholera epidemic in 1855 by simply removing the handle from the contaminated pump.Hygiene,antibiotics,and field medicine saved countless lives. However, disaster response remained largely an uncoordinated humanitarian effort. The dictum that there were “no rules” in a disaster became an excuse for response failures and deficient education and planning. Although disasters overwhelmed local response capability, certain types of disasters recurred, and response strategy could therefore be formulated. Subsequent efforts to plan for disaster response were well intentioned but failed because they diverged from daily practice. Complex plans involving communication,2 patient identification and documentation, and command systems that were literally pulled from cabinets or trailers only for annual drills failed in actual events. The military has learned that soldiers “fight like they train,” and they train frequently. Disaster responders need to learn this lesson; disaster response paradigms fail in proportion to their deviation from daily practice. 322

CURRENT PRACTICE Education Adequate disaster education should include ageappropriate guidelines and must follow a basic format for training that allows evaluation of effectiveness. One recommended format is the establishment of clearly stated objectives (e.g.,“The children will be evacuated from the school in under 5 minutes,” or “The physicians will properly recognize nerve agent exposure from symptoms presented during simulation.”). These objectives are next used to develop evaluation tools (e.g., a timed drill for the school, written testing or observed performance for the physicians). Training curricula are then developed to achieve the desired objectives as measured by the evaluation tool. The students, for example, may need little more than general principles (“Follow the teacher’s instructions in an emergency”) and awareness that the alarm bell signals such an emergency; therefore occasional drills may suffice to maintain the needed level of training. Physicians treating patients exposed to chemicals may be trained using a variety of adult learning techniques. Target audiences for disaster education include the general public, nonmedical responders, and medical responders. The same principles of effective education apply. General public topics include general disaster readiness, sheltering, evacuation, and first aid. Such education can reduce panic, minimize load on evacuation or shelter systems, and mitigate illness and injury. Nonmedical responder topics vary with the type of responder but should include awareness of medical response issues and plans. Nonmedical responders may include those who provide shelter, evacuation, security, law enforcement, administration, logistics, food and water supply, sanitation systems, transportation, and structural engineering, among many others. Medical responders should improve their readiness through training; including knowledge of education provided to the general public and nonmedical responders. This inclusive and coordinated approach will optimize readiness, prevention, and mitigation. Readiness is the ability to perform, on request, a specific action in the allotted time. To improve readiness, an agency may work on communication essential to notify personnel of a request for service and coordinate their

actions, optimal performance of specific tasks, or means to increase the efficiency of performance. Each of these areas can be the subject of a variety of types of research and training and can apply to the general public and nonmedical responders as well as medical responders. For example, is a population ready to evacuate? Are the regional water suppliers ready to secure their facilities and prevent an effort to contaminate public drinking water? A variety of research exercises linked to training programs can improve readiness in such areas. Communication, a common challenge in disaster response, can be improved with use of robust and redundant technology that is familiar to all users. Practical research can assist agencies in the selection and adoption of flexible communication systems likely to remain functional during disaster events. Research parameters for such systems might include features such as interagency interoperability, simplicity and flexibility of use, sufficient power source and range for anticipated events, and the ability to move data between variable system elements. Drills, technical demonstrations, and prospective datagathering during real events are some research methods for the evaluation of communication systems. Similar to readiness, prevention may encompass public health, engineering, zoning, security, or other measures that trap errors that would otherwise, in certain circumstances,lead to disaster. In some cases,a disaster (defined as “an overwhelmingly damaging event”) may result in few if any medical casualties. Loss of computer data, defective products, and financial crisis are a few events that can have disastrous results without illness or injury, depending on those affected. Nevertheless, “atraumatic” disasters should be considered in disaster planning, education, and research alongside casualty-producing disasters, at least for healthcare systems if not for all community entities. The disruption caused by a loss of computer data, by revelations of administrative scandal, or by bankruptcy of a relied-on local service can be significant and can create stress and damage comparable to an event that causes injury or illness. There are many models of adult education that can be used to train disaster responders: self study, distance learning, direct education, hands on learning, drills and exercises, and, most recently, simulation labs. The types of education must be matched to the audience as well as the task to be taught and must also take into account available resources. For example, although the best method of teaching personnel how to do a particular skill may be intensive hands-on experience, there may not be the time or money for large audience training of this type. Types of education include the following: • Self-study: Involves self-paced learning, either from a text or Internet source. This kind of learning lends itself well to those with limited downtime during their workdays and with time to study that may be off shift or off hours. • Distance learning: Currently well used by the U.S. Centers for Disease Control and Prevention, this type of learning is often accomplished by a satellite broadcast. It allows many to be trained in a “live environment” where their questions and issues can be addressed.

• Direct education:This involves a lecturer delivering content to a reasonably sized audience. Although this type of education facilitates questions and feedback to participants, it requires a ready pool of expert educators that may not exist in a particular subject or geographic area. • Hands-on learning: Particularly suited for teaching skills, such as the wearing of protective equipment, this training is labor and time intensive and requires the use of local expertise and small class size–to–instructor ratio. • Drills and exercises: Although the full-scale exercise with its cast of thousands is usually seen as the ultimate training experience, much can be accomplished by specific, task-oriented drills. Drills and exercises are an excellent place to solidify training, identify future needs, and conduct research.

Simulation Training Human patient simulation is reaching a larger audience as the technology has improved and become more accessible. Distinct from the training offered by cardiopulmonary resuscitation manikins or personal computer–based multimedia software, high-fidelity medical simulation features integrated life-sized “patients” with programmable, reproducible,and physiologic response capabilities. Interactive communication, the ability to undergo procedural interventions, and real-time recording of events are key features. The application of these tools and techniques to disaster medicine education is now taking place. Both manikin and virtual reality (VR) simulated patients have been implemented to train healthcare personnel in various fields. Detailed patient presentations in realistic treatment settings, accurate modeling of human physiology, and dynamic changes in response to interventions are contributing to unique educational experiences. Otherwise unachievable training is being made possible for clinical events and care settings that harbor significant risk and enormous consequences. Difficult medical resuscitation and intraoperative crisis management are representative subject areas. Manikin-based systems such as those using the Laerdal SimMan and METI HPS models are becoming widespread due to the relative ease of setup and maintenance compared to VR counterparts. Expanding from their original role in anesthesia and resuscitation instruction, these manikins are being applied to disaster training in an ongoing exploration of their capabilities. Re-creation of the physical barriers and material impediments to patient care at disaster scenes is a prime area of inquiry. For example, practicing of intravenous access, medication administration, and endotracheal intubation while garbed in personal protective equipment (PPE) is currently being investigated on manikins.3-6 Total-immersion virtual reality (TIVR) and associated technologies are also starting to be used for disaster education.7 Featuring fully computer-generated environments and patients with multisensory interactivity (i.e., visual, auditory, haptic),TIVR advances the “perceptual illusion of non-mediation.”8 This capacity to seamlessly establish the presence of participants within the TIVR-constructed world hints at the potential for tremendously flexible and virtually unlimited simulations for training. A case study in DISASTER EDUCATION AND RESEARCH 323

this endeavor is the University of Michigan 3D Lab, where researchers have implemented a disaster scenario inside a Cave Automated Virtual Environment.9,10 Additional examples are present at the University of Missouri–Rolla11 and the University of Padova.12 Lack of standardization and significant startup requirements limit TIVR’s accessibility for the time being.

Civilian and Commercial High-Fidelity Simulation Applications in Disaster and Weapons of Mass Destruction Education With the increasing number of civilian sites featuring various forms of patient simulators, training courses have begun to earnestly delve into disaster-specific content. The fundamentals of disaster medical response, such as situational and hazard assessment,triage,patient examination and treatment, decontamination/provider protection, and evacuation are being addressed.13 Focused task training as well as exercises fostering specific cognitive processes and teamwork behaviors14,15 is being undertaken. Increased funding for disaster and weapons of mass destruction (WMD) training has helped prehospital systems in several states experience sophisticated disaster exercises employing advanced medical simulation. These efforts in Florida, Maryland,16 and Rhode Island17 have been primarily based at university-affiliated academic simulation centers receiving state and/or federal support. Significant use of high-fidelity simulation technology for nuclear, biological, and chemical preparedness is most apparent internationally in the Israel Center for Medical Simulation’s activities. Their programs address the preparation of physicians, nurses, and paramedics for the casualties of nonconventional warfare.18-20 In the commercial sphere, at least two U.S. centers are offering courses using high-fidelity manikin patient simulators for training in WMD and hazardous materials (HazMat). Simulation Training in Emergency Preparedness courses21 supported by the Health Resources and Services Administration are in progress at the Rhode Island Hospital Medical Simulation Center. The Texas Engineering Extension Service provides another WMD-focused prehospital operations and planning curriculum.22 These courses for the emergency medical service (EMS) community contain assorted applications of patient simulation, ranging from isolated patient care duties to full-scale multi-manikin disaster drills. Military high-fidelity simulation applications in disaster and WMD education military forces have routinely been involved in training for disasters, either in support roles for natural calamities or in combat preparation duties. Consequently, many of the issues raised by terrorism and WMDs have been addressed by the military in their established training. Troops engaging in combat have been expected to encounter weaponized chemical toxins, bioweapons, explosives, and radioactive hazards. Whereas the settings in which such exposures can occur have changed, the knowledge and techniques involved in responding to them remain mostly unaltered. The U.S. military is developing and running training programs focused on the healthcare services specialist, 324 POST - EVENT TOPICS

known as a “91W,” with a particular interest in chemical, biologic,radioactive,nuclear,and explosive qualifications.23 Component modules include personal computer–based Simulation Technologies for Trauma Care (STATCARE)24 and Nuclear Biological Chemical Casualty Training System (NBCCTS)25 software. Advanced patient simulation within the various project efforts features prominently under the Medical Simulation Initiative. Several hundred high-fidelity manikins in on-site and distance-learning settings have already been integrated into 91W training at various locations.26-28 WMD-specific applications are being phased in. Additionally, logistical simulation of the mechanics and delivery of medical care at multiple levels in a realistic and complete battlefield environment is progressing with the Combat Trauma Patient Simulator program.29

Future Directions in Simulation Numerous simulation experts and groups are pursuing scientific validation of simulation techniques in healthcare education. The disordered environment of a true disaster make prospective, controlled, and objective studies of educational content transfer difficult. Retrospective analyses may have a role,whereas surrogate markers of training efficacy and improvement in emergency preparedness could serve to demonstrate simulation utility in the interim. Enhancement of independent disaster response abilities can be individually assessed at “skill stations” akin to those in advanced cardiac life support courses. Global rating scales have surfaced as potential indicators of overall learner competence in educational settings using high-fidelity simulation.30 Such instruments, using properly defined scoring systems, should help in investigating basic disaster response competencies in conjunction with fully immersive multiple-manikin disaster drills. Development and testing of tools to demonstrate improved medical responder preparedness with proper disaster training are taking place through federally and state-funded projects. Extensively incorporated into these activities, high-fidelity simulation has already allowed objective examination of EMS providers’ scene hazards assessment, triage decision-making, use of novel interventions,31 and resuscitative actions13 in PPE. Continued work through such ventures is hoped to establish causal associations between high-fidelity simulation training, enhanced responder readiness training, improved disaster medical response, and ultimately, better patient outcomes. The greatest challenge for disaster trainers is to maintain the training competencies and certifications initially acquired and to work on continual skill development in an environment where little is changing, and the next disaster may seem far away.

CATEGORIES OF RESEARCH Disaster research can be categorized and associated with educational objectives. Categories include after-action report/case studies; aftermath epidemiology; discussion of planning, training, and mitigation techniques; trials of specific techniques or equipment; organizational or analytical schemes; and randomized controlled trials.

After-Action Report/Case Studies A description of the first 10 cases of anthrax in the United States caused by a terrorist event32 provides an example of the after-action report/case study. These data are useful in planning response magnitude and type. Recurring failures in response are well elucidated in this type of report. While cogently documenting the events surrounding various natural and manmade tragedies, these papers also often report shockingly similar response failures, including those involving communication, logistics, clothing, equipment, interagency cooperation, perimeter control, patient care delays, and suboptimal distribution of casualties.33 Although various nonmedical entities such as the Federal Aviation Administration and National Transportation Safety Board have implemented various regulatory and technology improvements during the past few decades, reducing the incidence of manmade disasters and mitigating their severity, medical responders often face the same challenges reported 25 years ago.

Aftermath Epidemiology Descriptions of the delayed effects of a disaster point out needs for subsequent responders and planners. The need to rapidly reestablish infrastructure, to attend to chronic healthcare needs and sanitation, to distribute medications, etc., can all be noted in a review of these research papers. Additionally, descriptions of lingering effects, such as the description of eye injuries following the Tokyo sarin attack, can be illuminating. Cultural diversity may alter the expression of disaster effects, but awareness that disasters have long-lasting and significant effects can be important for planners and educators seeking to address these concerns.

Discussion of Planning, Training, and Mitigation Techniques A discussion of planning, training, and mitigation techniques might include a survey and discussion related to bioterrorism training for emergency medicine residents.34 These papers document current education and planning methodologies and are useful in two ways. First, they provide a benchmark for the schemes in place that can be compared with outcome when an event occurs. If a system has a plan in effect, with specific training methods and specific techniques, readiness (as measured in a wellrun drill or an actual event) can be compared with alternative systems. Second, these papers serve to distribute the ideas, good and bad, that others have developed. Planners should be familiar with this literature and should seek to learn from the mistakes and brilliant insights of others as they design training and response plans.

Trials of Specific Techniques or Equipment Although fairly rare in the disaster research literature, trials of specific techniques or equipment present various methodologies for care and use of equipment. Topics such as triage technique, categories of patient condition, patient identification tags, communications equipment,

training programs in specific scenarios or problems, and command structures fall into this literature category. A weakness of many of these papers is failure to document use of the topic item (method, equipment, etc.) in a real event or in a controlled series of drills where it can be realistically compared with an alternative. Papers that tout the utility of an item and offer only a single drill designed to showcase the item should be scrutinized carefully and critically.

Organizational or Analytical Schemes Organization and analytical schemes discuss progress in disaster management, or lack thereof, and offer schemes or suggestions to improve international coordination, planning focus, funding allocation, etc.35 They often report the collective wisdom of a group of experts, but occasionally offer the scheme of a single person. In either case, this body of literature should be familiar to all disaster researchers and educators because a certain level of standardization and commonality in definitions and language is essential to collaborative effort.

Randomized Controlled Trials Vanishingly rare in disaster research, randomized controlled trials are nonetheless very important. The potential to perform research on recurring disasters (e.g., floods, earthquakes, certain transportation disasters) exists, and a few researchers have attempted to gather data comparing use of techniques or equipment with some degree of randomization. Currently, the most feasible option is the use of recurring drills to conduct research. The Rhode Island Disaster Initiative (RIDI), a federally funded disaster research project that began in 1999, included a series of disaster drills performed in a high-fidelity multiplace simulation center. The ability to accurately reproduce a disaster drill allowed the RIDI team to compare training and equipment practices between randomized responder groups. Future initiatives should move this type of research into formal research formats, such as crossover control or randomized trial models. REFERENCES 1. Snow J. On the mode of communication of cholera. London: John Churchill, 1855:38-55. Available at: http://www.ph.ucla.edu/ epi/snow/snowbook2.html. 2. Yoho DR Jr. Wireless communication technology applied to disaster response. Aviation Space Environ Med. 1994 Sep;65(9):839-45. 3. Vardi A, Levin I, Berkenstadt H, et al. Simulation-based training of medical teams to manage chemical warfare casualties. Isr Med Assoc J. 2002;4(7):540-4. 4. Berkenstadt H, Ziv A, Barsuk D, et al. The use of advanced simulation in the training of anesthesiologists to treat chemical warfare casualties. Anesth Analg. 2003;96(6):1739-42. 5. Rhode Island Disaster Initiative Web site. Available at: http:// www.ridiproject.org. 6. Kobayashi L, Shapiro MJ, Suner S, et al. Disaster medicine education: the potential role of high fidelity medical simulation in mass casualty incident training. Med Health RI. 2003;86(7):196-200. 7. Beier K, Freer JA, Levine H, and the Medical Readiness Trainer Team. An immersive virtual reality platform for medical education: introDISASTER EDUCATION AND RESEARCH 325

8. 9. 10. 11.

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18. 19. 20.

duction to the Medical Readiness Trainer. Proceedings of the 33rd Hawaii International Conference on System Sciences (HICCS-33), 2000. Available at: http://csdl.computer.org/comp/ proceedings/hicss/2000/0493/05/04935025.pdf. Lombard M, Ditton T. At the heart of it all: the concept of presence. J Computer-Mediated Commun. 1997;3(2). Available at: http:// www.ascusc.org/jcmc/vol3/issue2/lombard.html. University of Michigan 3-D Lab. CAVE Technology Demonstration Disaster Scenario Web site. Available at: http://um3d.dc.umich.edu/ index.html. University of Michigan Virtual Reality Laboratory at the College of Engineering. Medical Readiness Trainer Web site. Available at: http://www-vrl.umich.edu/mrt. Leu MC, Hilgers MG, Agarwal S, et al. Training in virtual environments for first responders. Proceedings of the 2003 ASEE Midwest Section Meeting. Rolla: University of Missouri–Rolla, 2003. Available at:http://campus.umr.edu/venom/publications/Leu_ ASEE_midwest_meeting’03_paper_(TACOM).pdf. Gamberini L, Cottone P, Spagnolli A, et al. Responding to a fire emergency in a virtual environment: different patterns of action for different situations. Ergonomics 2003;46(8):842-58. Suner S, Williams K, Shapiro M, et al. Effect of personal protective equipment (PPE) on rapid patient assessment and treatment during a simulated chemical weapons of mass destruction (WMD) attack [abstract]. Acad Emerg Med. 2004;11(5):605. Kyle RR, Via DK, Lowy RJ, et al. A multidisciplinary approach to teach responses to weapons of mass destruction and terrorism using combined simulation modalities. J Clin Anesth. 2004;16(2): 152-8. Kobayashi L, Shapiro M, Hill A, Jay G. Creating a MESS for enhanced acute care medical education and medical error reduction: the multiple encounter simulation scenario [abstract]. Acad Emerg Med. 2004;11(8):896. Kyle RR, Via DK, Lowy RJ, et al. A multidisciplinary approach to teach responses to weapons of mass destruction and terrorism using combined simulation modalities. J Clin Anesth. 2004;16(2): 152-8. Kobayashi L, Shapiro M, Hill A, Jay G. Creating a MESS for enhanced acute care medical education and medical error reduction: the multiple encounter simulation scenario [abstract]. Acad Emerg Med. 2004;11(8):896. Vardi A, Levin I, Berkenstadt H, et al. Simulation-based training of medical teams to manage chemical warfare casualties. Isr Med Assoc J. 2002;4(7):540-4. Berkenstadt H, Ziv A, Barsuk D, et al. The use of advanced simulation in the training of anesthesiologists to treat chemical warfare casualties. Anesth Analg. 2003;96(6):1739-42. The Chaim Sheba Medical Center at Tel Hashomer. Israel Center for Medical Simulation Web site. Available at: http://eng.

326 POST - EVENT TOPICS

21. 22.

23. 24. 25. 26. 27. 28. 29. 30. 31.

32. 33. 34. 35.

sheba.co.il/main/siteNew/index.php?page=45&action=sidL ink&stId=435. Rhode Island Hospital Medical Simulation Center. Simulation Training in Emergency Preparedness (STEP) course Web site. Available at: http://www.lifespan.org/services/simctr. Texas Engineering Extension Service Emergency Services Training Institute (TEEX-ESTI). EMS operations and planning for weapons of mass destruction course Web site. Available at: http://www.teexesti.com/course_catalog_course.cfm?courseID=159&cid=535 &pid=505,535. U.S. Army. 91W Healthcare Specialist Web site. Available at: http://www.cs.amedd.army.mil/91w. RTI International. Simulation Technologies for Advanced Trauma Care (STATCare) Web site. Available at: http://www.rti.org/ page.cfm?objectid=3F6A5676-FEF7-423F-92479553E912FB73. U.S. Army Medical Department. Nuclear Biological Chemical Casualty Training System (NBCCTS) software Web site. Available at: http://www.cs.amedd.army.mil/simcenter/NBCCTS.htm. U.S. Army. Camp Shelby Medical Company Training Site Chemical, Biological, Radioactive, Nuclear & Explosive (CBRNE) Training Web site. Available at: http://www.ngms.state.ms.us/mcts/page9.html. MedSMART Inc. International and Distance-Enabled Offerings: U.S. And Global Range Operations. Available at: http://www.medsmart.org/services.html. Research, Development and Engineering Command (RDECOM) Web site. Available at: http://www.globalsecurity.org/military/ agency/army/rdec.htm. U.S. Army Program Executive Office for Simulation, Training, and Instrumentation. Combat Trauma Patient Simulator (CTSP) program Web site. Available at: http://www.peostri.army.mil/products/CTPS. Gordon JA, Tancredi D, Binder W, et al. Assessing global performance in emergency medicine using a high-fidelity patient simulator: a pilot study [abstract]. Acad Emerg Med. 2004;10(5):472. Vardi A, Berkenstadt H, Levin I, et al. Intraosseous vascular access in the treatment of chemical warfare casualties assessed by advanced simulation: proposed alteration of treatment protocol. Anesth Analg 2004;98(6):1753-8. Jernigan J, Stephens D,Ashford D, et al. Bioterrorism-related inhalational anthrax: the first 10 cases reported in the United States. Emerg Infect Dis. 2001;7(6):933-44. Williams A. Lessons learned from transportation disasters [unpublished thesis, MPH program] Cambridge, Mass: Harvard University; 1995. Pesik N, Keim M, Sampson TR. Do US emergency medicine residency programs provide adequate training for bioterrorism? Ann Emerg Med. 1999;34(2):173-6. Sundnes KO, Adler J, Birnbaum ML, et al. Health disaster management: guidelines for evaluation and research in the Utstein style: executive summary. Prehospital Disaster Med. 1996;11(2):82-90.

c h a p t e r

5 1

Practical Applications of Disaster Epidemiology P. Gregg Greenough and Frederick M. Burkle, Jr.

Regardless of whether a prolonged heat wave hits Europe, a spate of hurricanes occur in the southeastern United States, a volcano erupts in the Philippines, or a complex humanitarian emergency continues in Sudan, each type of disaster has a unique epidemiology. Broadly, epidemiology refers to the study of the distribution and determinants of health-related states or events in specified populations and the application of this study to managing and controlling health problems. In essence, epidemiology uncovers the way in which specific disasters generate specific predictable patterns of public health effects, usually disease or injury, in dimensions of time, space, or subgroup within a population.1 Disaster epidemiology has a role in every aspect of the disaster cycle, including the development of prevention strategies, the assessment of need and targeting of resources during the impact phase, and the measurement of the effectiveness of the disaster response. Every type of disaster can be classified both as a “disease process”and as a “disease generator.” Knowing the types of public health effects of a given disaster can guide disaster preparedness efforts. For instance, a population prone to earthquakes will present acutely en masse to emergency departments with fractures, closed head injury, lacerations, and soft tissue injury. Within days, patients may be at risk for complications such as renal failure and wound infection. Long-term effects such as mental health issues and disability will be public health problems well after the event itself. Advanced understanding of a specific disaster’s epidemiology can assist disaster managers and organizations in planning for a disaster response and directing critical resources before,during,and after the event. More importantly, disaster mitigation efforts guided by epidemiology can reduce the number of deaths and minimize the burden of disease caused by a given disaster. Epidemiology plays a role in the developing world where basic healthcare is lacking, preventable infectious diseases are endemic, famine is recurrent, and subsistentlevel poverty the norm. High mortality rates can be expected in places where disasters are superimposed on a baseline poor public health infrastructure. Populations displaced by natural or human-generated disasters are at risk for health, food, water, and shelter insecurities.

HISTORICAL PERSPECTIVE Epidemiology, which once simply concerned itself with infectious diseases and their relation to a population, has evolved over the years to comprise all hazards that affect the public health, including natural and human-generated disasters. The practical application of epidemiology began with the humanitarian assistance during the Nigerian (Biafran) War of the late 1960s and a variety of natural disasters in the 1970s (e.g., Bangladesh cyclone, 1972; Guatemala earthquake, 1976) and 1980s (e.g., Armenian earthquake, 1988).2,3,4 These events showed that epidemiologic methods could measure and minimize risk, assess the relief effort, describe patterns of morbidity and mortality, and suggest prevention and intervention strategies. To that end, the Center for Research on the Epidemiology of Disasters (CRED) at the University of Louvain in Belgium was created in the early 1970s; today it maintains a global emergency events database (EM-DAT) that provides information on the effects of the nearly 13,000 mass disasters since 1900. The existence of such a database allows for donors, disaster managers, researchers, and policy makers to make comparisons across disaster type and place and analyze vulnerability factors. Historically, large numbers of humanitarian relief and multilateral agencies with varying degrees of expertise in humanitarian response did not approach the humanitarian response in a unified, coordinated fashion. However, with the advent in the late 1990s of the Sphere Project, a collective effort of humanitarian nongovernmental organizations (NGOs) and the International Federation of the Red Cross and Red Crescent Societies to reach consensus on minimum standards in health, food, nutrition, shelter, water, and sanitation, a common understanding of the role of epidemiology in supporting the public health in disasters emerged.5

CURRENT PRACTICE Epidemiologic studies in disasters need to be proactive, timely, well-designed, and widely disseminated to all organizations involved in all phases of the disaster cycle. 327

In addition, the epidemiologic method used should be appropriate for the public health issue in question. The following field methodologies are the keys to critical information during all phases of the disaster.

Vulnerability Analyses The key purpose of vulnerability analyses is to identify populations at risk in an effort to implement preparedness and mitigation efforts as well as establish a baseline from which rehabilitation efforts can be measured. Thus, a variety of stakeholders—from disaster managers to urban planners to insurance representatives—find such information vital to their respective tasks. A more detailed discussion can be found in Chapter 17; the brief mention here is to highlight the role of epidemiology in the analysis. Vulnerability is defined as the degree to which one’s life and livelihood (or that of a population) is at risk by an encounter with a given hazard. The hazard is the potential for a specific harm-causing event which may directly or indirectly affect the population.6 Vulnerability is not only measured by degree of exposure of the hazard but also by the level of sensitivity and resilience of the population’s environment, or what is increasingly being referred to as the coupled humanenvironment system.7 Changes in a population’s environment affect its ability to absorb the shock of the hazard. Factors inherent in the system’s ability to absorb the shock and stresses of a given hazard or combination of hazards may include the level of environmental degradation and deforestation present, the degree of urbanization, the population’s socioeconomic status, and the types of livelihoods on which the population depends. On a macro level, transnational factors such as global climate change and debt-relief policies or national factors such as types of national land use planning and degree of communication and transportation infrastructure, degree of governmental stability, and adherence to the rule of law all directly contribute to a given population’s vulnerability. All of these factors are potential epidemiologic markers in a vulnerability analysis. Risk perception—the way a population understands the hazards it may be exposed to, its vulnerability related to that hazard, and the probability of a hazard occurring—may require a qualitative study to determine how a population is likely to prepare for and react to such an event. For instance, using a mental model with respondents affected by flooding, researchers from Carnegie-Mellon University found that most knew very little about the direct causes of flooding and how to protect themselves, and they perceived mitigative efforts such as flood insurance to be unwarranted despite a government effort to address those issues.8 Such methods provide the ability to get at the underlying thought processes of an at-risk population. Qualitative techniques bring other disciplines into the discourse, such as anthropology, sociology, communications, and social sciences, thus enabling researchers to gain insight into how and why things work in a population and to improve the ability of the population to address its own problems. 328 POST - EVENT TOPICS

Vulnerability analyses can draw from “lessons learned”–type studies in the postdisaster phase. A cohort study of the deaths following the Taiwan earthquake of 1999 showed that people with mental disorders, moderate physical disabilities,or recent hospitalization were the most vulnerable.9 Similarly, women and elderly groups were found to be at higher risk of injury during the 1994 earthquake in Northridge, California. Those who lived in mobile homes during the 1978 Wichita Falls, Texas, tornado had a significantly higher risk of injury or death.10 In populations at high risk for a given hazard, applied quantitative epidemiology can identify vulnerable groups for targeted interventions before the next disaster.

Rapid Assessments and Needs Evaluations The cornerstone of epidemiology’s role in disasters is during the response itself. The epidemiologic methods of rapid assessments, surveys, and surveillance should parallel the emergency response. The outcome measures of these methods are termed indicators—the quantitative or qualitative criteria used to correlate or predict the value or measure of a program, system, or organization—tools used to inform and guide decision-making during the crisis and beyond.11 A few examples of general indicators are listed in Box 51-1.

BOX 51-1 COMMON INDICATORS IN RAPID ASSESSMENT Demographics • Vulnerable group identification Health • Morbidity and mortality rates o Crude mortality o Under-5 mortality o Cause-specific attack ■ Diarrheal illness ■ Acute respiratory infection ■ Malaria (in non-immune) ■ Measles • Measles immunization coverage Nutrition • Global acute malnutrition (−2 z score weight for height) • Macronutrient intake o Energy (kcal/day) o Protein (% of total energy) Food Security • Household access Water and Sanitation • Quantity (liters/person/day) • Quality (fecal coliforms/100 ml) • Household access o Distance to source o Source/population Shelter • Area per person • Fuel availability (kg/household/day)

Rapid assessments answer the primary questions of “what has happened” and “what is needed”?12 In the chaos of the moment, multiple agencies will be attempting to get solid information for decision-making and coordination, and information sharing among various agencies will be critical. Often these assessments out of necessity will be “quick and dirty,” depending on the nature and timing of the disaster and the need to have information readily available. More important is for public health providers with expertise in field epidemiology to be able to use the right type of epidemiologic tool for the right information. A variety of sources from a variety of methods will allow for the triangulation of data, where multiple sources of information can lend verification to each other—a “cross-checking”reference point. Bradt and Drummond13 propose an assessment tool containing a “minimum essential data set” of health information that will be uniformly understood and used by all stakeholders partially or entirely. Similar assessment indicators can be found in a number of field-tested resources (Box 51-2). Rapid assessments are used to examine the situation and the needs, ideally within the first several days of the impact. In so doing, public health providers determine the magnitude of the emergency by characterizing and quantifying the affected population; they identify existing and potential public health problems; they measure present and potential impact, especially health and nutritional needs; they assess resources needed, including availability and capacity of a local response; they aid in planning and guiding an appropriate external or international response; they identify vulnerable groups; and they provide baseline data from which the public health system can be restored.14 Often it is the indirect effects of a disaster, the subsequent migration of populations, separation from food supplies, and destruction of public health infrastructure that eventually cause the greatest mortality and morbidity. After the Asian tsunami of December 26, 2004, a rapid assessment in the six affected provinces of Thailand identified a 1.7 times greater increase in the incidence of diarrheal illness and a significant increase in wound infections compared with normal.15 Because Hurricane Charley in August 2004 devastated several counties on Florida’s Gulf Coast having a large concentration of older adults, the U.S. Centers for Disease

BOX 51-2 RESOURCES FOR ASSESSMENTS WHO, 1999 UNHCR Médicins Sans Frontiéres, 1997 Sphere Project, 2004 Office of Foreign Disaster Assistance EpiCentre

Rapid Health Assessment Protocols for Emergencies Handbook for Emergencies, 2nd ed Refugee Health Humanitarian Charter and Minimum Standards in Disaster Response Field Operations Guide Rapid Health Assessment of Refugee or Displaced Populations

WHO, World Health Organization; UNHCR, United Nations High Commission for Refugees.

Control and Prevention (CDC) and Florida Department of Health performed a rapid assessment of households with adults over 60 years of age who were found to have disruption in medical care for chronic medical conditions.16 Rapid assessments and their interpretations critically depend on reliable population denominators. The count refers to the absolute number of a population in a specific area in a specific period of time. First-world countries will have background demographic statistics of the population before the disaster strikes, but less developed places or areas with migrating populations may have inexact or nonexistent numbers. Global sources such as the World Health Organization, CRED, Epicentre, or the CDC are sources of information and publications that include baseline data on endemic diseases, baseline mortality rates, morbidity incidence rates, nutritional status, sources of healthcare, and the level of health service disruption by past disasters (Table 51-1). Other non-health sources of population data include the U.S. Central Intelligence Agency (CIA)’s World Factbook, which provides individual country profiles on infrastructure and government, maps, and census data. In almost all cases, an effort at population reconnaissance must be made to determine the numbers of affected persons relative to the entire population. Fly overs using aerial photography, satellite images linked to geographic information systems, mapping strategies, or drive- or walk-throughs using handheld global positioning system receivers are typically done to get a rough idea of absolute numbers and degree of devastation. Using multiple approaches allows for the triangulation of population numbers. Denominators are necessary to calculate a rate, the frequency of an event (usually morbidity or mortality) in a population in a specific period of time. Crude rates are calculated for an entire population, whereas specific rates are computed for a specific subgroup of the population. Specific rates highlight vulnerable groups and may be age specific, sex specific, occupation specific, and so on. Death rates are one of the most sensitive indicators of the success (or failure) of emergency relief efforts. Crude mortality rates (CMR), also known as crude death rates (CDR), reflect deaths within a population over a period of time: Number of deaths in time period CMR = Total population at mid-period

×

K Number of days in time period

where K is a uniform constant by which rates or proportions can be multiplied for purposes of comparison and easy understanding—usually a multiple of 10 (such as 1000, 10,000, or 100,000). CMRs are usually expressed during the emergency phase in deaths per 10,000 population per day. CDRs are employed after the health crisis of the impact has passed and are expressed as deaths per 1000 population per year. For either figure, the formula for calculation is the same and the underlying rate does not differ. The consensus among humanitarian agencies is that successful humanitarian relief programs should aim for a PRACTICAL APPLICATIONS OF DISASTER EPIDEMIOLOGY 329

TABLE 51-1

RESOURCES FOR BASELINE PUBLIC HEALTH INDICATORS

ORGANIZATION

WEB SITE

MISSION

Center for Research on the Epidemiology of Disasters

http://www.cred.be

• •

U.S. Centers for Disease Control and Prevention World Health Organization

http://www.cdc.gov http://www.who.int

Pan American Health Organization EpiCentre

http://www.paho.org http://www.epiet.org/ institutes/Epicentre.htm

Measure DHS U.S. Central Intelligence Agency World Factbook

http://www.measuredhs.com http://www.cia.gov/cia/ publications/factbook

CMR at or below twice the population’s baseline (predisaster) CMR. A doubling of the baseline rate defines a humanitarian disaster and immediate response. The average baseline CMR in the least developed countries is 0.38 deaths/10,000 persons/day; in developed countries it is 0.25 deaths/10,000 persons/day.17 A robust system of recording births and deaths as well as a registration system for displaced populations are needed for accurate denominators. This baseline will serve as the foundation by which agencies and disaster managers can follow the trends of mortality and morbidity over time, the function of a surveillance system (see Chapter 37). Age- and sex-specific death rates—the under-age-5 mortality rate (U5MR) is a frequently used example—are used in emergencies to identify subgroups particularly at risk during the disaster and to further clarify the information buried in the CMR figures. Because young children are a vulnerable group in a disaster, a rise in death rates among children younger than 5 years of age is a warning indicator of significant public health disturbance. Similar to the CMR calculation, the U5MR uses the number of deaths in children younger than 60 months of age over a time interval divided by the total population of children younger than 5 years at the middle of that time period: Number of U.S. deaths in time period USMR = Total U.S. population at mid-period

×

K Number of days in time period

This is expressed in terms of under 5 deaths per 10,000 population per day (during the emergency phase) or per 1000 population per month (in the postemergency phase). U5MR and CMR are the most commonly used mortality indicators during a disaster. 330 POST - EVENT TOPICS

• • • • • • • • • • • • • •

Maintains the EMDAT disaster database Promotes disaster education and training activities through applied research Links disaster epidemiology with policy and programming Publish Morbidity and Mortality Weekly Reports Research and document emerging infectious diseases Monitor disease burden Provide tools for research and assessment Maintain mortality database Offer geographic information tools Provide baseline health indicators (Western Hemisphere) Monitor health trends Maintain CRID (Regional Disaster Information Center) disaster database Provide National Demographic and Health Surveys Document population and environment data Monitor governmental structures, communications, transportation Monitor current political issues

The causes of specific mortality rates can identify the common causes of death during the emergency. Aside from the mortal injury caused by the disaster itself, the developing world often suffers mortality from diarrheal diseases, measles, acute respiratory infections, malnutrition, and malaria. To be rapid and efficient while maintaining accuracy, uniform simple case definitions (as opposed to laboratory confirmations) should be used in such settings to classify cases. Cases classified by standard case definitions are the numerator with the other components of the formula similar to the previous mortality rate calculations: Number of deaths from specific cause in time period K Cause- = × specific Total population at Number of days MR mid-period in time period Cause-specific mortality rates can target interventions: if the incidence of deaths from diarrheal illness is high, then a focus on water, sanitation, and hygiene will be most important. Various causes of injury morbidity vary according to the disaster type. However, infectious diseases are common in all disasters that disrupt the public health infrastructure. The five diseases mentioned above, along with meningitis, should not be missed during a rapid assessment. Interviewing health workers, reviewing clinic records, or directly observing households are techniques to determine the incidence and prevalence of a disease. Incidence refers to the number of new cases of a disease that occur during a specific time period; prevalence is the number of cases present in the population at the time of assessment.18 As the emergency phase passes into the postemergency phase, secondary wound infections, acute exacerbations of chronic diseases, and men-

tal health issues add to the burden of the disease in the disaster-affected population.

Participatory Appraisals In an effort to enhance the role of the affected population in the decision-making process during the response and reconstruction, researchers use participatory methods. Typically these are qualitative unstructured interviews with key informants,persons specifically selected because of their unique role in the community. Such respondents provide insight into the dynamic of the affected community or group, its interpretation of its environment, level of migration, needs, behaviors, and attitudes. Mental health issues require this kind of participatory ethnographic approach. Assessment teams take a listener/observer role. Relatively simple, inexpensive, and fast, participatory appraisals provide subjective nongeneralizable data that often require alternative methods for confirmation. Group interviews can generate “problem trees,” a participatory exercise that identifies problems and their root causes.

Surveys: In-Depth Sectoral Assessments A survey involves a more in-depth study compared with a rapid assessment, usually by means of a detailed study design that employs a sampling methodology and relies on observations, interviews, or questionnaires to yield data on a specific aspect of the disaster. That data undergoes a formal analysis and interpretation. Surveys are used for “one-off” assessments of a given sector (e.g., shelter), subpopulation (e.g., children younger than 5 years), or public health problem (e.g., acute malnutrition). In general, a survey should be used when greater precision is needed to make informed decisions. Nutritional surveys are the common example. Since undernutrition rates are associated with excess mortality from complications of preventable illnesses such as diarrhea, measles, malaria, and acute respiratory infections, it is imperative to determine the level of acute malnutrition within the disaster-affected population. The severity of acute malnutrition in young children is expressed as a z score—that difference between the weight-for-height ratio for an individual child and the median value of the population of children divided by the standard deviation of the population. The measure of greatest interest is that segment of the population below −2 z score termed global acute malnutrition, or wasting. Finding the prevalence of wasting within the population of children requires the systematic measuring of weight and height—in essence, a probability sample. A sample is that subset of a population that represents the population well enough to make inferences about it. A sample may be one of two types: a probability sample or nonprobability sample. The former uses random selection to minimize inherent bias, ensuring that each person within the population has an equal chance of being selected; the latter implies that samples are chosen subjectively by the researcher. Nonprobability sampling is quick and easy because it does not require a full listing of the population. If a public health worker wanted to know the prevalence of crush injury after an earthquake

to determine the amount of supplies needed, he could visit clinics. However, this nonprobability sample would miss those in the population who still may suffer crush injury but could not make it to a health facility. Thus, nonprobability sampling makes it difficult to measure the level of uncertainty of the results. More often, a probability sample complete with a sampling frame is needed to answer the research question appropriately. Sampling frames are full listings of the population as persons or households arranged in units of analysis. Invariably such sample surveys are more expensive (and may be prohibitive in the setting of low resources), demand time (when often an answer is needed immediately), and require a certain level of training (often not found in developing countries). In addition to nutritional indicators, surveys are commonly used in disasters to measure level of food security, immunization coverage, prevalence of mental health problems, access to clean water, household use of water, hygiene practices, level of infrastructure damage, shelter density, and livelihood disruption, among many other areas of interest. Because they require expertise, planning, and time, surveys are done on any given area of interest usually as a “one-off” event, a snapshot in the disaster response continuum. To adequately follow indicators of interest in real time, a more flexible, rapid, and simple tool should be used.

Surveillance Monitoring the mortality and morbidity indicators mentioned above, observing for epidemic outbreaks, and monitoring trends in endemic diseases is the role of surveillance in the emergency phase. As the disaster response transitions from the emergency phase to the postemergency and rehabilitation phases, trends in key indicators will measure the effectiveness of the relief efforts. The role of a surveillance system and its applications are discussed in Chapter 37.

PITFALLS Each epidemiologic method has its drawbacks. Vulnerability analyses fail when they don’t take into account all the factors that contribute to the structure of the human environment, particularly the knowledge, attitudes, and behaviors of the population at risk. Rapid needs assessments continue to suffer from lack of common shared indicators between donor agencies, NGOs, and international organizations. Mortality rates may be inappropriately inflated or deflated if the population estimates are not accurate. Respondents may easily introduce biases in participatory appraisals, for example, exaggerating the needs of the community knowing that the interviewer will likely have access to outside resources or, because of mistrust or pride, will minimize the needs. Bias is also inherent in nonprobability sample surveys; critical errors can result when such samples are generalized to a population. Since the humanitarian response depends on each of these methods, it is critical that they are used correctly and appropriately. PRACTICAL APPLICATIONS OF DISASTER EPIDEMIOLOGY 331

REFERENCES 1. Binder S, Sanderson LM. The role of the epidemiologist in natural disasters. Ann Emerg Med. Sep 1987;16:1081-84. 2. Sommer A, Mosley WH. East Bengal cyclone of 1970: epidemiological approach to disaster assessment. Lancet 1972;1(7759):1029-36. 3. deVille deGoyet C, del Cid E, Romero A, et al. Earthquake in Guatemala: epidemiologic evaluation of the relief effort. Bull Pan Am Health Organ. 1976;10(2):95-109. 4. Armenian HK, Melkonian A, Noji EK, et al. Deaths and injuries due to the earthquake in Armenia: a cohort approach. Int J Epidemiol. 1997;26:806-13. 5. The Sphere Project: Humanitarian Charter and Minimum Standards in Disaster Response. Available at: http://www.sphereproject.org. 6. World Health Organization. Community Emergency Preparedness: A Manual for Managers and Policy-makers. Geneva:World Health Organization; 1999. 7. Turner BL, Kasperson RE, Matson PA, et al. A framework for vulnerability analysis in sustainability science. Proc Natl Acad Sci U S A. 2003;100(14):8074-9. 8. Lave TR, Lave LB. Public perception of the risks of floods: implications for communication. Risk Analysis. 1991;11(2):255-67. 9. Chou YJ, Huang N, Lee CH, et al. Who is at risk of death in an earthquake? Am J Epidemiol. 2004;160(7):688-95. 10. Glass RI, Craven RB, Bergman DJ, et al. Injuries from the Wichita Falls tornado: implications for prevention. Science 1980;207:734-8.

332 POST - EVENT TOPICS

11. Spiegel PB, Burkle FM, Dey CC, et al. Developing public health indicators in complex emergency response. Prehospital Disaster Med. 2001;16(4):281-5. 12. Robinson WC. Demographic Assessment in Disasters: A Guide for Practitioners. Baltimore: Center for International Emergency, Disaster & Refugee Studies, Johns Hopkins Bloomberg School of Public Health. In press. 13. Bradt DA, Drummond CM. Rapid epidemiological assessment of health status in displaced populations: an evolution toward standardized minimum data sets. Prehosp Disast Med. 2003;17(4): 178-85. 14. Burkle FM. The epidemiology of war and conflict. In:Cahill JD, ed. Bioterrorism and Complex Emergencies. New York: Springer Press; submitted for publication. 15. Centers for Disease Control and Prevention. Rapid health response, assessment, and surveillance after a tsunami—Thailand, 2004-2005. MMWR. Jan 2005:54(3):61-4. 16. Centers for Disease Control and Prevention. Rapid assessment of the needs and health status of older adults after Hurricane Charley—Charlotte, DeSoto, and Hardee Counties, Florida, August 27-31, 2004. MMWR. 2004:53(36);837-40. 17. The Sphere Project. The Humanitarian Charter and Minimum Standards in Disaster Response. Geneva: 2004. 18. Gordis L. Epidemiology. 2nd ed. Philadelphia: WB Saunders; 2000.

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5 2

Measures of Effectiveness in Disaster Management Frederick M. Burkle, Jr. and P. Gregg Greenough

Measures of effectiveness (MOEs) are operationally quantifiable management tools that provide a means for measuring effectiveness, outcome, and performance (including success or failure) of disaster management.1,2 The foundation units or elements for developing MOEs are found in indicators used to assess, monitor, and evaluate services provided by disaster relief agencies and organizations.3 Most importantly, MOEs have the capability to serve as an integration performance tool that speaks to the disaster timeline or critical pathway and allows for the horizontal crossing of sector and professional boundaries that may influence both policy decisions and the operationalizing of policy.4

HISTORICAL PERSPECTIVE MOEs were first used in industry to measure the performance of products.2 Disaster research and application of MOEs were directed primarily toward disaster sectorspecific indicators, such as mortality rates, under-age-5 mortality rates, case fatality rates, and water requirements per person per day, to name but a few.1 Eventually, multiple indicators were studied to determine the influence of multiagency and multisectoral indicators on overall performance. For example, in Somalia, the military developed over 500 security-related indicators, only a small number of which actually were essential to assessing the success or failure of security on the mission. By applying these security indicators against other humanitarian indicators used by relief agencies and logisticians, a clearer picture was gained as to what might be contributing to or detracting from the performance of the mission. For example, failures to adequately mitigate malnutrition in some geographic sectors were found by MOE analysis to be more related to lack of security and access to aid for the intended recipients of care rather than lack of supplies delivered to the local warehouses.2

CURRENT PRACTICE Currently, MOEs are used as combined “essential indicators”to gain an overview of management performance and

to help define critical pathways (e.g., the multisectoral/ agency organizational response), to assess performance, and to define the end state or sustainability of operations. Essential indicators are MOEs as they subsume the essential indicators, often from each sector, into a definable horizontal measure of overall disaster management. As such, they are the quantifiable language of a critical pathway that disaster managers follow, initially on an hourly and subsequently daily basis, to ensure that management requirements are being met.3 If expected requirements are not met across the management timeline, this becomes a negative variance that must be investigated as to the cause and solved as soon as possible. Also, there may be an unexpected improvement or acceleration of the disaster response timeline that becomes a positive variance, which may eventually alter the way the timeline process of management will be defined in future disasters. Most critical is that MOEs have the capability to unify the language of the disaster event, thereby bringing together the strange bedfellows made up of the varied disaster response agencies and organizations. If disaster organizations agree to share information and work for a common goal, MOEs are a priority in management, evaluation, and monitoring for all concerned, especially the beneficiaries of relief and development. Whereas MOEs must be quantifiable in nature, this does not exclude semiquantitative or -qualitative indicators that often successfully provide a reliable measure of social, cultural, behavioral, and mental health disasterrelated services. To be useful, indicators and the MOEs they support must be defined as precisely as possible, easily understood, reliable, valid, simple, and informative. MOEs must be consistently measurable, cost-effective, sensitive, timely, mission related, and appropriate to the developed critical pathway followed by disaster managers. The key to understanding MOEs and the process by which they are generated lies in (1) the recognition of which indicators are considered essential measures of sector performance; (2) the assessment of the applicability and reliability of these essential indicators and whether they meet usefulness criteria; and lastly (3) the ability of these essential indicators to provide the coordinating language of the timeline or critical pathway specific to the disaster event (Fig. 52-1). 333

MOEs

Incorporation of essential indicators on to disaster timeline template

Indicators assessed for applicability and reliability as essential indicators

Individual sector and multi-agency indicators gained from planning, assessment, monitoring and evaluation of disaster services

FIGURE 52–1 Measures of effectiveness are based on essential indicators.

MOEs have been applied to complex humanitarian emergencies to study complex multiagency performance as well as in narrowing the field of multiple available indicators in a large-scale bioterrorism event to a workable number of essential indicators that will readily weather management success.1,2,5 Here the essential indicators that make up the operational MOEs include: • Measuring response capacity of deployed biologic sensor devices linked to a real-time public health surveillance system; • Measuring how rapidly a full-coverage health information system is mobilized with timely dissemination of accurate information; • Measuring variance compliance to a bioagentspecific management timeline; • Measuring decline in mortality and morbidity; • Measuring control of transmission rate (Ro) in communicable outbreaks; and • Measuring management resource distribution across the entire cohort of a vulnerable population.

334 POST - EVENT TOPICS

In this regard, indicators for education of suspected or exposed victims may indeed be useful but may contribute more critically to the knowledge base of more essential indicators such as health information system and decline in mortality and morbidity. If mortality and morbidity is not declining as expected, then the contributing indicators are analyzed for cause.

PITFALLS The main pitfalls of MOEs are organizational ones. In the heat of a disaster event, they are often neglected or forgotten. It takes some agency leadership to organize a multiagency effort, and although the United Nations (UN) includes MOEs as a need in peacekeeping missions, this is often left to the discretion of the mission commander. That said, the after-action report for UNPROFOR, the UN mission to the Former Yugoslavia, criticized the lack of MOEs in the mission planning. The inherent verticality of agencies and organizations in disasters prohibits the horizontal cooperation needed to get MOEs operational. Timelines or critical pathways, although available for natural and chemical disasters management, have not been developed for complex emergencies and large-scale bioterrorism events, the two disasters where they are most needed. REFERENCES 1. Burkle FM. Complex, humanitarian emergencies: III. measures of effectiveness. Prehospital Disaster Med. 1995;10(1):48-56. 2. Dworken JT. Measures of effectiveness (MOEs) for humanitarian intervention: Restore hope and beyond. Working paper 27. Washington DC: Center for Naval Analyses; 1993. 3. Spiegel PB, Burkle FM, Dey CC, Salama P. Developing public health indicators in complex emergency response. Prehospital Disaster Med. 2001;16(4):281-5. 4. Burkle FM. Complex emergencies: measuring effectiveness across a multitude of indicators. Standardized monitoring and assessment of relief and transition (SMART) workshop. Washington, DC, 26 July 2002. Available at: http://www.smartindicators.org/workshop/ agenda2.htm. 5. Burkle FM. Measures of effectiveness in large-scale bioterrorism events. Prehospital Disaster Med. 2003;18(3):258-62.

S E C T I O N

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Topics Unique to Terrorist Events

5 3

Lessons Learned as a Result of Terrorist Attacks* Mark E. Keim

The threat of terrorism is a high-priority national security and law enforcement concern in the United States. Modern policy on combating terrorism against the United States has been evolving over the past 30 years. A series of presidential decision directives, implemented guidance, executive orders, interagency agreements, and legislation now provide the basis for counterterrorism programs and activities in more than 40 federal agencies, bureaus, and offices. Unfortunately, societal reactions and public policy regarding disasters do not always translate into effective outcomes of “lessons learned.” Traditionally, after-action studies and reports have been composed of largely anecdotal observations offered by relatively small consensus groups. Although helpful, these methods frequently lack scientific validity. Since most responders (and political policy makers) do not experience a statistically significant number of disaster events themselves, so-called lessons learned often represent the same redundant themes and epiphanies of a relatively novice cohort. In one 2-year comparative study of catastrophes in disaster-prone India, many of the same problems listed as “lessons learned”from one national disaster were only to be repeated just 2 years later and, ironically, were again listed as lessons learned in yet another after-action report (Giannone P., personal correspondence, 2004). As another example, remarkable parallels may also be drawn between lessons learned at the Pan American Health Organization Meeting on Evaluation of Preparedness and Response to Hurricanes Georges and Mitch (held over a decade ago)1 and recent U.S. Government Accountability Office (GAO) reports involving federal and state efforts related to terrorism preparedness.2-5 Unfortunately, it has also been the case that even when sound findings are identified within an after-action review, these lessons are “learned” by the group but not implemented into an effective policy. New policies may even become implemented but never validated by realworld experience. And finally, even the best-validated *The material in this chapter reflects solely the views of the authors. It does not necessarily reflect the policies or recommendations of the Centers for Disease Control and Prevention or the U.S. Department of Health and Human Services.

public policies may not be maintained in the absence of an ongoing risk-reduction program. Terrorism itself has been an age-old threat to the public health and security of many populations throughout the world. During the past three decades, terrorist attacks against the United States have led to a significant number of legislative, regulatory, organizational, and programmatic actions associated with very comprehensive and ambitious expectations. More study is needed before we can conclude to what extent these major changes will have a lasting and significant impact on capacity and capability to deal with future disasters or the practice of disaster medicine as a health science. Even though the extent of long-term impact remains uncertain, two major accomplishments have become realized: (1) national capacity of emergency management appears to have been increased, and (2) awareness and possibly even commitment to the issue of emergency preparedness also appear to be greater.6 It would appear that the information and knowledge about what to do in response to the terrorist threat already existed before September 11, 2001. What was lacking was the political backing for change and the political will to act. A rapid series of events involving emergency management and protection of critical infrastructure then followed. This chapter identifies recent terrorist events that have had a significant impact upon U.S. society and public policy. The discussion correlates these policies with widely accepted doctrines of incident management and disaster risk reduction. From this perspective, these lessons learned represent a recent trend for implementation of what may be more accurately described as already well-established doctrines of disaster medicine and emergency management.

HISTORICAL PERSPECTIVE Development of Modern U.S. Emergency Management Policy Modern emergency management policy in the United States began with the “Unlimited National Emergency” 335

(Proclamation 2487 of May 27, 1941) immediately before World War II. Over three decades later, out of concern for a catastrophic earthquake predicted to occur in the central United States, the Earthquake Hazards Reduction Act of 1977 mandated the development of a Federal Response Plan for a Catastrophic Earthquake. In July 1979, Executive Order 12148 delegated authority to the U.S. Federal Emergency Management Agency (FEMA) to establish federal policies and to coordinate all civil defense and civil emergency planning, management, mitigation, and assistance functions of executive agencies. At this time, FEMA was also assigned the lead responsibility for response to consequences of terrorism. The Robert T. Stafford Disaster Relief Act PL 100-707 was enacted in 1986 to formalize a coordinated federal policy. In 1990, FEMA issued the Federal Response Plan to establish a process for coordinated delivery of federal disaster assistance. After significant criticism of the response to Hurricane Andrew in 1992, Congress adopted a formal all-hazards approach to emergency management in the National Defense Authorization Act of 1994, PL 103-160. In June 1995, President Clinton issued Presidential Decision Directive 39 (PDD 39), the central blueprint for the U.S. counter-terrorism strategy. PDD 39 elaborated a strategy for combating terrorism consisting of three main elements: (1) reduce vulnerabilities and prevent and deter terrorist acts before they occur, (2) respond to terrorist acts that do occur, including managing crises and apprehending and punishing terrorist perpetrators, and (3) manage the consequences of terrorist attacks. All three elements of the strategy include terrorism involving weapons of mass destruction.7 Emergency managers will recognize these elements as phases of the risk reduction cycle including disaster prevention, mitigation, and response. The Defense Against Weapons of Mass Destruction Act of 1996, Public Law 104-201, September 23, 1996 (also known as the Nunn-Lugar-Domenici Act), drew on the convergence of federal assets at the Atlanta 1996 Olympic Science and Technology Center8,9 and directed this momentum to set in place a long-term effort to prepare domestic response for terrorist threats.

Development of Incident Management Systems The Incident Command System (ICS) was conceptualized more than 30 years ago, in response to a devastating wildfire in California. As a result, Congress mandated that the U.S. Forest Service design a system that would improve wildland fire protection agencies to effectively coordinate interagency action and allocate suppression resources in dynamic situations. This system became known as FIRESCOPE (FIrefighting RESources of California Organized for Potential Emergencies) ICS. Although FIRESCOPE ICS was originally developed to assist in the response to wildland fires, it was quickly recognized as a system that could help public safety responders provide effective and coordinated incident management for a wide range of situations, including 336 TOPICS UNIQUE TO TERRORIST EVENTS

floods, hazardous materials accidents, earthquakes, and aircraft crashes. In 1982, all FIRESCOPE ICS documentation was revised and adopted as the National Interagency Incident Management System (NIIMS). In Homeland Security Presidential Directive-5 (HSPD-5), President Bush called on the Secretary of Homeland Security to develop an NIMS to provide “a consistent nationwide approach for federal, state, tribal, and local governments to work together to prepare for, prevent, respond to and recover from domestic incidents,” regardless of cause, size, or complexity.10 On March 1, 2004, after close collaboration with state and local government officials and representatives from a wide range of public safety organizations, Homeland Security issued the NIMS guidelines.10 These incorporate many existing best practices into a comprehensive national approach to domestic incident management and are applicable at all jurisdictional levels and across all functional disciplines or public sectors.

Development of Disaster Risk Reduction Strategies In 1994, the States Members of the United Nations, having met at the World Conference on Natural Disaster Reduction in the city of Yokohama, Japan, in partnership with nongovernmental organizations and with the participation of international organizations, the scientific community, business, industry, and the media affirmed that “Disaster prevention,mitigation,and preparedness are better than disaster response in achieving the goals and objectives of the Decade. Disaster response alone is not sufficient, as it yields only temporary results at a very high cost. We have followed this limited approach for too long. This has been further demonstrated by the recent focus on response to complex emergencies, which, although compelling, should not divert from pursuing a comprehensive approach. Prevention contributes to lasting improvement in safety and is essential to integrated disaster management” [emphasis added].11

Development of Disaster Medicine During the late 1980s, disaster medicine began to develop in the United States as a subspecialty of emergency medicine.12,13 In the 1990s, several disaster medicine fellowships were established and graduated at least six disaster medicine subspecialists. None of these programs received earmarks for federal or state support of disaster medicine. All were closed by the end of the decade.

Recent Terrorist Events That Have Influenced U.S. Policy The development of new disaster policy is dependent on a society’s perception of risk. Public perception of risk is known to be higher immediately after the occurrence of a major disaster. During this time there is a notable window of opportunity for change in disaster-reduction policy. Table 53-1 is a listing of recent terrorist events and their corresponding influence on resultant U.S. policy.

LESSONS LEARNED AS A RESULT OF TERRORIST ATTACKS 337

Bhagwan Rajneesh Salmonella Release

Bombing of Pan Am Flight 103

World Trade Center (WTC) Bombing

1984

1988

1993

1996

Crash of TWA Flight

Chechnyan Threaten to Use Radiologic Dispersion Device (RDD) Bombing of Lebanon Marine Barracks Bombing of Khobar Towers

1995

1996

Bombing of the Murrah Federal Building in Oklahoma City

1995

1994-1995 Aum Shinrikyo Sarin Attacks

EVENT

DATE

•

•

• • •

• •

•

•

• •

•

•

• •

•

• •

•

• •

•

•

SIGNIFICANCE

Truck bomb detonated near U.S. military barracks in Lebanon Linked to MIE Truck bomb detonated near U.S. military barracks in Dhahran, Saudi Arabia Linked to MIE Killed 19 Americans, injured 500 Explosion of airliner during takeoff in New York. Initially believed to be result of a terrorist attack using surface-to-air missile Later ruled to be accidental

•

• •

•

This event was an asymmetric attack on U.S. military facility by MIE.

(Continued)

There was an unprecedented state and federal preparedness activities related to the 1996 Olympic games. In 1997, the White House Commission on Aviation Safety and Security (Gore Commission) issued a report recommending that “The federal government should consider aviation security as a national security issue and provide substantial funding for capital improvements.” The Department of Homeland Security 2005 budget includes $61 million for the research and development of countermeasures to protect commercial aircraft from shoulder-fired, surface-to-air missiles.

This was an asymmetric attack on U.S. military facility by MIE.

•

Salmonella bacteria released in • This was the first large-scale biologic attack in the United States with a high morbidity rate. 10 Dalles, Oregon, restaurants • For years, this outbreak went largely unrecognized as an intentional event. Outbreak linked to Bhagwan Rajneesh religious cult years later No deaths, over 800 infected Parcel bomb detonated on plane • In 1989, President George H. W. Bush issued Executive Order 12686, which formed the Presidential Commission while en route from London to on Aviation Security and Terrorism. New York, explodes over Lockerbie, Scotland Linked to Libyan Militant Islamic • President George H.W. Bush signed the Aviation Security Improvement Act of 1990. Extremist (MIE) terrorist cell Killed 270 Truck bomb detonated in the • Congress enacted the “National Defense Authorization Act for Fiscal Year 1995, which directed FEMA to: WTC parking garage Linked to MIE including multiple (1) Prepare federal response plans and programs for the emergency preparedness of the United States; and Arab nationalities. Killed 6, wounded 1042 (2) Sponsor and direct such plans and programs to coordinate such plans and programs with state efforts. 1994: Japanese religious cult, Aum • This was the first time that a nonstate group used a chemical weapon against civilians. Shinrikyo, released sarin nerve agent • Demonstrated how terrorist groups could recruit scientists, obtain deadly chemical or biologic agents, and put in a residential area of Matsumoto, Japan. plans into action. This event killed 7 and injured 500. • President Clinton released PDD 39. 1995: Same group released sarin in the • The 1996 Nunn-Lugar-Domenici Act (a.k.a., Defense Against Weapons of Mass Destruction [WMD] Act of 1996) Tokyo subways, killing 12 and injuring was passed. hundreds. • In 1997, the Terrorist Annex to the Federal Response Plan was adopted by FEMA. • These events provided evidence of extensively coordinated planning and execution. Truck bomb detonated near the Alfred • This was the first instance of large-scale bombing caused by U.S. domestic terrorists. P. Murrah Federal Building in Oklahoma • This was the first use of the President’s authority under the Stafford Act to “self-initiate” an emergency declaration City, Oklahoma. for emergencies with federal involvement. Linked to U.S. right-wing extremists • Experts other than foreign policy and security specialists became more involved in terrorist preparedness and Killed 169, injured more than 500 response (most notably, disaster medicine). • This event initiated increased awareness of occupational health concerns among disaster responders (most notably, behavioral health). Chechnyan separatists direct news • First credible threat for use of an RDD (a.k.a.“dirty bomb”) by a sub-national group. reporter to Moscow park where cesium-137 RDD weapon is found

DESCRIPTION

TABLE 53-1 RECENT TERRORIST EVENTS THAT HAVE INFLUENCED U.S. POLICY

338 TOPICS UNIQUE TO TERRORIST EVENTS

Bombing of Atlanta Olympic Games

U.S Embassy Bombings in Kenya and Tanzania

Attack of the U.S.S. Cole

WTC and Pentagon Attacks

Anthrax Letter Attacks

1996

1998

2000

2001

2001

2002-2004 Bombings and attacks in Russia, Indonesia, Philippines, Kenya, Saudi Arabia, Afghanistan, Iraq, and Spain 2004 Attack on US Consulate in Jeddah, Saudi Arabia

EVENT

Letters containing anthrax spores mailed to news media personnel and Congress Leads to the first cases of intentional anthrax infection in the United States Infections follow a 3-year history of over 1500 anthrax letter hoaxes. Perpetrators remain at large Killed 5, infected 18 A series of terrorist bombings and attacks involving numerous nations Most attacks are linked to MIEs and some to national separatist movements Most events kill a few to several hundred victims A car bomb detonation and subsequent small arms attack of the US consulate in Jeddah, Saudi Arabia. Linked to MIE, possibly Al-Qaeda

•

• •

•

•

• • •

•

•

•

•

• •

•

• •

•

• •

•

•

Occurred within days of the start of the 1996 Olympics Shoulder-fired surface-to-air missiles were used by MIE to attack aircraft in Kenya, Saudi Arabia, and Iraq during 2003-2004 Pipe bomb explodes at Centennial Olympic Park, in Atlanta, Georgia, during the ninth day of the 1996 Summer Olympics Killed one, injured 112 Truck bombs detonated simultaneously near U.S. embassies in Nairobi and Dar es Salaam Linked to MIE,Al-Qaeda terrorist network Killed 280, injured over 5000 Explosion occurred on the destroyer U.S.S. Cole docked at the harbor in Aden,Yemen Linked to MIE,Al-Qaeda terrorist network Killed 17, injured 39 Hijacked airliners deliberately flown into WTC towers in New York City and the Pentagon in Washington, DC Linked to MIE,Al-Qaeda terrorist network Killed over 3000, injured hundreds

•

DESCRIPTION

•

•

• •

•

• • • • •

•

•

• •

• • •

• • • • • •

• •

Recent U.S. activities resulting in hardening and increasing security of U.S. embassies and consulates proved valuable in mitigating the impact of the attack

These events illustrated MIE tactics for attacks against broader pro-Western interests. Events related to national separatist movements revealed a growing level of sophistication in coordination and execution of attacks. Nations other than the United States became frequent targets.

This attack has had a significant long-term economic impact as well as symbolic significance. U.S. response included at least 10 pieces of national legislation, two Executive Orders, one Homeland Security Decision Directive, one new federal department (i.e., Department of Homeland Security), and several significant reports. There was unprecedented speed in the passage of major federal legislation, in absence of Congressional hearings or task forces. A major reorganization of U.S. intelligence organizational structure occurred in 2004 consistent with recommendations of the 9/11 Commission report. This event was the second-largest-scale biologic attack in the United States and had the highest mortality rate. Reports cited speculation regarding U.S. domestic origin of terrorism. The challenges and shortcomings facing the nation’s public health system were revealed. The Federal Concept of Operations Plan (CONPLAN) for responses to terrorist attacks was not used. The FBI did not exercise its crisis management authority, nor did FEMA exercise consequence management authority as called for by PDD 39. The Federal Response Plan was never activated.

This bombing occurred during first interagency coordination of federal WMD response teams. Title XIV of the Defense Authorization Act of 1996,The Defense Against WMD Act (a.k.a. Nunn-Lugar-Domenici Act) was adopted. The Terrorist Annex to the Federal Response Plan was adopted by FEMA. The first forward staging of a medical stockpile in preparation for WMD casualties was created. This was the first large-scale attack on U.S. embassies or consulates caused by MIE terrorists. The event provided evidence of extensively coordinated planning and execution. The United States responded with cruise missile strikes in Afghanistan and Sudan. U.S. policy shifted focus toward proactive and global policy that is less constrained about targeting terrorists, their bases, and their infrastructure. First HHS public health and medical response to overseas terrorism This was the first asymmetric attack on a U.S. naval warship perpetrated by MIE. The Department of Defense subordinated its terrorism analysis capability under the Joint Chief of Staff/ Intelligence. This reduced confusion and clarified responsibility for warning.

SIGNIFICANCE

RECENT TERRORIST EVENTS THAT HAVE INFLUENCED U.S. POLICY—Cont’d

DATE

TABLE 53-1

CURRENT PRACTICE AND LESSONS LEARNED Lessons learned as result of recent terrorist attacks can be divided into two main categories: those involving a trend toward a more comprehensive disaster risk reduction strategy (Table 53-2), and those building capacity for more effective models of incident management (Table 53-3).

PITFALLS Homeland Security and Emergency Management Remain Poorly Defined Although a new homeland security emphasis is under way throughout the federal government, the process is still evolving. Additional actions to clarify missions and activities will be necessary, and some agencies will need to determine how best to support both homeland security and nonhomeland security missions.14 Many people are not clear on just what homeland security is and how it is in fact quite different from all-hazard emergency management. People tend to use the terms homeland security and emergency management synonymously. The extent to which the homeland security mission is displacing the natural and technologic disaster function is also an important question. Related to this question is the degree to which extensive experience in natural hazards has been leveraged (or ignored) in the new reality of homeland security.

The Need for an All-Hazard Strategic Approach and National Strategy According to WL Waugh in 2000,“For the most part, policies and programs have been instituted and implemented in the aftermath of a disaster, based almost solely on that disaster experience, and with little investment in capacity building to deal with the next disaster.”15 After the events of September 11, 2001, national legislation was enacted and organizational changes occurred in the absence of any hearings or studies being ordered to determine what went wrong and what remedies were needed. Another unusual characteristic of the aftermath of this disaster was the speed with which the major federal organizational and coordination changes occurred, even before Congressional hearing or special task forces were formed.16 Because the drafters of Public Health Security and Bioterrorism Preparedness Act (June 12, 2002), Public Law 107-188, “did not have detailed information as to how other federal response plans operated or were designed to operate, the statute tends to encourage stove-piping of information, planning and response by the medical community.” Additionally, the principal assets of the medical community, including personnel and institutions, are private; therefore, statutory mandates are difficult to apply.16

The first step toward disaster risk reduction involves adopting a strategic national approach. The first annual Gilmore report (REF) to the President and the Congress of the Advisory Panel explored a broad range of issues regarding weapons of mass destruction and details of actual terrorist attacks. The report formulated several initial policy recommendations, one of which included “the need for a national strategy to address domestic response to terrorism.”17 The second annual Gilmore report re-sounded the alarm in 2000, stating,“The United States needs a functional, coherent national strategy for domestic preparedness against terrorism.”18 Comprehensive disaster risk-reduction measures include prevention, mitigation, response, and recovery phases. Recent terrorist attacks have driven emergency management policy toward prevention, preparedness, and mitigation as the most cost-effective interventions. However, these three pre-event disaster risk-reduction activities and programs remain underdeveloped for natural disasters in the United States.

The Need for National Threat and All-Hazard Risk Assessment According to a Government Accountability Office report in 2001, “The first step toward developing a national strategy is to conduct a national threat and risk assessment.”2 By 1999, a national-level risk assessment of potential chemical and biologic terrorist incidents had not yet been performed.19 A risk assessment is a decision-making process that is used to estimate risk and then to establish requirements and priorities. The components of risk assessment include asset and loss impact assessment, threat assessment, and vulnerability analysis.20 Comprehensive risk management strategies involve risk assessment, cost-benefit analysis, risk communication, and risk-reduction activities. The Department of Justice and the Federal Bureau of Investigation (FBI) have collaborated on such an assessment, but as of September 2001, they had not formally coordinated with other departments and agencies on this task.2 Many conflicting statements have been made in public testimony before Congress and in the press concerning the risk of dissemination of a chemical or biologic agent on U.S. soil.6 The Centers for Disease Control and Prevention (CDC), in partnership with other military and civilian federal governmental organizations, has developed a list of priority agents for biologic warfare.21 The intelligence community has recently produced National Intelligence Estimates and other high-level analyses of the foreign-origin terrorist threat that include judgments about the more likely chemical and biologic agents that would be used. In the Homeland Security Act of 2002, Congress required the Homeland Security Department to implement a system for analyzing information on terrorist threats. The Terrorism Threat Integration Center was announced in February 2003 and is housed within the Central Intelligence Agency, serving as a central repository for all government intelligence information. However, this repository does not integrate significant LESSONS LEARNED AS A RESULT OF TERRORIST ATTACKS 339

TABLE 53-2 DISASTER RISK REDUCTION LESSONS LEARNED AS A RESULT OF RECENT TERRORIST EVENTS LESSON

REPORTS AND FEDERAL ACTIONS

Need for a comprehensive and coordinated disaster risk-reduction strategy

REPORTS AND RECOMMENDATIONS

• • • • • • • • • • • • • •

Seiple C. Consequence management: domestic response to weapons of mass destruction. Parameters. 1997;Autumn:119-34. Gilmore Report I: Identified as the “need for national strategy to address domestic response to terrorism.” December 15, 1999. GAO-01-14, Combating Terrorism: Federal Response Teams Provide Varied Capabilities; Opportunities Remain to Improve Coordination. November 30, 2000. Gilmore Report II: Restated “The US needs a functional coherent strategy for domestic preparedness against terrorism.” December 15, 2000. U.S. Commission on National Security/21st Century. Seeking a National Strategy:A Concert for Preserving Security and\Promoting Freedom:The Phase II Report on U.S. National Security Strategy for the 21st Century. April 15, 2000, 17 pp. GAO-01-822, Combating Terrorism: Selected Challenges and Related Recommendations, September 20, 2001. GAO-01-915, Bioterrorism: Federal Research and Preparedness Activities, September 28, 2001. Gilmore Report III:“Recommended clarifying the role of the military for domestic preparedness against terrorism.” December 15, 2001. GAO-02-893T, Homeland Security: New Department Could Improve Coordination but May Complicate Priority Setting. June 28, 2002. GAO-02-924T, Homeland Security: New Department Could Improve Biomedical R&D Coordination but May Disrupt Dual-Purpose Efforts. July 9, 2002. GAO-02-954T, Homeland Security: New Department Could Improve Coordination, but Transferring Control of Certain Public Health Programs Raises Concerns. July 16, 2002. GAO-03-260, Homeland Security: Management Challenges Facing Federal Leadership. December 20, 2002. GAO-04-100, Homeland Security: Effective Regional Coordination Can Enhance Emergency Preparedness. September 15, 2004. Burkle F, Noji E. Health and politics in the 2003 war with Iraq: lessons learned. Lancet. 2004;364(9442): 1371; criticized U.S. military-led humanitarian efforts.

FEDERAL ACTIONS

• • • • Need for a comprehensive analytical risk assessment

100 meters

strous storms cause over 50% of the tornado-related fatalities in the United States each year.3 Tornadoes occur with equal frequency in all countries of the world that have land mass in the middle latitudes, but the unique landscape and weather patterns of the United States cause it to have the most intense tornadoes of any country. Between 1950 and 2003, over 4663 deaths and 80,376 injuries were reported as directly related to tornadic storms in the United States. In addition to the loss of life and the frequent injuries, tornadoes were responsible for over $20 trillion in property and crop damage between 1950 and 2003.4 Tornadoes come in all shapes and sizes and can occur anywhere in the United States at any time of the year. In the southern states, peak tornado season is March through May, whereas peak months in the northern states are during the summer.2 Because of the consistent high frequency of tornadoes seen in the region including northern Texas, Oklahoma, Kansas, and Nebraska, this area has become known as “Tornado Alley.”5 The probability that any one particular city in North America will be struck by a tornado has been calculated as once every 250 years.6 This probability is much higher for communities in Tornado Alley. For example, Oklahoma City has been struck by significant tornadoes 26 times in the past 100 years.7 Tornadoes strike with little or no warning. Because of investments in research and observation systems such as the NEXRAD Doppler radar, interactive computer systems, and other forecasting technology, the lead time for tornadoes has nearly doubled from a national average of 5 minutes in the early 1990s to nearly 11 minutes today. Major storms are often picked up or spotted and warnings made more than 20 minutes before the tornado touches down.1 In the United States, all severe weather watches and warnings are issued by the Storm Prediction Center (SPC) in Norman, Oklahoma. The SPC is a division of the National Weather Service (NWS). The SPC issues a tornado watch when their forecasting systems indicate there is a region where tornadoes and other kinds of severe weather are possible in the next several hours. This is the time to turn on the TV or radio to the local weather channel and quickly review tornado disaster plans. The SPC issues a tornado warning only when a tornado has been spotted or when Doppler radar has detected a thunderstorm circulation that can spawn

a tornado at any moment.8 When a tornado warning is issued, immediate action to ensure safety during a tornado should be undertaken. Despite the improved surveillance and severe weather warning systems, communities that hope to prevent unnecessary death and injury from tornado disasters must prepare long before the warning sirens are sounding.

Pre-Incident Actions The most important preincident action is to develop a tornado disaster plan and to rehearse that plan regularly. Such rehearsals should be especially frequent in communities within Tornado Alley. The Federal Emergency Management Agency (FEMA) has published a State and Local Guide for All-Hazard Emergency Operations Planning (SLG 101), which can be downloaded from their Web site.9 The SLG 101 has an appendix addressing specific issues for tornado planning.

Communication Command/Control Designate a clear command and control structure involving police, fire, EMS, and local hospital emergency rooms with capability for these entities to communicate on radio devices that do not depend on the local power grid for functionality. Warning Systems Make certain all public buildings, trailer home parks, nursing homes, and all hospitals have 24/7 access to local weather reports and a method for receiving severe weather watch and warning information from the SPC. Active warning systems (weather alert sirens, weather alert radios, and loudspeakers) are more effective than passive warning systems (conventional radio and TV).10

Injury Prevention Warning/Shelter Timely warning of an approaching tornado and appropriate sheltering have proved to be the most important factors in preventing injury and death in the face of tornadic storms.11-13 Focused Education Public health education regarding tornado warning systems and safe sheltering during tornados should be provided to the populations most at risk. These include: 1. People in mobile homes 2. The elderly, very young, and physically or mentally impaired. 3. People who may not understand the warnings because of a language barrier.1,9 Sheltering Guidelines FEMA, the Centers for Disease Control and Prevention (CDC), and the NWS have published guidelines detailing

the safest sheltering actions to take in case of a tornado warning. These are summarized in Table 74-2.

Emergency Medical Response Hospital Power/Water Supply Medical facilities are not immune from tornado damage.14 Electrical power and clean, running water are essential to medical care following a tornado. All hospitals should have plans for short-term back-up power and water supply should the main power and water lines be damaged. Trauma System Triage/Transport An organized trauma system with a centralized communication system has been shown to be highly effective and efficient in ensuring that the sickest patients go to the highest level care facilities following a tornado disaster.15 Even with such a system in place, a significant minority of patients will require transfer from community hospitals to higher-level trauma centers. Agreements for such transfers should be worked out before a mass casualty incident occurs. Aeromedical transport has been shown to be of great benefit when they come to rural hospitals, or when the normal urban roadways are damaged or closed because of the disaster.16 Traffic Control at Hospitals Traffic control has consistently been reported as a problem in and around emergency departments following a tornado disaster. Disaster plans should include

TABLE 74-2 SHELTERING GUIDELINES IN CASE OF TORNADO WARNING In General: 1. 2. 3. 4.

Stay away from windows. When a warning is issued, move to the safest area immediately. If possible, put on a helmet. Get under a sturdy piece of furniture and cover yourself with a blanket, pillows, or mattress.

IF YOU ARE:

YOU SHOULD:

Outside

Get inside a building. If stuck outside, stay away from cars and trees. Lie down in a ditch or culvert and cover your head and neck with your hands. Leave the mobile home. Go to a community shelter. If no shelter is available, see “Outside” above. Move the car off the road. Leave the vehicle. Do not seek shelter under an overpass. If stuck outside, see above. Go to the designated interior room or hallway away from windows, and get under a sturdy piece of furniture. Go to the basement. If there is no basement, go to an interior room or hallway away from windows, get under a sturdy piece of furniture, and cover yourself with a blanket.

In a mobile home In a car At work or school In a house

TORNADO 485

directions for hospital security or local police to secure the access and egress routes from local hospitals. These agencies should understand where to direct the walking wounded, privately owned vehicles, and EMS vehicles for appropriate triage and evaluation.17 Healthcare Provider Training The majority of patients arriving at hospitals following a tornado disaster will arrive by private vehicles. Some of these patients may have severe injuries. Healthcare personnel should be trained in proper spinal immobilization and vehicle extraction techniques in order to avoid further injury to these patients who have not benefited from prehospital medical care.8,17

Postincident Actions Search/Rescue Reports of tornado disasters—including the 1970 tornado in Lubbock, Texas and the 1996 tornado in Topeka, Kansas—support the intuitive idea that the most severely injured victims and the majority of those killed will be found in the core area of the tornado strike.8 Severely injured victims are likely to be thrown by the tornado, struck by flying debris, or found in buildings with the greatest structural damage. An aerial survey using fire, EMS, or police helicopters can greatly assist rescue efforts by defining the regions of greatest damage and guiding search teams to locations where the most injured patients are likely to be found. Such surveys may be hindered by severe weather still lingering in the region. Search-and-rescue teams and first responders should protect themselves from hazards such as downed power-lines, gas leaks, and potentially unstable building structures. This is especially important since most tornado fatalities are not prevented by rapid EMS transport. Most patients that die in tornado disasters do so at the scene prior to EMS arrival.8 Multiple reports of tornado disasters confirm that very few patients that arrive at the hospital alive die during hospitalization.8,15,18,19 EMS Triage EMS units should be deployed carefully along the area of the tornado strike. Early responding units will likely become overwhelmed with casualties and must be supported by other units or aeromedical transport systems that can move the severely injured patients to the area hospitals and resupply the units in the field. Casualty collection points should be set up using mobile EMS vehicles or public buildings such as schools or churches. These collection points should be carefully selected to avoid radio blackout zones so that the medical command/control personnel can stay in close contact with the providers in the field to coordinate evacuation resources. If aeromedical transport is to be used, personnel must be trained in selecting and marking safe landing zones for the helicopters. 486 NATURAL DISASTERS

Hospital Triage As in any mass casualty situation, it is imperative that open and precise communication channels are in place to allow triage personnel, emergency department physicians, and operating room personnel and surgeons to communicate as casualties arrive. Casualties following a tornado usually arrive in a bimodal fashion, with the least severely injured arriving first, usually within 5 to 30 minutes after the disaster. The severely wounded will arrive by EMS transport and by privately owned vehicles usually 1-4 hours after the tornado strike.17,20 Plans should be designed to allocate appropriate resources to the least injured without overwhelming personnel and space that will be needed by critically injured patients. Monitor Ongoing Weather Alerts It is not uncommon for multiple tornadoes to touch down in a region over a period of several hours. The emergency response teams and emergency departments should have access to NOAA weather alert radios and should constantly monitor the storm. Heavy flooding and/or hail may alter the medical response as well.

Medical Treatment of Casualties Types of Injuries The majority of injuries from tornado disasters are complex, contaminated soft-tissue wounds. Fractures are the second most common injury and the most common cause for hospitalization.8,10-12,15,19-20 Many fractures are open and require surgical wash-outs and reductions.21 Head injuries are the most common fatal injuries following tornado disasters.20,22 Nearly 50% of patients seen in emergency departments following tornado disasters will have soft tissue wounds as their chief complaint. Many of these wounds will be severely contaminated with mud and debris.8,9,22 Wound infections caused by gram-negative bacteria such as Escherichia coli, Klebsiella, Serratia, Proteus, and Pseudomonas are common in wounds sustained during tornadoes.23-25 A clean water supply, good lighting, large numbers of suture repair kits, and ample wound care materials are essential resources for emergency departments in a tornado response. In the case of water line damage, emergency departments must have access to a shortterm emergency water supply. Some have suggested that without clean water, emergency departments should not even attempt to treat patients following a tornado but instead act as triage or command/control headquarters.8,26 An emergency supply of high-powered flashlights should be kept in all emergency departments and the batteries checked regularly. Car headlights have been used as a temporary lighting mode in tornado disasters that caused loss of power to hospital centers.

CASE PRESENTATION At 6 PM on May 15, you are working in a community hospital on the outskirts of Kansas City and your triage nurse comes running into the emergency department (ED) screaming “A huge tornado has been spotted just 5 miles from here. The news says it’s headed right into the metropolitan area!!!” Because of the frequency of tornadoes in the region, your head nurse knows the drill and immediately activates the hospital tornado response plan. Suddenly the power goes out in the hospital. Thanks to the backup generator, the lights, monitors, and computers are back up within minutes. One of the new techs is assigned to watch three local news stations on the TVs in the waiting room and keep the head nurse posted on any new weather advisories or other public emergency announcements. This tech is also provided with a battery-powered weather alert (NOAA) radio that is kept in the emergency department for use during weather-related disasters. The operating room (OR) is notified of the possibility of mass-casualty incoming traumas, and the in-hospital radio system is tested to ensure adequate communications between the ED and the OR. All on-call physicians are alerted of the impending mass casualty and asked to respond ASAP. A call is made to the local police asking for assistance in organizing a controlled traffic pattern into and away from the ED. The hospital public affairs director is alerted via beeper and asked to organize a press-briefing area away from the ED. Over the next 5 hours your hospital receives some 200 tornado-related patients. Almost 70% of these patients arrive by private vehicle and must be triaged by ED and hospital staff.Thanks to recent training, all victims of blunt trauma or other high-risk injuries are carefully immobilized and c-collars are placed by the triage personnel. Again, thanks to the well-rehearsed hospital and regional disaster plan, you are able to provide appropriate care for all of these patients. During your shift, you and your colleagues treat 70 patients with soft tissue injuries, including

Unique Considerations Most tornado-related deaths occur prior to arrival at the hospital. Rapid EMS transport may not affect mortality from tornadoes. Soft tissue wounds from tornadoes should be considered highly contaminated, and delayed primary closure may be a prudent approach to wound management.

PITFALLS Up to 50% of soft tissue wounds and contusions from tornado disasters are sustained during search-and-rescue efforts. REFERENCES 1. National Oceanic and Atmospheric Administration. Available at: http://www.noaa.gov/. 2. National Severe Storms Laboratory. Available at: http://www. nssl.noaa.gov/.

30 lacerations, 2 corneal abrasions, and 38 contusions. Halfway through the shift the city water is shut off because of tornado damage to several of the main lines. Luckily the hospital has an emergency hot and cold water supply that allows for continued appropriate cleansing of your patients wounds, most of which are highly contaminated with soil and other debris. Almost 50 of the 200 patients are not physically injured but just don’t know where to go and need direction to the emergency shelters in the area being set up by the Red Cross and other relief agencies. Twenty-six patients present with head injuries ranging from mild concussions to skull fractures and ICH. Three of these patients require emergent transfer to the regional tertiary care facility for neurosurgical intervention. The local fire and EMS system provides two air ambulances, which make these transfers possible despite extensive damage and congestion on the local highways between your facility and the receiving hospital. During the shift you and your colleagues manage 18 patients with fractures and dislocations, 14 patients with blunt trauma to the chest and abdomen (one of whom has a pneumothorax requiring tube thoracotomy and 6 of whom are sent to the OR for emergent operative procedures), 18 sprains/strains, and one patient with a penetrating injury to the neck resulting in spinal cord injury. (This patient is also transferred via air ambulance to the regional tertiary care facility.) In all, you admit 35 patients with tornado-related injuries. Four of these go to the regional trauma center, four go to your ICU, six go to the OR, and 21 go to ward beds. Driving home after your shift you contemplate the magnitude of the disaster you have just witnessed. You realize how grateful you are for all those “mandatory” disaster response drills the city has required you to reluctantly participate in over the past several years. You shudder to think what might have happened had you, the hospital, and your staff been totally unprepared for the events of the past 12 hours. 3. Lillibridge S. Tornadoes. In:Noji E,ed.The Public Health Consequences of Disasters. New York: Oxford University Press; 1997, pp 228-44. 4. National Climatic Data Center. Available at: http://www.ncdc. noaa.gov/oa/ncdc.html. 5. Concannon P, Brooks H, Doswell C. Climatological Risk of Strong and Violent Tornadoes in the United States. Second Conference on Environmental Applications of the American Meteorological Society. 2000. Available at http://www.nssl.noaa.gov/users/brooks/ public_html/concannon/. 6. Saunderson L. Tornadoes. In: Gregg M, ed. The Public Health Consequences of Disaster, 1989. Atlanta, GA: Centers for Disease Control; 1989;127:39-49. 7. Galway J. Ten famous tornado outbreaks. Weatherwise 1981; 34:100-9. 8. Bohonos J, Hogan D. The medical impact of tornadoes in North America. J Emerg Med. 1999;17:67-73. 9. Federal Emergency Management Agency. Available at: http:// www.fema.gov/fema/first_res.shtm. 10. Liu S, Wuenemoen L, Malilay J, et al. Assessment of a severeweather system and disaster preparedness, Calhoun county, Alabama, 1994. Am J Pub Health. 1996;86:87-9. 11. Duclos P, Ing R. Injuries and risk factors for injuries from the 29 May 1982 tornado, Marion, Illinois. Int J Epidemiol. 1989;18:213-9. 12. Brenner S, Noji E. Tornado injuries related to housing in the Plainfield tornado. Int J Epidemiol. 1995;24:144-9. 13. Glass R, Craven R, Bregman D, et al. Injuries from the Wichita Falls tornado: implications for prevention. Science 1980;207:734-8.

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14. Anonymous. Salt Lake hospital survives close brush with twister, power outage. Profiles in Healthcare Marketing. 1999;15(6):48-9. 15. May A, McGwin G, Lancaster L, et al. The April 8, 1998 Tornado: Assessment of the trauma system response and the resulting injuries. J Trauma. 2000;48:666-72. 16. Hogan D, Askins D, Osburn A. The May 3, 1999, tornado in Oklahoma City. Ann Emerg Med. 1999;34:225-6. 17. Hogan D. Tornadoes. In: Hogan D, Burstein DE, eds: Disaster Medicine. Philadelphia: Lippincott-Williams and Wilkins; 2002, pp 171-8. 18. May B, Hogan D, Feighner K. Impact of a tornado on a community hospital. JAOA 2002;102:225-8. 19. Millie M, Senkowski C, Stuart L, et al. Tornado disaster in rural Georgia: Triage response, injury patterns, lessons learned. Am Surgeon. 2000;66:223-8. 20. Mandelbaum I, Noahrwold D, Boyer D. Management of tornado casualties. J Trauma. 1966;6:353-61.

488 NATURAL DISASTERS

21. Rosenfield L, McQueen D, Lucas G. Orthopedic injuries from the Andover, Kansas tornado. J Trauma. 1994;36:676-9. 22. Brenner S, Noji E. Head and neck injuries from 1990 Illinois tornado. Am J Pub Health. 1992;82: 1296-7. 23. Brenner S, Noji E. Wound infections after tornadoes. J Trauma. 1992;33:643. 24. Ivy J. Infections encountered in tornado and automobile accident victims. J Indiana State Med Assoc. 1968;61:1657-61. 25. Gilbert D, Sanford J, Kutscher E, et al. Microbiologic study of wound infections in tornado casualties. Arch Environ Health. 1973;26:125-30. 26. Johnson J. Tornado as teacher: lessons learned in caring for tornado victims lead to revision of one hospital’s disaster plan. Hospitals JAHA. 1970;44:40-2.

chapter

75

Flood Sylvia H. Kim

DESCRIPTION OF EVENT Floods are the most common natural disasters. They cause greater mortality than any other natural disaster.1 Worldwide, floods account for approximately 40% of natural disasters. In the United States, approximately 146 deaths are caused by floods each year, the majority associated with flash floods.2 Floods cost the nation $3.8 billion each year.3 Floods continue to be the No. 1 natural disaster in the United States in terms of lives lost and property damage. In 1889, more than 2200 deaths were due to flash flooding from a dam break in Johnstown, Penn. In 1976, a 19 foot wall of water near the Big Thompson River near Denver, Colo., killed 140 people camping nearby.4 More recently, in 2001, Tropical Storm Allison resulted in 41 deaths, $2 billion in property damage, and decades of research lost by scientists at the Texas Medical Center.5 Floods may be caused by an abundance of rainfall; melting snow; or the expanding development of wetlands, which reduces absorption of rainfall. Flash floods occur within 6 hours of a rain event, after a dam or levee fails, or after the sudden release of water from an ice or debris jam. Flash floods are the No. 1 cause of natural disaster–related death.3 Most communities in the United States can experience flooding. In fact, flash floods occur in all 50 states.6 Communities at greatest risk are those in low-lying areas, near water, and located downstream from a dam.4 In October 1998, flooding in Central Texas resulted in 31 deaths. Of the 16 incidents of vehicles being driven across flood waters, 11 (69%) occurred in areas with a prior history of flooding.7

PREINCIDENT ACTIONS Hospitals should determine whether they are located in a flood-prone area. The National Weather Service issues flood watches and warnings, which are organized by state, and publishes these listings at www.nws.noaa.gov. These projections are based on precipitation and lake and river levels.8 Flood watches are posted 12 to 36 hours before possible flooding events. Flood watches indicate a hazardous event is occurring or will occur

within 30 minutes.3 A flood watch should be used for early evacuation planning. Evacuation routes should be planned and practiced. For planning purposes, flood hazard maps are available from the Federal Emergency Management Agency at www.fema.gov/mit/tsd. The usual routes of access to and from the hospital may be flooded, therefore alternative routes should be planned in advance. As with any natural disaster, transport times will likely increase, and hospital personnel should expect ambulance arrival without prior dispatch. There will be greater reliance on alternative means of transport, including aeromedical and marine units.8 In one extreme case, flood waters isolated a community in Grand Forks, N.D. A temporary shelter for medical care that was capable of laboratory tests, radiology and other ancillary services was established.9 An emergency communications system should be available. Communication lines among hospitals, prehospital staff, and patients may be affected by floods. Telephone lines, 911 dispatch lines, and emergency medical service communication with hospitals may be impaired. Create a plan for redundant communications capabilities,including two-way radios and dedicated channels, cell phones, and Internet connectivity.10 An emergency communications system plan should be in place to request further staffing, services, or evacuation assistance. Floods are long-term events and may last days to weeks, or longer.6 Therefore, disaster supplies should be available and include a portable battery-operated radio, flashlights, batteries, first aid kits, nonperishable food, and water.4

POSTINCIDENT ACTIONS During a flood, battery-operated radios or televisions should be used. The National Oceanic and Atmospheric Administration (NOAA) Weather Radio broadcasts warnings from the National Weather Service 24 hours a day. Hospitals not equipped with the special radio receiver to pick up the signal can obtain timely information at iwin.nws.noaa.gov/iwin/nationalwarnings.html or from television and radio. Hospital staff and patients should immediately be evacuated according to a pre-established disaster plan. If no 489

plan is in place,seek shelter at higher ground. Avoid walking or driving through flood water. The force from 6 inches of flood water can cause one to fall. Cars can easily be swept away by just 2 feet of flood water.4 Research from the Georgia flood in 1994 showed that 71% of flood deaths were associated with submersion in vehicles.2

MEDICAL TREATMENT OF CASUALTIES Approximately 0.2% to 2% of flood survivors will require urgent medical care.1 The main cause of death during floods is drowning, with victims typically found some time after the flood recedes. Because it is often difficult to reach victims during the acute phase of a flood, it is relatively uncommon for near-drowning victims to present to emergency departments..11 Fast-flowing flood waters carry cars, trees, and other large debris that can result in trauma, including orthopedic injuries and lacerations.1,11 In addition, there have been reports of flood waters displacing snakes and other animals, resulting in increased animal bites.12,13 Also, the preponderance of water during the event and still water postevent results in an increase in insect bites and vectorborne illnesses. Flood waters also may contaminate the local water supply and sewage system.1,13 The Centers for Disease Control and Prevention13 analyzed data from emergency departments in 20 hospitals during Hurricane Floyd in North Carolina during September and October 1999. The medical examiner found that 52 deaths were directly related to the storm. Four causes of injury/illness accounted for 63% of all emergency room visits during this period: orthopedic and soft tissue injury (28%), respiratory illness (15%), gastrointestinal illness (11%), and cardiovascular disease (9%). The majority (24/52, or 67%) of deaths was due to drowning, primarily associated with vehicles. There were 19 cases of hypothermia and 10 cases of carbon monoxide poisoning. There was also an increase in suicide attempts, violence, dog bites, and arthropod bites compared with the same period the prior year. Finally, five deaths occurred among prehospital personnel.13 Not surprisingly, drowning is the primary cause of death during floods. Patients who are submerged in cold water for 40 minutes have been successfully resuscitated to attain complete neurologic recovery secondary to the neuroprotective effects of hypothermia.1 Therefore, cardiopulmonary resuscitation should be performed as soon as possible after securing the scene. Cervical spine injuries should be suspected, and immobilization should be maintained.14 The patient should be rewarmed using external and internal rewarming techniques, as indicated. Resuscitation efforts should be continued until the patient’s temperature is 32° to 35°C (90° to 95°F); at that point, decisions regarding the utility of continuing resuscitation are made.15 Flood waters carry a large amount of debris, such as cars and tree limbs, and result in traumatic injuries. Orthopedic injuries should be reduced, splinted, and managed accordingly. Most injuries during floods that require urgent medical attention include lacerations, 490 NATURAL DISASTERS

rashes, and ulcers. These wounds are contaminated and should be conservatively managed by irrigation and healing by secondary intention. Among those lacerations that are closed primarily, the majority require reopening secondary to infection.1 Floods cause water contamination and an increase in vectorborne illnesses. Water contamination often results from damage to the water purification and sewage systems. Contaminated water sources result in waterborne disease transmission, including Escherichia coli, Shigella, Salmonella, and hepatitis A virus. The large areas of stagnant water that typically remain days or weeks after the initial flood event create a breeding medium for vector-borne illnesses.. Flood waters may also result in the spread of chemicals stored above ground. In addition, temporary shelters to house those displaced by flooding may result in crowded and unsanitary living conditions, increasing the incidence of gastrointestinal illness among other infectious illnesses.1 The force from flood waters may also down power lines, flood electrical circuits, and submerge electrical equipment, increasing the risk of fires and electrical hazards.4,8 Finally, victims of floods, as well as other natural disasters, are at an increased risk of mental illness and substance abuse. In one study, there was an increase in suicide rates of 13.8% compared with predisaster rates.16 As of this writing we are beginning to see evidence of this in the flood regions resulting from Hurricane Katrina that struck the Gulf Coast of the United States in 2005.

UNIQUE CONSIDERATIONS Floods are the most common natural disasters and affect all 50 states. Flood waters can remain for days, weeks, or longer. As a result, flood-related injuries and illnesses may continue to present over a long period of time. Drowning is the No. 1 cause of death and is often related to vehicles attempting to cross flood waters. Deaths also occur among healthcare providers, but increased natural disaster training may decrease this occurrence. In addition to drowning, flood victims are at an increased risk for hypothermia, contaminated wounds, and waterborne infections. Water and sewage treatment facilities may be damaged by flood waters and result in water contamination. Most communities in the United States can experience flooding. Flash floods occur in all 50 states and most countries. Areas at greatest risk are low-lying, near water, and located downstream from a dam.4 For planning purposes, flood hazard maps should be obtained in advance and evacuation routes planned accordingly. In the event of flood warnings, evacuate early because a vehicle can be swept away with the force from as little as 2 feet of water.

PITFALLS • Failure to plan flood evacuation routes before a flood event • Delayed evacuation by those in a flood watch area

CASE PRESENTATION While seeing patients in your emergency department, one of your staff members informs you that she just heard a flood watch for the local area over the radio.What should you do next?

• Failure to know who is in command of disaster operations in the local area • Closing contaminated lacerations • Failure to continue resuscitation of a patient who is hypothermic • Notify the unified command/management structure and obtain directions • Listen to a radio or television for local flood information • Obtain your emergency kit and emergency communication (including battery-operated radio) • Be prepared to evacuate patients and staff and know the evacuation route • Communicate with other facilities to determine who has the capacity to accept your patients REFERENCES 1. Noji E. Natural Disaster Management. In: Auerbach P, ed. Wilderness Medicine: Management of Wilderness and Environmental Emergencies. 3rd ed. St. Louis: Mosby; 1995:644-63. 2. Centers for Disease Control and Prevention. Flood-related mortality—Georgia, July 4-14, 1994. MMWR. 1994;43(29):526-30.

3. National Disaster Education Coalition. Flood and Flash Flood. Available at: http://www.disastercenter.com/guide/flood.html. 4. Federal Emergency Management Agency. Fact Sheet: Floods and Flash Floods. Available at: http://www.fema.gov/library/prepandprev.shtm#floods. 5. Sirbaugh P, Bradley R, Macias C, et al. The Houston flood of 2001: the Texas Medical Center and lessons learned. Clin Pediatr Emerg Med. 2002;3:275-83. 6. US Department of Commerce, National Oceanic and Atmospheric Administration, National Weather Service. Floods: The Awesome Power. Available at: http://www.nws.noaa.gov/om/brochures/ Floodsbrochure_9_04_low.pdf. 7. Centers for Disease Control and Prevention. Storm-related mortality—Central Texas, October 17-31, 1998. MMWR. 2000;49(7): 133-5. 8. Floyd K. Floods. In: Hogan D, Burstein J, eds. Disaster Medicine. Philadelphia: Lippincott Williams & Wilkins; 2002:187-93. 9. Stensrud K. Floodwaters bring docs to the front. Minnesota Med. 1997;80(8):14-19. 10. Joint Commission on Accreditation of Healthcare Organizations. Health Care at the Crossroads: Strategies for Creating and Sustaining Community-wide Emergency Preparedness Systems. Available at: http://www.jcaho.org/about+us/public +policy+initiatives/ emergency_preparedness.pdf. 11. Pan American Health Organization. Emergency Health Management after Natural Disaster. Scientific Publication 407.Washington DC: Pan American Health Organization; 1981. 12. Ussher J. Philippine flood disaster. J R Nav Med Serv. 1973; 59(2):81. 13. Centers for Disease Control and Prevention. Morbidity and mortality associated with Hurricane Floyd—North Carolina, September-October 1999. MMWR. 2000;49(23):518. 14. Braun R, Kristel S. Environmental emergencies. Emerg Med Clin North Am. 1997;15:451. 15. Jolly B, Ghezzi K. Accidental hypothermia. Emerg Med Clin North Am. 1992;10:311. 16. Axelrod C, Killam PP, Gaston MH, Stinson N. Primary health care and the Midwest flood disaster. Public Health Rep. 1994: 109(5):601-5.

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Tsunami Prasanthi Ramanujam and Thea James

DESCRIPTION OF EVENT Tsunami is a series of waves formed by displaced water due to disturbance of the sea floor that enters the coastal areas, causing serious damage. Tsunami (pronounced tsoo-nahmee) is a Japanese word that literally means “harbor wave.” Tsunamis are appropriately named so because they are silent and unseen in the ocean waters, but are fierce on the shallow coastal waters. They are commonly referred to as tidal waves or seismic sea waves. This is entirely misleading because neither of these terms fully characterizes tsunamis. Tidal waves are caused by the gravitational pull of the moon, sun, or planets, whereas seismic sea waves are the result of earthquakes. Tsunamis can also be caused by nonseismic activity and usually occur due to the following three major geologic movements: 1. A fault movement on the sea floor occurring during an earthquake: When tectonic earthquakes (those associated with the crustal deformation of earth) occur in the ocean floor, the harmony of the ocean is disturbed.This results in the displacement of the water mass, creating a wave. When a large area of the sea floor is involved, tsunami waves are created. Tsunamis can occur in any oceanic region of the world but are more common in the Pacific coast. The zone of Earth where tsunamis terrorize the Pacific Island coast is called the “Ring of Fire.” This zone of extreme seismic activity circles the Pacific Ocean from south of Chile to the coast of North America and westward along the Aleutian Islands arc, extending south to Japan and the Philippines, westward to Malaysia and Indonesia, and eastward through New Guinea, the Southern Pacific Island groups, and New Zealand.1 2. A landslide: This begins above the sea, plunges into the water, or occurs under water and creates a violent disturbance in the waterfront as the landslide disseminates into the ocean floor, generating a tsunami. 3. A sub-marine explosion: This is the result of a volcanic eruption, creating a mechanical force that lifts the water column, which generates a tsunami. Landslides and cosmic-body impacts thrust the water from above, as the energy and force from falling debris are transferred to the water, stirring up a tsunami wave.2 492

Categories of Tsunamis There are three categories of tsunami. Depending on the area affected, they are categorized as local, regional, or Pacific. Local tsunamis are confined to small areas and are commonly caused by coastal or sub-marine landslides and volcanic explosions. Regional tsunamis are the most common and are undersized because of deficient energy or lack of a favorable geographic location. Pacific-wide tsunamis are less common but have the potential for causing major damage.1

Characteristics of a Tsunami Once tsunamis are generated, the energy propagates a horizontal wave through the ocean, similar to ripples formed by tossing a rock into a pond. A series of waves, called a tsunami wave train, spreads outward in all directions from the source of activity. The waves follow each other in 5- to 90-minute intervals.2 The original tsunami then divides into two types: one goes to the nearest coast (a local tsunami) and the other one travels into the deep ocean (a distant tsunami).1 The speed at which the waves travel varies depending on the ocean depth, which implies that the local tsunami travels at slower speeds than the deep ocean wave. Tsunamis in deep water may travel as fast as 500 mph, compared with the normal wave speed of around 60 mph. Despite traveling at such great speeds on the open ocean, at that depth, they only reach one or two feet, producing a small uprise of the sea surface, often going unnoticed by sea travelers. However, as a tsunami comes closer to the coast, the wave height increases due to a decrease in ocean depth. People who have survived tsunamis describe them as giant “walls of water.” On shore, the initial sign of a tsunami depends on what part of the wave first reaches the land: a wave crest causes a rise in water level, but a wave trough causes a recession.2 The terminology used to measure the height of water above the referenced sea level is called run up.3 Tsunamis may reach a maximum run up on shore of 10, 20, and even 30 meters. Unlike many descriptions of tsunami-like monster waves, the waves come onto the shore more like uncontrollable fast tides, and much of the damage inflicted is caused by their strong currents and debris.

The small number of tsunamis that form vertical walls of turbulent water near the shore line are called bores.1 Once a tsunami hits the shore, some of its energy reverts into the ocean. In some cases, a tsunami can generate a particular type of wave called an edge wave, which swings back and forth along a coastal shore, resulting in successive multiple waves.3

PREINCIDENT ACTIONS Once tsunamis are formed, they cannot be stopped; hence, strategies to lessen their effects are crucial. Salient features of a preparedness program include improving awareness and mitigation of the hazards. The foremost step is to increase knowledge among decisionmaking authorities, emergency personnel, and the public. Mitigation involves steps to decrease the impact of the event at the time of occurrence. The features recommended by the 1995 National Oceanic and Atmospheric Administration’s (NOAA) Tsunami Hazard Mitigation plan4 are as follows: 1. Identifying an approaching tsunami and attempting to reduce false alarms: The Pacific Tsunami Warning Center (PTWC) is an operational center for the Tsunami Warning System in the Pacific coast (TWSP). It has been the international warning center since 1965, when a formal arrangement was made. PTWC is able to locate seismic activities that are potentially tsunami-generating in the Pacific coast or surrounding areas by continuously obtaining seismographic data from more than 150 stations around the Pacific and other international agencies running such stations and networks.5 6 This method is not foolproof; false alarm rates are extremely high. To improve the accuracy of reporting, Japan and NOAA have planted multiple bottom-pressure sensors that detect a tsunami traveling overhead. This information is communicated to the shore via satellite links using a buoy in the ocean. If the extent of destruction is determined to be wide, entire Pacific coastal areas are given a warning. Regional warning centers exist, which are responsible for the issuing warnings to specific countries and their coastal areas. For example, the Japan Meteorological Agency provides tsunami warnings to Japan and also to Korea and Russia for events occurring in the Sea of Japan or East Sea. The Center Polynesien de Prevention des Tsunamis provides warnings to French Polynesia and Chile. In the United States, West Coast/Alaska Tsunami Warning Center (WC/ATWC) provides tsunami warnings to the U.S.West Coast and Canada, and PTWC provides tsunami warnings to Hawaii and all other U.S. interests in the Pacific.6 2. Utilization of resources for communication and evacuation: Local preparedness planning consists of determining safe evacuation pathways, setting up shelters,critical facilities,and strengthening structures that cannot be relocated and are in the path of inundation of a tsunami. As preparations are being undertaken, alerting systems are used to spread the information

and to communicate effectively about the evacuation measures. Local tsunamis pose major challenges. They are associated with earthquakes that cause damage to the infrastructure, leading to difficult evacuation plans. This is further complicated by a tsunami arriving minutes after events like earthquakes leaving less time for emergency response. Planning committees have made recommendations for this setting. They include disseminating an inundation map obtained using computer-generated simulations to plan mapping of the critical zones and to predict the areas prone to devastation. Other strategies are improvising warning systems and notifying the public immediately after earthquakes of the likelihood that a tsunami will result.4 3. Support for state and local agencies’ long-term tsunami mitigation program: Multistate projects have been proposed, along with individual state programs, to raise the public’s level of awareness and preparation for an event. Apart from federal and state actions, various organizations exist to help coordinate federal, state, and local emergency management agencies; the public; and the NWS (National Weather Service) tsunami warning system. This helps maintain the safety of the public by increasing awareness. The various guidelines at the community level include: • Establish minimum community standards, which depend on the size of the community. Create a 24hour operations system, with the ability to receive, disseminate, and activate warning systems in the community. There also should be communicative abilities between other emergency centers and tsunami warning centers.7 • Disseminate information to the public using means such as NWS (NOAA weather radio), television, and a statewide telecommunications network located at public buildings.7 • Improve awareness and preplanning among the community by conducting awareness programs in schools, hospitals, and community meetings. Define the areas in the community for shelter, provide hazard zones and evacuation maps, and conduct practice evacuation drills in schools.7

POSTINCIDENT ACTIONS Preventing a disaster from happening is paramount, but when it is impossible to avert the natural disaster, timely applications of management strategies gain importance. The postincident action phase is composed of emergency response activities that transition into rehabilitation phase activities that culminate in the reconstruction phase. Emergency response efforts actually evolve from the final stages of the preincident phase and have many overlapping features. Examples include (a) evacuation of people to safe places, which in the case of a tsunami can be inland or to a higher altitude, and (b) provisions for emergency shelter and temporary lodging to people who are displaced after the event. The next stage begins TSUNAMI 493

with the dispatch of search and rescue teams to look for injured people who need medical assistance. Because damage to water pipes in the affected areas is likely, provision of short-term food and water is essential for the displaced population. Water disinfection and purification become important after the disaster to prevent epidemics from water contamination. Public announcements regarding safety standards for water storage and disinfection, even after flooding, should be made as a preventive health measure. Epidemiologic surveillance in areas affected by flooding is important because overcrowding among the displaced population and overflow of industrial, agricultural, and sewage systems can pose serious health hazards. Subsequent management steps consist of reestablishing communication with remote areas, restoring infrastructure by re-opening roads, clearing debris, and repairing damaged housing and public buildings. The final phase consists of providing employment by creating opportunities, offering technical assistance to industries and for agricultural recovery, and encouraging activities that help rebuild the area.8 9

MEDICAL TREATMENT OF CASUALTIES Mass casualties can exceed system capabilities during disasters. This becomes a burden on the local system until outside help arrives. Steps to hasten the delivery of treatment to the injured include triage, on-site stabilization, and transportation to the local hospital. The goal of triage is to prioritize injured patients by identifying those whose injuries are critical and in need of prompt medical attention and arranging for either on-site treatment or quick transfer. Patients who have minimal likelihood of survival from major injuries despite optimal care are provided only comfort measures. There are two different systems of triage for mass casualties, and they are qualitative and quantitative. The former system is based on the patient’s injury relative to others who are injured and to available care and requires timely reassessment. The latter is based on a clinical score for the patient at time of initial presentation to predict outcome. Triage begins with arrival of the emergency medical personnel onscene. This is followed by relative assessment of the demand on available supplies. If the numbers overwhelm available help, the need for additional services is rapidly communicated to the emergency dispatch center. Triage set up begins with designating the most qualified medical person to be the provisional triage officer. With the arrival of more help from outside, this role should be taken by the most knowledgeable person with triage experience. Various adjuncts to triage help with the identification of which triage category the patient is placed in and with enforcing the use of a classification system, such as immediate, delayed, minor, and expectant, depending on the injury severity and prognosis. Priority one triage, based on the initial clinical picture, includes patients with impending airway issues, such as asphyxia, respiratory obstruction, sucking chest wounds, tension pneumothorax, maxillofacial wounds with impending air494 NATURAL DISASTERS

way compromise, shock, and major medical problems. Delayed triage, or priority two, includes patients with visceral, vascular, facial, spinal cord, and genitourinary injuries; thoracic injuries without asphyxia; and victims with less chance of survival. Once patients are triaged, a decision must be made as to whether to transport them to a nearby hospital or provide on-site care by setting up the necessary facilities. This decision is based on the number of available qualified transport personnel. If the system is overwhelmed by the number of patients awaiting rapid transportation, advanced-field medical treatment may be necessary. If rescue personnel or patients are in an unsafe environment, rapid transport becomes a necessity. Emergency communications should be used to alert local hospitals about the mass casualty situation and the need for resources to handle multiple-trauma patients. Hospitals, in turn should, report to the disaster operations center the current status on bed availability, the number of casualties they have received, and the availability of supplies to manage the crisis.9

UNIQUE CONSIDERATIONS • Tsunami is rightfully called the harbor wave because its effects are devastating on coastal areas. • Tsunamis are not one single wave but consist of a wave train and travel at great speeds in the ocean. • Unlike other tides,tsunamis are caused mostly by seismic activity, which adds to the damage caused by a tsunami. • Tsunamis are unique in that their propagation involves the entire depth from the ocean surface to the bottom, accounting for their tremendous energy.1 • The issuance of a tsunami warning means that evidence exists for a potentially destructive tsunami and evacuation is strongly advised. On the other hand, a watch status means that a tsunami may have been generated, the wave travel time is more than 3 hours, and evacuation is needed if the watch is upgraded to a warning.1 • For tsunamis of distant origin, the danger areas are 50 feet above sea level and within 1mile of the coast. • For tsunamis of local origin, potential danger areas are those less than 100 feet above sea level and within 1 mile of the coast.8

PITFALLS • Tidal wave is a misnomer for tsunami because the latter can be extremely dangerous with devastating effects. • Tsunami run up (height of the water above sea level) varies with the geography of the land, leading to different degrees of damage along the coastline. • Local tsunamis can follow a seismic activity very quickly, leaving less time for incident preparation. • False alarms during the preincident phase can pose a major drain on available resources. • Early return of people to their settlements without anticipating the wave train or to witness the tsunami can result in significant morbidity and mortality.

CASE REPORT Papua New Guinea is a group of islands including the eastern half of the island of New Guinea between the Coral Sea and the South Pacific Ocean, east of Indonesia. On July 17, 1998, at 6:49 PM local time, these islands experienced an earthquake with a magnitude of 7.1 near the northwest coast. This was soon followed by three dreadful tsunamis that killed about 2182 people and left more than 10,000 people in the villages of Sissano, Warupu, and Arop homeless. The tsunamis affected a 40-km coastline of a narrow strip of land, largely a swamp area between the ocean and a lagoon that was home to 15,000 tribal people who subsisted on farming and fishing. About 20 minutes after the first earthquake, the trough of the first tsunami arrived with a 7- to 10-meter crest that destroyed the village and swept the debris into the lagoon 500 meters inland from the coast. The destruction was enormous and included three schools, a heath center, mission buildings, churches, bridges, and the government administration center. Common injuries included multiple bony and soft tissue injuries, development of gangrene, near-drownings, and loss of lives from impalement onto tree stumps.10 The tsunami of southeast Asia on Dec. 26, 2004, deserves mention for the death and devastation it caused in the region. An undersea earthquake with a magnitude of 9.0 on the Richter scale in the Indian Ocean originated off the western coast of Northern Sumatra. This fourth-largest earthquake since 1900 resulted in the generation of a tsunami, which affected the coastal regions of Indonesia, Thailand, Sri Lanka, and South India. Waves were as tall as 50 feet and traveled more than 1 mile inward in some areas. Damage also was recorded in South Africa, about 5000 miles from the epicenter. The estimated number of deaths

REFERENCES 1. British Columbia Ministry of Public Safety & Solicitor General. British Columbia Tsunami Warning and Alerting Plan 2000. Available at: http://www.pep.bc.ca/hazard_plans/tsunami 2001/ Tsunami_Warning_and_Alerting_Plan-2001.pdf. 2. Reed SB. Natural and human-made hazards: mitigation and management issues. In: Auerbach, PS ed. Wilderness Medicine. 4th ed. St. Louis: Mosby; 2001. 3. U.S. Geological Survey. Tsunamis and Earthquakes: Tsunami Research at the USGS. Available at: http://walrus.wr.usgs.gov/ tsunami/. 4. National Oceanic and Atmospheric Administration. National Tsunami Hazard Mitigation Program. Available at: http://www. pmel.noaa.gov/tsunami-hazard 5. The University of Washington Earth and Space Sciences. The Tsunami Warning System. Available at: http://www.ess.washington.edu/ tsunami/general/warning/warning.html

in the affected region was about 300,000 and the displaced population about 1.5 million. The waves also inflicted major environmental damage on the regions. There was infiltration of fresh water supplies, spread of solid and liquid wastes, damage to ecosystems, and much more. The economic damages are unquantifiable and included loss of industrial infrastructure on the coastline, destruction of fishing fleet, and a breakdown of the tourism industry. The devastation has created a lot of awareness in the region about tsunamis and has created a need for establishing warning systems in the Indian Ocean.11 Multiple case reports from different parts of the world have resulted in improvements to existing disaster mitigation plans. Lessons learned from historic events include the following:

• Establish a global communication network that recog• • • •

nizes and warns the population in high-risk areas about possible tsunamis Quickly sense an approaching tsunami after groundshaking and loud oceanic noises.10 Identify areas of land between a lagoon and the ocean as high-risk areas for inundation, thereby avoiding rebuilding after a tsunami10 Train the local population to handle the immediate disaster needs in case of a tsunami strike until further support systems can be deployed Recognize that mangroves are a source of floating debris that can cause more physical damage and that lagoon areas are less of an impediment for tsunamis, exposing more inland to destruction10

6. National Weather Service. Tsunami Warning Centers. Available at: http://www.prh.noaa.gov/itic/library/pubs/great_waves 7. State of Alaska Division of Homeland Security and Emergency Management. Tsunami Mitigation. Available at: http://www. ak-prepared.com/plans/mitigation/tsunami.htm. 8. University of Wisconsin Disaster Management Center. Natural Hazards: Causes and Effects. Lesson 3: Tsunamis. Available at: http://dmc.engr.wisc.edu/courses/hazards/BB02-03.html 9. Noji EK. Natural disaster management. In: Auerbach PS, ed. Wilderness Medicine.4th ed. St. Louis: Mosby; 2001. 10. James F, Lander LS, Whiteside PA, Lockridge PA. Two decades of global tsunamis 1982-2002. Science of Tsunami Hazards. 2003; 21(1):3. 11. Wikipedia. 2004/Indian Ocean Earthquake. Available at: http://en.wikipedia.org/wiki/ 2004/Indian_Ocean_Earthquake.

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Heat Wave Alison Sisitsky

DESCRIPTION OF EVENT A heat wave is a prolonged period of heat and humidity. The duration of heat plays an important role in how people are affected. Illness tends to occur within 2 days of excessive heat. However, there are certain populations who are at increased risk, and may exhibit symptoms earlier. The elderly, very young, those with preexisting diseases, those taking various drugs/medications, and urban dwellers are more susceptible to heat-related illness. Each year, hundreds of people die from heat-related illnesses. The Centers for Disease Control and Prevention estimated that from 1979 to 1997 there were 7000 U.S. deaths attributable to extreme heat. There were 600 deaths during the Chicago heat wave of July 1995. The next summer, during the 1996 Summer Olympics in Atlanta, Ga., 1059 people were treated for heat-related illness. Of those who died, 89% were either spectators or volunteers.1 There are four mechanisms by which the human body is able to dissipate heat. Radiation is the passive transfer of heat by electromagnetic waves. This accounts for 65% of heat transfer. Evaporation is the transition of liquid into gas. This only occurs when the outside temperature reaches 95˚F, and it accounts for 30% of heat transfer. Convection is heat loss to air and water vapor molecules that surround the body. It only accounts for 10% of heat transfer. Finally, conduction is heat transfer via direct physical contact. It is only responsible for 2% of heat transfer.2 Heat waves are among the most common emergencies and are the leading environmental cause of death in the United States, followed by cold-related deaths during winter months (Fig. 77-1).

PREINCIDENT ACTIONS The most important action in preventing illness during a heat wave is public education before the heat wave begins. The National Weather Service issues alerts when a potential heat wave is near. The heat index (HI) is the temperature the body feels when heat and humidity are combined. For example, if the air temperature is 90°F and the relative humidity is 60%, the HI is 99°F.1 496

Educating the public allows people to protect themselves from excessive heat exposure. If the following recommendations are adhered to, the risk of heat-related illnesses could be reduced. Reduce strenuous activity or reschedule outdoor activities until the coolest time of day. Dress with lightweight clothing and light colors. Avoid restrictive hats that will block sweating and evaporation of heat. Drink large amounts of water or other nonalcoholic beverages. Avoid alcohol intake. Spend as much time as possible in air-conditioning and avoid direct sun exposure.3

POSTINCIDENT ACTIONS In the prehospital setting, remove the patient from the heat. Disrobe the patient and apply ice packs to the neck, axilla, and groin. In addition, placing a wet sheet over the body will encourage heat loss from the body to the environment. Intravenous fluid should be started. If the patient has an altered mental status, consider administering glucose, thiamine, and naloxone. Always assess vital functions, and obtain an accurate core temperature with a rectal probe. Laboratory evaluation should include a complete blood count to assess for leukocytosis as well as electrolyte levels and a urinalysis. Hypernatremia can exist with severe dehydration. Acute renal failure and myoglobinuria may be present with rhabdomyolysis. If heat stroke is suspected, liver function tests and coagulation studies are needed to assess for hepatic necrosis or disseminated intravascular coagulation. Further diagnostic tests should include an electrocardiogram in an elderly patient or anyone with cardiac risk factors, head computed tomography for patients with an altered mental status, and a chest x-ray for evidence of respiratory distress.4,5

MEDICAL TREATMENT OF CASUALTIES Immediate cooling should include spraying the disrobed patient with cool mist; fanning mist with bedside fans; and applying ice packs to the neck, axilla, and groin.

1000

800

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Cold

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0 1995

1996

1997

1998

1999

2000

2001

2002

FIGURE 77–1. Heat fatalities. Between 1995 and 2002 in the United States heat-related deaths outnumbered both hurricane- and cold-related deaths. (Graph adapted from data collected at http://www.disastercenter.com.)

Immersion in cold water is effective if the patient’s condition is stable, but it is difficult to manage patients who have any evidence of cardiovascular compromise. For patients whose hyperthermia (temperature >104˚F) persists, iced peritoneal lavage and cardiopulmonary bypass should be considered. While active cooling is taking place, hydration should be started with 0.5 to 1 L of normal saline. Pediatric patients should receive a 20-mL/kg bolus. Medications to consider include analgesics for muscle cramps; benzodiazepines for seizures or severe shivering; and glucose, thiamine, and naloxone for altered mental status. Patients with evidence of heat stroke (hyperthermia, anhidrosis, and altered mental status) should be admitted to an intensive care unit. Patients with heat exhaustion (hyperthermia [temperature >104oF], central nervous system dysfunction, dehydration, nausea/vomiting, and diaphoresis) or the elderly should be admitted for electrolyte abnormalities and evidence of rhabdomyolysis.4,5

UNIQUE CONSIDERATIONS Patients at extremes of age are at increased risk of heatrelated illnesses. Children have an increased body surface area to mass ratio, which increases their risk. Hydration of pediatric patients consists of a 20-mL/kg bolus of intravenous fluid. If hypoglycemia is present, give 2 mL/kg of D25W over 1 minute intravenously. Elderly patients are at increased risk secondary to underlying medical conditions and medications that worsen heat illness. Taking a thorough history and a physical examination will help guide therapy. Risk factors for serious heat injury are outlined in Table 77-1.2,4,5

PITFALLS Consider other causes of hyperthermia in patients with altered mental status. The differential diagnosis includes

TABLE 77-1 RISK FACTORS FOR SERIOUS HEAT INJURY Dehydration Obesity Heavy clothing Poor physical fitness Cardiovascular disease Skin diseases (burns, eczema, scleroderma, psoriasis) Febrile illnesses Hyperthyroidism Alcoholism Drug use (cocaine, amphetamines, opiates, LSD, PCP) Poor socioeconomic conditions Medications (antipsychotics, anticholinergics, calcium-channel blockers, beta blockers, diuretics, alpha agonists, sympathomimetics)

CASE PRESENTATION Today is the local marathon.There are 2000 runners participating in the event.The local temperature is predicted to reach 99˚F. The race started 2 hours ago and medical control is calling with questions. Not only do they have runners with symptoms of heat-related illness, many of the spectators are symptomatic. Currently, they would like to bring three patients. Patient 1 is a 40-year-old male with vomiting and severe abdominal pain who was unable to finish the race. Patient 2 is a 4-year-old female spectator who had a syncopal episode while waiting for her mom to finish the race. Patient 3 is an 85-year-old female who was providing water for the participants, but became diaphoretic and short of breath and is now unresponsive. While you are online with medical control, the triage nurse is handing you a note with five expected patients that were called in. How can you prepare to treat these people, and what care do they need? HEAT WAVE 497

alcohol withdrawal, neuroleptic malignant syndrome, malignant hyperthermia, toxicities (anticholinergics, salicylates, PCP, cocaine, amphetamine), infectious sources (tetanus, sepsis, encephalitis, meningitis, brain abscess, typhoid fever, malaria), endocrine abnormalities (thyroid storm, diabetic ketoacidosis), status epilepticus, and cerebral hemorrhage. For patients with hyperthermia, do not forget to consider an acute cardiac event or a severe electrolyte abnormality. Consider other causes of altered mental status, including hypoglycemia, thiamine deficiency, or opiate overdose.6 REFERENCES 1. Wetterhall SF, et al. Medical care delivery at the 1996 Summer Games. JAMA 1998:279, 1463-1468. 2. Moran DS, Gaffin SL. Clinical management of heat-related illnesses. In:Aurebach PS, ed. Wilderness Medicine. 4th ed. St. Louis: Mosby; 2001:290-317.

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3. The Disaster Center. Available at: http://www.disastercenter.com 4. Walker JS, Barnes SB. Heat emergencies. In: Tintinalli JE, ed. Emergency Medicine: A Comprehensive Study Guide. 5th ed. New York: McGraw-Hill; 2000:1237-42. 5. Doucette M. Hyperthermia. In: Schaider J, et al, eds. Rosen and Barkin’s 5-Minute Emergency Medicine Consult. 2nd ed. Philadelphia: Lippincott Williams & Wilkins; 2003:562-3. 6. Schmidt E, Nichols C. Heat- and sun-related illnesses. In: HarwoodNuss A, Wolfson AB, Linden CH, Shepherd SM, Stenklyft PH, eds. The Clinical Practice of Emergency Medicine. 3rd ed. Philadelphia: Lippincott Williams & Wilkins; 2001:1667-70.

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Winter Storm Alison Sisitsky

DESCRIPTION OF EVENT Heavy snow, high winds, and freezing rain can combine to create winter storms. The National Weather Service provides public information related to the severity of the storm expected. The various types of winter storm are blizzard, heavy snow, sleet, and ice storm. A blizzard is a combination of low temperatures, snow, and wind speeds up to 35 miles per hour resulting in less than a quarter mile of visibility. Heavy snow is 6 or more inches of falling snow in less than 12 hours. Sleet is frozen raindrops that bounce when hitting the ground. Finally, ice storms occur when rain hits the ground and freezes. The ice can accumulate on roads and power lines, causing damage and creating dangerous electrical hazards.1 The incidence of winter storms is approximately 105 per year in the continental United States. Causes of death related to winter storms include traffic accidents, overexertion, and exposure.2 Of these deaths, 70% occur in automobiles, and 25% occur out in the storm.1

PREINCIDENT ACTIONS Before a winter storm hits, the most important action is to prepare the public. This includes educating the public about when to expect a storm, how to find out if one is coming, and how to handle the possible dangers associated with it. The National Weather Service will issue alerts on the radio and television within 24 hours of a possible storm. The alerts are graded from watch to advisory to warning. When dangerous weather is predicted, a watch is issued. During the storm, an advisory is issued that alerts the public to dangerous winter weather. When a warning is issued, the weather is very dangerous and could be lifethreatening.1 The public should have a winter storm plan as well as various supplies. Every home should have extra blankets and warm clothing, including coats, gloves, hats, and water-resistant boots. A disaster kit should be assembled. The American Red Cross recommends a first aid kit, a battery-powered weather radio, extra batteries, canned food, can opener, bottled water (1 gallon per person per day for 3 days), and extra warm clothing. In

addition, cars should be winterized in the late fall, including placing a disaster kit inside the car.1 When a winter storm warning is issued, the public should follow these general rules: stay indoors but if one must go outside, wear several light layers of clothing, a hat, and gloves; protect the skin from wind chill; walk carefully on snow and ice; and avoid overexertion when removing snow. If one gets stuck in a car, it is advised to stay inside the car after placing a bright cloth on the antenna. To stay warm, start the car and use the heater for 10 minutes every hour. Continue to move the arms and legs while sitting in the car to keep the body warm.1 Prehospital treatment consists of keeping the patient warm with minimal movement if the patient is hypothermic. Assess vital functions, remove cold or wet clothing, and apply dry blankets. Refer to hypothermia treatment described later in the chapter. It is not recommended to begin cardiopulmonary resuscitation if a pulse is palpable and transport time is brief.

POSTINCIDENT ACTIONS Remove the patient from the cold environment as soon as possible. Remove all wet and cold clothes to prevent further heat loss.3 The medical conditions to consider in a patient caught in a winter storm are hypothermia (mild, moderate, and severe), frostbite, carbon monoxide poisoning, and overexertion injuries.3 It is important to keep roads clear of snow and ice as soon as possible. Driveways and sidewalks around the hospital also must be clear to keep patients safe upon arrival.

MEDICAL TREATMENT OF CASUALTIES Assess vital functions, and determine core temperature. Blood should be evaluated for possible complications, including lactic acidosis, rhabdomyolysis, and bleeding diatheses. A toxicology screen is recommended as well. An electrocardiogram should be obtained to evaluate for 499

prolongation of the intervals, elevation of the J point (Osborne wave) (Fig. 78-1), and dysrhythmias.3 Mild hypothermia is when the core temperature is between 32° and 35°C. Patients with mild hypothermia may experience tachypnea, tachycardia, shivering, or mild altered mental status. Passive external rewarming should be initiated after removing wet clothing. Blankets or any other insulation should be adequate to assist endogenous thermogenesis. Moderate hypothermia is when the core temperature is between 28° and 32°C. These patients may have decreased heart rate and cardiac output and generalized central nervous system depression. They are at risk for renal failure, atrial fibrillation, and bradycardia. Paradoxical undressing may be witnessed. Immediate passive and active external rewarming should be initiated. Warm blankets, heating pads, and warm air should be applied to the patient to decrease further heat loss. The heat should be applied to the patient’s torso to prevent core temperature afterdrop. The goal is to prevent extensive peripheral vasodilation that occurs naturally after the patient is removed from the cold and is rewarmed. Cold blood is shunted to the core, causing decrease in body temperature as well as hypotension, poor cardiac perfusion, and risk of ventricular fibrillation.4–6 Severe hypothermia is when the core body temperature is below 28°C. Patients with severe hypothermia are at risk for hypotension, bradycardia, ventricular fibrillation, pulmonary edema, and coma. Move these patients carefully to avoid inducing ventricular fibrillation. Active internal rewarming is necessary in these patients and can be done with the external techniques previously described. Humidified oxygen and warm intravenous fluids are minimally invasive ways to warm the severely hypothermic patient. The peritoneal cavity, pleural spaces, and bladder can be irrigated with 45°C fluid.

Pleural irrigation should be reserved for those without a cardiac rhythm to avoid inducing ventricular fibrillation with chest tube placement. Blood warming by hemodialysis and cardiopulmonary bypass are acceptable means to raise the core body temperature. Protocols for aggressive and invasive rewarming procedures should be developed in cooperation with other departments involved in these processes prior to an incident requiring such measures.4–6 Arrhythmias related to hypothermia were formerly treated with bretylium, but this medication is no longer available. Arrhythmias should be treated according to advanced cardiac life support (ACLS) guidelines and may be refractory until the patient is normothermic.5 Cold-induced tissue injuries are common during winter storms. Risk factors include altered mental status, advanced age, malnutrition, and peripheral vascular disease. Tissue injuries range from mild (frostnip) to severe (frostbite). Frostbite is local injury from contact with temperatures below 2°C. The first phase of frostbite is the initial freeze injury when cell damage occurs. The second phase is the reperfusion injury that occurs while rewarming. The full extent of the injury may not be obvious on initial presentation. Do not rub or manipulate the frozen part. Treatment should consist of rapid rewarming in a water bath kept between 40° and 42°C. The affected extremity should be immersed for 15 to 30 minutes. Blisters should be left intact, and a sterile dressing with antibiotic ointment should cover any that have burst. Other remedies include aloe vera and ibuprofen. Tetanus status needs to be updated. Patients should be advised to avoid smoking as well.3,7,8 Carbon monoxide poisoning should be considered in patients with headache, dizziness, nausea, vomiting, confusion, seizures, or coma. Apply 100% oxygen, and consider hyperbaric oxygen therapy if the patient’s condition is stable and a chamber is easily accessible.

FIGURE 78–1. Electrocardiogram of a hypothermic patient with characteristic J waves after the QRS complexes. 500 NATURAL DISASTERS

Arterial blood gas and carboxyhemoglobin levels will help guide therapy.9 Epidemics of carbon monoxide toxicity may be encountered when heat and electricity are cut off for prolonged periods due to storms. The indoor use of heat generation utilizing fossil fuels contributes to cases (as was seen in the 1999 ice storms in upstate New York).

UNIQUE CONSIDERATIONS Extremes of age are risk factors for cold-induced illnesses. As one ages, the shivering mechanism may not be adequate, and therefore there is an increased risk of hypothermia. Infants have a large body surface to mass ratio and can lose heat quickly. The elderly and children may be unable to carry out actions to warm themselves. Medications such as barbiturates, benzodiazepines, chlorpromazine, and tricyclic antidepressants can increase the risk of hypothermia.

PITFALLS • Always assess the entire patient. • Think of other causes of altered mental status and consider giving naloxone, thiamine, and glucose.

CASE PRESENTATION Yesterday, the National Weather Service issued a winter storm warning. A blizzard is expected to hit this morning. Snow began falling late last night, and local schools are closed. Emergency medical services have just arrived with a homeless man found unresponsive under a bridge. He is naked, feels frozen, and has a thready pulse. They have intubated him in the field and started intravenous fluid, but they cannot get a blood pressure reading. What else can be done to save this patient?

• Do not forget to evaluate for hypothermia in the patient who presents with frostbite. • For patients with frostbite, do not rub the affected part. Monitor the rewarming bath temperature to avoid extremity refreezing. Obtain surgical consult for severe frostbite that involves structures below the subcutaneous tissues. Warn patients about the dangers of reexposing the area to cold temperatures. • For patients with hypothermia, always obtain an accurate rectal temperature. Remember that arrhythmias are best treated with rewarming. Do not handle the patient roughly because it may induce arrhythmias. Continue to resuscitate patients until the core temperature is at least 32˚C. Continue fluid resuscitation, and watch for core temperature afterdrop.3,5 REFERENCES 1. Thousands Without Power After Southeast Ice Storm, 2000, CNN.com.Available at: http://edition.cnn.com/2000/WEATHER/ 01/24/ice.storm.02/ 2. Spitalnic SJ, Jagminas L, Cox J. An association between snowfall and ED presentation of cardiac arrest. Am J Emerg Med. 1996; 14(6):572-3. 3. Schaider J. Hypothermia. In: Schaider J, et al, eds. Rosen and Barkin’s 5-Minute Emergency Medicine Consult. 2nd ed. Philadelphia: Lippincott Williams & Wilkins; 2003:584-5. 4. UpToDate. Available at: http://www.uptodate.com. 5. Currier J. Hypothermia. In: Harwood-Nuss A, Wolfson AB, Linden CH, Shepherd SM, Stenklyft PH, eds. The Clinical Practice of Emergency Medicine. 3rd ed. Philadelphia: Lippincott Williams & Wilkins; 2001:1664-7. 6. Danzl D. Accidental hypothermia. In: Aurebach PS, ed. Wilderness Medicine. 4th ed. St. Louis: Mosby; 2001:135-77. 7. Gonzalez F, Leong K. Cold-induced tissue injuries. In: HarwoodNuss A,Wolfson AB, Linden CH, Shepherd SM, Stenklyft PH, eds. The Clinical Practice of Emergency Medicine. 3rd ed. Philadelphia: Lippincott Williams & Wilkins; 2001:1661-4. 8. Arnold P. Frostbite. In: Schaider J, et al, eds. Rosen and Barkin’s 5-Minute Emergency Medicine Consult. 2nd ed. Philadelphia: Lippincott Williams & Wilkins, 2003:436-7. 9. Chang A, Hamilton R. Direct relationship between unintentional workplace carbon monoxide deaths and average U.S. monthly temperature. Academic Emergency Medicine AEMJ 2002;9:531.

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79

Volcanic Eruption Gregory Jay

DESCRIPTION OF EVENT Volcanic eruptions have the potential to produce significant loss of life and far-reaching medical and socioeconomic disruption. More than 270,000 volcano-related fatalities have been recorded since 1700, with the number of fatal eruptions averaging two to four events per year.1–3 Eighty percent of the world’s active volcanoes are located around the Pacific Basin where continental and seafloor plate subduction occurs.1,4 In 1990 approximately 10% of the world’s population lived within 100 km of an active volcano.1 With the continued growth in world population and urbanization, the risk of trauma and death from volcanic eruptions will only increase. The violence or force of a volcanic eruption determines the characteristic of injuries produced. A volcanic eruption is the ejection of gases and solid material from a vent or hole in the Earth’s surface. Outgassing, or release of volatiles dissolved in magma, provides the motive force for an eruption. While magma rises to the Earth’s surface, the decreasing pressure on molten rock allows volatiles and gases in the melt to be released.5 The higher the silica content of the melt, the more viscous and polymerized it remains, stabilizing volatiles and gases.1 When pressure is suddenly released on magma with a high dissolved volatile concentration, rapid and explosive outgassing may occur.This produces the typical violent or explosive eruption during which lava bombs and plumes of ash are ejected. When magma has a low silica content, outgassing occurs more gradually, and a more gentle, or effusive, eruption ensues.6 The volcanoes located along plate subduction zones tend to produce more violent eruptions because of the high silica and dissolved volatile concentration in their magma.1 A variety of physical and chemical hazards are associated with volcanic eruptions. Lava is responsible for very few fatalities. The flow is often slow and can be easily avoided. Pyroclastic flows are responsible for the most deaths.2 A pyroclastic flow is a mass of hot volcanic ash, lava fragments, and gases that erupts from a volcano and moves rapidly down its slope at speeds of up to a few hundred miles per hour.6–8 Rocks and debris within the flow may be hurled at great speed, causing severe secondary blast injury. Pyroclastic flows are extremely destructive and fatal to nearly all life in the 502

area through which they travel. The temperatures in a pyroclastic flow may be as high as 600° to 900°C, causing severe, if not fatal, burns.6 Pyroclastic flows may extend a great distance from the site of an eruption. Flows commonly travel up to 15 km from a vent; during the Mount St. Helens eruption in 1980, flows reached 17 miles.7 Pyroclastic flows often occur multiple times during an eruption and have also been reported in the absence of violent eruption.9,10 Another common cause of volcanic eruption–related fatalities is tephra. Tephra includes all of the solid fragments of magma and volcanic rock ejected from a volcano during an eruption.6,8 Ejecta can cause severe head injury, burns, and blunt trauma.11 Tephra fragments less than 2 mm are termed ash, 2- to 64-mm fragments are called lapilli, and fragments larger than 64 mm are often called lava bombs or blocks. Lava blocks and bombs generally follow a more ballistic trajectory after ejection, landing a few meters to several kilometers away from the site of eruption. The path and final point of impact is dependent on the initial “muzzle velocity” of the fragment.6 Ballistic fragments are a serious hazard near a vent, but become a more minor hazard as distance increases from the site of eruption. Air resistance also prevents ballistic fragments less than a few centimeters in diameter from being hurled more than a few hundred meters from a vent.6 Ash clouds pose a potential health hazard. Small particles of tephra rise on convection currents within a hot eruption cloud and may drift for hundreds of kilometers downwind from the active volcano.6 Tephra deposits tend to become finer grained farther downwind because the coarser particles of ash and lapilli fall nearer the volcano.6 In very large eruptions, tephra accumulations may reach several meters in depth, and the associated lapilli and ashfall may be heavy enough to induce darkness at midday.6 Although the mean diameter of tephra grains decreases with distance from a vent, the percentage of respirable ash, particles less than 10 μm in diameter, does not necessarily increase.6 Currently very little research is available regarding the respiratory effects of volcanic ash. There was concern about the development of acute silicosis from exposure to ash with high silica and cristobalite content.12,13 However, no cases of acute silicosis were reported in

studies of eruptions at Soufriere Volcano in Montserrat and of the Mount St. Helens eruption in 1980, where high concentrations of cristobalite and silica were recorded in ash samples.12,13 These studies did note a slight increase in bronchial reactivity and wheeze in children during the Montserrat eruptions and a doubling of asthma- and bronchitis-related emergency department (ED) visits, compared with the previous year, during the Mount St.Helens eruption.13,14 It is believed that no cases of acute silicosis were reported because people were not exposed to high enough concentrations of silica-laden ash for a long enough duration to develop the condition.13 The risk of silicosis from prolonged ash exposure may be more substantial, but it is difficult to quantify.13 During ashfalls, the amount of total suspended particles (TSP) in the air is a useful predictor of ED visits for some respiratory conditions. The number of ED visits for respiratory complaints during the Mount St. Helens eruption was highest when the TSP concentration was greater than 30,000 μg/m3.14 The number of ED visits did decline with decreasing TSP levels, but it did not return to normal levels until 3 weeks after peak TSP levels were recorded.14 The increase in ED visits during high TSP levels was greatest for asthmatics.14 (An important factor to remember is that rain significantly reduces TSP levels.14) Volcanic gases also pose a potential health threat. To determine the hazards from volcanic gas, the composition of the volcanic gas emissions and the prevailing weather conditions should be assessed.6,15,16 Water vapor is the most abundant volcanic gas released, followed by carbon dioxide and sulfur dioxide.5,6 Volcanic emissions may also include smaller amounts of hydrogen sulfide, hydrogen, carbon monoxide, hydrogen chloride, hydrogen fluoride, helium, and trace amounts of other gases.5 The volcanic gases that pose the greatest threat to people, animals, and agriculture are sulfur dioxide, carbon dioxide, and hydrogen fluoride.5 Sulfur dioxide may produce an irritant effect in the upper and lower airways, on mucosal surfaces, in the eyes, and on the skin.5,17 Few studies have been performed to assess the health risk of volcanic gas emissions. One study, performed in Hawaii, of volcanic sulfur dioxide emissions was inconclusive in respect to its effect on reactive airway disease.18 Sulfur dioxide does produce acid rain, which may react with zinc in galvanizing on sheet metal roofs and release heavy metals into drinking water and catchments.16 Hydrogen fluoride also induces an irritant response in the upper and lower respiratory tracts, but it is of greatest risk to livestock secondary to ingestion. Ash becomes impregnated with hydrogen fluoride, and upon ingestion, the fluoride produces fluorosis and death of the animal.5 Fluorosis is a theoretical risk to a human population posteruption, but it can be avoided by cleaning ash off of food before ingestion and checking the fluoride levels of local drinking water. Carbon dioxide is the second most common gas released during volcanic activity. Carbon dioxide is odorless, colorless, and heavier than air, thus it will collect in low-lying areas. Breathing air with a carbon dioxide concentration greater than 20% to 30% can rapidly induce unconsciousness and death through asphyxiation.5 If a substantial release of carbon dioxide has occurred or is sus-

pected, venturing into depressions or cellars in the area should be avoided. The carbon dioxide and air boundary can be sharply demarcated, with one step placing a person within a lethal concentration of carbon dioxide.5 The other gases tend to be released in much smaller quantities during an eruption. An important consideration is hydrogen sulfide. It is a highly toxic gas that is relatively dense and may collect in depressions and low-lying areas.6 Hydrogen sulfide gives off a “rotten egg” odor and can cause eye and upper respiratory tract irritation, pulmonary edema with prolonged exposure, and death through cellular asphyxiation.5,17 It is important to determine the emissions spectrum of a volcano to ensure that larger concentrations of dangerous trace gases are not present. Volcanic debris flows, termed lahars, and mudslides can be very destructive. Loose fragments of rock mixed with water from rainfall, melted snowpack, or another source forms a thick slurry that travels down the mountain side or valley at speeds that may be greater than 50 km per hour.6,19 The high sediment concentration of the flow destroys buildings, bridges, and other structures, which would usually survive a flood.6 People caught in the flows almost universally perish.6 Lahars also occur when a volcano is quiescent. Both the heavy rainfall from hurricanes and the disruption of volcanic debris and sediment by earthquakes have produced lahars and mudslides.20,21 Lahars may also be formed by lake breakouts. This happens weeks to months after an eruption when a river blocked by a mudslide or other volcanic deposit overflows the newly formed dam. Erosion of the blockage and the walls of the river channel downstream from the initial surge of water allows tremendous volumes of sediment to be incorporated into the flow.22 This is termed a cold lahar; in comparison, the lahar formed by hot volcanic debris may remain hot far downstream.6 Volcanoes pose a unique threat in regard to gas release in the absence of visible eruption. In 1984 at Lake Monoun in Cameroon, 73 people were killed by carbon dioxide released by lake water turnover.23 A similar event occurred in 1986 at Lake Nyos in Cameroon, a crater lake. Approximately 1700 people in low-lying areas were killed by a massive release of carbon dioxide.23 Carbon dioxide is believed to have gradually accumulated in the deep waters of the lake. Rain or a landslide may have been responsible for the lake water turnover and gas release at Lake Nyos. Other risks associated with volcanic eruptions are lightning, tsunamis, and earthquakes. Lightning discharges and lightning strikes from ash clouds occur during eruptions and have caused electrocution injuries.24 Please see the chapters on tsunamis (Chapter 76) and earthquakes (Chapter 73) for further information about these forms of disaster.

PREINCIDENT ACTIONS The following are important preincident questions to ask: • Is there a volcano in close proximity to your medical facility that may be at risk of eruption? To determine VOLCANIC ERUPTION 503

•

•

•

•

•

•

this, contact the U.S. Geological Survey or an equivalent authoritative source. Does your facility have a mass casualty plan in case of an eruption? Refer to the section on the basics of disaster management (Part 1 of the book) for assistance in developing an organized strategy for dealing with mass casualties. Does your medical facility need to be evacuated in the event of an eruption? Medical facilities were evacuated during the eruption of the Rabaul Volcano in Papua New Guinea in 1994 because it was in the fallout zone.24 If your facility is in a valley or plain with a history of lahars or mudslides, it may need to be evacuated. Is a disaster plan prepared, and has it been practiced to allow the timely notification and evacuation of your hospital and the populations at risk? Preparation is crucial, considering that the majority of the deaths during an eruption occur within the first 24 hours.2 Please refer to the basics of disaster management of this book (Chapter 1) for assistance in creating a disaster plan appropriate for your facility. If your facility may require evacuation during an eruption, is there an evacuation plan prepared and coordinated with the appropriate nearest medical facilities outside of the potential fallout zone? Does your facility have appropriate supplies and personal protective equipment? Your facility may benefit from having detectors for sulfur dioxide, hydrogen sulfide, carbon dioxide, and carbon monoxide available in case of gas release.15 Special masks may be needed for protection from gases and dust. Particulate masks do not provide adequate protection. Based on experience from the World Trade Center disaster, the New York Committee for Occupational Safety and Health has recommended the use of National Institute for Occupational Safety and Health (NIOSH)–approved air-purifying respirators of N-100 or N-95 grade.25 Other useful protective equipment would include hard hats or helmets and heat-resistant clothing.11 Does your facility have adequate internal resources for continued short-term operation if isolated by disruption of local infrastructure? If not, do you have a plan for communication and procurement of needed assistance?

POSTINCIDENT ACTIONS 1. Activation of disaster plan with appropriate allocation of resources. 2. Distribution and use of appropriate personal protective equipment. 3. Situational awareness. Avoid low-lying areas where lahars or pyroclastic flows have occurred because of the risk of repeat episodes. Avoid basements or depressions where toxic gases may have accumulated unless air quality has been tested. 4. Be alert for repeat eruptions. The volcano may erupt multiple times. 5. Monitor ash and tephra accumulation on buildings in the medical facility. Tephra causes the most injuries 504 NATURAL DISASTERS

through building collapse. If ash clearing is undertaken, make sure that appropriate personal protective equipment is worn and that the conditions are safe enough to allow removal of the ash. If there is any concern about the risk of building collapse, consider evacuating the facility or building. 6. Monitor air quality and provide appropriate public health warnings. Those at risk for chronic obstructive pulmonary disease and asthma exacerbations may benefit from staying indoors, if it is safe to do so, while TSP concentrations are high.

MEDICAL TREATMENT OF CASUALTIES Casualties during a volcanic eruption can be complex and require sophisticated and intensive multisystem trauma care. Detailing of all the medical treatments potentially required is beyond the scope of this chapter. The important factor to consider is the mechanism of volcanicrelated injury in anticipating patient care needs. The broad categories of injuries seen are burns, crush injuries, head trauma, inhalation injuries, toxic exposure to gases, blunt force trauma, and amputations. For further information and recommendations please refer to the basics of disaster management of this book (Part 1), the accidental disaster section (chapter 57), and the following chapters: accidental versus intentional event (Chapter 57) building and bridge collapse (Chapters 169 and 170), landslide (Chapter 81) and building fires (Chapter 156).

UNIQUE CONSIDERATIONS 1. Gas release from lake water turnover in the absence of visible volcanic activity. 2. Dormant or suspected dormant volcano reactivation.

PITFALLS 1. Failure to assess whether your medical facility is at risk from volcanic eruption and failure to incorporate this eventuality into the hospital disaster plan. 2. Lack of consideration for a volcano’s historic eruptive pattern when preparing a disaster plan. 3. Failure of your medical facility to procure adequate and appropriate supplies to deal with a volcanic eruption. Personal protective equipment should include heat-resistant coveralls, hard hats, and NIOSHrecommended respirators. 4. Failure to appreciate the risk for volcanic-related injuries in the absence of visible volcanic activity. Examples include mudslides, lahars, and volcanic gas release. 5. Failure to consider the need to evacuate a hospital posteruption and to determine whether the receiving facility is in a safe zone that will not be endangered by future or repeated eruptions.

CASE PRESENTATION The eruption of the Galeras Volcano in Colombia in 1993 provides a better understanding of the need for adequate personal protective equipment and a more clear understanding of the injury spectrum that may be suffered during a volcanic eruption. Six volcanologists and three tourists were killed when the volcano erupted without warning. Autopsies showed that individuals closest to the eruption site within the caldera were torn apart by the force of the eruption. Those farther away from the eruption suffered burns from ejecta, fractures, concussions, and other head injuries from bombardment with ejecta. Analysis of the tragedy suggested that hard hats would provide some protection from head injuries during escape. Heat-resistant and water-repellent coveralls could limit the risk of burns and clothing ignition.11

REFERENCES 1. Small C, Naumann T. The global distribution of human population and recent volcanism. Environmental Hazards. 2001;3:93-109. 2. Simkin T, Siebert L, Blong R. Disasters: volcanic fatalities—lessons from the historical record. Science. 2001;5502:255. 3. US Geological Survey. Types and Effects of Volcanic Hazards. Available at: http://volcanoes.usgs.gov/Hazards/What/hazards.html. 4. Bernstein RS, Baxter PJ, Buist AS. Introduction to the epidemiological aspects of explosive volcanism. Am J Public Health. 1986; 76(3 Suppl):3-9. 5. US Geological Survey. Volcanic Gases and Their Effects. Available at: http://volcanoes.usgs.gov/Hazards/What/VolGas/volgas. html. 6. Newhall CG, Fruchter JS. Volcanic activity: a review for health professionals. Am J Public Health. 1986;76(3 Suppl):10-24. 7. US Geological Survey. Effects of Pyroclastic Surge at Mount St Helens, Washington, May 18, 1980. Available at: http:// volcanoes.usgs.gov/Hazards/Effects/MSHsurge_effects. html. 8. Decker RW, Decker BB. Mountains of Fire: The Nature of Volcanoes. New York: Cambridge University Press; 1991:1-40. 9. US Geological Survey. Dome Collapses Generate Pyroclastic Flows at Unzen volcano, Japan. Available at: http://volcanoes.usgs. gov/Hazards/What/PF/PFUnzen. html.

10. US Geological Survey. Effects of Pyroclastic Flows and Surges at Soufriere Hills Volcano, Montserrat. Available at: http://volcanoes. usgs.gov/Hazards/Effects/Soufrie reHills_PFeffects.html. 11. Baxter PJ, Gresham A. Deaths and injuries in eruption of Galeras Volcano, Colombia, 14 January 1993. J Volcanology Geothermal Research. 1997;77:325-38. 12. Martin TR, Covert D, Butler J. Inhaling volcanic ash. Chest. 1981;80(1 Suppl):85-8. 13. Searl A, Nicholl A, Baxter PJ. Assessment of the exposure of islanders to ash from the Soufriere Hills volcano, Montserrat, British West Indies. Occup Environ Med. 2002;59:523-31. 14. Baxter PJ, Ing R, Falk H, Plikaytis B. Mount St. Helens eruptions: the acute respiratory effects of volcanic ash in a North American community. Arch Environ Health. 1983;38(3):138-43. 15. Baxter PJ, Berstein MD, Buist AS. Preventative health measures in volcanic eruptions. Am J Public Health. 1986;76(3 Suppl):84-90. 16. US Geological Survey. Long-lasting Eruption of Kilauea Volcano, Hawai`i Leads to Volcanic-Air Pollution. Available at: http://volcanoes.usgs.gov/Hazards/What/Vol Gas/VolGasPollution.html. 17. Olson KR, et al. Poisoning and drug overdose. 3rd ed. Stamford, Conn:Appleton & Lange; 1999:181-8. 18. Mannino DM, Ruben S, et al. Emergency department visits and hospitalizations for respiratory disease on the island of Hawaii, 1981 to 1991. Hawaii Med J. 1996;55:48-54 19. US Geological Survey. “What’s That Cloud Upriver?”An Eyewitness Account of a Lahar by USGS Geologist Jeff Marso. Available at: http://volcanoes.usgs.gov/Hazards/What/Lahars/ Santiaguito_89. html. 20. US Geological Survey. Intense Rainfall During Hurricane Mitch Triggers Deadly Landslide and Lahar at Casita Volcano, Nicaragua, on October 30, 1998. Available at: http://volcanoes.usgs.gov/ Hazards/What/Lahars/Cas itaLahar.html. 21. US Geological Survey. Earthquake on June 6, 1994, Triggers Landslides and Catastrophic Lahar Near Nevado del Huila Volcano, Colombia. Available at: http://volcanoes.usgs.gov/Hazards/What/ Lahar s/HuilaLahar.html. 22. US Geological Survey. Lahars Caused by Lake Breakouts. Available at: http://volcanoes.usgs.gov/Hazards/What/Lahars/LakeLahar.html. 23. Baxter PJ, Kapila M, Mfonfu D. Lake Nyos disaster, Cameroon, 1986: the medical effects of large scale emission of carbon dioxide? BMJ. 1989;298:1437-41. 24. Dent AW, Davies G, Barrett P, de Saint Ours PJ. The 1994 eruption of the Rabaul volcano, Papua New Guinea: injuries sustained and medical response. Med J Aust. 1995;163:536-9. 25. New York Committee for Occupational Safety and Health. NYCOSH WTC Factsheet 4: Cleaning Up Indoor Dust and Debris in the World Trade Center Area. Available at: http://www.nycosh.org/ environment_wtc/wtc-dust-factsheet.html.

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80

Famine Laura Macnow and Hilarie Cranmer

DESCRIPTION OF EVENT Famine is the most extreme form of lack of access to enough food and is often the result of natural or manmade disasters. Famine has been defined as “a condition of populations in which a substantial increase in deaths is associated with inadequate food consumption.”1 Natural disasters such as drought, floods, crop infestations, and livestock diseases that limit a population’s food production are often popularly thought of as the events precipitating famine; however, insufficient access to food is now more commonly the result of war, civil strife, and economic collapse. Famine is usually caused by an exacerbation of preexisting conditions of poverty, debt, underemployment, and high malnutrition prevalence in a population, so that when added burdens arise, widespread starvation can occur rapidly.2 Famine is a complex emergency often involving massive population displacements between and within countries, and as such, complicates the ability of agencies to coordinate relief efforts and provide ongoing surveillance of the emergency. The usual consequences of mass starvation during famine are increased malnutrition and mortality.3 Manifestations of starvation depend on the individual’s previous nutritional status, age, and severity of food deprivation.4 Malnutrition is the objective physical or laboratory findings of physical deterioration as a result of inadequate nutrient intake and encompasses a range of conditions, including acute malnutrition (characterized by wasting), chronic malnutrition (characterized by stunting or nutritional edema), and micronutrient deficiencies.5 To assess the prevalence of moderate-to-severe malnutrition in a population, it is a commonly accepted practice to do anthropometric surveys in a random sample of children younger than 5 years using the weightfor-height (WFH) index2,5; these data are a reliable indicator of malnutrition in the wider population. Because weight is more sensitive to sudden changes in food availability,2 the WFH index is used instead of height-for-age (which measures stunting). Mean upper arm circumference (MUAC) can also be measured to screen for acute malnutrition. The presence of edema, however, may confound these indices, and clinical judg506

ment must be used in their evaluation. Additionally, anthropometric data may be skewed by concurrent mortality rates. Anthropometric data are commonly interpreted using z scores (or standard deviation [SD] scores) where: Observed Value − Median Value of the z score = Reference Population (or SD score) Standard Deviation Value of Reference Population The WHO Global Database on Child Growth and Malnutrition6 uses a z-score cut-off point of less than −2 SD to classify low weight-for-age, low height-for-age, and low weight-for-height as moderate and severe undernutrition, and less than −3 SD to define severe undernutrition.6 If more than 8% of the children samples have a z score of less than −2, a nutritional emergency exists. An excess of even 1% of children with z scores of less than −3 indicates a need for immediate action.2 Famines are often assessed and reported in terms of cases, rates, or degrees of malnutrition, or the number of deaths from malnutrition and its complications. Crude mortality rates (CMRs) can be useful for evaluating the severity of a disaster, using 1 death/10,000 population/ day as the cut-off for an emergency.2 Although the most direct and obvious results of famine are severe malnutrition and death, the immediate cause of death in affected individuals is usually a communicable disease, most commonly measles, diarrheal illness, acute respiratory infections (ARIs), and malaria. Displaced populations and refugees almost always experience higher CMRs compared with nondisplaced populations, and this is likely due to increased risk of communicable disease associated with crowded, often unsanitary camps. Malnutrition predisposes individuals to certain micronutrient deficiencies, notably vitamin A deficiency; communicable diseases such as measles and diarrhea further deplete vitamin A stores and can cause worsening immune compromise and xerophthalmia, corneal xerosis, and ulceration and scarring, and can eventually lead to blindness.2 Other important micronutrient deficiencies include vitamin C, niacin, iron, iodine, and thiamine deficiency.

PREINCIDENT ACTIONS • Advance detection and monitoring of economic, social, and environmental factors that influence the development of food shortages and famine. Early warning systems may rely on community involvement. Local people can collect data on what they see as signs of growing food insecurity;for example,an increase in the number of animals sold in local markets may indicate that families need cash to buy food because their crops have failed.7 This information is used in conjunction with satellite imaging and meteorologic data to create the whole picture of drought and its effects. • Support of socially responsible community development, including education about preserving the huge local ranges of hardy crop types and encouraging food production of a wide variety of crops, bred to be hardy and grown together in a robust mixed-crop pattern. This will help communities recover quickly in the event of natural disasters.7 Mono-cropping can increase vulnerability in times of natural or economic disasters, as can deforestation, desertification, and poor agricultural practices.2 • Coordination of relief agencies. • Development of standard case management protocols. • Establishment of reserves of essential supplies (medical and nutritional). • Development of environmental management plans.

POSTINCIDENT ACTIONS • Media and worldwide notification. • Perform field assessment: determine total refugee or displaced population, determine age-sex breakdown and average family/household size, identify at-risk groups (children 11.

the clinician to exclude other diagnoses, including infectious etiologies, because these patients will often present with temperature elevation (due to psychomotor agitation and anhidrosis) and an altered mental status.

UNIQUE CONSIDERATIONS Complications resulting from exposure to BZ include acute-angle closure glaucoma secondary to the mydriasis, rhabdomyolysis due to psychomotor agitation, ileus, urinary retention requiring Foley catheterization, pneumonia or hypoxia due to prolonged stupor or aspiration, and heat damage from heat retention secondary to anhidrosis. 3-Quinuclidinyl benzilate is a bicyclic ester that will hydrolyze in an alkaline solution of pH > 11 to benzylic acid and 3-quinuclidinol within minutes; both of these hydrolysis products are much less toxic than the parent compound (Figure 95-1).5,11 This may be relevant in decontamination of surfaces and medical equipment.

PITFALLS Several potential pitfalls in response to a nerve agent attack exist. These include the following: • Disorganization of hospital and local emergency medical services, should they become overwhelmed by many patients with agitated delirium • Failure to recognize that numerous patients requiring attention (including restraint in many cases) will mandate efficient allocation of hospital resources and personnel to avoid resource depletion and staff exhaustion • Inadequate decontamination of patients exposed externally, resulting in secondary exposure to healthcare workers, particularly rescue workers and paramedics • Failure to be diligent in identifying other injuries when confronted with multiple patients • Failure to suspect the diagnosis of an antimuscarinic agent, resulting in the administration of medications with antimuscarinic effects (e.g., haloperidol) that may worsen the patient’s condition 584 NATURAL DISASTERS

• Failure to restrain potentially disruptive patients who have been exposed to BZ • Failure to recognize the potential for heat stress in anhidrotic patients who have been exposed to BZ REFERENCES 1. Ketchum JS. The Human Assessment of BZ. Edgewood Arsenal, Md: Chemical Research and Development Laboratory; 1963. Technical Memorandum 20-29. Cited in: Ketchum JS, Sidell FR. Incapacitating agents. In: Sidell FR, Takafuji TE, Franz DR, eds. Textbook of Military Medicine: Medical Aspects of Chemical and Biological Warfare. Falls Church, Va: Office of the Surgeon General, U.S. Army; 1997:287-305. 2. U.S. Army Center for Health Promotion and Preventive Medicine: Psychedelic agent 3: quinuclidinyl benzilate (BZ). The Deputy for Technical Services’ Publication: Detailed Chemical Facts Sheets; 1998. Available at: http://chppm-www.apgea.army.mil/dts/ dtchemfs.htm. 3. Wyper DJ, Brown D, Patterson J, et al. Deficits in iodine-labelled 3-quinuclidinyl benzilate binding in relation to cerebral blood flow in patients with Alzheimer’s disease. Eur J Nucl Med. 1993; 20:379-86. 4. Hiramatsu Y, Eckelman WC, Baum BJ. Interaction of iodinated quinuclidinyl benzilate enantiomers with M3 muscarinic receptors. Life Sci. 1994;54:1777-83. 5. Guidelines for 3-quinuclidinyl benzilate. In: Subcommittee on Guidelines for Military Field Drinking-Water Quality, Committee on Toxicology, Board on Environmental Studies and Toxicology, National Research Council. Guidelines for Chemical Warfare Agents in Military Field Drinking Water. The National Academies Press; 1995:15-8. 6. Hay A. Surviving the impossible: the long march from Srebrenica. An investigation of the possible use of chemical warfare agents. Med Confl Surviv. 1998;14:120-55. 7. Byrd GD, Paule RC, Sander LC, et al. Determination of 3-quinuclidinyl benzilate (QNB) and its major metabolites in urine by isotope dilution gas chromatography/mass spectrometry. J Anal Toxicol. 1992;16:182-7. 8. Burns MJ, Linden CH, Graudins A, et al. A comparison of physostigmine and benzodiazepines for the treatment of anticholinergic poisoning. Ann Emerg Med. 2000;35:374-81. 9. Ketchum JS. The Human Assessment of BZ. Technical Memorandum 20-29. Edgewood Arsenal, Md: Chemical Research and Development Laboratory; 1963. 10. U.S. Centers for Disease Control and Prevention. Scopolamine poisoning among heroin users—New York City, Newark, Philadelphia, and Baltimore, 1995 and 1996. JAMA 1996;276:92-3. 11. Hull LA, Rosenblatt DH, Epstein J. 3-Quinuclidinyl benzilate hydrolysis in dilute aqueous solution. J Pharm Sci. 1979;68:856-9.

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96

LSD, Other Indoles, and Phenylethylamine Derivative Attack Fiona E. Gallahue

DESCRIPTION OF EVENT d-Lysergic acid diethylamide (LSD), an indole alkylamine, also known as LSD-25, was discovered by Albert Hofmann in 1938 while he was working for Sandoz Company. In 1943, Hofmann became intoxicated by LSD through accidental exposure, and 3 days later he intentionally took LSD. His experience with LSD paved the way for neuropsychiatric studies using LSD and later, in 1951, for U.S. Central Intelligence Agency (CIA) experimentation with human subjects using LSD and similar mind-altering drugs. The results of most of these CIA experiments are still classified, but some documents that have been made available describe how the American government intended for LSD to be used as a weapon. Psilocin and psilocybin, indole alkylamines derived from hallucinogenic mushrooms, were also considered and allegedly tested. Mescaline, a phenylethylamine derivative derived from the peyote cactus, was also reportedly selected for testing on human subjects. Because these substances have cross-tolerance and similar side effects and treatment, and because they were once considered by the American government as potential chemical weapons,we will narrow our focus to these hallucinogens rather than including the entire spectrum of phenylethylamine derivatives (e.g., 3,4-methylenedioxyamphetamine [MDA] and related amphetamines) or the other indole alkylamines (e.g., bufotenine, ibogaine).1,2 LSD, mescaline, peyote, psilocin, and psilocybin have all been classified as Schedule I drugs since the passage in 1970 of the Controlled Substance Act. These agents have somewhat similar (although not identical) effects but differ in potency: 1000 mcg of mescaline is equivalent to 1.0 mcg of LSD or 100 mcg of psilocybin.3 LSD, the most potent of these drugs, is generally taken orally at doses between 1 and 16 mcg/kg. There is a proportional relationship between the dose and the psychophysiologic effect of LSD, with 50 to 100 mcg constituting a mild dose, 100 to 250 mcg representing a moderate dose, and 250 to 500 mcg considered to be a strong dose.4,5 LSD is odorless and tasteless and is usually ingested orally, although it can be smoked, snorted, or injected. It has a plasma half-life of 100 minutes but can

be detected in plasma or urine for up to 3 days, and it is metabolized in the liver, with urinary excretion of metabolites.6 The clinical effects begin within 30 to 60 minutes and peak at 2 to 4 hours; the majority of the symptoms resolve within 12 hours.5,7,8 Studies conducted in simulated military settings demonstrated that even well-trained units become totally disorganized after ingesting total oral doses of less than 200 mcg.9 Affected persons usually cannot carry out a series of instructions or concentrate on a complex task, but they might be capable of isolated impulsive actions. Behavior is said to unpredictable although well coordinated.9 Although LSD has an LD50 (the amount needed to kill 50% of an exposed group) of 14,000 mcg (nearly 30 times the 500-mcg strong dose), LSD is not considered a safe drug.10 Acute psychotic reactions have been reported. Trauma resulting from accidents or selfdestructive behavior, suicide, or homicide can occur; deaths from LSD are more likely from these effects than from the direct toxicity of the compound.1,7,11 LSD resembles serotonin chemically and acts on serotonin and dopamine receptors. Sympathomimetic effects commonly seen with LSD intoxication include dilated pupils, tachycardia, hypertension, and hyperreflexia.5,6 The mind-altering properties of LSD can cause euphoria, anxiety, and paranoia with intense visual and auditory hallucinations that tend to be abstract,colorful,expansive,and often ineffable (in contrast to the concrete, lilliputian, and easily describable hallucinations from anticholinergic compounds). Synesthesia (sensory crossover) is frequently present, although tactile hallucinations are uncommon.6,7 Abnormalities of serotonin-induced platelet aggregation may result in abnormal clotting and poor clot retraction. Although cardiovascular complications are infrequent, reports exist of supraventricular tachycardia and myocardial infarction.6 Severe manifestations of toxicity include hyperthermia, seizures, and rhabdomyolysis.8 Mescaline is a hallucinogenic alkaloid derived from the North American peyote cactus and that also occurs in several species of the genus Trichocereus of South American cacti. Mescaline, or 3,4,5-trimethoxyphenylamine, can be taken directly from the peyote cactus or derived synthetically. The ritual use of mescaline-containing cacti is 585

documented from the sixteenth century; mescaline itself was first isolated from peyote in 1896 and was first synthesized in 1918. Peyote is commonly ingested in the form of brown discoid “mescal buttons,” which are the sun-dried crowns of the cactus. Each button may contain 45 to 100 mg of mescaline. The hallucinogenic dose is 5 mg/kg. Taken orally, mescaline is rapidly absorbed from the gastrointestinal tract and has an unpleasantly bitter taste. It can also be taken intravenously with similar side effects and with a similar duration of effects. (The popular Mexican liquor called mescal does not come from peyote and does not contain mescaline.) The effects of mescaline begin within 30 minutes to 2 hours of ingestion and peak at about 4 hours,with a total duration of 8 to 14 hours. Like LSD, mescaline is metabolized in the liver and excreted in the urine. Clinically, the effects are similar to those of LSD but with the additional initial symptoms of nausea, vomiting, sweating, generalized discomfort, dizziness, and headache, all of which generally occur during the first hour after ingestion and shortly before the onset of hallucinogenic effects. Large doses can produce hypotension, bradycardia, and respiratory depression.5,7 Psilocybin (4-phosphoryloxy-N,N-dimethyltryptamine) and psilocin (4-hydroxyl-N,N-dimethyltryptamine) are members of the indole alkylamine hallucinogens derived from tryptophan. These drugs were first isolated in 1958 from hallucinogenic mushrooms used by Mexican Indians for centuries. Psilocybin is more resistant to oxidation than psilocin and retains its activity in dried mushrooms. Psilocin is approximately 1.5 times as potent as psilocybin, but otherwise these two drugs are pharmacologically similar; in fact, psilocin is the active metabolite of psilocybin in the body. A 100-mcg dose of psilocybin is equivalent to 1 mcg of LSD and 1000 mcg of mescaline. The LD50 of intravenous psilocybin has been reported to be 280 mg/kg.3 Peyote mushrooms can be ingested raw, dried, as a brew, or stewed. The dose to produce hallucinogenic effects in nontolerant adults is approximately 6 to 12 mg. Little correlation has been found between clinical effects and the number of mushrooms ingested. Approximately 50% of the hallucinogenic compounds are absorbed via the gastrointestinal tract, and distribution occurs to most tissues, including the brain; most excretion is renal. Signs and symptoms develop within 30 to 60 minutes, with the psychedelic effects peaking between 30 minutes and 2 hours and lasting from 3 to 15 hours.3,5,10 Both compounds primarily affect serotonergic neurotransmission. Clinical effects of the drug are mostly sympathomimetic and include pupillary dilation, piloerection, tachycardia, and hyperreflexia. The hallucinations are usually visual but may be auditory or tactile. Both dysphoria and euphoria are commonly reported mood alterations. Nausea, cramping, abdominal pain, and a sensation of swelling of parts of the body are potential adverse responses. Deaths from psilocin and psilocybin are rare but have been reported from ingestion by a 6-year-old child who experienced hyperthermia and status epilepticus.5 All of these drugs have cross-tolerance to each other; the tolerance develops rapidly (within days) without the 586 NATURAL DISASTERS

development of physical dependence and also regresses rapidly, within 3 to 4 days of withdrawal. Flashbacks, or recurrences of hallucinogenic imagery days to years after the initial experience, have been described often with LSD but also with mescaline. Their etiology is unknown, but these flashbacks do decrease in their intensity with time and can be treated adequately with benzodiazepines in significantly affected patients. Flashbacks can be precipitated by triggers such as stress, exercise, and illness.5 LSD chemically resembles serotonin and interacts with the 5-hydroxytryptamine, or 5-HT, receptor. As might be expected, there is evidence (from a small retrospective cohort study by Bonson and Murphy12) of cross-reactivity between LSD and various antidepressants. In this study, patients taking selective serotoninreuptake inhibitors (SSRI agents) and monoamine oxidase inhibitors reported decreased responses to LSD, whereas those taking tricyclic antidepressants and lithium experienced increased responses. Psilocybin also chemically resembles serotonin, and similar interactions might be expected between psilocybin and these antidepressants. Since LSD is the most potent of these agents, the most difficult to detect (being odorless and tasteless), and the compound that was reportedly most tested by governmental agencies in the 1960s, this agent may be the most likely of the indoles and phenylethylamine derivatives to be used in an attack.13 Difficulties in covert distribution of LSD limit its utility as a chemical weapon. The compound could be released into water, but impossibly high quantities would be needed to contaminate a large water source such as a reservoir. Moreover, chlorine in concentrations found in water-treatment plants can deactivate LSD by oxidation. Delivery distal to such treatment facilities is possible but also impractical (because of dilution) even for someone intent on targeting a single building.1 LSD could also be delivered in an aerial drop so that a bomb filled with LSD would explode at ground level or several feet above the ground. The local population would become intoxicated through inhalation.1 LSD could potentially be aerosolized, but it would have to be dispersed relatively close to the intended targets, a mode of delivery that might be acceptable to some but perhaps not all terrorists, depending on the situation. With a particle size of approximately 5 microns, the ID50 (the dose that incapacitates 50% of the exposed population) was estimated to be 5.6 mcg/kg, approximately twice the ID50 of the parenteral route.9 If an immediate effect in a particular location is desired, the fact that LSD has a latent period of 30 minutes or longer might be a disadvantage, since exposed victims might well have moved to different areas by the time that they begin hallucinating. However, this delay in action might be advantageous in a covert release of agent. Another potential problem is the fact that SSRI antidepressants are used commonly in the American populace and might have protective effects in these patients. Nevertheless, biologic variability is likely to ensure that a significant proportion of intended victims will still be affected.

CASE PRESENTATION

PREINCIDENT ACTIONS Hospitals and emergency personnel should be well trained for the event of a potential chemical weapons attack. Protocols for these events should include removal of the victims from the contaminating source and the use of protective equipment to avoid inhalation, ingestion, or transdermal exposure to the toxicant. Although person-to-person transmission of LSD from a terrorist attack would not be expected, aerosolized LSD could theoretically remain on skin, clothing, or environmental surfaces; whether secondary aerosolization would be significant for this compound would depend on a multitude of as-yet-uninvestigated variables. If settling of aerosolized product on skin or clothing is of concern, washing of the skin with water (with or without soap) and washing of clothes would likely suffice. Since LSD detection equipment is not readily available, the detection of small amounts covertly released into the environment could be difficult.

POSTINCIDENT ACTIONS LSD and similar hallucinogenic agents in a mass-casualty event should be relatively easy for most clinicians to detect clinically, given the onset of action of approximately 30 to 60 minutes, the sympathomimetic effects, and the types of hallucinations induced. LSD intoxication would be difficult to distinguish from poisoning by the other psychedelic indoles and by phenylethylamine derivatives, but management of all these types of cases is similar. The differential diagnosis also includes acute panic reactions, schizophrenia, and exposure to phencyclidine (PCP), amphetamines, and anticholinergic compounds.14 The appropriate authorities should be contacted to identify and eliminate the contaminating source.

MEDICAL TREATMENT OF CASUALTIES Treatment is usually supportive, and patients can often be managed adequately without medications if they can be reassured and treated in a calm, quiet area.15 Some patients with more severe agitation may require medication. In this situation, a moderately long-acting benzodiazepine such as lorazepam 2 mg or diazepam 5 mg administered intravenously would be the best choice. Although haloperidol 5 mg given intramuscularly/intravenously or 10 mg given orally can also be used effectively for LSD-induced agitation not responding adequately to benzodiazepines, it should not be used routinely for drug-induced hallucinations. Haloperidol and the phenothiazines are contraindicated for patients with anticholinergic poisoning, which could be mistaken for LSD psychosis without a careful examination.

A number of patients are brought from an insurance office in the middle of the week to your emergency department with the complaint of “agitation.” On arrival, they appear to be hallucinating. Some are intensely panicked, whereas others appear to be distracted and calm. You examine one of these patients, a 40-year-old administrative assistant with no past medical history. She has no complaints, although some of her answers to you are incoherent and inappropriate. On examination, her blood pressure is 160/90 mm Hg, her heart rate is 110 beats per minute, and her oral temperature is 37.8˚C (100.0˚F). Her pupils are dilated, she is slightly diaphoretic but otherwise well, and she seems relatively calm in the quiet area to which she has been taken. A few minutes later, one of her coworkers, who has been positioned near the busy ambulance bay, starts thrashing around requiring benzodiazepines for sedation. Another coworker, who had left the office for a meeting but returned to find a number of his colleagues in this state, asks to speak with you. In trying to recall any unusual events in the office, he mentions a bottled-water delivery from a new supplier today. Shortly after your conversation, you get a call notifying you to expect another group of patients who are “agitated” from a legal office in the same building as your current group of agitated patients. Later, while discussing the cases with a coworker, you find out that the legal office also had a bottled-water delivery that day.

UNIQUE CONSIDERATIONS Because LSD can be oxidized by large amounts of chlorine, contaminated water sources could potentially be appropriately treated and used safely. Because LSD, mescaline, and psilocybin are rapidly metabolized and are excreted primarily in the urine, these drugs can be most easily detected in the urine through an immunologic method such as the enzyme multiplied immunoassay technique (EMIT) for confirmatory testing.16 Some studies have suggested that SSRI agents may decrease the severity of the effects of LSD and psilocybin. In certain situations, it may be useful to consider using SSRIs as protective medications for personnel at high risk for being exposed to LSD. However, more testing needs to be done before a definitive recommendation can be made.

PITFALLS Several potential pitfalls exist in responding to an attack. These include the following: • Failure to notify the appropriate agencies to find the source of the contaminating drug • Failure to use proper protective equipment in removal of patients, causing additional victims

LSD, OTHER INDOLES, AND PHENYLETHYLAMINE DERIVATIVE ATTACK 587

• Failure to remove hallucinating patients to a quiet, controlled area • Failure to consider amphetamines, anticholinergic agents, schizophrenia, and acute panic reactions in the differential diagnosis • Use of haloperidol for hallucinations without being certain of the cause

ACKNOWLEDGMENTS I would like to especially thank Dr. Lewis Nelson, Dr. Robert Hoffman, and Mary Ann Howland, PharmD, from the New York Poison Control Center for their help and support. REFERENCES 1. Buckman J. Brainwashing, LSD, and CIA: historical and ethical perspective. Int J Soc Psychiatry. 1977;23:8-19. 2. Lee MA, Schlain B. Acid Dreams: The Complete Social History of LSD: The CIA, the Sixties and Beyond. Grove Press; 1985. 3. Passie T, Seifert J, Schneider U, et al. The pharmacology of psilocybin. Addict Biol. 2002;7:357-64. 4. Lycaeum Web site. Available at: http://www.lycaeum.org. 5. Leikin JB, Krantz AJ, Zell-Kanter M, et al. Clinical features and management of intoxication due to hallucinogenic drugs. Med Toxicol Adverse Drug Exp. 1989;4:324-50.

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6. Ghuran A, Nolan J. Recreational drug misuse: issues for the cardiologist. Heart 2000;83:627-33. 7. Williams LC, Keyes C. Psychoactive drugs. In: Ford MD, Delaney KA, Ling LJ, et al, eds. Ford: Clinical Toxicology. Philadelphia:WB Saunders; 2001:640-9. 8. Lemke T, Wang R. Emergency department observation for toxicologic exposures. Emerg Med Clin North Am. 2001;19:155-67, viii. 9. Ketchum JS, Sidell FR. Incapacitating agents [Chapter 11]. In: Zajtchuk R, ed. Textbook of Military Medicine, Part I: Warfare, Weaponry, and the Casualty: Medical Aspects of Chemical and Biological Warfare. Washington, DC: Office of the Surgeon General, U.S.Army,TMM Publications, Border Institute; 1997:293. 10. Clark RF, Williams SR. Hallucinogens. In: Marx JA, ed. Rosen’s Emergency Medicine: Concepts and Clinical Practice. St Louis: Mosby; 2002:2137-50. 11. Sotiropoulos A. Injury to the bladder: unusual complication of lysergic acid diethylamide. Urology 1974:3:755-8. 12. Bonson KR, Murphy DL. Alterations in responses to LSD in humans associated with chronic administration of tricyclic antidepressants, monoamine oxidase inhibitors or lithium. Behav Brain Res. 1996;73:229-33. 13. Yensen R. LSD and psychotherapy. J Psychoactive Drugs. 1985;17:267-77. 14. Perry P. LSD psychosis. In: Clinical Psychology Seminar, Virtual Hospital. Available at http://www.vh.org/adult/provider/psychiatry/CPS/28.html. 15. Schlicht J, Mitcheson M, Henry M. Medical aspects of large outdoor festivals. Lancet 1972;1(7757):948-52. 16. Bodin K, Svensson JO. Determination of LSD in urine with highperformance liquid chromatography—mass spectrometry. Ther Drug Monit. 2001;23:389-93.

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97

Opioid Agent Attack Rick G. Kulkarni

DESCRIPTION OF EVENT In cultivation since circa 300 BCE, pure opium is a mixture of alkaloids extracted from the sap of unripened seedpods of Papaver somniferous (the Asian, or opium, poppy). Opiates, such as heroin, codeine, and morphine, are natural derivatives of these alkaloids. Synthetic opium-like narcotic compounds, such as oxycodone, meperidine, and fentanyl and its derivatives (e.g., carfentanil and sufentanil) are also available. Originally, opioid meant a synthetic narcotic not derived from opium, but the term is increasingly applied to opiates as well as to synthetic narcotics; opiate is still reserved for the naturally occurring alkaloids with a morphine or thebaine backbone.1,2 The postsynaptic binding of opioids to receptors in the central nervous system (CNS) and in the gastrointestinal tract leads to hyperpolarization of neuronal cell membranes, inhibition of neurotransmission, and, depending on the affected cell population, either depression or excitation of end organs. The physiologic effects of opioids are mediated principally through three major kinds of opioid receptors: OP1 (δ), OP2 (κ), and OP3 (μ). All three types of receptors can mediate analgesia and respiratory depression, but OP1 (δ) receptors are responsible primarily for spinal analgesia, OP2 (κ) receptors are more selective for sedation (although they also mediate miosis, analgesia, and respiratory depression), and OP3 (μ) receptors are the most important for respiratory depression, miosis, constipation, and euphoria (with subsequent dependence in chronic users).3 The opioid antagonists (e.g., naloxone, nalmefene, naltrexone) have greater affinity for OP3 (μ) receptors than for OP1 or OP2 receptors and are all effective in reversing the respiratory depression associated with acute opioid overdoses. Naltrexone, however, is usually reserved for the treatment of opioid addiction.1,2

CLINICAL PRESENTATION Opioid toxicity characteristically presents with a depressed level of consciousness and should be suspected when the clinical triad of CNS depression, respiratory depression, and pupillary miosis are present. The

differential diagnosis of miosis also includes clonidine, cholinergic crisis (from cholinergic agents, organophosphorous pesticides, or nerve agents), phenothiazines, phencyclidine, and sedative-hypnotic drugs as well as pontine and subarachnoid hemorrhage. However, pupillary dilatation can be seen in hypoxic opioid patients as well as in persons exposed to mixtures containing both an opioid and an anticholinergic agent such as atropine or scopolamine. Drowsiness, euphoria, ventricular arrhythmias, and acute mental status changes are frequently seen. Often, intoxication leads to respiratory impairment with bradypnea and hypopnea. In moderate-to-severe opioid intoxication, the respiratory rate can be as low as four breaths per minute; and frank respiratory arrest can occur. Generalized seizures are infrequent and occur mostly in infants and children because of initial excitation of the CNS. Nystagmus is also infrequent but has been reported.1,2

LIKELY AGENTS IN AN ATTACK Oral ingestion and respiratory exposure are the two most likely routes of absorption in an opioid agent attack. Both routes provide easy absorption for most opioids. Peak effects are reached by 90 minutes after ingestion and within 10 minutes of inhalation.4 The synthetic opioid fentanyl and its derivatives as a group are the most likely agents to be used in a terrorist attack (Table 97-1).5 Their high potency (approximately 10 to 10,000 times that of morphine) and the fact that they can be aerosolized to induce unconsciousness and longlasting respiratory depression in animals make them ideal agents in this regard.6-8

PREINCIDENT ACTIONS Preparedness is the single most important action that can be taken to prevent mass casualties from an opioid attack. The critical factors in minimizing the number of casualties in such an attack are as follows: (1) reaching casualties as soon as possible; (2) securing the airway. (3) implementing assisted ventilation either noninvasively or invasively; and (4) rapid treatment with the 589

TABLE 97-1 CHARACTERISTICS OF OPIOIDS, INCLUDING FENTANYL DERIVATIVES AGENT

OPIOID POTENCY (COMPARED WITH MORPHINE)

THERAPEUTIC INDEX*

Morphine Meperidine Fentanyl Sufentanil Alfentanil Remifentanil Carfentanil

1 0.5 300 4500 75 220 10,000

70 5 300 25,000 1100 33,000 10,600

*Therapeutic index = median lethal dose (LD50)/lowest median effective dose (ED50).

specific opioid antagonist naloxone. Recognition of the use of opioid agents as the primary contributing factor to the state of the victims is paramount, and in view of the relatively high profile given to chemical warfare agents such as nerve agents, a number of unconscious victims with respiratory depression (or apnea) and miosis who are not responsive to nerve agent antidotes should initiate the suspicion of other causes, including opioid agent attack. Communities at high risk for such an attack must familiarize their first responders, including firefighters, police personnel, and emergency medical technicians/paramedics, with the typical presentation and the differential diagnosis of a person exposed to such agents. In addition, consideration should be given to equip such personnel not only with devices to assist ventilation but also with naloxone. Training and equipping of healthcare facilities in highrisk metropolitan areas for the treatment of a large number of patients exposed to an opioid agent is also an important link in the chain of adequate preparedness. Although there are no official position statements from government agencies or professional organizations addressing this specific possibility at this time, hospital disaster committees should include this topic in their general emergency preparedness plan. At a minimum, high-risk areas should be able to provide on-scene emergency medical services (including fast rescue and supportive care during transport), noninvasive and invasive artificial ventilation to affected persons, and sufficient doses of naloxone.1,2

POSTINCIDENT ACTIONS Once an opioid agent attack is identified, a preformulated action plan must be activated immediately. An attack with an opioid agent will likely take place in an enclosed area containing hundreds of people. Implementation of the facility evacuation plan is the first step to isolate persons not already under the effects of the agent and to remove them from the affected area. For those persons who are affected, rescue personnel wearing personal protective equipment should imple590 NATURAL DISASTERS

ment rapid control measures even before the arrival of medical personnel. These measures are fundamental for three important reasons: 1. Proper positioning of the patient in the left-lateraldecubitus position can prevent aspiration of gastric contents and can minimize the risk of the tongue falling back to occlude the airway. 2. The ability of the medical rescue team to deliver artificial ventilation and naloxone can be severely limited if the victims cannot be accessed easily (for example, victims sitting in the middle seats of rows in a theater may be difficult to reach where they are). 3. Without intervention, the ensuing confusion can create a situation in which persons are not properly categorized or treated. Because local supplies of antidotes can be rapidly depleted in a mass-casualty situation, additional stocks of naloxone should be requested early from adjoining communities.1,2 Appropriate local, state, and federal public-health and law-enforcement authorities should be notified.

MEDICAL TREATMENT OF CASUALTIES Treatment should be tailored to the clinical presentation of victims. For those who are awake and not disoriented, the only intervention necessary may be to escort the victims into an open area outside the zone of contamination. Those who are sleepy or just lethargic but who are easily arousable should also be escorted to an open area and kept under observation for progression of symptoms. Patients who are unconscious but still breathing should also be moved to an open area and administered adequate intramuscular doses of naloxone in 2.0-mg increments (0.1 mg/kg for pediatric patients) to awaken them. The onset of antidotal effects after intramuscular naloxone administration is 1 to 3 minutes, with maximal effects observed within 5 minutes. Repeat doses are indicated for partial response and can be repeated as often as needed. Because the clinical half-life of naloxone is between 20 and 60 minutes, assigned medical staff should observe patients for a period of no less than 1 hour to ensure that opioid effects do not recur. Nalmefene, if available, could be used in intramuscular doses of 0.5 to 1.0 mg, with a maximal efficacy seen at a total dose of 1.5 mg. Finally, those patients who are unconscious with significantly depressed respirations or who are frankly apneic should receive immediate artificial ventilation, preferably with noninvasive techniques such as a bag-valve-mask device connected to 100% oxygen. They should also be given naloxone until they are awake and breathing spontaneously. These persons should be triaged and transported to local hospitals for continued administration of naloxone as needed and for further monitoring for at least 12 to 24 hours. All affected victims should be examined and assessed for blunt trauma from possible falls resulting from

opioid-induced unconsciousness. If there is concern regarding neck injury or head injury, the patient should be placed on a backboard and into a cervical collar and should be transported to a local hospital for further evaluation and treatment. Although opioids have not been used directly by terrorists in large-scale attacks, the potential of these agents to create mass casualties is illustrated by their use in October 2002 by Spetsnaz commando units of the Russian Federal Security Service (FSB) against Chechen terrorists who had taken control of a theater in Moscow.9,10 Minister of Health Yuri Shevchenko later identified the agent used as a fentanyl derivative, and it has been speculated that this opioid compound had been aerosolized either alone or in combination with an anesthetic agent. Approximately 120 hostages died. Shevchenko asserted that over a thousand doses of “antidote” were available and were used, but many casualties appear to have been removed from the theater and placed into positions, either on the ground or in buses, in which their airways were not secured.9,10 This incident demonstrates that use of an opioid agent on a large group of people can represent a major medical disaster and that proper evacuation of casualties and careful attention to airway and ventilation can be matters of life and death quite apart from the issue of antidotes. An attack can quickly overwhelm limited medical resources available in the affected area. Proper preparation and planning can help save lives in a catastrophic event.11-13

UNIQUE CONSIDERATIONS An opioid agent attack will likely take place in a closed space filled with hundreds of people because this combination presents an ideal opportunity for causing mass casualties. Because respiratory depression is the usual mechanism of death from opioid intoxication, absolutely crucial elements of response will include speed in reaching victims, evaluation of airway and breathing, and maintenance of airway and ventilation during and after evacuation from the scene. Naloxone should be administered as soon as is practical but is not so important in the immediate response as securing and maintaining an open airway and ensuring adequate ventilation. Naloxone stocks may become quickly depleted during an outbreak, and early consideration should be given to ordering more antidote. Awareness for blunt trauma from falls sustained due to unconsciousness induced by the opioid agent and from potential mass hysteria during exit from an enclosed space should be considered. Recognition by first responders, hazardous-materials teams, and other rescue personnel of the clinical picture of opioid exposure in humans and of the essentials of speedy rescue, appropriate evacuation, and the primacy of airway support and ventilation can make the difference between a relatively good outcome and a catastrophe involving hundreds of casualties. Although there have been no reported incidents of a terrorist attack

CASE PRESENTATION The grand opening of a new concert hall in Los Angeles is today. The auditorium has a maximum capacity of 800 patrons and accommodates an additional 200 performers and support staff. During the first intermission, several patrons in the back of the concert hall report hearing a hissing sound. Two security-staff personnel are called to the scene of the noise and locate three large canisters hidden behind the curtains and vigorously discharging an odorless substance into the hallway. Before they can remove the canisters, they succumb to the unknown gas and fall unconscious to the floor. Moments later, several of the patrons in the vicinity of the reported noise begin to slump into their seats or to sit down in the hallways. Others complain of nausea and begin to vomit. In a few minutes, more patrons begin to experience similar symptoms in a progressive fashion toward the front of the stage. Approximately 5 minutes after the first group of people have begun to experience symptoms, the majority of the persons in the theater are unconscious. The performers and those at the front of the stage have panicked and are rushing for two clearly marked exits at the front of the concert hall. Hazardous materials staff arrive at the scene, which was cordoned off by the police within 10 minutes of the first report. Entering the concert hall in personal protective equipment, they find hundreds of unconscious victims.

Many of the victims are not breathing. When the unit commander notes pinpoint pupils in every victim he examines, he immediately suspects a nerve agent attack and radios the operational commander to have nerve agent antidotes brought to the scene. Rescue team members inside the hall pull victims from their seats, move them to the aisles, and then remove them from the concert hall. Outside, the victims are placed on their sides to prevent aspiration of gastric contents, and their airways are secured. Two of the apneic patients are successfully intubated by paramedics, and artificial ventilation by bag-valve-mask is begun with no significant airway resistance noted. The lack of airway resistance and the failure of victims to respond to nerve agent antidotes leads to a consideration of the differential diagnosis of pinpoint pupils and to the possibility of an opioid agent attack. Naloxone from arriving ambulances is administered via intramuscular injection first to the apneic but not intubated patients, and when spontaneous respiration resumes within 2 or 3 minutes of injection in two of these patients, this finding is reported to the hospital and additional naloxone is requested. Most of the unconscious persons wake up and resume adequate respirations, but approximately 80 persons are declared dead at the scene despite receiving large amounts of naloxone. An additional five persons are declared dead at local hospitals. None of the rescuers are affected or succumb to the agent. OPIOID AGENT ATTACK 591

involving an opioid agent, the possibility of such an attack cannot be excluded. Increased vigilance among enclosed venues capable of holding hundreds of people is indicated.

PITFALLS Several potential pitfalls in response to an opioid agent attack exist. These include the following: • Failure to create a plan for mass treatment in the event of an attack • Failure to staff and supply a high-risk area with adequate stocks of naloxone • Failure to recognize or report an attack from an opioid agent • Misdiagnosis of a victim of an opioid agent attack as one of nerve agent attack • Delay in reaching casualties with respiratory depression or apnea • Failure to position victims properly and to attend to airway and ventilation issues • Failure to recognize the clinical presentation of opioid toxicity and to institute specific antidotal treatment with naloxone REFERENCES 1. Wax PM, Becker CE, Curry SC. Unexpected “gas” casualties in Moscow: a medical toxicology perspective. Ann Emerg Med. 2003;41:700-5.

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2. Toxicity, Narcotics. eMedicine.com. Available at: http://www. emedicine.com. 3. Worsley MH, Macleod AD, Brodie MJ, et al. Inhaled fentanyl as a method of analgesia. Anesthesia 1990;45:449-51. 4. Mather LE,Woodhouse A,Ward ME, et al. Pulmonary administration of aerosolized fentanyl: pharmacokinetic analysis of systemic delivery. Br J Clin Pharmacol. 1998;46:37-43. 5. Van Bever WF, Niemegeers CJ, Schellekens KH, et al. N-4Substituted 1-(2-arylethyl)-4-piperidinyl-N-phenylpropanamides, a novel series of extremely potent analgesics with unusually high safety margin. Arzneimittel-Forschung. 1976;26:1548-51. 6. Jaffe AB, Sharpe LG, Jaffe JH. Rats self-administer sufentanil in aerosol form. Psychopharmacology 1989;99:289-93. 7. Kreeger TJ, Seal US. Immobilization of gray wolves (Canis lupus) with sufentanil citrate. J Wildlife Dis. 1990;26:561-3. 8. Baker JR, Gatesman TJ. Use of carfentanil and a ketamine-xylazine mixture to immobilise wild grey seals (Halichoerus grypus). Vet Rec. 1985;116:208-10. 9. Lethal Moscow gas an opiate? CBS News Web site. October 29, 2002. Available at: http://www.cbsnews.com/stories/2002/10/29/ world/main527298.shtml. 10. Ruppe D. CWC: Experts differ on whether Russian hostage rescue violated treaty. Global Security Newswire. October 30, 2002. Available at: http://www.nti.org/d_newswire/issues/thisweek/ 2002_11_1_chmw.html. 11. Lakoski JM, Murray WB, Kenny JM. The advantages and limitations of calmatives for use as a non-lethal technique. The Sunshine Project Web site. Available at: http://www.sunshine-project.org. 12. Glenski JA, Friesen RH, Lane GA. Low-dose sufentanil as a supplement to halothane/N2O anaesthesia in infants and children. Can J Anaesth. 1988;35:379-84. 13. Committee for an Assessment of Non-Lethal Weapons Science and Technology, National Research Council. An Assessment of NonLethal Weapons Science and Technology. Washington, DC: National Academies Press; 2003.

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Riot-Control Agent Attack Sam Shen

DESCRIPTION OF EVENT Riot-control agents are commonly known as “tear gas,” irritants, harassing agents, and lacrimators. These agents are used by the military for training purposes and by law enforcement officers for riot control. The North Atlantic Treaty Organization (NATO) has assigned these compounds two-letter codes.The agents include 1-chloroacetophenone (NATO code, CN), o-chlorobenzylidene malononitrile (CS), bromobenzylcyanide (CA), and dibenz (b,f)-1:4-oxazepine (CR). Oleoresin capsicum (OC), an oily extract of the capsaicin found in pepper plants, is also used by law enforcement officers and, often mixed with CN, in products for personal protection. Because of their long chemical names, they are generally referred to by their NATO codes except for OC, which is often called pepper spray. These compounds are similar in the following respects1: • Production of sensory irritation causing severe discomfort • Quick onset of action • Short duration of effects after exposure • High safety profile (ratio of lethal to effective dose) Diphenylaminearsine, or adamsite (DM), is an agent that causes vomiting and is also used for riot control, but it differs in several aspects1: • Its onset of action is delayed for several minutes after exposure. • It produces nausea, vomiting, diarrhea, abdominal cramping, and other systemic effects (including headache and depression) in addition to the mucosal irritation characteristic of the other riot-control agents. • It produces less severe effects on the skin. When properly used, these agents can cause extreme discomfort and temporarily disable the victim.2 Due to the high safety profile of these compounds, riot-control agents are an attractive option for incapacitation by military and law enforcement personnel. They are sometimes called nonlethal, or less-lethal, agents because their intent is to incapacitate rather than to produce serious injury or death and because of their high safety ratios; however, it should be kept in mind that a sufficiently high dose can prove fatal.

The first widely used agent was CN, which was developed in 1871; in about 1912, ethylbromoacetate was used to control riots in Paris.1 As Mace, CN was also subsequently marketed for personal protection. Subsequent agents were developed that produced similar results but possessed better safety profiles, higher potencies, or both.3 CS is more potent and less toxic.3 It is the agent most commonly used today and was introduced for common civil use in 1967.4,5 CA was developed toward the end of World War I but is rarely used today. CR is the newest compound in this class and is the most potent, with a high safety profile and such low volatility that its effects deep in the lungs are minimal.1 DM is primarily a vomiting agent but will be discussed as a riot-control agent because of its similar effects and management steps. Riot-control agents are liquids or solids (“tear gas” is a misnomer) and can be dispersed as fine droplets or particles or in solution. They may be combined with an explosive substance in grenades or released as a smoke of particles from handheld devices.6,7 Consequently, the effects are from direct contact with skin, eyes, or mucous membranes and from inhalation.

EFFECTS OF RIOT-CONTROL AGENTS Riot-control agents are nonlethal when used properly. Reports of death are infrequent and are usually due to toxic pulmonary damage leading to pulmonary edema.2 Symptoms usually occur within 1 minute of exposure and last approximately 30 minutes.6 These agents have minimal long-term effects.5 The predominant systems affected are the eyes, nose, lungs, and skin.3

Eyes The eye is extremely sensitive to irritants. Exposure to an agent will produce an intense burning sensation leading to tearing, blepharospasm, photophobia, and conjunctival injection.6,8 The victim will subsequently close his or her eyes reflexively. Although the vision of the victim will be near normal, the blepharospasm will hinder the ability of the victim to see. Most of these effects disappear in 20 minutes,although conjunctivitis may persist for 24 hours.3 593

In addition to the sensory effects, the ejection of the agent particles can cause blunt trauma to the cornea, and small particles can be embedded in the tissue of the eye.

Nose

cians should wear impermeable gloves and goggles to avoid exposure to the agents before treating casualties.3,6 Facilities should be prepared for the disrobing and showering of patients before they enter the emergency department.8

If riot-control agents make contact with the mucous membranes of the nose, they will produce rhinorrhea, sneezing, and burning.3,8

POSTINCIDENT ACTION Since the agents are released into the air, evacuation is important to eliminate further exposure. Therefore, victims must be advised to do the following11:

Lung One of the more serious effects of riot-control agents involves the airways. In addition to a burning sensation, irritation of the bronchial lining can produce bronchoconstriction, coughing, and dyspnea. Effects from higher doses include pulmonary edema and chemical pneumonitis.2 The agents can also worsen underlying lung disease such as asthma or chronic obstructive pulmonary disease.2 Due to numerous reported deaths in custody patients who had been exposed to OC, many of whom had been restrained, pulmonary function testing was studied in normal subjects given OC or placebo to inhale. OC does not result in abnormal spirometry, hypoxemia, or hypoventilation in either the sitting, or prone–maximal restraint position.9

Skin If riot-control agents make contact with the skin, they will produce erythema and a burning or tingling sensation.2 Prolonged exposure can produce vesicles and burns similar to thermal burns. These symptoms are exacerbated in hot or humid weather.2

Metabolic System Some studies have suggested that CS can be metabolized to cyanide in peripheral tissues.2,10 However, the risk of cyanide toxicity from inhalational exposure to CS appears to be minimal.1

Gastrointestinal System Exposure can produce nausea, vomiting, and diarrhea.2 DM is the riot control agent responsible for predominantly gastrointestinal symptoms in addition to mucosal irritation.

Pregnancy One animal study showed no significant effects from CS on pregnancy.2,8

PREINCIDENT ACTION The effects of riot-control agents are usually self-limiting. Therefore, victims often will not seek medical care initially. Victims may seek assistance if symptoms persist or if complications develop. Emergency medicine physi594 NATURAL DISASTERS

• Immediately leave the scene where riot control agents were released. • Move to an area where fresh air is available. • Move to higher ground, since riot-control agents can linger as dense, low-lying clouds.

MEDICAL TREATMENT OF CASUALTIES There is no antidote for riot-control agents. Their effects are self-limiting and usually last no more than 15 to 30 minutes, although erythema of the skin may persist longer.1 Medical management consists primarily of supportive care for each affected system. Initially, it is important to decrease any possible further contact with the agents through the following decontamination methods11: • Remove clothing that may have agent particles on it. Do not pull clothing over the victim’s head. Instead, clothing should be cut off to minimize potential further contact. • The victim should be washed with copious amounts of soap and water even though wetting of the skin may temporarily increase the severity of the burning sensation from the agent. The specific management steps are directed to each system affected.

Eye The first step involves blowing dry air into the eyes to help the dissolved agents vaporize.6 This should be followed by irrigation of the eyes with cold water or saline. If irrigation is performed before drying the eyes, one can prolong the burning sensation in the eyes. Although 5% sodium bisulfite was once recommended for treatment of exposure, its use is no longer advised.12 A careful slitlamp examination should be performed to evaluate for corneal impaction injuries secondary to the blast of the agent particles. If a corneal injury is present, any visible foreign bodies should be removed and topical antibiotics should be prescribed.

Lungs The most serious complications occur in the lungs. Initially, humidified oxygen can provide relief. Inhaled beta-2 agonists may be given for dyspnea and bron-

chospasm.6 Because the clinical onset of pulmonary injury, especially pulmonary edema, can be delayed, patients should be admitted for observation. Victims should also be admitted if they have respiratory complaints or underlying lung disease.2

Skin Any solid powder or smoke particles should be gently brushed from the skin. After copious irrigation with soap and water (a measure that may be briefly painful), burns should be treated the same as any other types of burns. If dermatitis or erythema persists, topical steroids or antipruritic agents may be applied.2,6

CASE PRESENTATION There has been an ongoing strike by workers at a local factory.The local news has reported that many protesters have become disruptive and violent. In fact, law enforcement officers were called to the site of the factory strike to restore order. Unfortunately, there were too many demonstrators to control safely. As the crowd of angry factory workers became more agitated, they began throwing objects at the police. Consequently, the officers had to use riot-control agents to contain the situation. In the emergency department, emergency medical services personnel start to bring you patients complaining of shortness of breath, tearing, and burning sensation in their eyes, nose, and skin.

UNIQUE CONSIDERATIONS Riot-control agents are fast-acting compounds that cause significant discomfort but are nonlethal when used properly. Whereas other chemical agents may cause worsening of symptoms over time, symptoms of riot-control agents often recede with time. Death is rare and, when it occurs, usually ensues from pulmonary complications. Symptoms will improve over time without long-term sequelae, so supportive care is the main treatment.

• Failure to blow dry eyes before irrigating them with water or saline after exposure • Failure to brush affected skin before washing with soap and water to eliminate further exposure • Use of bleach for skin decontamination13 • Failure to admit patients with respiratory symptoms or underlying lung disease • Failure to decontaminate any patient with riot-control agent contamination before loading onto a medical helicopter; the spread of such agents around the cockpit during flight could immobilize the pilot and endanger the lives of the patient and crew REFERENCES 1. Sidell F. Riot control agents. In: Medical Aspects of Chemical and Biological Warfare. Borden Institute, Walter Reed Army Medical Center Office of the Surgeon General, U.S. Army U.S. Army Medical Dept. Center and School, U.S. Army Medical Research and Material Command Uniformed Services University of the Health Sciences; 1997:307-24. 2. Hu H, Fine J, Epstein P, et al. Tear gas: harassing agent or toxic chemical weapon? JAMA 1989;262:660-3. 3. Beswick FW. Chemical agents used in riot control and warfare. Hum Toxicol. 1983;2:247-56. 4. Kalman SM. Riot control agents. Introduction. Fed Proc. 1971 Jan-Feb; 30(1):84-5. 5. Karagama YG, Newton JR, Newbegin CJ. Short-term and long-term physical effects of exposure to CS spray. J R Soc Med. 2003;96:172-4. 6. Yih J-P. CS gas injury to the eye. BMJ 1995;311:276. 7. Smith J. The use of chemical incapacitant sprays: a review. J Trauma. 2002;52:595-600. 8. Sanford JP. Medical aspects of riot control (harassing) agents. Ann Rev Med. 1976;27:421-9. 9. Cucunell SA, Swentzel KC, Biskup R, et al. Biochemical interactions and metabolic fate of riot control agents. Fed Proc. 1971;30:86-91. 10. U.S. Army Medical Research Institute of Chemical Defense. Riot control agents. In: Medical Management of Chemical Casualties Handbook. 2nd ed. Md: 1995. 11. Lee BH, Knopp R, Richardson ML. Treatment of exposure to chemical personal protection agents. Ann Emerg Med. 1984;13:487-8. 12. Harrison JM, Inch TD. A novel rearrangement of the adduct from CS-epoxide and dioxin-2-hydroperoxide. Tetrahedron Lett. 1981;22:679-82. 13. Chan TC, Vilke GM, Clausen J, et al. The effect of oleoresin capsicum “pepper spray” inhalation on respiratory function. J Forensic Sci. 2002;47:299-304.

PITFALLS Several potential pitfalls exist in treating injuries involving riot-control agents. These include the following: • Failure to evacuate victims from area of exposure • Failure to remove clothing or any materials that may have come in contact with the agents from the victims

RIOT-CONTROL AGENT ATTACK 595

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99

Nicotinic Agent Attack Sage W. Wiener and Lewis S. Nelson

DESCRIPTION OF EVENT Nicotine has long been recognized as a toxin in humans by reason of its action as a direct agonist at the nicotinic family of acetylcholine receptors (a family in fact defined by the affinity for nicotine). These receptors are present at the neuromuscular junction (NMJ), in both sympathetic and parasympathetic ganglia, and in the central nervous system (CNS).1 More recently recognized nicotinic acetylcholine receptor agonists include epibatidine and anatoxin-a, among others.1-3 Epibatidine is derived from the skin of the Epibatobades frog (a species of “poison dart” frogs) and has been studied as an analgesic that acts through incompletely understood central nicotinic cholinergic pathways.4 Anatoxin-a is found in species from several genera of cyanobacteria (formerly known as blue-green algae).3 It should not be confused with amatoxin, a cyclopeptide RNA polymerase inhibitor found in several hepatotoxic mushrooms, or with anatoxin-a(s), a cyanobacterial toxin that acts purely as a cholinesterase inhibitor without accompanying nicotinic agonist activity (the s refers to the salivation caused from excess acetylcholine at muscarinic receptors). Anatoxin-a and epibatidine differ from nicotine primarily in potency. The LD50 (the dose required to kill 50% of those exposed) of anatoxin-a is 200 to 250 μg/kg body weight (mouse, ip),3 and the LD50 of epibatidine (rat, iv) is less than 125 nmol/kg.5 By comparison, a lethal dose of nicotine is estimated to be between 0.5 and 1.0 mg/kg in humans.6 Epibatidine is also more specific than nicotine at the ganglionic and CNS subtypes of nicotinic receptor and does not act at the NMJ.1 Another difference between these agents is that in vitro, epibatidine appears to have some agonist action at muscarinic acetylcholine receptors as well.7 It is unclear, however, whether muscarinic effects would be seen clinically after human exposure. Although nicotine has never been known to be developed as a chemical weapon by any government, it has been weaponized more than once by domestic criminals. In 1997,Thomas Leahy was found to possess ricin and botulinum toxins as well as a spray bottle filled with nicotine sulfate dissolved in dimethyl sulfoxide (an organic solvent also known as DMSO). Because his 596

intent with the other agents was difficult to prove, he was initially only charged and convicted for the weaponization of the nicotine sulfate, although he subsequently pled guilty to the other charges.8 Another incident of domestic terrorism involving nicotine is discussed in the case at the end of this chapter. Neither epibatidine nor anatoxin-a is known to have been developed for state, terrorist-group, or individual use. The potential for the use of nicotine in a chemical attack is enhanced by its many possible means of delivery and routes of absorption. Nicotine freebase is an oily liquid but is relatively unstable in air. Nicotine salts, however, are solids that are readily dissolved in water or organic solvents. Therefore, these salts could potentially be dispersed as an aerosol of liquid or powder. Nicotine can be absorbed transdermally, as evidenced by “green tobacco sickness.” In this illness, acute nicotine toxicity occurs in those who harvest wet tobacco without protection for their skin.9 Nicotine patches for smoking cessation take advantage of this principle. Clearly, if nicotine were suspended in a solvent with good dermal penetration (DMSO would be an option) and then aerosolized, the potential for systemic toxicity from dermal exposure would be great. Nicotine is also stable to pyrolysis and may be absorbed through inhalation, as in tobacco smoking. Nicotine is orally bioavailable, and numerous case series exist of children with nicotine toxicity from ingestion of tobacco products.10-18 Much less is known about the absorption and bioavailability of epibatidine and anatoxin-a through different routes. Epibatidine is available as an off-white powder and is soluble in organic solvents including alcohol. Anatoxin-a is a light brown solid that is soluble in water. Anatoxin-a appears to cause illness through ingestion in animal models.19 Few data exist regarding the oral bioavailability of epibatidine or the inhalational absorption of either toxin. One feature of anatoxin-a that might make it illsuited to chemical terrorism is that it is susceptible to photolysis, rapidly breaking down in the presence of sunlight.20 Thus, while an incident involving contamination of food is possible, an incident involving outdoor dispersion of an aerosol seems extremely unlikely. The clinical effects of nicotinic poisoning depend in part on the route of absorption. Most data have been gathered in the context of exposure through ingestion, in

which significant nausea and vomiting are early features. In one review of 143 children with symptoms after ingestion of cigarettes or cigarette butts, 99% (138 children) vomited; 74% (104 children) did so within 20 minutes.10 These features are also seen in toxicity from dermal absorption, but they may not be the first sign of exposure. Other early findings include dizziness and dyspnea. In one reported case of dermal exposure, dizziness, dyspnea,“unsteadiness,” and nausea occurred within 30 minutes.21 Flushing and pallor of the skin have both been reported after nicotine exposure, and diaphoresis may be present as well.11,12,14 Cardiac effects include both hypertension and hypotension as well as palpitations and dysrhythmias ranging from sinus bradycardia and sinus tachycardia to sinoatrial block, atrial fibrillation, and asystole.10,12-14,16,17 These seemingly contradictory effects are better understood when one considers that the effects of nicotine on the autonomic nervous system are mediated through its action at both sympathetic and parasympathetic ganglia. Which effects predominate in any individual patient can be difficult to predict. Nicotine also acts as a depolarizing neuromuscular blocker at the NMJ.1 Thus, early muscle spasms and fasciculations may occur, followed by weakness, hypotonia, and even flaccid paralysis.10,12,13 Nicotinic cholinergic agonism in the CNS leads to seizures and altered mental status. In children, both lethargy and irritability have been reported after tobacco ingestion.10-14,16 Patients with less severe poisoning may present with headache or dizziness.10,11,15 Seizures are uncommon in typical cases of cigarette ingestion and when present suggest a more severe exposure.10 Severe exposures can lead to permanent neurologic devastation.22 Little is known about clinical findings in humans after poisoning with epibatidine or anatoxin-a; there are no reported cases. Presumably, because of the greater potency of these agents, patients would clinically resemble those with severe nicotine toxicity. If epibatidine were used, it is possible that muscarinic findings would be present as well, which would make the distinction from nerve agent poisoning even more challenging; however, the absence of neuromuscular signs and symptoms might actually clarify the diagnosis.

PREINCIDENT ACTIONS Disaster planning and education are the most important preincident actions that can be taken in preparation of an attack involving cholinergic agents. Coordination between the U.S. Department of Agriculture, the Food and Drug Administration, and law enforcement and counterterrorism agencies is likely to facilitate early detection of incidents involving food and water contamination. Syndromic surveillance of emergency department triage complaints may also play a role because food and water contamination may initially appear as gastrointestinal (GI) illness. Although atropine is already stockpiled in many hospitals because of preparations for nerve agent attack, this measure is unlikely to be helpful because muscarinic effects will be inconsequential in most patients. Other than basic preparedness for chemical terrorism such as personal protective equipment and

decontamination facilities, no specific physical infrastructure or supplies are required in the hospital for preparation for a nicotinic agonist attack. Technology originally developed for workplace monitoring exists for detection of small amounts of nicotine in the air.23 It is also possible to test water supplies for cyanobacteria,3 and anatoxin-a can be detected by gas chromatography with an electron-capture detector.24 In the future, it may be possible to deploy chemical detectors in strategic sampling locations to provide early warning of a chemical attack.

POSTINCIDENT ACTIONS The most important actions after a nicotinic agent attack (besides rescue and care of exposed patients) are prompt notification of the appropriate authorities and decontamination of affected areas. This differs little from the response to other types of chemical attack. If anatoxin is known to have been the agent involved, maximizing exposure of the involved area to sunlight will help to rapidly destroy the toxin; anatoxin-a spontaneously degrades in direct sunlight, with a half-life of about 1 hour.20

MEDICAL TREATMENT OF CASUALTIES Although nicotinic cholinergic antagonists exist, there are no clinical data on their use in human poisoning with nicotinic agents. In addition, of the ganglionic blockers, hexamethonium and trimethaphan are not available for clinical use, and mecamylamine is available in tablet form only, making it unsuitable for use in an emergency. Furthermore, nicotinic cholinergic antagonists at the NMJ are not useful to treat paralysis, as they are themselves paralytic agents. There is thus no useful antidote to nicotine or nicotinic-agonist exposure, and supportive care is the mainstay of therapy. As in most chemical-attack scenarios, rapid removal of just that clothing that has been soaked and of agent visible on the skin (local, or “spot,” decontamination) is crucial to prevent continued absorption and should be accomplished in concert with attention to airway, breathing, and circulation. Patients without a secure airway or who need ventilatory support need these interventions at approximately the same time that local decontamination is being done and before full-body disrobing and decontamination. Mouth-to-mouth ventilation should never be performed because it can pose risks to the rescuer, particularly after a GI exposure.25 For fullbody decontamination, removal of the patient’s clothes, shoes, belt, watch, and jewelry should be followed by irrigation of the skin with copious amounts of water with or without soap (soap may be useful for oily substances such as nicotine freebase or any of these agents dissolved in an organic solvent). Hemodynamic support should include intravenous fluid boluses followed by vasoconstrictor agents such as norepinephrine as needed to treat hypotension. NICOTINIC AGENT ATTACK 597

Therapy for hypertension should be approached with caution, because hemodynamic collapse may be precipitous.26 In the absence of end-organ effects of severe hypertension, pharmacologic intervention should probably be avoided. Dysrhythmias should be managed according to the usual practice. Seizures should be treated with benzodiazepines or barbiturates. Other anticonvulsants are unlikely to be helpful and are not indicated. Vomiting should be managed with antiemetics, and oral activated charcoal should be administered, particularly after GI exposures.27 Because nicotine exhibits a certain degree of enteroenteric circulation, oral activated charcoal even after dermal or inhalational exposure could theoretically be of benefit.26 Suspected cases should be reported to the regional poison control center. Poison control centers can recognize developing epidemics, assist with patient management, and help contact other health and law enforcement authorities in the event of an attack. Because symptoms occur early after exposure, minimal observation is required for patients who present with no clinical abnormalities. Poisoning by a nicotinic agonist may be difficult to distinguish from nerve agent poisoning, and it is possible that patients exposed to these agents might conceivably be treated in the field with Mark I kits containing atropine and pralidoxime. If possible, this should be avoided. Although there may be some role for atropine in patients with bradydysrhythmias, bronchorrhea, or other severe muscarinic symptoms, there is no role for pralidoxime, an oxime cholinesterase reactivator. In

CASE PRESENTATION In 2003, a total of 18 patients from four different families developed nausea, vomiting, dizziness, and burning of the mouth after eating ground beef. One of the patients required evaluation in the emergency department for atrial fibrillation.The pattern of illness suggested contamination at a single store rather than at a meat-processing plant. A recall was issued for approximately 1,700 pounds of ground beef with sell-by dates including the 3 days potentially involved. Samples of the ground beef were sent for analysis. Although testing for food-borne pathogens was negative, it was quickly determined that the samples contained nicotine at a concentration of 300 mg/kg of ground beef. Since a lethal dose of nicotine is about 50 mg, about one-third pound of beef would have represented a life-threatening ingestion. Investigators thus became suspicious of contamination with a nicotine-containing pesticide because these were widely available in the community. However, none of these pesticides was used or sold in the store where the contamination occurred. Several weeks later, a man formerly employed as a meat cutter in the supermarket was arrested and charged with poisoning the meat with Black Leaf 40, a pesticide containing 40% nicotine.A public health notice was issued, and 148 people were interviewed after reporting illness; 92 were ultimately determined to have suffered illness consistent with nicotine poisoning.6 598 NATURAL DISASTERS

fact, aggressive oxime therapy may do more harm than good because pralidoxime is itself a weak cholinesterase inhibitor with the potential to cause cholinergic excess.

UNIQUE CONSIDERATIONS The most notable feature of nicotinic-agonist poisoning is its similarity to poisoning by cholinesterase inhibitors such as organophosphate pesticides and nerve agents. Enhanced parasympathetic outflow (with resulting muscarinic effects) due to ganglionic stimulation may further confuse the clinical findings and mimic organophosphate poisoning. Without identification of the product at the scene, it is unlikely that this distinction will be possible in the event of a chemical attack. Failure to respond to atropine and oximes (or worsening of symptoms with oxime therapy) may be the only clue. Fortunately, as there is no specific therapy for nicotinic-agonist poisoning, chemical attacks with these agents are otherwise managed as are any generic chemical exposure; good decontamination and supportive care is the only therapy needed.

PITFALLS Several potential pitfalls exist in responding to an cholinergic agent attack. These include the following: • During disaster planning and provider education, failure to consider the possibility of nicotinic agonists as mass-casualty chemical agents • Failure to consider a chemical attack with a nicotinic agonist after an epidemic of a GI illness • Misdiagnosis of nicotinic-agonist poisoning as poisoning by organophosphate pesticides or nerve agents • Administration of atropine therapy to patients with nicotinic-agonist poisoning and with no significant muscarinic signs or symptoms • Administration of oxime therapy to patients with nicotinic-agonist poisoning • Failure to involve public health and law enforcement authorities when a chemical attack is suspected • Failure to call the regional poison control center to report cases and to get assistance with management REFERENCES 1. Hoffman BB,Taylor P. Neurotransmission. In: Hardman JG, Limbird LE, Gilman AG, eds. Goodman & Gilman’s The Pharmacological Basis of Therapeutics. 10th ed. New York: McGraw-Hill Medical Publishing Division; 2001:115-53. 2. Rupniak NM, Patel S, Marwood R, et al. Antinociceptive and toxic effects of (+) epibatidine oxalate attributable to nicotinic agonist activity. Br J Pharmacol. 1994;113:1487-93. 3. Hitzfeld BC, Höger SJ, Dietrich DR. Cyanobacterial toxins: removal during drinking water treatment, and human risk assessment. Environmental Health Perspectives. 2000;108:113-22. 4. Dukat M, Glennon RA. Epibatidine: impact on nicotinic receptor research. Cellular and Molecular Neurobiology. 2003;23:365-78. 5. Kassiou M, Bottlaender M, Loc’h C, et al. Pharmacological evaluation of a Br-76 analog of epibatidine: a potent ligand for studying brain nicotinic acetylcholine receptors. Synapse 2002;45:95-104.

6. Boulton M, Stanbury M, Wade D, et al. Nicotine poisoning after ingestion of contaminated ground beef. MMWR 2003;52:413-6. 7. Kommalage M, Hoglund AU. (+/−) Epibatidine increases acetylcholine release partly through an action on muscarinic receptors. Pharmacol Toxicol. 2004;94:238-44. 8. Threat of Bioterrorism in America. Statement for the Record of Robert M. Burnham, Chief, Domestic Terrorism Section before the United States House of Representatives Subcommittee on Oversight and Investigations, May 20, 1999. Available at: http://www.fas.org/irp/congress/1999_hr/990520-bioleg3.htm. 9. Ballard T, Ehlers J, Freund E, et al. Green tobacco sickness: occupational nicotine poisoning in tobacco workers. Arch Environ Health. 1995;50:384-9. 10. McGee D, Brabson T, McCarthy J, et al. Four-year review of cigarette ingestions in children. Pediatr Emerg Care. 1995;11:13-6. 11. Lewander W,Wine H, Carnevale R, et al. Ingestion of cigarettes and cigarette butts by children—Rhode Island, January 1994-July 1996. MMWR 1997;46:125-8. 12. Smolinske SC, Spoerke DG, Spiller SK, et al. Cigarette and nicotine chewing gum toxicity in children. Human Toxicol. 1988;7:27-31. 13. Oberst BB, McIntyre RA. Acute nicotine poisoning. Pediatrics 1953;11:338-40. 14. Mensch AR, Holden M. Nicotine overdose after a single piece of nicotine gum. Chest 1984;86:801-2. 15. Haruda F. “Hip-pocket” sign in the diagnosis of nicotine poisoning. Pediatrics 1989;84:196. 16. Malizia E,Andreucci G,Alfani F, et al. Acute intoxication with nicotine alkaloids and cannabinoids in children from ingestion of cigarettes. Human Toxicol. 1983;2:315-6.

17. Petridou E, Polychronopoulou A, Kouri N, et al. Childhood poisoning from ingestion of cigarettes. Lancet 1995;346:1296-7. 18. Sisselman SG, Mofenson HC, Caraccio TR. Childhood poisoning from ingestion of cigarettes. Lancet 1996;347:200-1. 19. Stevens DK, Krieger RI. Effect of route of exposure and repeated doses on the acute toxicity in mice of the cyanobacterial nicotinic alkaloid anatoxin-a. Toxicon. 1991;29:134-8. 20. Stevens DK, Krieger RI. Stability studies on the cyanobacterial nicotinic alkaloid anatoxin-a. Toxicol. 1991;29:134-8. 21. Davies P, Levy S, Pahari A, et al. Acute nicotine poisoning associated with a traditional remedy for eczema. Arch Dis Childhood. 2001;85:500-2. 22. Rogers AJ, Denk LD,Wax PM. Catastrophic brain injury after nicotine insecticide ingestion. J Emerg Med. 2004;26:169-72. 23. Pendergrass SM, Krake AM, Jaycox LB. Development of a versatile method for the detection of nicotine in air. AIHAJ. 2000;61:469-72. 24. Stevens DK, Krieger RI. Analysis of anatoxin-a by GC/ECD. J Anal Toxicol. 1988;12:126-31. 25. Koksal N, Buyukbese MA, Guven A, et al. Organophosphate intoxication as a consequence of mouth-to-mouth breathing from an affected case. Chest 2002;122:740-1. 26. Salomon ME. Nicotine and tobacco preparations. In: Goldfrank LR, Flomenbaum NE, Lewin NA, et al. Goldfrank’s Toxicologic Emergencies. 7th ed. New York: McGraw-Hill Medical Publishing Division; 2002:1075-84. 27. Geller RJ, Singleton KL, Tarantino ML, et al. Nosocomial poisoning associated with emergency department treatment of organophosphate toxicity—Georgia, 2000. J Toxicol Clin Toxicol. 2001;39: 109-11.

NICOTINIC AGENT ATTACK 599

chapter 100

Anesthetic-Agent Attack Kinjal N. Sethuraman and K. Sophia Dyer

DESCRIPTION OF EVENT In the 1830s, ether, the earliest anesthetic agent, began to be used for sedation and pain control in the United States.1 Today, however, ether and various other anesthetics such as chloroform and cyclopropane are no longer in use because of the danger of explosion and the potential for fatal consequences from their use. Initially, they were replaced by nonflammable agents such as halothane and nitrous oxide; however, halothane itself, because of its hepatotoxicity and cardiotoxicity, has now been largely superseded by halogenated ethers such as isoflurane and enflurane. These drugs are typically delivered via inhalation after intravenous sedation. A major advantage of inhaled anesthetics for anesthesiologists is that the level of sedation can be rapidly modified to remain within the therapeutic window and to achieve desired analgesia, amnesia, muscle relaxation, and paralysis.2 Anesthetic agents are not known to have been used on the battlefield or by terrorists, but recently an event in Russia brought the issue of the topic of anesthetic agents as potential mass-casualty weapons into sharp focus.3-5 In 2002, a “knockout gas,” bluish-gray in color and with a sweet taste, was used by the Russian Army to incapacitate Chechnyan hostage-takers while elite Spetsnaz forces of the Russian army attempted to rescue 800 hostages in a Moscow theater.6 It has been speculated that the gas contained halothane or another anesthetic agent mixed with an opioid compound (see Chapter 97).7,8 One hundred twenty-seven hostages, including several children, died from the gas. It was reported that the gas was released for over 20 minutes at an unknown concentration. The preincident health of some of the victims may have led to the high mortality rate, but some hostages had virtually no response to the agents.7 Hospitals that received victims of the attack were allegedly not informed of the gases used and thus had to experiment with reversal agents.8,9 As television footage shows, many affected hostages removed from the theater were placed onto the ground or onto buses in positions that risked airway compromise and underscored the necessity of attention to airway and breathing in these casualties quite apart from considerations of specific antidotal treatment.7 600

Although newer anesthetic gases are relatively safe, older agents have several properties that could make them appealing for criminal purposes: • • • • • • • • • •

Ease of availability Portability Volatility Mass dissemination Rapid onset of action Low warning properties Potential to incapacitate or kill Possible use of remote trigger Novel to first responder Can also be used as explosives in high concentrations

In this chapter, we will focus on some of the more common agents. If a terrorist attack occurs with any agent, first responders need to be well prepared. The response team needs to act quickly to triage, evacuate, and attend to airway and breathing in affected casualties and to determine which agent or agents were used, the agent concentration, and the method of distribution. The odor, taste, color, signs, and symptoms will vary by agent. Therefore, interviewing victims can be helpful in identifying the gas or gases used. Since these agents share significant inhalational hazards with a quick onset of action, they could pose a hazard both to original victims and also first responders.

CHARACTERISTIC PROPERTIES OF POTENTIAL TERROR AGENTS The following agents are described as examples of the range of physicochemical properties and effects of the many compounds that have been used as inhalational anesthetics. Clinicians should always be aware of potential interactions from combinations of agents, as in the Moscow theater incident. Attention to presenting symptoms, descriptions by victims, and information from hazardous materials specialists can aid in clarification of the chemical used. Victims of inhaled anesthetic agents will experience confusion, relaxation, dizziness, drowsiness, and various respiratory symptoms that can include choking, a burning sensation in the mouth or nose, and respiratory

distress. Less water-soluble agents such as nitrous oxide will stealthily cause effects in the smaller, peripheral airways but less pronounced skin, mucous-membrane, or central-airway damage.10 The mean alveolar concentration (MAC) is used as a measure of the strength of an anesthetic. It represents the minimum concentration necessary to cause unresponsiveness in 50% of the general population.11 Simply put, the higher the MAC, the less potent the gas. The MAC is influenced by many factors including age of victim, the victim’s comorbidities and metabolism, combination with another anesthetic or analgesic agent, and preexposure vital signs.2 The solubility of an anesthetic in blood is described by the blood-gas partition coefficient (BGPC), which expresses, in liters, the amount of an agent that will dissolve in 1 liter of blood exposed to air containing the anesthetic. The lower the BGPC, the faster the onset of an anesthetic and the faster it will wear off.

Diethyl Ether Diethyl ether (C4H10O) is a flammable, volatile, colorless liquid with a sweet taste and ethereal odor.12 It is soluble in alcohol, acetone, benzene, and chloroform. Its boiling point is only 94˚F (34.5˚C). When exposed to fire or heat, ether releases carbon monoxide; exposure to light causes ether to break down into flammable peroxides.12 Ether, with a BGPC of 12, is more soluble in blood than either halothane or nitrous oxide. The MAC of ether is 2.0%. Because of the explosive nature of ether, the National Fire Protection Association has given ether a flammability rating of 4, corresponding to an extreme fire hazard.13 Although ether works well as an anesthetic, its propensity to explode prompted anesthetists to find alternative inhaled agents such as chloroform, cyclopropane, and halothane. Anesthesia induction occurs at a concentration of 100,000 to 150,000 ppm and is maintained with 50,000 ppm.13 Very small doses to eyes or skin can cause corneal injury and burns.14 Toxic exposures to ethers (as with other anesthetics) can occur through inhalation, eye or skin contact, and ingestion. The effect of ether is dose dependent. Symptoms consist of skin, eye, and mucosal irritation leading to an increase in bronchial secretions. Dizziness, drowsiness, bradycardia, hypothermia, or acute excitement may also occur. Laryngospasm, loss of consciousness, and death may result. The aftereffects of emergence from ether-induced anesthesia include nausea, vomiting, and headache.15 Newer ethers are halogenated and include enflurane, desflurane, and sevoflurane. They are not flammable, have fewer side effects, are efficient as anesthetic agents, and cause less end-organ damage.1 They may be potentially used by terrorists as incapacitating agents.

Nitrous Oxide Nitrous oxide (N2O)16 is a weak anesthetic (MAC of 105) often combined with other agents to produce adequate analgesia and anesthesia. Induction and maintenance of anesthesia require very high concentrations of nitrous oxide, and hypoxia may result if high concentrations of

oxygen are not coadministered. During minor procedures, lower concentrations are used for sedation. Nitrous oxide is found commonly in aerosol sprays, and its abuse potential is accordingly high. Prolonged use can cause peripheral nerve damage, psychosis, perceptual impairment, and hyperpyrexia.17 Nitrous oxide administered in high doses has been found to cause arrhythmias, malignant hyperthermia, seizures, pneumomediastinum, and subcutaneous emphysema. Nausea and vomiting are early signs of nitrous oxide toxicity.18

Chloroform Chloroform (CHCl3)18 is a colorless, volatile chlorinated hydrocarbon that is often mixed with ethanol. It has a sweet, burning taste and a pungent odor. As a byproduct of chlorination, chloroform is present in low concentrations in chlorinated water19 but exposure to these low concentrations is insufficient to cause anesthesia. It is also produced from the reduction of carbon tetrachloride (CCl4) with moist iron. Although no longer used as an anesthetic,1 chloroform is still used an intermediate in chemical syntheses. One of the Freon refrigerants is an example of the current use of chloroform. Moreover, chloroform has been widely popularized as a knockout agent to induce consciousness when poured onto a handkerchief or other cloth and held over the mouth and nose. And its well-known use for this purpose may make it a more likely choice for terrorists for either small-scale or mass-casualty use. The toxic dose of chloroform is 7 to 25 mg/dL (0.59 to 2.1 mmol/L).20 At inhaled concentrations of less than 1500 ppm, physical effects of dizziness, tiredness, and headache are reported; and anesthesia occurs at a range of 1500 to 30,000 ppm. Chloroform causes irritation to the respiratory tract. It will cause dry mouth, sedation, confusion, and loss of consciousness within 5 to 10 minutes, and unconsciousness may last up to 30 minutes after removal from exposure. Fatalities occur after 5 to 10 minutes at doses of 25,000 ppm or greater by inhalation.20 Death can occur from cardiac arrest and hepatic toxicity with peak elevation of hepatic enzymes 3 to 4 days after exposure and a subsequent return of liver-function tests to normal in survivors.20 Pulmonary toxicity from intravenous injection of chloroform peaks after 3 days. Renal and hepatic toxicity may also occur from phosgene (COCl2), a byproduct that results from exposure of chloroform to sunlight and air (see Chapter 95).21 Other byproducts include hydrochloric acid (HCl), carbon monoxide (CO), inorganic chloride, and formaldehyde.21 Pulmonary exposure to HCl and phosgene can result in pulmonary edema, bronchial pneumonia, and subsequent lung abscesses. Victims exposed to chloroform need supportive care, including cardiac and pulmonary monitoring in an intensive care unit as clinically indicated. While there is no antidote for chloroform, liver toxicity in animals may be prevented by using N-acetylcysteine (NAC) after exposure, since chloroform and its byproducts deplete glutathione stores.20,22 However, no studies have evaluated the use of NAC for this purpose in humans.23 ANESTHETIC-AGENT ATTACK 601

Cyclopropane Cyclopropane (C3H6) is a hydrocarbon ring that was discovered in 1882; it began to be used as an anesthetic in 1933.1 It is extremely flammable and is thus no longer used clinically. Cyclopropane, a gas at room temperature, is caustic to eyes but not to the skin. At concentrations greater than 40%, cyclopropane causes irritation to the eyes and respiratory tract. Its density is greater than air, and if released into the environment, it will hug the ground.14 At higher concentrations, it causes nausea, disorientation, dizziness, and incoordination. If released in a closed area, cyclopropane, as is the case with all hydrocarbons, will displace oxygen and cause asphyxiation.24 Autopsy results from accidental death after cyclopropane ingestion showed hemorrhagic edema of the lungs.14 Cardiac output, stroke volume, and heart rate are all affected by high concentrations of cyclopropane, but these parameters return to normal a few minutes after the agent is removed.25 Cyclopropane causes decreases in renal blood flow and glomerular filtration rate.26 Malignant hyperthermia from cyclopropane has been reported; it can be resolved with cooling and perhaps by the administration of dantrolene.27 Cyclopropane has also been shown to alter cognitive function, especially the ability to learn, for up to a week after exposure.28

Halothane Halothane (C2HBrClF3) continues to be used occasionally as an anesthetic, analgesic, and amnesic. Halothane is a colorless, volatile, nonflammable liquid unique for its sweet taste and odor. It is the most potent inhaled anesthetic, with a MAC of 0.77.2 The MAC is commonly reduced by administering a coagent. The MAC for patients who are older, hypothermic, hypotensive, or hypoxic will be lower.29 Halothane is highly soluble in both blood and fat; this behavior accounts for its prolonged emergence from anesthesia.2 When exposed to light, heat, flames, and acids, halothane will decompose into other toxic fumes or metabolites (e.g., bromide, chlorine, and fluorine). The dose used for anesthesia ranges between 5000 to 30,000 ppm,30 or 0.5% to 3% concentration in oxygen.31,32 Even if victims are exposed to less than 5000 ppm, they will show impaired manual dexterity and word-finding difficulties. Acute exposure to this agent causes severe irritation to all exposed areas. Hypotension, dizziness, somnolence, lethargy, and changes in mental status are all potential symptoms. Exposure to halothane may lead to hepatic failure, cardiac arrhythmias, and malignant hyperthermia.31,33,34 Liver failure from other halogenated anesthetics is less common. Long-term, chronic exposure to halothane can increase the risk of some cancers and can increase rates of spontaneous abortions and of congenital abnormalities in newborns of exposed mothers.35 Diagnosis of halothane toxicity is based mainly on history, physical examination, and basic laboratory analyses. Attributing hepatic failure to halothane is difficult, since the clinical presentation is identical to other causes of hepatitis. An assay for halothane-related antibodies is available for experimental use but is not practical in emer602 NATURAL DISASTERS

gency or disaster settings. Halothane metabolites can be detected in the urine up to 1 week after exposure.31

PREINCIDENT ACTIONS Because terrorist attacks are for the most part unpredictable, it is important for emergency medical services, law enforcement, and local, state, and national agencies to be prepared for any type of attack at any given time. For attacks using anesthetic agents, the focus should be on rapid access to casualties, prompt evacuation, careful attention to airway and ventilation (especially during transport and positioning), general supportive care, identification of agent, and ample supply of reversal agents. In Moscow, although the Russian military had an “antidote” (probably naloxone) to the agents used, claims were made that there were not enough medical personnel to administer the drug.7 There are no antidotes to ether, chloroform, cyclopropane, or halothane, and the importance of attention to airway, breathing, and circulation cannot be overemphasized. The first gas masks were developed as a response to the use of inhaled gases at Ypres during World War I.3 In any given situation, appropriate respiratory protection should be worn by emergency medical services personnel, healthcare workers, and law enforcement personnel until the area in question has been cleared of inhalation risk. Many first-responding agencies may not have the available detection equipment to identify exactly the type of anesthetic gas used or even the general class of anesthetic gases used, thus making it even more important to use proper equipment. The typical canister respirator either with a full face piece or partial face piece, which is very portable and varying in comfort, will not offer protection in an atmosphere of depleted oxygen. If oxygen displacement has occurred, a supplied air respirator (either through a tank or air line) is the only appropriate respiratory protection. Many portable sensors are available for measuring ambient oxygen concentrations, either as individual items or components in other detection equipment. Several companies market canister respirators for application in event of the use of weapons of mass destruction. In general, these products are not specifically tested against many of the anesthetic agents discussed in this chapter, as of the time of this writing. An organic vapor canister might trap some of these agents, with the obvious exception of the inorganic nitrous oxide. However, this will depend on concentration values within the acceptable range. In addition, the canister testing information should be evaluated to see whether it has been tested against the known agent. Given that this might be difficult to accomplish in a critical time period, a self-contained breathing apparatus will offer the best protection for an unknown environment.

POSTINCIDENT ACTIONS As with any potential exposure to an inhalational toxin, protection of the victims from further exposure and guarding against exposure in responders is vital. If in

doubt as to the type of chemical, the highest level of respiratory protection is recommended—in many cases, this is a supplied air respirator. Because some of these products are volatile, precautions against direct flame and any equipment that could potentially generate a spark are prudent. The most important immediate actions to take are to reach victims (who may already be apneic) as soon as possible, to ensure a patent and protected airway, to increase ventilation, to decrease exposure, and to provide oxygen to victims.

MEDICAL TREATMENT OF CASUALTIES It is important to interview survivors and gather as many data as possible to determine the agent used. The volatility of anesthetic agents may decrease the utility of air samples, but such samples can help to identify other agents that may have been used in combination with the agents. It is important to consider the potential of a mixture of agents even after the identification of a specific agent. Once victims are at a hospital, laboratory studies that can be obtained relatively quickly can be helpful in the management of exposed patients. These studies include arterial-blood-gas and carboxy-hemoglobin determinations, liver-function tests, a complete blood count, and a comprehensive metabolic panel. A chest radiograph is also useful in the setting of suspected chemical pneumonitis or pulmonary edema, although dyspnea is usually the first indicator of incipient pulmonary edema.

CASE PRESENTATION It is a hot and humid summer day on a holiday weekend in Baltimore. Air conditioners are working overtime. The threat of rain forever looms overhead, as it always seems to do in the mid-Atlantic region of the United States. As shopping continues to be a national pastime, several hundred shoppers have packed into a local mall. Security is nonexistent due to budget cuts and the economic slump. Nearly 20 men holding machine guns, wearing masks, and carrying cylinders that could be mistaken for helium tanks easily enter the mall. They strategically release the gas in the cylinders into the air-conditioning system. After a few minutes, people with asthma start feeling their chests tighten. Others start to choke, as their eyes burn. Still more involuntarily fall asleep. Those near the doors try to run outside for fresh air, but the electrically controlled doors are locked shut. The masked men make their presence known to the few who are fighting off the weight of their eyelids.They have taken the mall over for two purposes: to steal, and to make it known to the Westerners that they are not safe.

PITFALLS Several potential pitfalls exist in response to an anesthetic opioid nerve agent attack. These include the following:

• Failure to recognize that an attack has taken place • Failure to reach potentially apneic patients as soon as possible • Failure to attend adequately to airway, breathing, and circulation in casualties before, during, and after transport to medical treatment facilities • Failure to notify proper local, state, national, and international agencies • Failure to identify the agent or agents used • Failure to follow the identification of a specific chemical agent by consideration of the possibility of simultaneous use of an anesthetic agent • Failure to remove igniting factors or flammable objects from scene • Failure to use gloves and appropriate respiratory protection • Failure to evacuate or ventilate area • Failure to notify hospitals • Failure to have enough personnel available REFERENCES 1. Vandam L. History of anesthetic practice. In: Miller RD, ed. Anesthesia. Vol V. Philadelphia: Churchill Livingston; 2000. 2. Schwinn DA, Shafer SL. Basic principles of pharmacology related to anesthesia. In: Miller RD ed. Anesthesia. Vol V. Philadelphia: Churchill Livingston; 2000. 3. Gas killed hostages in raid. CNN Web site. October 27, 2002. Available at: http://www.cnn.com/2002/WORLD/europe/10/27/ moscow.putin/index.html. 4. Moscow doctor: gas killed 116 hostages. CBS News Web site. October 27, 2002. Available at: http://www.cbsnews.com/stories/ 2002/10/28/world/main527107.shtml. 5. Bismuth C, Borron S, Baud FJ, et al. Chemical weapons: documented use and compounds on the horizon. Toxicol Lett. 2004;149:11-8. 6. Reed D. Terror in Moscow. HBO Documentaries; June 2004. 7. Wax PM, Becker CE, Curry SC. Unexpected “gas” casualties in Moscow: a medical toxicology perspective. Ann Emerg Med. 2003; 41:700-5. 8. Lethal Moscow gas an opiate? CBS News Web site. October 29, 2002. Available at: http://www.cbsnews.com/stories/2002/10/29/ world/main527298.shtml. 9. Anger grows over gas tactics. CNN Web site. October 28, 2002. Available at: http://archives.cnn.com/2002/WORLD/europe/10/ 28/moscow.gas/. 10. Greenfield RA, Brown BR, Hutchins JB, et al. Microbiological, biological, and chemical weapons of warfare and terrorism. Am J Med Sci. 2002;323:326-40. 11. Marshall BE, Longenecker DE. General anesthetics. In: Hardman JG, Limbird LE, Molinoff PB, et al, eds. Goodman and Gilman’s The Pharmacological Basis of Therapeutics. Vol IX. New York: McGraw-Hill; 1996. 12. Occupational Health and Safety Administration, US Department of Labor. Ethyl ether: material data safety sheet. April 27, 1999.Available at: http://www.osha.gov/SLTC/healthguidelines/ethylether/. 13. Hathaway GJ, Proctor NH, Hughes JP, et al. Proctor and Hughes’ Chemical Hazards of the Workplace. Vol III. New York: Van Nostrand Reinhold; 1991. 14. Grant WM. Toxicology of the Eye. Springfield, Ill: Charles C Thomas; 1962. 15. Clayton G, Clayton F. Patty’s Industrial Hygiene and Toxicology. 3rd ed. New York: John Wiley & Sons; 1981. 16. OSHA Health Guidelines. Occupational Safety and Health Guideline for nitrous oxide. Available at: http://www.osha.gov/ SLTC/healthguidelines/nitrousoxide/recognition.html. 17. Murray MJ, Murray WJ. Nitrous oxide availability. J Clin Pharmacol. 1980;20:202-5. 18. Haddad K, Pearson C. Chlorinated hydrocarbons. In: Ellenhorn MJ, Barceloux DG, eds. Medical Toxicology: Diagnosis and Treatment of Human Poisonings. Philadelphia:WB Saunders; 1998. ANESTHETIC-AGENT ATTACK 603

19. Rook JJ. Formation of haloforms during chlorination of natural waters. Water Treatment Exam. 1974;23:234-43. 20. Maynard SM. Appendix D: drugs and toxins: therapeutic and toxic levels. In Ford MD, ed. Clinical Toxicology. Vol 1. Philadelphia: WB Saunders; 2001. 21. Van Dyke RA. On the fate of chloroform. Anesthesiology 1969; 30:264-72. 22. el-Shenawy NS,Abdel-Rahman MS. The mechanism of chloroform toxicity in isolated rat hepatocytes. Toxicol Lett. 1993;69:77-85. 23. Flanagan RJ, Meredith TJ. Use of N-acetylcysteine in clinical toxicology. Am J Med. 1991;91:131S-9S. 24. Barasch ST, Booth S, Modell JH. Hypercapnia during cyclopropane anesthesia: a case report. Anesth Analg. 1976:55:439-41. 25. Cullen DJ, Eger EI, Gregory GA. The cardiovascular effects of cyclopropane in man. Anesthesiology 1969;31:398-406. 26. Deutsch S, Pierce EC, Vandam LD. Cyclopropane effects on renal function in man. Anesthesiology 1967;28:547-58. 27. Lips FJ,Newland M,Dutton G. Malignant hyperthermia triggered by cyclopropane during cesarean section. Anesthesiology 1928;56: 144-6.

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28. James FM. The effect of cyclopropane anesthesia without surgical operation on mental function of normal man. Anesthesiology 1969;30:264-72. 29. Dale O, Brown BR. Clinical pharmacokinetics of the inhalational anesthetics. Clin Pharmacokinet. 1987;145-67. 30. OSHA Health Guidelines. Occupational Safety and Health Guidelines for Halothane. Available at: http://www.osha.gov/ SLTC/healthguidelines/halothane/recognition.html. 31. Halothane: Drugdex Drug Evaluations. DRUGDEX® System. Greenwood Village, Colo:Thomson MICROMEDEX. 32. Product Information: Fluothane®, Halothane (Liquid for Vaporization). Philadelphia:Wyeth-Ayerst Laboratories; 1998. 33. Viitanen H, Baer G, et al. The hemodynamic and Holter-electrocardiogram changes during halothane and sevoflurane anesthesia for adenoidectomy in children aged one to three years. Anesth Analg. 1999;87:1423-5. 34. Humphrey DM. Technical Info Fluothane®, Halothane. Philadelphia:Wyeth-Ayerst Laboratories; 2002. 35. Material Safety Data Sheet 2-Bromo-2-chloro-1,1,1-trifluoroethane. Milwaukee,Wisc:Aldrich Chemical Co; May 1992.

S E C T I O N

T E N

Biologic Events

chapter 101

Introduction to Biologic Agents Andrew S. Nugent and Eric W. Dickson

On Aug. 6, 1945, at 8:16 AM, the detonation of “Little Boy” over the city of Hiroshima, Japan, ushered in the age of nuclear weapons and warfare. The first known use of the second element of NBC (nuclear, biologic, and chemical) weapons of mass destruction is not as dramatic nor as well documented but likely took place in 6th century BC, when the Assyrians used rye ergot to poison the wells of their adversaries.1 Knowing a good idea when they saw it, Scythian, Roman, Greek, and Persian archers tipped their arrows with manure and other biologic agents circa 400 to 300 BC. Many other uses of human sickness to wage war followed; perhaps the most destructive occurred when the Tartars used trebuchets to hurl plague-infected corpses into the city of Caffa in the year 1346. Sailors fleeing the ensuing epidemic may have inadvertently initiated the Great Plague by spreading the illness to Genoa, Italy (although this has been recently questioned).2–4 Biologic warfare was not limited to the “Old World.” Pizzaro, the British, and the Americans used smallpox-infected blankets to produce mass casualties among their adversaries.5 U.S. research into offensive biologic weapons continued until 1969,when President Richard Nixon renounced the use of biologic weapons as killing or incapacitating agents. Although most nations signed the Biological Weapons Convention in 1975, many experts believe that biologic weapons programs still exist in Russia, North Korea, and until recently, Iraq. It is estimated that 10 countries have stockpiled biologic weapons either now or in the recent past.6 Since the early 1980s, the risk of the use of biologic weapons has increased dramatically with the rise of modern terrorism because these agents are relatively easy and inexpensive to make and weaponize and have the potential to kill large numbers of individuals,while sowing terror into millions of survivors. The organisms and toxins that can be used as biologic weapons have been categorized by the U.S. Centers for Disease Control and Prevention (CDC) into three categories (A, B, and C [Table 101-1]). Agents classified as Category A by the CDC are of the highest priority because of the risk of their imminent use. Each of the Category A agents is easily disseminated, may result in much mortality, and has the ability to cause public panic, outcomes that are perceived to be among the main goals of a terrorist attack. All other significant bacteria that could possibly be used as bioweapons fall into the CDC’s

Category B; these are moderately easy to disseminate and have much less potential for severe mortality, although morbidity may be high. Category C is reserved for emerging infectious illnesses that may be bioengineered in the future as weapons. Beyond the psychologic impact of a biologic weapon attack, several conditions must be met in order for a biologic agent to be useful as a weapon; lethality and infectivity of an organism alone are not sufficient. For example, Ebola is highly transmissible unless proper precautions are used and has a high mortality rate. However, Ebola does not persist in the environment and kills too quickly to allow for widespread exposure to infected individuals. This limits dissemination (e.g., formation of an epidemic) in the population. Thus, Ebola is unlikely to make an ideal weapon unless weaponized in a form that rapidly infects a large segment of the population. With that in mind, several criteria must be met for an organism or toxin to be an effective biologic weapon, including the following: (1) the organism or toxin must be easily obtainable, culturable, and stable in the environment; (2) the organism or toxin must have the ability to be weaponized with a delivery system that allows widespread dissemination and/or be highly transmissible (by human, insect, or animal vector) while also allowing time for individuals to infect others in society; (3) the organism or toxin must be able to incapacitate or kill a large segment of the population (e.g., there is no innate resistance or easy treatment). The first barrier to weaponization is delivery. Biologic agents can be delivered by several routes: inhalation of an aerosol, such as with anthrax; ingestion, such as with enterohemorrhagic Escherichia coli; or transcutaneously (e.g., the use of plague-infected fleas in Manchuria during World War II). Delivering and disseminating biologic agents effectively is not easy. Distribution via explosive device can reduce the efficiency of the delivered organisms to as low as 5%. However, it is not only delivery to a location that is important. Aerosolized particles that are too large will settle out of the atmosphere, and particles that are too small will not be trapped effectively in the lung, reducing infectivity. For this reason, aerosolized particles must be between 1 and 10 μm, and an efficient delivery system must be used; aerosolization using compressed gas can achieve 70% efficiency.7 Weather and 605

TABLE 101-1 CDC CATEGORIES OF BIOLOGIC WEAPON AGENTS CATEGORY

DEFINITION

AGENTS

A

Organisms that pose a high risk to national security because they are easily disseminated or transferred from person to person, they can result in high mortality rate and have the potential for major public health impact, may cause public panic and social disruption, and require special action for public health preparedness. Organisms that are moderately easy to disseminate, result in moderate morbidity and low mortality rates, and require the CDC’s diagnostic capacity and enhanced disease surveillance.

Bacillus anthracis (anthrax) Yersinia pestis (plague) Francisella tularensis (tularemia) Botulinum toxin Variola (smallpox) Viral hemorrhagic fevers (Marburg, Ebola, etc.) Brucella (brucellosis) Coxiella brunetti (Q fever) Rickettsia rickettsii (Rocky Mountain spotted fever) Vibrio cholerae (cholera) Shigella dysenteriae (shigellosis) Salmonella species (salmonellosis) Salmonella typhi (typhoid fever) Burkholderia mallei (glanders) Burkholderia pseudomallei (melioidosis) Chlamydia psittaci (psittacosis) Escherichia coli 0157:H7 and others(enterohemorrhagic E. coli) Hantavirus, flavivirus, and others

B

C

Emerging pathogens capable of being engineered for mass dissemination in the future due to availability, ease of production and dissemination, and potential for high morbidity and mortality resulting in a major health impact.

electrical charge are other barriers to the effective dispersion of a biologic agent. For example, rain will remove particles from the atmosphere, and high wind speed can disperse an agent away from the intended target, whereas low wind speed will allow the aerosol to settle too rapidly. Electrical forces affect distribution as well.There is a natural electrostatic attraction between particles and surfaces. Unless compensated for, this electrostatic charge limits aerosolization.The problem of electrostatic charges can be overcome but is difficult and requires expertise.8 Alternatively, electrostatic charge can be used as an advantage when designing environmental filtering systems.9,10 Because of the variability of outdoor conditions, an indoor release of a biologic agent may be more desirable for terrorists since it requires a smaller amount of the agent and can be targeted to a specific population of interest (as was accomplished with anthrax in the Hart Office building in 2001). Conversely, an indoor release is not as likely to cause mass casualties unless the organism is highly infective during an asymptomatic incubation period and can be disseminated person to person. A second route of delivery is by oral ingestion. There are barriers to the effective transmission of biologic agents in the water system, primarily the use of water purification in the United States. For this reason, the release of a biologic agent in the water supply may be less effective than contaminating the food supply. The archetype for biologic weapons is anthrax. Anthrax is easily obtainable, easily weaponized, stable when released (spores can persist in the environment for up to 40 years), and highly lethal. One hundred kilograms of aerosolized anthrax spores have the potential to kill up to 3 million people. Because of efficient delivery, the lack of person-to-person infectivity and limited secondary aerosolization are not barriers to its effective use as a biologic weapon. Thus, even though it is unlikely that infection will persist or spread much beyond the initial casualties, anthrax still makes an ideal weapon. 606 BIOLOGIC EVENTS

SURVEILLANCE The role of surveillance is a subject of much debate. Surveillance depends on the recognition of occurrences of diseases/organisms/symptoms beyond that which would be expected as a background rate or outside of a disease’s natural range. One of the major weaknesses in surveillance systems is the lack of sensitivity and specificity. Even though it is critical to detect the presence of a pathogen, it is also important to avoid mobilizing a response to false-positive tests. A second weakness is that by the time symptom or organism surveillance is able to pick up a pattern of illness in a community, the illness may already be well established. Environmental monitoring, on the other hand, has the potential to identify pathogens before they become ensconced in the community. Environmental monitoring includes the routine monitoring of food and water supplies as well as the general environment. Autonomous monitoring devices are available (August 2004) that perform testing (e.g.,on air) at a predefined interval for infectious,chemical, and radiologic agents.11 More information on surveillance is available at the CDC Web site (www.cdc.gov) and in Morbidity and Mortality Weekly Report.12 Readers with an interest in worldwide surveillance may wish to subscribe to ProMed-mail (www.promedmail.org), which is a free mailing list that reports symptomatic outbreaks of known diseases and unidentified symptom complexes worldwide. Each of the chapters in Section 10 will review the likely scenario and consequences of an attack with a specific biologic agent. Much of the information provided is based on our understanding of the agent’s pathogenicity in nature. In many cases, how a given agent will behave when delivered as a weapon is extrapolated from these data. Early recognition and isolation minimize morbidity and mortality of the primarily exposed and reduce secondary infection. For the clinician, this is implemented by early identification of a cluster of patients with similar symptoms or the occurrence of a

TABLE 101-2 DIFFERENTIAL DIAGNOSIS OF SYNDROMES POSSIBLY CAUSED BY BIOLOGIC WARFARE AGENTS CATEGORY A BIOTERRORISM DISEASES

CATEGORY B BIOTERRORISM DISEASES

CATEGORY C BIOTERRORISM DISEASES

NATURALLY OCCURRING DISEASES

Respiratory tract infection with fever

Inhalational anthrax Tularemia Pneumonic plague

Inhalational glanders Inhalational ricin Melioidosis Q fever Typhus

Legionellosis SARS, Hantavirus (2nd stage)

Gastroenteritis

Anthrax Tularemia Ebola Plague Marburg

Hantavirus Norovirus Legionellosis

Rash with fever

Ebola Marburg Pneumonic plague Smallpox

Acute brucellosis Cholera Giardia Cryptosporidium Q fever Ricin/abrin toxins Paralytic shellfish toxins Glanders typhus

Influenza-like illness

Plague Smallpox Anthrax Tularemia Ebola

Q fever Typhus Brucellosis Glanders

Hantavirus Nipah virus Legionellosis Lyme disease SARS

Sepsis, nontraumatic shock

Ebola Lassa fever Marburg

E. coli

Hantavirus

Meningitis, encephalitis-like syndrome

Anthrax Ebola Lassa fever

Eastern equine Encephalitis Venezuelan equine encephalitis Q fever

St. Louis encephalitis West Nile virus Lyme disease Japanese encephalitis Nipah virus

Botulism-like illness

Botulism

Diphtheria E. coli Histoplasmosis Influenza Malaria Measles Respiratory syncytial virus Cestodes Clostridium difficile Helicobacter pylori Hepatitis A & E Leishmaniasis-Visceral Rocky Mt. spotted fever Typhoid fever Chickenpox Measles Monkeypox Mumps Rubella Rocky Mt. spotted fever Diphtheria Influenza Malaria Measles Mononucleosis Rift Valley fever Respiratory syncytial virus Yellow fever Cytomegalovirus Enterococcus faecium Histoplasmosis Listeriosis Staphylococcus epidermidis Streptococcus pneumonia Toxic shock syndrome Yersinia entercolitica Chickenpox Dengue Epstein-Barr virus Haemophilus influenza Influenza A & B Malaria Measles Viral meningitis Rift Valley fever Rocky Mt. spotted fever Diphtheria Listeriosis

SYNDROME

Lyme disease Dengue fever

(Table reproduced with permission Kristin Uhde, PhD, and Center for Biological Defense, College of Public Health, University of Southern Florida.)

disease outside of its normal range. Table 101-2 provides a summary of the symptoms and a differential diagnosis that are observed during a possible bioterrorism attack.13 REFERENCES 1. Kortepeter M, Christopher G, Cieslak T, Culpepper R, Darling R, Pavlin J, eds. Medical Management of Biological Casualties Handbook. Fort Detrick, Frederick, Md: US Army Medical Research Institute of Infectious Diseases; 2001:1-12. 2. Derbes VJ. De Mussis and the great plague of 1348: a forgotten episode of bacteriological warfare. JAMA. 1966;196(1):179-82. 3. Christopher GW, Cieslak TJ, Pavlin JA, Eitzen EM. Biological warfare: a historical perspective. JAMA. 1997;278(5):412-17. 4. Wheelis M. Biological warfare at the 1346 siege of Caffa. Emerg Infect Dis. 2002;8(9):971-5. Available at: http://www.cdc.gov/ ncidod/EID/vol8no9/01-0536.htm. 5. Noah DL, Huebner KD, Darling RG, Waeckerle JF. The history and threat of biological warfare and terrorism. Emerg Med Clin North Am. 2002;20(2):255-71.

6. Jakobs MK. The history of biologic warfare and terrorism. Dermatol Clin. 2004;22:231-46. 7. Federation of American Scientists. Militarily Critical Technologies List. (MCTL) Part II: Weapons of Mass Destruction Technologies. Section III: Biological Weapons Technology. Available at: http://www.fas.org/irp/threat/mctl98-2/. 8. Gomez A. The Electrospray and its application to targeted drug inhalation. Respir Care. 2002;47:1419-31. 9. Utrup LJ, Frey AH. Fate of bioterrorism-relevant viruses and bacteria, including spores, aerosolized into an indoor air environment. Exp Biol Med. 2004;229:345-50. 10. Weber RW. Meteorologic variables in aerobiology. Immunol Allergy Clin North Am. 2003;23:411-22. 11. Bravata MD, McDonald KM, Smith WM, et al. Systematic review: surveillance systems for early detection of bioterrorism-related diseases. Ann Intern Med. 2004;140:910-22. 12. Syndromic surveillance. Reports from a national conference, 2003. Morb Mortal Wkly Rep. 2004;53(Suppl):1-264. 13. Center for Biological Defense, College of Public Health, University of Southern Florida. Syndromic Surveillance. Available at: http://www.bt.usf.edu/files/SurveillancePacket%20Draft.pdf. INTRODUCTION TO BIOLOGIC AGENTS 607

S E C T I O N

T E N

( P A R T

O N E )

Bacterial Agents

chapter 102

Bacillus Anthracis (Anthrax) Attack Christo C. Courban

DESCRIPTION OF EVENT Anthrax,a category A bioterrorism agent,is a zoonotic disease caused by Bacillus anthracis, an aerobic, nonmotile, spore-forming, gram-positive bacillus that is ubiquitous in soil. Anthrax is primarily a disease of herbivores, including sheep; cattle; goats; horses; and, less commonly, pigs. The first known description of anthrax (approximately 1400 BC) is in the Old Testament where it represented the fifth plague on Egypt, the killing of the Egyptian cattle. The “Black Bane”outbreak (named after the black eschars caused by cutaneous anthrax) took place in Europe in the 1600s and killed 60,000 people and many more cattle. In 1881, Robert Koch definitively identified B. anthracis as the cause of cutaneous anthrax, making it the first disease for which a microbial cause was identified. Soon thereafter, Pasteur developed an effective vaccine. Despite all efforts, anthrax remains a sporadic problem in Africa, the Middle East, some parts of South America, and Asia. B. anthracis makes an almost perfect biologic weapon—it is easily weaponized; can be aerosolized; has a high mortality rate; and the spores are highly resistant to drying, heat, gamma radiation, ultraviolet light, and many disinfectants. Additionally, the spores can remain dormant in the environment for up to 40 years. Several countries have developed weaponized anthrax, which was used during WWII by the Japanese in Manchuria. It is estimated that the release of 100 kg of anthrax spores in a major city could lead to up to 3 million deaths, making anthrax potentially as lethal as a hydrogen bomb. For comparison, it is estimated that Iraq had 8500 L of concentrated B. anthracis in 1991, all of which was subsequently destroyed. Concern about the use of anthrax spores as a biologic weapon was heightened dramatically in 1979 when an epidemic of inhalation anthrax occurred downwind of a weapons research facility in Sverdlovsk, Russia, with cases occurring up to 50 km away and almost 6 weeks after the release. Indeed, anthrax was used as a biologic weapon in 2001 when anthrax spores were disseminated via the U.S. Postal Service along the Eastern Seaboard of the United States. Twenty-two cases of anthrax were identified, half of which were inhalation type anthrax and half cutaneous, resulting in five fatalities among those with inhalation anthrax. 608

Transmission Anthrax infection occurs by three methods: contact with broken skin, inhalation of spores, and ingestion. Naturally occurring infections are due mainly to contact with infected animals or animal products, such as hides or poorly cooked meats. Historically, the number of inhaled spores required to cause infection in 50% of individuals was thought to be approximately 10,000. More recent data suggest that as few as 1 to 3 spores may be sufficient to cause disease, depending on particle size. This estimate is tempered somewhat by the observation that many hide and wool workers are exposed to high concentrations of aerosolized spores on an ongoing basis with subsequent infection occurring only in a minority of individuals. There is no person-to-person transmission of anthrax, with the exception of the cutaneous form, which can be spread by skin contact.

Virulence The virulence of anthrax is dependent on its ability to produce three distinct proteins: lethal factor (LF), protective antigen (PA), and edema factor (EF). Edema toxin, formed when edema factor and protective antigen bind, interferes with water homeostasis, causing severe, localized edema seen in cutaneous anthrax. Edema toxin also inhibits neutrophil function, impairing the host’s ability to defend itself against infection. Lethal toxin is also composed by the binding of two subunits: the lethal factor and protective antigen. Lethal toxin is responsible for, among other things, the release of TNFalpha and interleukin B-1, which are responsible for the systemic reaction leading rapidly to death. One area of investigation has been the search for an inhibitor that can block the binding of protective antigen with lethal factor and edema factor, thus preventing the formation of lethal toxin and edema toxin.

Inhaled Anthrax Inhaled anthrax is the most serious form likely to occur after a bioterrorism event. Inhalational anthrax victims typically present 1 to 5 days after exposure, with a median incubation time of 4 days.1 However, cases have

occurred up to 6 weeks after exposure to anthrax spores (thus the suggestion for prolonged prophylaxis). Inhaled anthrax does not cause a true pneumonia. Rather, the lungs act only as a portal for infection. After the inhalation of anthrax spores into the alveoli, the spores are picked up by macrophages that transport them to the mediastinal and peribronchial lymph nodes. Activated spores divide rapidly, causing hemorrhagic mediastinitis and subsequent dissemination to the rest of the body via the blood, causing toxemia and sepsis.2 Presenting complaints are that of a nonspecific flulike illness, often including occasional nonproductive cough, fevers, chills, sweats, malaise, myalgia, and chest discomfort. Rhinorrhea is notably absent. If untreated, this prodrome can last for 48 to 72 hours, after which the patient’s condition may improve before a severe and precipitous decline. Within 24 to 48 hours of the onset of respiratory disease, patients develop bacteremia, with disease progression to hemorrhagic mediastinitis, pleural effusions, and septic shock. Patients often become dyspneic and cyanotic, with increasing chest and/or abdominal pain and diaphoresis. Stridor may also be present because of obstruction of the trachea by enlarged lymph nodes. Up to 50% of patients with pulmonary anthrax develop meningitis with associated subarachnoid hemorrhages. The detection of hemorrhagic cerebrospinal fluid with gram-positive bacilli and polymorphonuclear pleocytosis can aid in making the diagnosis.3 Chest radiographs characteristically show a widened mediastinum with pleural effusions and relative sparing of the lung parenchyma. Computed tomography (CT) of the chest should be considered if inhalation anthrax is suspected and the diagnosis is in doubt. CT scan is more sensitive and specific for detecting mediastinal lymphadenopathy, in which there is a normal white cell count or a mild leukocytosis with a left shift.4 The differential diagnosis of inhalational anthrax is wide and includes mycoplasma, influenza, legionella, tularemia, and psittacosis. Characteristics that differentiate anthrax from influenza and other influenza-like illnesses include the following: wide mediastinum on radiograph (70%), pleural effusion (80%), absence of rhinorrhea (only 10% of patients with anthrax infection will have rhinorrhea), absence of sore throat (found in only 20%), dyspnea (80%), and nausea and/or vomiting (80%). Before September 2001, inhalation anthrax was estimated to have a mortality rate of up to 95%. With modern antibiotics and aggressive supportive care, the mortality rate has been reduced to 50%. This reduction in mortality is attributed to prompt recognition of the disease, aggressive concomitant antimicrobial therapy, and improvements in supportive care techniques. However, in the face of a major attack, medical services will likely be overwhelmed and it will not be possible to provide intensive care for all cases. Thus, the mortality of cases may be higher than 50% and possibly approach 95%.

Cutaneous Anthrax As seen during 2001, cutaneous anthrax is likely to occur regardless of the mode of attack. Cutaneous anthrax represents 95% of background cases of anthrax in the United

States. Cutaneous anthrax presents as a painless pruritic papule generally appearing 1 to 7, but up to 12, days after exposure in an area of compromised skin integrity. Within 48 hours, vesicles containing a serosanguineous fluid surround the papule, with extensive associated edema. The vesicles rupture, necrose, and enlarge, forming the characteristic painless, black (hence “anthrax” from the Greek “anthracis,” or coal), ulcerated lesion. Debridement of such lesions should be avoided because this may facilitate bacteremia. However, with concurrent administration of antibiotics, this prohibition does not extend to diagnostic skin biopsies, which is part of the recommended evaluation for cutaneous anthrax.5 The eschar dries and falls off in 1 to 2 weeks, leaving little or no scar. Lymphangitis and painful lymphadenopathy associated with systemic symptoms occur in some patients. Mortality is due to systemic invasion and may be as high as 20% of those with cutaneous anthrax without treatment. Even though antibiotics do not affect the course of the local eschar, they can prevent systemic infection. The differential diagnosis of cutaneous anthrax includes ecthyma gangrenosum, brown recluse spider bite, orf, and glanders among others. The presence of purulence suggests an etiology other than anthrax unless there is a secondary infection.

Gastrointestinal Anthrax Gastrointestinal anthrax occurs 2 to 5 days after ingestion of poorly cooked, contaminated meat or poisoned food sources. Patients generally develop ulcers in the mouth, esophagus, terminal ileum, or cecum. Symptoms initially include nausea, vomiting, fever, and abdominal discomfort that progress rapidly to bloody diarrhea and signs suggestive of peritonitis. Gastric ulcers with associated hematemesis, hemorrhagic mesenteric lymphadenitis, and massive ascites may also occur.6 Gastrointestinal anthrax can mimic an acute abdomen, ascites with peritonitis, and a perforated viscus. The mortality rate of gastrointestinal anthrax approaches 100%. It has been suggested that early aggressive therapy may reduce the mortality rate. However, the diagnosis is often overlooked until the patient’s condition is already terminal.

Specimen Collection and Organism Identification Anthrax is so prolific that the organism may be seen on a Gram stain of blood. Cultures of blood, pleural fluid, and cerebrospinal fluid may be used to identify the organism in suspected cases. Surveillance cultures in exposed individuals (e.g., nasal swabs) are used as an epidemiologic tool and should not be routinely obtained. If possible, cultures should be obtained prior to the initiation of antibiotic therapy, since blood can be sterilized after only one or two doses of antibiotics. The organism can be easily cultured on 5% sheep blood agar or MacConkey’s agar; growth can be expected in 6 to 24 hours. Treatment should be initiated on clinical grounds. Withholding treatment while waiting for culture results will lead to increased mortality. Although initial identification of the organism can be done in a local laboratory, specialized BACILLUS ANTHRACIS (ANTHRAX) ATTACK 609

testing must be done in one of the laboratories certified to do so. More information about these laboratories is available at www.bt.cdc.gov/labissues. Identification of anthrax spores at the site of an attack is problematic. Handheld identification devices generally require 10,000 or more spores. Additionally, there is a cross-reactivity between B. cereus and other bacillus species. Several rapid identification techniques have been developed since 2001, including a nucleic acid-based test that can identify as few as 10 spores within 4 hours,a polymerase chain reaction (PCR) based test, and others. Autonomous detection systems (ADS) that perform a PCR or immunoassay test at a defined interval (e.g., 1.5 hours) have been developed for anthrax and are being deployed in 300 high-speed mail handling facilities. Further details about ADS, including necessary criteria for deployment, can be found at the Centers for Disease Control and Prevention Web site (www.cdc. gov/mmwr/preview/mmwrhtml/rr53e430-2a1.htm).

TABLE 102-1

Isolation There are no data suggesting that person-to-person transmission of inhalational anthrax occurs;hence,patients with suspected anthrax may be hospitalized in a standard hospital room with standard universal precautions. Contact precautions should be used with patients who have cutaneous lesions because direct exposure to vesicle secretions of such lesions may result in secondary cutaneous infection.7

MEDICAL TREATMENT OF CASUALTIES Guidelines for therapy are subject to change and may vary at the time of an anthrax attack. This is because weaponized B. anthracis may be engineered to be resistant to multiple antibiotics. A summary of current treatment suggestions is found in Tables 102-1 and 102-2.

INHALATIONAL ANTHRAX TREATMENT PROTOCOL*,† FOR CASES ASSOCIATED WITH BIOTERRORISM ATTACK

CATEGORY

Adults

INITIAL THERAPY (INTRAVENOUS)‡§ Ciprofloxacin 400 mg every 12 hrs* or Doxycycline 100 mg every 12 hrs¶ and One or two additional antimicrobials§

Children

Ciprofloxacin 10-15 mg/kg every 12 hrs **,†† or Doxycycline:¶,‡‡ >8 yrs and >45 kg: 100 mg every 12 hrs >8 yrs and 45 kg: 100 mg po BID >8 yrs and 45 kg: 100 mg every 12 hrs >8 yrs and 45 kg: 100 mg po BID >8 yrs and ≤45 kg: 2.2 mg/kg po BID ≤8 yrs: 2.2 mg/kg po BID

60 days

Children

60 days

* Ciprofloxacin dose should not exceed 1 g per day in children. (From Morb Mortal Wkly Rep. 2001; 50:909-19.)

on the Centers for Disease Control and Prevention’s Web site at www.bt.cdc.gov.

UNIQUE CONSIDERATIONS Isolation of the source of infection may be valuable for public health and law enforcement officials. If, for example, an envelope is the source of infection, the source

CASE PRESENTATION An envelope containing anthrax is sent to a member of Congress. There are several infected individuals. Other sources of anthrax are found in the mail throughout the country. Because of concern about anthrax, every person who finds a white powder presents to the emergency department convinced he or she needs antibiotic prophylaxis for anthrax or at least cultures, as do close relatives and co-workers and everyone who was in the mall last Saturday when someone scattered baking soda. The emergency department is overwhelmed by the walking well.What are some of the steps necessary to manage this event?

612 BIOLOGIC EVENTS

should be placed in a plastic bag. If a plastic bag is not available, the source should be covered with a sheet or other barrier. All windows in the infected building should be closed, the ventilation system should be turned off, and exposed individuals should be instructed to remove possibly contaminated clothing and shower before presenting to the emergency department.

PITFALLS • Failure to remain vigilant. • Failure to treat for an adequate length of time and with multidrug regimens. • Failure to consider inhalation anthrax as the cause of flulike symptoms. • Failure to notify appropriate authorities in suspected or confirmed cases of anthrax. REFERENCES 1. Dixon TC, Meselson M, Guillemin J, Hanna PC. Anthrax. New Engl J Med. 1999;341:815-26. 2. Inglesby TV, Henderson DA, Bartlett JG, et al. Anthrax as a biological weapon: medical and public health management [Erratum appears in JAMA. 2000;283:1963]. JAMA. 1999;281:1735-45. 3. Friedlander AM. Anthrax: clinical features, pathogenesis, and potential biological warfare threat. In: Remington JS, Swartz MN, eds. Current Clinical Topics in Infectious Disease. Vol. 20. Malden, Mass:Blackwell Science; 200:335-49. 4. Jernigian DB, Raghunathan PL, Bell BP, et al. Investigation of bioterorism-related anthrax, United States, 2001: epidemiologic findings. Emerg Infect Dis. 2002;8:1019-28. 5. Update: investigation of bioterrorism-related anthrax and interim guidelines for clinical evaluation of persons with possible anthrax. Morb Mortal Wkly Rep. 2001;50:941-8. 6. Swartz MN. Recognition and management of anthrax—an update. New Engl J Med. 2001;345:1621-6. 7. Anonymous. Bioterrorism alleging use of anthrax and interim guidelines for management—United States, 1998. Morb Mortal Wkly Rep. 1999;48:69-74. 8. Bell DM, Kosarsky PE, Stephens DS. Conference summary: clinical issues in the prophylaxis, diagnosis and treatment of anthrax. Emerg Infect Dis. 2002;8:222-5. 9. Centers for Disease Control and Prevention. Use of anthrax vaccine in response to terrorism: supplemental recommendations of the Advisory Committee on Immunization Practices. MMWR Morb Mortal Wkly Rep. 2002;51(45):1024-6. 10. Centers for Disease Control and Prevention. Update: investigation of anthrax associated with intentional exposure and interim public health guidelines, October 2001. MMWR Morb Mortal Wkly Rep 2001;50:889-97. 11. APIC Bioterrorism Task Force, Centers for Disease Control and Prevention Hospital Infections Program Bioterrorism Working Group. Bioterrorism Readiness Plan: A Template for Health care Facilities. Available at: http://www.cdc.gov/ncidod/hip/ Bio/13apr99APIC-CDCBioterrorism.PDF.

chapter 103

Yersinia Pestis (Plague) Attack Jeremiah D. Schuur and Jonathan Harris Valente

DESCRIPTION OF EVENT A bioterrorism event leading to multiple cases of the plague would likely result from airborne dispersal of a weaponized form of Yersinia pestis and would cause a pulmonary variant of the plague called pneumonic plague.1 During World War II, in two separate incidents, the Japanese dropped clay pots filled with Y. pestis–contaminated rice and fleas over the Chinese cities of Shusien in Chekiang province and Changteh in Hunan province. This tactic led to outbreaks of bubonic plague.2,3 However, this would not be the optimal way for terrorists to spread the plague because bubonic plague requires a bite from a flea. In addition, bubonic plague is not spread directly from person to person like the pneumonic form. Pneumonic plague may occur as a secondary pneumonia due to hematogenous spread from bubonic plague. This is the most common form of naturally occurring pneumonic plague. Primary pneumonic plague occurs after inhalation of aerosolized Y. pestis bacilli, either from person-to-person transmission or via an intentional attack. Pneumonic plague is rapidly progressive and can spread from person to person via aerosolized droplets. The incubation period for pneumonic plague (1 to 6 days) is shorter than that of the bubonic form (2 to 8 days).4,5 Control of the disease would be complex because affected people without knowledge of the exposure could spread disease by travel to other regions.6–8 Pneumonic plague presents clinically as a rapidly progressive respiratory syndrome that is often associated with fever, cough, shortness of breath, chest pain, hemoptysis, malaise,myalgia,nausea and vomiting,sputum or blood cultures with gram-negative rods,and radiographic findings of pneumonia. Chest roentgenograms of patients with pneumonic plague usually show patchy bronchopneumonic infiltrates as well as segmental or lobar consolidation with or without confluence. They may show cavitary lesions or bilateral diffuse infiltrates characteristic of acute respiratory distress syndrome.9 It has been estimated that if 50 kg of weaponized Y. pestis were released as an aerosol over a city of 5 million people, pneumonic plague could occur in as many as 150,000 persons, 36,000 of whom would be expected to die.10

PREINCIDENT ACTIONS An intentional plague outbreak should be considered one of the most likely bioterrorism scenarios for which emergency providers need to prepare. Pneumonic plague would most likely occur naturally as a complication of bubonic plague in the setting of a major bubonic plague outbreak.11 Y. pestis is not stable in the environment, and it is readily destroyed by drying and sunlight exposure. If Y. pestis were released into the air in a bioterrorism attack, it would likely survive for less than an hour. Due to these factors, preparation for environmental decontamination is less important than in other similar attacks, such as with anthrax.7,8,10 No vaccine is currently available. The U.S. manufactured vaccine (Greer) was discontinued in 1999 and was not protective for the pneumonic form of the plague. Research is under way, and a new vaccine protective against pneumonic plague is in advanced development.6,8 There are no early warning systems for the detection of Y. pestis if an aerosolized form were dispersed. In addition, there are no rapid diagnostic tests to detect Y. pestis in suspected patients.8,12

POSTINCIDENT ACTIONS All cases of pneumonic plague should be considered terrorism-related until proven otherwise. Hospital infection control officers and local and state, national health, and law enforcement officials should be notified immediately of any suspected cases of the plague. The risk for reaerosolization of Y. pestis from the contaminated clothing of exposed persons is low. Under ideal conditions, Y. pestis can survive in the environment for about 1 hour, and since patients will present with symptoms after 24 hours, there is no need for routine decontamination. In situations where there may have been recent, gross exposure to Y. pestis, decontamination of skin and potentially contaminated fomites (e.g., clothing or environmental surfaces) may be considered to reduce the risk of cutaneous or bubonic forms of the disease. The plan for decontaminating patients may include several steps. Patients should be instructed to remove contaminated clothing. Clothing should be stored in 613

labeled, plastic bags and gently handled to avoid dispersal of Y. pestis. Patients should be instructed to shower thoroughly with soap and water. Environmental surface decontamination may be performed using an Environmental Protection Agency–registered, facility-approved sporicidal/germicidal agent or a 0.5% hypochlorite solution (one part household bleach added to nine parts water).1,13,14 In its natural form, pneumonic plague is transmitted person to person via large droplets (not via fine-particle aerosol) and requires close personal contact (2 meters or less) for effective transmission.4,15,16 Patients with symptoms suggestive of pneumonic plague should be isolated using droplet precautions in addition to standard precautions. Patients with suspected pneumonic plague should be placed in a private room when possible. It is appropriate to cohort symptomatic patients with similar symptoms and the same presumptive diagnosis (i.e., pneumonic plague) when private rooms are not available. Maintain spatial separation of at least 3 feet between infected patients and others when cohorting is not possible. Avoid placement of patients requiring droplet precautions in the same room with an immunocompromised patient. Special air handling is not necessary, and doors may remain open. Patient transport should be limited to essential medical purposes. When transport is necessary, minimize dispersal of droplets by placing a surgical-type mask on the patient. Isolation precautions should be continued for 2 days after initiation of antibiotics and until some clinical improvement occurs in patients with pneumonic plague.8

MEDICAL TREATMENT OF CASUALTIES Specific antibiotic treatment must be initiated within 24 hours after symptom onset, otherwise pneumonic plague is nearly uniformly fatal.6,8 Table 103-1 shows the Working Group on Civilian Biodefense’s antibiotic recommendations for pneumonic plague.8 These consensus-based recommendations cover contained exposures, mass casualty exposures, and postexposure prophylaxis. They are based on the best available evidence. However, it should be noted that there is a lack of published trials in treating plague in humans and a limited number of studies in animals. A number of possible therapeutic regimens for treating plague have not been prospectively studied or approved by the Food and Drug Administration. In a contained casualty setting, parenteral antibiotics are recommended for all symptomatic patients. In a mass casualty incident, local resources must be evaluated and if sufficient supplies of parenteral antibiotics are not available, oral antibiotics may be used. Oral antibiotics should also be given for 7 days as postexposure prophylaxis. Individuals refusing postexposure antibiotics should be observed for fever or cough for 1 week, although isolation is not recommended.6,8 Several antibiotics that should not be used for pneumonic plague include rifampin, aztreonam, ceftazidime, cefotetan, and cefazolin.20 614 BIOLOGIC EVENTS

Laboratory testing is needed to confirm pneumonic plague. A sputum Gram stain should be used emergently because it may reveal bipolar staining gram-negative bacilli or coccobacilli. Y. pestis is described as having a bipolar (also termed “safety pin”) staining best seen with Giemsa or Wayson stains.21 The only gramnegative bacilli to cause rapidly progressing pulmonary symptoms are Y. pestis and Bacillus anthracis. Blood or sputum cultures should demonstrate growth within 24 to 48 hours, although some laboratory systems may misidentify Y. pestis. 22 Laboratory personnel should be notified when Y. pestis is suspected to decrease the chance of laboratory exposure and to increase the diagnostic yield. Biosafety Level 2 conditions are acceptable for routine laboratory procedures.8 Serologic tests are useful for bubonic plague, but since patients do not seroconvert until between 5 and 20 days postexposure, they would be of little use in a pneumonic plague outbreak.4 Due to the severity of pneumonic plague, patients may require advanced supportive measures including mechanical ventilation, pressors, and invasive monitoring. Clinical deterioration despite appropriate antimicrobial treatment should raise the possibility of an antimicrobial-resistant strain of Y. pestis. This has been reported to occur naturally as well as via genetic engineering by Soviet scientists.23

UNIQUE CONSIDERATIONS Y. pestis must be considered one of the most likely bacteria to be used as a bioterrorism agent. Y. pestis has been used as a biowarfare agent throughout history, it is readily available worldwide in nature and biologic laboratories, and mass production is relatively simple. Although aerosolized Y. pestis is not known to have ever been used, it has been successfully weaponized by the former Soviet Union and could be effectively dispersed as an aerosol.8,23 Under proper conditions, such a release could lead to widespread epidemic pneumonic plague with continued human-to-human transmission. Cases would not present for at least 24 hours after exposure. Pneumonic plague is highly contagious and virulent, and antimicrobial treatment must be initiated within 24 hours to improve survival. Without appropriate antibiotic treatment and supportive care, numerous casualties would result.

PITFALLS • Failure to notify appropriate public health and law enforcement agencies when an outbreak of pneumonic plague is suspected or confirmed • Failure to consider pneumonic plague as the etiologic agent in major pneumonia endemics or pandemics • Failure to use droplet precautions and standard precautions in potential cases of pneumonic plague • Failure to initiate specific antibiotic therapy within 24 hours of symptom onset • Failure to provide postexposure antibiotic prophylaxis

TABLE 103-1 RECOMMENDATIONS FOR ANTIMICROBIAL TREATMENT OF PNEUMONIC PLAGUE* PATIENT CATEGORY

RECOMMENDED THERAPY

Contained Casualty Setting Adults

Children⎪⎪

Pregnant women¶

Preferred choices Streptomycin, 1 g IM twice daily Gentamicin, 5 mg/kg IM or IV once daily or 2 mg/kg loading dose followed by 1.7 mg/kg IM or IV 3 times daily† Alternative choices Doxycycline, 100 mg IV twice daily or 200 mg IV once daily Ciprofloxacin, 400 mg IV twice daily‡ Chloramphenicol, 25 mg/kg IV 4 times daily§ Preferred choices Streptomycin, 15 mg/kg IM twice daily (maximum daily dose, 2 g) Gentamicin, 2.5 mg/kg IM or IV 3 times daily† Alternative choices Doxycycline, If >45 kg, give adult dosage If 50 cfu/mL).7 In addition, no effective vaccine currently exists, and successful treatment requires broad-spectrum, potent antibiotics. Because of the variable presentations of melioidosis,the unpredictable incubation period, and the possibility that many carriers will remain asymptomatic, the medical and public health community may not recognize a bioterrorist attack involving B. pseudomallei until the organism is cultured from acutely septic persons. The attack would likely involve aerosolization of media containing B. pseudomallei and distributing it over a heavily populated, urban area. Over a period of days to weeks, affected persons would visit healthcare facilities with symptoms ranging from fevers, chills, and cough to fulminant multisystem organ failure. The diagnosis of melioidosis in the absence of travel to an endemic area should be presumed to be evidence of bioterrorism until proven otherwise, and appropriate authorities should be notified. The outcome of infection with B. pseudomallei depends on a balance between the virulence of the organism, the size of inoculum, the point of entry, and the underlying immunologic status of the host. During a bioterrorist event, immunologically compromised hosts

and those who received the largest inoculum would likely be the first to manifest symptoms and would develop the most severe illness. Long periods of latency (up to 29 years) have been reported before the disease becomes clinically apparent.8 Melioidosis septicemia typically presents with high fever and rigors, although some patients will present with a recurrent fever. About half of patients will have a primary focus of infection, typically in the lung or skin. Patients may develop confusion, jaundice, and diarrhea. They often develop diffuse metastatic foci, acidosis, and shock, and many die within 48 hours. Poor prognostic features include absence of fever, leukopenia, azotemia, and abnormal liver function test results.3 The disease is characterized by abscess formation.9 The lung is the most commonly affected organ, and lung abscesses may rupture into the pleural space to cause empyema. The liver, spleen, kidney, and prostate are also common sites for abscess formation. In one third of children with melioidosis in Thailand, the infection was found to present with acute suppurative parotitis.10 Melioidosis presents as brainstem encephalitis or flaccid paraparesis in 4% of cases from Northern Australia.11 Laboratory data may reveal anemia, leukocytosis with neutrophilic predominance, evidence of hepatic and renal impairment, and coagulopathy. An abnormal chest x-ray is found in up to 80% of patients, most commonly with widespread, nodular shadowing.8 B. pseudomallei can be readily cultured from infected sites or the blood.12 Cultures should be grown on routine blood agar and Ashdown’s selective medium. The median time taken to obtain a positive blood culture result is 48 hours. Latex agglutination tests based on monoclonal antibodies to lipopolysaccharide can then be undertaken for definitive identification.13

PREINCIDENT ACTIONS Preparation for a mass-casualty event requires coordination of local, state, and federal officials and resources. Cities, hospitals, and emergency departments should have disaster plans developed and tested before the advent of a terrorist attack. The diagnosis of melioidosis in the absence of travel to an endemic area should be presumed to be evidence of bioterrorism until proven otherwise, and appropriate authorities should be notified. In the event of large numbers of people presenting with symptoms suspicious for a bioterrorist attack, symptomatic persons should be isolated pending further investigation, and the CDC must be rapidly notified. Healthcare workers must remain vigilant in identifying trends that may correspond with an outbreak of melioidosis. These trends may become apparent over weeks to months, initially involving those with underlying, chronic illness and then possibly spreading to involve otherwise healthy persons presenting with skin infections, pneumonia, and multisystem organ failure. Mechanisms to detect progressively increased emergency department volume and symptom trends should continue to be developed and implemented, and further research into the development of a vaccine against melioidosis is warranted.

POSTINCIDENT ACTIONS Appropriate federal, state, and local healthcare authorities and the CDC must be notified if any clinician has a high level of suspicion of a melioidosis outbreak or if a confirmed case of melioidosis is diagnosed in an individual without a known history of travel to an endemic area. Implementation of disaster plans may be warranted if several cases are simultaneously reported or emergency department volume is noted to be significantly increased. Mobilization of resources including expansion of intensive care units and release of antibiotic stockpiles may be required.

MEDICAL TREATMENT OF CASUALTIES Patients presenting with melioidosis septicemia require aggressive supportive care, including hemodynamic and respiratory support and correction of volume depletion and shock. Abscesses should be drained whenever possible. The antibiotics of choice are ceftazidime, imipenem-cilastatin, or meropenem with or without trimethoprim-sulfamethoxazole.14-17 These should be given in full doses (1 g every 8 hours, or a dose appropriately adjusted for renal function or size) for 2 to 4 weeks, according to the clinical response. This should be followed by a 20-week course of doxycycline (100 mg twice a day) and trimethoprim-sulfamethoxazole (160 mg trimethoprim plus 800 mg sulfamethoxazole twice per day), which has been associated with a lower relapse rate than amoxicillin-clavulanic acid (500 mg amoxicillin/125 mg clavulanic acid three times a day). Prolonged oral antibiotics are needed to prevent relapse, which occurs in up to 23% of patients and is more common in patients who have more severe disease.17 Other agents with activity against B. pseudomallei include

CASE PRESENTATION Over the past week you have noted an increased volume of patients visiting your emergency department. You see a 28-year-old female with fever and cough. Her examination is notable for a temperature of 40˚C, heart rate of 140, respiratory rate of 28, blood pressure of 95/60, and oxygen saturation of 88% on room air. She has diffuse bibasilar crackles on her pulmonary examination and a diffuse pustular rash. Her laboratory results reveal a hematocrit of 24, a white blood cell count of 23 with a neutrophilic predominance, a creatinine level of 2.0, a glucose level of 433, and an international normalized ratio of 2.0. Her chest x-ray reveals widespread, nodular shadowing. Blood cultures are sent for evaluation; the patient is treated with oxygen, insulin, intravenous fluids, and antibiotics; and she is admitted to the intensive care unit. Meanwhile, intensive care units throughout the city are becoming overwhelmed. BURKHOLDERIA PSEUDOMALLEI (MELIOIDOSIS) ATTACK 651

ceftriaxone, aztreonam, doxycycline, and ticarcillin-sulbactam. The role of granulocyte colony-stimulating factor, which has also been used as adjunctive treatment in Australia, remains to be determined. Currently, no vaccine exists for melioidosis.

UNIQUE CONSIDERATIONS During a bioterrorist event, affected persons would present to healthcare facilities over a period of days to weeks with symptoms ranging from fevers, chills, and cough to fulminant multisystem organ failure. Because of the variable presentations of melioidosis, the medical and public health community may not recognize a bioterrorist attack involving B. pseudomallei organisms until the organism is successfully cultured. In addition, B. pseudomallei pneumonia could be confused with plague given a similar appearance of stained organisms, and the diffuse, pustular eruption could be confused with smallpox or varicella.18 Healthcare providers need to be aware that melioidosis should be treated with either ceftazidime, imipenem-cilastatin, or meropenem in the acute phase, and a prolonged antibiotic course is also required to prevent relapse.

PITFALLS Several potential pitfalls in response to an attack involving melioidosis exist. These include the following: • Failure to prepare for potential bioterrorist attacks prior to the event • Failure to consider melioidosis attack in the context of multiple persons presenting to healthcare facilities over a period of days to weeks with symptoms ranging from fevers, chills, and cough to fulminant multisystem organ failure • Failure to treat melioidosis with ceftazidime, imipenem-cilastatin, or meropenem in the acute phase, and a prolonged antibiotic course to prevent relapse • Failure to notify appropriate law enforcement and public health officials in the event of a suspected melioidosis attack or outbreak, or in the event of a con-

652 BIOLOGIC EVENTS

firmed case of melioidosis in a person without a known history of travel to an endemic area REFERENCES 1. White N. Melioidosis. Lancet 2003;361:1715-22. 2. Leelarasamee A, Bovornkitti S. Melioidosis: review and update. Rev Infect Dis. 1989;11:413-25. 3. Chaowagul W, White N, Dance D, et al. Melioidosis: a major cause of community-acquired septicemia in northeastern Thailand. J Infect Dis. 1989;159:890-9. 4. Horn J. Bacterial agents used for bioterrorism. Surg Infect. 2003;4:281-7. 5. Wuthiekanun V, Smith M, Dance D, et al. The isolation of Pseudomonas pseudomallei from soil in northeastern Thailand. Trans R Soc Trop Med Hyg. 1995;89:41-3. 6. Wuthiekanun V, Smith M, White N. Survival of Burkholderia pseudomallei in the absence of nutrients. Trans R Soc Trop Med Hyg. 1995;89:491. 7. Walsh A, Smith M,Wuthiekanun V, et al. Prognostic significance of quantitative bacteremia in septicemic melioidosis. Clin Infect Dis. 1995;21:1498-500. 8. Dance, D. Melioidosis. In: Cohen J, Powderly W, eds. Infectious Diseases. 2nd ed. London: Mosby; 2004:1637-9. 9. Vatcharapreechasakul T, Suputtamongkol Y, Dance D, et al. Pseudomonas pseudomallei liver abscesses: a clinical, laboratory, and ultrasonographic study. Clin Infect Dis. 1992;14:412-7. 10. Dance D, Davis T, Wattanagoon Y, et al. Acute suppurative parotitis caused by Pseudomonas pseudomallei in children. J Infect Dis. 1989;159:654-60. 11. Currie B, Fisher D, Howard D, et al. Endemic melioidosis in tropical northern Australia: a 10-year prospective study and review of the literature. Clin Infect Dis. 2000;31:981-6. 12. Walsh A, Wuthiekanun V. The laboratory diagnosis of melioidosis. Br J Biomed Sci. 1996;53:249-53. 13. Steinmetz I, Reganzerowski A, Brenneke B, et al. Rapid identification of Burkholderia pseudomallei by latex agglutination based on an exopolysaccharide-specific monoclonal antibody. J Clin Microbiol. 1999;37:225-8. 14. White N, Dance D, Chaowagul W, et al. Halving of mortality of severe melioidosis by ceftazidime. Lancet 1989;2:697-701. 15. Simpson A, Suputtamongkol Y, Smith M, et al. Comparison of imipenem and ceftazidime as therapy for severe melioidosis. Clin Infect Dis. 1999;29:381-7. 16. Cheng AC, Fisher DA, Anstey NM, et al. Outcomes of patients with melioidosis treated with meropenem. Antimicrob Agents Chemother. 2004;48:1763-5. 17. Chaowagul W. Recent advances in the treatment of severe melioidosis. Acta Trop. 2000;74:133-7. 18. McGovern T, Christopher G, Eitzen E. Cutaneous manifestations of biological warfare and related threat agents. Arch Dermatol. 1999;135:311-22.

chapter 116

Chlamydia psittaci (Psittacosis) Attack Hans R. House

DESCRIPTION OF EVENT Psittacosis, also known as parrot fever, is caused by Chlamydia psittaci, an obligate intracellular bacterium. Clinical cases of psittacosis are sporadic and have a worldwide distribution. Approximately 100 to 200 cases are reported annually in the United States.1 The true incidence, however, is likely higher. Since psittacosis carries a nonspecific presentation and is difficult to culture, many cases go unnoticed or are simply attributed to “atypical pneumonia.” The association of bird ownership or bird exposure with psittacosis is well known. Parrots, parakeets, cockatiels, and canaries are the species most commonly associated with C. psittaci infection. More than 130 avian species have been documented as hosts of C. psittaci, including pigeons, sparrows, ducks, egrets, chickens, and turkeys.2 Not all cases of human psittacosis derive from avians; case reports describe transmission from infected sheep, cattle, cats, and dogs.3,4 Human-to-human transmission has been described, but it is rare.5 C. psittaci is categorized as a Centers for Disease Control and Prevention (CDC) class B biologic warfare agent for its potential to spread via aerosol and infect victims with a relatively low mortality rate.6 The United States, the former Soviet Union, and Egypt have all conducted research into its use as a weapon, but none is known to have deployed it. To date, no known incidents of intentional infection by C. psittaci have occurred.7 The few incidents of large-scale outbreaks of psittacosis involved the distribution or industrial processing of birds. The largest outbreak, from 1929–1930, involved 750 to 800 cases and was linked to the importation of exotic birds from Argentina to Europe and the United States. Epidemiologic data from the 1970s and 1980s in the United Kingdom, the United States, and Sweden show a direct relationship between increased importation of exotic birds and rising numbers of cases of psittacosis.8,9 More recent outbreaks occurred in workers at a duck farm and at turkey processing facilities.10–12 C. psittaci is usually acquired by inhalation or direct contact with the infectious discharges from infected animals. Infected birds may transmit the disease while asymptomatic, but the greatest number of organisms is expressed during periods of obvious illness (shivering, emaciation, anorexia,

dyspnea, and diarrhea). Since the discharge from the beaks and eyes,feces,and urine are all infectious,feathers and dust in and around the birds’ cages become infectious.13 Aerosolization of infectious material, such as bird excreta, is one possible route of infection that might be attempted in a biologic attack. However,a weaponized agent could also be used. According to Bill Patrick, who headed a component of the U.S. biologic weapons program at Fort Detrick, Md., in the 1950s and 1960s,C. psittaci was high on the list to be produced and stockpiled as a biologic weapon just before President Richard Nixon terminated the program in 1969 (Bill Patrick, personal communication, July 30, 2004). The organism, measuring 300 nm in its infectious form (or elementary body), is resistant to drying and may be viable for up to 1 week at room temperature.14 After inhalation of C. psittaci and establishment of an infection in the epithelial cells of the lower respiratory tract, psittacosis may follow one of two routes of pathogenesis. Direct local invasion of the pulmonary parenchyma results in a disease with a relatively short incubation period (1 to 3 days). More commonly, a primary bacteremia leads to infection of the reticuloendothelial cells of the liver and spleen. This results in an incubation period of 1 week to 15 days. Based on this bimodal pathogenesis, it can be presumed that a biologic attack on a large population would lead to an epidemic with two spikes in cases. The first, smaller peak would occur only days after the attack, and a second, larger peak may be seen 1 to 2 weeks after the release of the agent. Cases would probably go unnoticed initially. Although there may be clues on history and physical examination, psittacosis does not have a distinctive presentation; it usually presents as an atypical pneumonia with varying degrees of severity—from an unapparent mild disease to a severe, life-threatening systemic illness and respiratory failure. Untreated, up to 20% of cases may be fatal. With proper treatment,however,the mortality rate is around 1%. The most common symptoms of psittacosis are cough, fever, headache, and vomiting. Most patients (about two thirds) describe a dry cough with scant sputum. Malaise, anorexia, and diarrhea are also common symptoms. Many other symptoms have been associated with cases of C. psittaci infection, including photophobia, tinnitus, ataxia,deafness,sore throat,hemoptysis,epistaxis,and rash. 653

Typical findings on physical examination include fever, rales, consolidation, and tachypnea.15,16 Two unusual findings that may alert the examiner to the possibility of psittacosis are splenomegaly and relative bradycardia (a normal heart rate in the presence of a high fever). Many other signs have also been described in reviews of psittacosis cases. These include somnolence, confusion, pleural rub, adenopathy, palatal petechiae, herpes labialis, and Horder’s spots. Horder’s spots are pink, blanching maculopapular eruptions similar to the rose spots seen in typhoid fever. As the disease progresses, multiple systemic complications may develop (see Postincident Actions). The most important laboratory finding involves the chest x-ray, which usually demonstrates a variable degree of consolidation. Most often, this consolidation exceeds the clinical severity of the patient. The white blood cell count is usually normal, but often demonstrates a left shift. More than one-half of patients have moderately elevated transaminases levels, and many demonstrate mild hyponatremia. Although isolation of the organism from the blood in cell culture is possible, it can be difficult and is dangerous for laboratory personnel. The preferred method of diagnosis is by serology; antibodies are measured by complement-fixation (CF) or microimmunofluorescence (MIF) during the acute illness and after recovery. A single convalescent titer of 1:32 in a patient with a compatible clinical picture is considered by the CDC to be a presumptive case. A four-fold rise in titer between acute and convalescent specimens in a consistent clinical setting is defined as a confirmed case. The presence of IgM antibody to C. psittaci in either specimen is also considered to be a confirmed case.17

PREINCIDENT ACTIONS A biologic attack with psittacosis does not necessarily call for unique preparations. As with any potential incident, the emergency department, hospital, and local emergency services should have an integrated disaster response plan. This plan should provide for security and isolation of the treating facility; the triage of potential patients; a mechanism for liberating hospital beds and other treatment space; and the rapid recruitment of local police, fire, and healthcare personnel. Above all, the plan should provide for redundancy in communication methods—the element most commonly deficient in disaster scenarios. This plan should be reviewed and practiced annually. Person-to-person transmission of psittacosis has been documented, but no specific isolation beyond universal precautions is indicated. The treating hospital should have a sufficient supply of antibiotics (tetracycline or doxycycline [see Medical Treatment of Casualties]) available to initiate therapy in suspected cases. The disaster plan should then include a mechanism for recruiting more doses from local and state suppliers within 1 day. After 48 to 72 hours, the federal stockpiles should be mobilized to the affected area. The most significant challenge in addressing a C. psittaci attack is recognizing the event at all. A large 654 BIOLOGIC EVENTS

number of patients presenting with a nonspecific, febrile, respiratory illness would present over 1 to 2 weeks. Such a scenario would probably be interpreted as an influenza outbreak. Establishing a local or statewide syndromic surveillance system might assist in identifying psittacosis and other subtle biologic attacks using nonspecific diseases. A syndromic surveillance system that depends on observed rates of certain symptoms, such as cough, fever, or shortness of breath, would more rapidly detect a psittacosis attack than the conventional public health reporting system. A surveillance system that monitors pharmaceutical sales (such as the National Retail Data Monitor) may also be helpful. It may detect a spike in sales of antipyretics/analgesics or antitussives. The hospital laboratory should not be expected to culture C. psittaci. The CF or MIF test for C. psittaci should be readily available. If the local facility cannot provide these tests, it must provide for rapid referral of specimens to the next level in the Laboratory Response Network (LRN). The LRN laboratories are a defined hierarchy of increasingly specialized and sophisticated testing institutions available for the confirmation of suspicious agents.18 The earlier the outbreak is identified, the sooner specific treatment can be initiated. Early therapy of psittacosis is important to minimize mortality, prevent secondary and recurrent cases, and reduce the rates of systemic complications.

POSTINCIDENT ACTIONS If a case of psittacosis has been confirmed, the appropriate local public health authority should be notified (psittacosis is considered a reportable disease). In the event that multiple cases from different households are diagnosed, the possibility of a biologic attack must be considered. Alerting the disaster chain of command up to the federal level would be indicated. Isolation of patients is not necessary, but decontamination of the affected area may help prevent additional cases. Patients’ clothing should be discarded in a safe manner. Any surface possibly contaminated by infectious particles should be disinfected with 70% isopropyl alcohol or a 1:100 dilution of household bleach. Note that C. psittaci is susceptible to heat and most detergents, but it is resistant to acid and alkali. Avoid using a vacuum cleaner because it can aerosolize particles; sweep or wet mop the floor after spraying it with a disinfectant. The use of a N95 respirator and disposable protective clothing (gown, gloves, and mask) is advisable for those cleaning infectious dust. If the outbreak is associated with a known bird population, isolate or cull the birds. Infected avians can be successfully treated with medicated water or feed or can be administered antibiotics. Wash and disinfect all cages or other containment areas. After the initial acute cases have presented, the affected population can expect sporadic complications of systemic C. psittaci infection. In addition to the expected respiratory illness, psittacosis has been known to cause pericarditis, myocarditis, and “culture-negative” endocarditis. Unless the diagnosis is specifically sought,

a patient with C. psittaci endocarditis might be subjected to repeatedly negative evaluations, delaying definitive therapy and risking valve destruction. Psittacosis has also been associated with hepatitis and jaundice, glomerulonephritis, hemolytic anemia, pancytopenia, and disseminated intravascular coagulation. A reactive, polyarticular arthritis is seen 1 to 4 weeks after the initial illness. Neurologic complications are common and diverse. Cranial nerve palsies, cerebellar dysfunction, transverse myelitis, confusion, meningitis, encephalitis, and seizures have all been described. The lumbar puncture is usually normal, but the protein level may be greatly elevated.

• Failure to consider psittacosis as a possible diagnosis in a patient who does not have contact with birds • Failure to directly test for C. psittaci by serology in a patient with a history of bird contact or in a group of patients with similar, unexplained cases of “atypical pneumonia” • Failure to design, practice, and implement a disaster plan to cope with the increase in patient load seen during a biologic attack • Failure to stock adequate supplies of antibiotics or to request early mobilization of state and federal stockpiles • Failure to treat infected patients with a sufficient duration of therapy to prevent relapses

MEDICAL TREATMENT OF CASUALTIES Tetracyclines are the treatment of choice for psittacosis. Satisfactory response is seen with oral therapy and doxycycline 100 mg twice per day or tetracycline 500 mg four times per day. Intravenous treatment can be initiated in the severely ill with doxycycline 2.2 mg/kg (up to 100 mg) twice per day. Defervescence is expected after 24 to 48 hours of therapy. Treatment should continue for 10 to 14 days after the fever resolves. Relapses can occur, so adequate duration of therapy is essential. Although in vivo data are lacking, erythromycin is presumed to be the best alternative agent for patients with a contraindication to tetracyclines, such as children and pregnant women. Antibiotic prophylaxis is not specifically addressed by psittacosis infection control guidelines, but preventative therapy for exposed persons (doxycycline 100 mg by mouth once per day) was demonstrated to be effective in at least one outbreak.19 There is no vaccine for psittacosis in either humans or animals.

CASE PRESENTATION “Another Z PAK (azithromycin)?” you think, as you write yet another prescription for yet another case of atypical pneumonia. That makes three today alone. Add that to the four from the previous shift and the 12 cases last week, and this is starting to be the worst winter flu season in years. The only problem is that the calendar still reads September. The latest case is a 24-year-old female student complaining of a severe headache, fever, dry cough, sweats, and nausea for 5 days. On physical examination, you find bilateral crackles, splenomegaly, and photophobia, but no meningismus. Her chest x-ray reveals the same bilateral interstitial infiltrates that were seen in the other patients, and her laboratory results include moderately elevated transaminases levels. This prompts you to ask for further history; she denies smoking and alcohol or drug use. She also denies any recent travel, except to the state capital last week for a rock concert. By a strange coincidence, the last patient with pneumonia you treated also mentioned he had been at that particular concert.

UNIQUE CONSIDERATIONS REFERENCES Psittacosis is an unusual disease that is rarely seen. Every medical student recognizes it as the “pneumonia caused by living with a parrot.” But would this disease be considered in a large number of patients who lack a history of exposure to birds? Very little has been written about the use of C. psittaci as a biologic weapon, so most would probably consider other agents before testing for psittacosis. Clinical clues to the possibility of psittacosis include a respiratory illness with unusual systemic symptoms and signs. Severe headache, neurologic abnormalities or complications, splenomegaly, or elevated transaminases levels in a patient with x-ray findings consistent with atypical pneumonia should suggest psittacosis as a possible diagnosis.

PITFALLS • Failure to identify that a biologic attack has occurred; dismissing a spike in respiratory illnesses as a routine influenza outbreak

1. Gregory DW, Schaffner W. Psittacosis. Semin Respir Infect. 1997;12:7-11. 2. Macfarlane JT,Macrae AD. Psittacosis. Br Med Bull.1983;39:163-87. 3. Schlossberg D. Chlamydia psittaci (psittacosis). In: Mandell GL, Bennet JE, Dolin R, eds. Principles and Practice of Infectious Diseases. 4th ed. New York: Churchill Livingstone; 1995:1693-96. 4. Gresham AC,Dixon CE,Bevan BJ. Domiciliary outbreak of psittacosis in dogs; potential for zoonotic infection. Vet Rec. 1996;138:622-3. 5. Ito I, Ishida T, Mishima M, et al. Familial cases of psittacosis: possible person-to-person transmission. Intern Med. 2002;41:580-3. 6. U.S. Centers for Disease Control and Prevention. Emergency Preparedness & Response. Available at: http://www.bt.cdc.gov. 7. Davis JA. The looming biological warfare storm. Air Space Power J. 2003;17:57-68. 8. Wreghitt TG,Taylor CED. Incidence of respiratory tract chlamydial infections and importation of psittacine birds. Lancet. 1988; 8585:582. 9. Reeve RVA, Carter LA, Taylor N. Respiratory tract infections and importation of exotic birds. Lancet. 1988;8589:829-30. 10. Hinton DG, Shipley A, Galcin JW, et al. Chlamydiosis in workers at a duck farm and processing plant. Aust Vet J. 1993;70:174-6. 11. Hedberg K,White KE, Forfang JC, et al. An outbreak of psittacosis in Minnesota turkey industry workers: implications for modes of transmission and control. Am J Epidemiol. 1989;130:569-77. CHLAMYDIA PSITTACI (PSITTACOSIS) ATTACK 655

12. U.S. Centers for Disease Control and Prevention. Psittacosis at a turkey processing plant—North Carolina, 1989. Morb Mortal Wkly Rep. 1990;39:460-1. 13. Grimes JE. Zoonoses acquired from pet birds. Vet Clin. 1987;17:209-18. 14. U.S. Centers for Disease Control and Prevention. Psittacosis Surveillance, 1975-1984. Atlanta: Centers for Disease Control and Prevention, June 1987. 15. Yung AP, Grayson ML. Psittacosis—a review of 135 cases. Med J Aust. 1988;148:228-33.

656 BIOLOGIC EVENTS

16. Crosse BA. Psittacosis: a clinical review. J Infect. 1990;21:251-9. 17. U.S. Centers for Disease Control and Prevention. Compendium of measures to control Chlamydia psittaci infection among humans (psittacosis) and pet birds (avian chlamydiosis), 2000. Morb Mortal Wkly Rep Recomm Rep. 2000;49:RR-8,1-18. 18. Pavlin JA, Gilchrist MJR, Osweiler GD, Woollen NE. Diagnostic analyses of biological agent-caused syndromes: laboratory and technical assistance. Emerg Med Clin North Am. 2002;20:331-50. 19. Broholm KA, Bottiger M, Jernelius H, et al. Ornithosis as a nosocomial infection. Scand J Infect Dis. 1977;9:263-7.

chapter 117

Escherichia coli O157:H7 (Hemorrhagic E. Coli ) Attack Roy Karl Werner

DESCRIPTION OF EVENT Escherichia coli is a ubiquitous, gram-negative, rodshaped bacterium that can be located throughout the environment, including water and soil. It is most commonly found as normal flora of the intestinal tract of most mammals, including humans, where it lives to suppress growth of more harmful bacteria. In addition to the enterohemorrhagic E. coli, which is of concern as potential biologic weapons, there are four other types of E. coli that cause gastrointestinal disease.1 A detailed discussion of these is beyond the scope of this chapter. However, their characteristics are summarized in Table 117-1. E. coli O157:H7, an enterohemorrhagic strain, is considered a category B threat by the Centers for Disease Control and Prevention (CDC)2 since it is easily spread via the fecal-oral route3 and has moderate morbidity but low mortality. The O157:H7 serotype produces a Shiga-like toxin that can cause a significant inflammatory response within the intestines without direct invasion of cells. The toxin is encoded on a plasmid and can be readily passed from one bacterium to another.1 This bacterium is quite facile in its ability to obtain new genetic information and incorporate it into its arsenal for defense and infectivity in its hosts. E. coli O157:H7 can persist for significant lengths of time in hostile environments and may even require a slightly acidic environment to grow.4–6 Most E. coli 0157:H7 outbreaks are linked to fecal-oral transmission due to poor handwashing techniques and unhygienic food handling. Sources of human infection have included, among others, poorly cooked meat (especially hamburger), apple juice, water (including water parks), vegetables and fruit from salad bars, and milk products such as yogurt and unpasteurized milk.7–11 There are reported cases of aerosolized spread of E. coli, usually in sewage, but only under very specific circumstances and conditions. E.coli O157:H7 can infect anyone,but more severe symptoms are found among patients at the extremes of age or in immunocompromised individuals.12 The endotheliocidal properties of E. coli O157:H7 affect the intestinal endothelium as well as the renal and vascular endothelium, leading to the development of hemolytic uremic syndrome (HUS)

and thrombotic thrombocytopenic purpura (TTP).1,2,7,12–14 It is noteworthy that other enterohemorrhagic E.coli exist with different serotypes. Thus, a bioterrorism attack need not be of the 0157:H7 serotype. For purposes of this chapter,the term E.coli 0157:H7 will be used since it is the most common serotype, but the reader should understand that the clinical syndrome could be caused by other enterohemorrhagic serotypes as well. Symptomatic E. coli O157:H7 infection affects approximately 75,000 individuals in the United States yearly and was first identified as a human pathogen in 1982 when it was isolated in the stool of individuals who had eaten raw or undercooked meat. In 1993 there was an outbreak from hamburgers served at a regional fast food chain, causing HUS and several deaths.8,15,16 The incubation period of E. coli O157:H7 is between 3 and 9 days.6,14 Patients initially complain of symptoms similar to viral gastroenteritis: abdominal cramping with significant abdominal pain and tenderness; flatulence; elevated temperatures; and voluminous, watery diarrhea. The diarrhea eventually becomes bloody; 91% of patients report bloody stools at some time during the course of the disease. This likely overestimates the prevalence of bloody diarrhea since patients with less severe disease likely don’t present to physicians. Approximately 30% of symptomatic patients require hospitalization, and the mortality rate is approximately 1%. Shigella, Vibrio parahaemolyticus, Campylobacter, and Salmonella species; cancerous lesions; ulcerative colitis; incomplete obstruction; gastrointestinal bleeding; and recent antibiotic usage (e.g., for Clostridium difficile)13 should all be included in the differential diagnosis of hemorrhagic diarrhea. Treatment for E. coli O157:H7 infection is limited to supportive measures to prevent dehydration and other complications. The use of antibiotics is contraindicated and has been associated with increased incidence of hemolytic complications.2,7,13,14,17,18 Antimotility medications are appropriate in afebrile patients without bloody diarrhea. Early re-feeding of patients with a lactose-free diet can reduce the duration of diarrhea. The disease is generally self-limited and resolves approximately 1 week after the onset of symptoms. 657

TABLE 117-1 E.COLI CAUSING GASTROINTESTINAL SYMPTOMS TYPE OF GI DISORDER

SOURCE / GEOGRAPHY

TOXIN

INVASIVENESS

CLINICAL

DIARRHEA

Water sources

Cytotoxic heat stabile and/or heat labile

None; no cellular changes or bacteremia

No fever, mild dehydration, self-limited illness

Watery, voluminous; originates in proximal small bowel

Asia

Shigella-like

Epithelial cells of intestine

Fever, tenesmus, dehydration, abdominal cramps

Blood-tinged with many polymorphonuclear lymphocytes

Less developed countries

Some have a heat stabile

Aggregative adherence

No fever, mild dehydration, selflimited illness

Watery, nonbloody, and persistent

Nurseries

None

Adherence, causing effacement

No fever, acute-onset diarrhea in neonates, dehydration

Nonbloody

Foods, raw beef

Shiga-like

Effacement of intestinal mucosa

Vomiting, no fever, nausea, chills, HUS,TTP

First nonbloody, then grossly bloody

Enterotoxigenic Traveler’s diarrhea (children and travelers) Enteroinvasive Dysentery syndrome (children and adults) Enteroaggregative Children

Enteropathogenic Children and newborns Enterohemorrhagic Children and adults

HUS, Hemolytic uremic syndrome; TTP, thrombotic thrombocytopenic purpura

The most feared sequela of enterohemorrhagic E. coli is HUS, a triad of acute renal failure, thrombocytopenia, and microangiopathic hemolytic anemia. This is especially common in infants and children. Patients with the additional findings of fluctuating neurologic symptoms and fever are classified as having TTP. This may be more common in geriatric or infirm populations.19 Blood urea nitrogen (BUN) should be monitored because an increase may signal extraintestinal endothelial involvement and potential progression to TTP or HUS. Urine should also be monitored for hematuria and/or proteinuria, again suggesting progression to TTP or HUS. Discussion of the treatment of TTP and HUS is beyond the scope of this chapter. All E.coli is easily cultured on sorbitol-MacConkey agar. Laboratory analysis will seldom identify the causative organism unless E. coli O157:H7 is specifically sought. However, the CDC recommends that all stools from patients with bloody diarrhea be screened for the 0157:H7 serotype. Antisera to the O157:H7 antigen can be used to screen isolates. Any isolates that screen positive should be sent to a reference laboratory for further characterization. Isolation of the bacteria is most likely during the first 6 days of diarrhea. Many times the O157:H7 serotype cannot be isolated from even bloody diarrheal stools that commonly have high concentrations of this pathogen.20,21 Obtaining stool samples from multiple patients will increase isolation yield and assist with characterization of E. coli O157:H7 when present. Stool studies should include a search for other etiologic factors of the diarrheal disease, including those previously noted. Multiplex PCR (polymerase chain reaction using multiple primers) studies, fingerprinting, and rapid identification22,23 studies should be used to assist in determining the specific cause. If E. coli O157:H7 is identified, it is 658 BIOLOGIC EVENTS

mandatory that it be reported to the CDC; this allows centralized monitoring of outbreaks.

PREINCIDENT ACTIONS The greatest potential for limiting the impact of a terrorist attack involving the dissemination of E. coli O157:H7 is the readiness of the “front-line fighters” of the healthcare system—emergency medical personnel, outpatient clinics, and emergency departments. The presentation of an escalating number of patients with severe diarrheal disease along with similarities in medical, travel, or exposure history should alert medical and public health personnel to the possibility of a nonaccidental exposure.24 Continuous water and food production monitoring by the appropriate local, state, and federal agencies as well as routine testing and retesting of in-place barriers to terrorism by Homeland Security task forces25,26 will also contribute to the safety of citizens. Computer-aided programs, passive surveillance of foodstuffs, random testing of food processing areas, irradiation and filtration of airborne particles, and tighter control of treatment areas for national food and water supplies are all methods currently in place to decrease the impact of bioterrorism.24,26 Handwashing and glove use at patient points of contact or before handling foodstuffs are ways spread can be minimized.

POSTINCIDENT ACTIONS When an outbreak of E. coli O157:H7 infection is suspected, hospital laboratories should be alerted, and

agent-specific cultures of stool samples should be obtained. Stool samples can also be tested for fecal leukocytes,13,28 although results are not particularly sensitive or specific. Fecal lactoferrin assays have the potential to be beneficial but their utility is also debated; fecal lactoferrin is considered more specific for bacterial causes of diarrhea29 but cannot help with determining the specific etiologic factor. If the source of the outbreak can be readily identified, it should be contained and eliminated immediately. Foodstuffs in the area should be incinerated to decrease perpetuation of the infection.30,31 Surface areas can be decontaminated with a 5% to 10% bleach solution.

MEDICAL TREATMENT OF CASUALTIES Oral rehydration solutions are helpful in patients with E. coli O157:H7 infection since most patients have minimal vomiting. The World Health Organization recommends solutions containing: 2.6 g sodium chloride, 2.9 g trisodium citrate dihydrate, 1.5 g potassium chloride, and 13.5 g anhydrous glucose, all dissolved in 1 L of clean water for a total osmolarity of 245 mOsm/L solution.13,28,32–34 Appropriate infection control practices should be instituted for E. coli and include body substance isolation and handwashing. Masks are optional for E. coli because airborne spread is inconsequential (unless contaminated feces are aerosolized). Rehydration should include intravenous solutions if oral intake is poorly tolerated or if the patient fails to improve.

UNIQUE CONSIDERATIONS The relatively benign symptoms of fevers, abdominal cramping, and diarrhea are commonly minimized; therefore, E. coli O157:H7 infection is not suspected and thus fecal-oral spread continues before hemorrhagic diarrhea commences or E. coli O157:H7 infection is considered. Identification of E. coli O157:H7 requires specialized testing that may not be readily available at the local laboratory. Harbingers of a possible bioterrorism event with E. coli O157:H7 include a clustering of infectious diarrhea in a previously healthy population, all of whom have similar exposures (e.g., water, food). Travel to an area with a known outbreak of disease should also raise the clinician’s level of suspicion.24,35 REFERENCES 1. Eisenstein BI, Zaleznik DF. Enterobacteriaceae. In: Mandell GL, Bennett JE, Dolin R, eds. Principals and Practice of Infectious Diseases. 5th ed, vol 2. Philadelphia: Churchill Livingstone; 2000:2294-2310. 2. U.S. Centers for Disease Control and Prevention. General and Technical Information. Available at: http://www.cdc.gov/ncidod/ dbmd/diseaseinfo/escherichiacoli_g.htm. 3. Todar K. Todar’s Online Textbook of Bacteriology. Available at: http://www.textbookofbacteriology.net. 4. Rhee MS, Lee SY, Dougherty RH, et al. Antimicrobial effects of mustard flour and acetic acid against Escherichia coli O157:H7, Listeria

CASE PRESENTATION A carnival is in town for a July 4th celebration being held at an old farm that was recently converted into a recreational area. There are rides for all ages, games of skill, a large variety foods and fresh vegetables, and tents containing many attractions. Many of the town’s people attend the festivities, including significant numbers of the hospital staff. The carnival ends without incident. One week later a number of children seek care at their doctors’ offices with complaints of diarrhea and abdominal cramping. Most are sent home with antimotility drugs and prescribed a “BRAT” (bananas, rice, applesauce, toast) diet, and some are given oral antibiotics. There is also an increase in the number of geriatric visits for similar complaints. Three days later, these same people begin presenting to the emergency department due to bloody diarrhea and lethargy. Laboratory analysis is unremarkable, other than for mild leukocytosis and borderline electrolyte abnormalities. Some patients have elevated levels of protein and casts present on urinalysis. Many patients presenting to the emergency department with children or elderly family members are complaining of similar symptoms and easy bruisability. Laboratory studies on these otherwise healthy young adults show renal insufficiency and mild hemolytic anemia. Patients presenting with confusion or weakness are sent for computed tomography of the brain. An emergency medical technician in a town the carnival visited died approximately 2 weeks after the carnival left. She died from complications from treatment of severe dehydration and cerebral vascular accident. A husband and wife, both emergency medical technicians, who worked at a previous site the carnival visited also died after an infant son of theirs died. They all had a similar disease course as described above and had no predisposing factors. Individuals of a terrorist group obtained part-time employment with the carnival company cleaning animals or common areas. These areas all contained a pressurized watering system used to clean these sections. These areas were theorized to have enormous concentrations of the aerosolized (36) Escherichia coli O157:H7 for periods of time throughout the day, usually at times of patron egress through causeways of the carnival. Small Petri dishes were found at the encampment containing genetically identical E. coli O157:H7 by multiplex PCR evaluation. After a thorough investigation, the CDC strongly suspects that the carnival was the site of a bioterrorism attack where the perpetrators disseminated E. coli O157:H7 via food and water contamination.

monocytogenes, and Salmonella enterica serovar Typhimurium. Appl Environ Microbiol. 2003;69:2959-63. 5. Reinders RD, Biesterveld S, Bijker PGH. Survival of Escherichia coli O157:H7 ATCC 43895 in a model apple juice medium with different concentrations of proline and caffeic acid. Appl Environ Microbiol. 2001;67:2863-6. 6. Cody SH, Glynn MK, Farrar JA, et al. An outbreak of Escherichia coli O157:H7 infection from unpasteurized commercial apple juice. Ann Intern Med. 1999;130: 202-9. 7. U.S. Food and Drug Administration, Center for Food Safety & Applied Nutrition. Foodborne Pathogenic Microorganisms and Natural Toxins Handbook. The Bad Bug Book. Available at: http://www.cfsan.fda.gov/~mow/intro.html. ESCHERICHIA COLI O157:H7 (HEMORRHAGIC E. COLI ) ATTACK

659

8. Feng P. Escherichia coli serotype O157:H7: novel vehicles of infection and emergence of phenotypic variants. Emerg Infect Dis. 1995;1(2):47-52. 9. U.S. Centers for Disease Control and Prevention. Lake-associated outbreak of Escherichia coli O157:H7—Illinois, 1995. Morb Mortal Wkly Rep. 1996;45(21):437-9. 10. U.S. Centers for Disease Control and Prevention. Outbreaks of Escherichia coli O157:H7 infection and cryptosporidiosis associated with drinking unpasteurized apple cider—Connecticut and New York, October 1996. Morb Mortal Wkly Rep. 1997;45(21):4-8. 11. U.S. Centers for Disease Control and Prevention. Outbreak of Escherichia coli O157:H7 infections associated with drinking unpasteurized commercial apple juice—British Columbia, California, Colorado, and Washington, October 1996. Morb Mortal Wkly Rep. 1996;45(44):975. 12. Guerrant RL, Steiner TS. Principles and syndromes of enteric infections. In: Mandell GL, Bennett JE, Dolin R, eds. Principals and Practice of Infectious Diseases. 5th ed. Vol 1. Philadelphia: Churchill Livingstone; 2000:1080-5. 13. Hamer DH, and Gorbach SL. Infectious diarrhea and bacterial food poisoning. In: Feldman M, Scharschmidt BF, and Sleisenger MH. Editors. Gastrointestinal and Liver Disease. 6th ed. Vol 2. Philadelphia:WB Saunders; 1998:1594-1632. 14. Tauxe RV, Swerdlow DL, Hughes JM. Foodborne disease. In: Mandell GL, Bennett JE, Dolin R, eds. Principals and Practice of Infectious Diseases, 5th ed. Vol 1. Philadelphia: Churchill Livingstone; 2000:1150-65. 15. U.S. Centers for Disease Control and Prevention. Preliminary report: foodborne outbreak of Escherichia coli O157:H7 infections from hamburgers—Western United States, 1993. Morb Mortal Wkly Rep. 1993;42(4):85-6. 16. U.S. Centers for Disease Control and Prevention. Update: multistate outbreak of Escherichia coli O157:H7 infections from hamburgers—Western United States, 1992-1993. Morb Mortal Wkly Rep. 1993;42(14):258-63. 17. Weinstein RS, and Alibek K. Shigellosis. In: Biological and Chemical Terrorism—A Guide for Healthcare Providers and the First Responders. New York: Thieme Medical Publishers; 2003:96-7. 18. Weinstein RS, and Alibek K. Biological weapon syndromic crossreferences. In: Biological and Chemical Terrorism—A Guide for Healthcare Providers and the First Responders. New York:Thieme Medical Publishers; 2003:13. 19. Richards A, Goodship JA, Goodship TH. The genetics and pathogenesis of haemolytic uraemic syndrome and thrombotic thrombocytopenic purpura. Curr Opin Nephrol Hypertens. 2002;11(4):431-5. 20. Osterholm MT, Hedberg CW, Moore KA. Epidemiologic principles. In: Mandell GL, Bennett JE, Dolin R, eds. Principals and Practice of Infectious Diseases. 5th ed. Vol 1. Philadelphia: Churchill Livingstone; 2000:157-9. 21. Gill VJ, Fedorko DP,Witebsky FG. The clinician and the microbiology lab. In: Mandell GL, Bennett JE, Dolin R, eds. Principals and Practice of Infectious Diseases. 5th ed. Vol 1. Philadelphia: Churchill Livingstone; 2000:191-2.

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22. Vidal R, Vidal M, Lagos R, et al. Multiplex PCR for diagnosis of enteric infections associated with diarrheagenic Escherichia coli. J Clin Microbiol. 2004;42(4):1787-9. 23. Fratamico PM, Bagi LK, Pepe T. A multiplex polymerase chain reaction assay for rapid detection and identification of Escherichia coli O157:H7 in foods and bovine feces. J Food Prot. 2000;63(8):1032-7. 24. Burkle FM. Mass casualty management of a large-scale bioterrorist event: an epidemiological approach that shapes triage decisions. Emerg Med Clin North Am. 2002;20(2):409-36. 25. Kahn AS, Swerdlow DL, Juranek DD. Precautions against biological and chemical terrorism directed at food and water supplies. Public Health Rep. 2001;116(1):3-14. 26. Filoromo C, Macrina D, Pryor E, et al. An innovative approach to training hospital-based clinicians for bioterrorist attacks. Am J Infect Control. 2003;31(8):511-14. 27. Brickner PW,Vincent RL, First M, et al. The application of ultraviolet germicidal irradiation to control transmission of airborne disease: bioterrorism countermeasure (practice articles). Public Health Rep. 2003;118(2):99-114. 28. Lung E. Acute diarrheal diseases. In: Friedman SL, McQuaid KR, Grendell JH, eds. Current Diagnosis and Treatment in Gastroenterology. 2nd ed. New York: Lange Medical Books/ McGraw-Hill; 2003:131-50. 29. Huicho L, Campos M, Rivera J, Guerrant RL. Fecal screening tests in the approach to acute infectious diarrhea: a scientific overview. Pediatr Infect Dis J. 1996;15(6):486-94. 30. Bosilevac JM, Arthur TM, Wheeler TL, et al. Prevalence of Escherichia coli O157 and levels of aerobic bacteria and Enterobacteriaceae are reduced when hides are washed and treated with cetylpyridinium chloride at a commercial beef processing plant. J Food Prot. 2004;67(4):646-50. 31. Oldfield EC 3rd. Emerging foodborne pathogens: keeping your patients and your families safe. Rev Gastroenterol Disord. 2001;1(4):177-86. 32. World Health Organization. 13th Expert Committee on the Selection and Use of Essential Medicines, 31 March to 3 April 2003. Available at: http://whqlibdoc.who.int/trs/WHO_TRS_920.pdf. 33. World Health Organization. WHO Essential Medicines Library. Oral rehydration salts (for glucose-electrolyte solution). Available at: http://mednet3.who.int/EMLib/DiseaseTreatments/MedicineDetails. aspx?MedIDName=235@oral%20rehydration%20salts%20(for%20 glucose-electrolyte%20solution). 34. World Health Organization. Oral Rehydration Salts (ORS): A New Reduced Osmolarity Formulation. Available at: http://www.who. int/child-adolescent-health/New_Publications/NEWS/Statement. htm. 35. Weinstein RS, and Alibek K. Basic bioterrorism. In: Biological and Chemical Terrorism—A Guide for Healthcare Providers and the First Responders. New York: Thieme Medical Publishers; 2003: 2-12. 36. Teltsch B, Shuval HI, Tadmor J. Die-away kinetics of aerosolized bacteria from sprinkler application of wastewater. Appl Environ Microbiol. 1980;39(6):1191-7.

S E C T I O N

T E N

( P A R T

T W O )

Viral Agents

chapter 118

Viral Encephalitides (Alphaviruses) Attack Matthew Berkman and Kelly J. Corrigan

DESCRIPTION OF EVENT The Alphaviruses are one of the three families of the arthropod-borne viruses (arboviruses) that can cause encephalitis.Three Alphaviruses currently cause human disease in the United States: the Eastern equine encephalitis (EEE), Western equine encephalitis (WEE), and Venezuelan equine encephalitis (VEE) viruses. All three are transmitted through mosquitoes and can initially present as a flulike illness. The EEE virus is maintained through a bird-mosquito-bird lifecycle. The most important vector is the mosquito Culiseta melanura.1 These mosquitoes are often found in coastal areas and near freshwater swamps. Hence, most U.S. cases have been reported in Florida, Georgia, Massachusetts, and New Jersey. EEE has a high case fatality rate—35% reported by the Centers for Disease Control and Prevention (CDC). Of those who survive, an estimated 35% will have permanent mild to severe neurologic deficits. There have been approximately 200 human cases in the United States since 1964, with two fatalities in August 2004 in Massachusetts.2 The closely related WEE has a reported 10% case fatality rate. Like EEE, it is a summertime disease but is found in states west of the Mississippi River and in some western Canadian provinces. It is also maintained by a birdmosquito-bird lifecycle, with its primary vector the mosquito Culex tarsalis. The worst outbreak recorded was 3336 human cases in 1941. Since 1955, a varied range of 0 to 200 cases per year have been reported, with no human cases reported since 1994.1,2 VEE is found in South and Central America. It is maintained by a rodent-mosquito lifecycle and claims at least 10 mosquito species as its vector. The fatality rates have been approximately 0.6% in reported outbreaks. Past epidemics include 32,000 human cases in Venezuela from 1962-64, and in 1971, more than 10,000 horses died from a VEE epidemic. Human cases have been sporadic since then.1,2 All three of these Alphaviruses can present clinically with nonspecific flulike symptoms, but many may include high fever, headache, photophobia, stiff neck, nausea, and vomiting. In cases of encephalitic invasion, symptoms can progress to confusion, obtundation, seizures, and focal neurologic deficits.

PREINCIDENT ACTIONS Humans who live in high-risk areas or work or play outside frequently in these areas should be sure to wear mosquito repellant that contains DEET and wear longsleeved shirts and pants. During outbreaks, outdoor activity should be limited. Widely available vaccines are being developed and are undergoing validity testing. In preparation for potential biologic terrorist attacks, the Institute of Medicine Committee on Research and Development to Improve Civilian Medical Response recommends that major hospitals conduct mass casualty planning and training and that they have isolation rooms available for infectious diseases; have decontamination capacity; and be fully supplied with drugs, ventilators, and personal protective equipment. The committee also encourages the CDC to keep medical care providers up-to-date on current dangerous biologic materials.3

POSTINCIDENT ACTIONS All cases are to be reported to the CDC. Public health warnings are then issued, and prevention measures are initiated. Eradicating potential arthropod vectors and vaccinating equine reservoirs may help to prevent the spread of encephalitis in the event of a biologic attack.4 Since no person-to-person spread is know to be possible, only universal precautions must be maintained in patients infected with one of the arboviruses.4,5

MEDICAL TREATMENT OF CASUALTIES As in the case of most viral illnesses, treatment of the Alphavirus encephalitides consists primarily of supportive care.2,6–9 Patients suspected of having viral encephalitis should undergo a workup for concomitant meningitis with computed tomography of the head and lumbar puncture and be admitted to the hospital for further serologic testing. The airway should be protected; nutrition, fluids, and electrolytes should be optimized; pyrexia should be aggressively treated; and vigilance in preventing secondary infections should be maintained.7,9 In the 661

setting of increased intracranial pressure, patients should be managed in the intensive care setting with hyperventilation, head elevation, diuresis, and possibly steroids or intravenous immunoglobulin.9 Prevention of seizures is important, and consideration for administering temporary anticonvulsant therapy should be given.2 Consultation with a neurologist and infections disease specialist is recommended. Neurosurgical consultation may be necessary if a brain biopsy is considered.8 Although there is no specific medical treatment available for the arboviruses, the use of ribavirin and recombinant interferon alpha is being assessed.2,8 Prognosis depends not only on the particular type of arbovirus responsible for the encephalitis, but also on the age and prior health of the individual infected. Children 1 year old or younger and adults 55 years old or older are at increased risk of life-threatening complications.

UNIQUE CONSIDERATIONS Although the effects of Alphavirus encephalitis can be devastating with persistent neurologic sequela or death, the vast majority of patients exposed to these viruses will be asymptomatic or present with nonspecific flulike symptoms.4 An early Alphaviral attack will be difficult to identify and distinguish from routine “viral syndrome” due to the similarity of illness presentation and lack of routine laboratory testing for the viruses. The viral encephalitides are CDC category B biologic agents, which are moderately easy to disseminate and have low mortality rates. In their natural state, these viruses require arthropod vectors for transmission and have a variable seasonality dependent on the geography, local climate, and virus-specific lifecycle. These qualities make the use of the Alphaviruses as a terrorist agent more difficult to control and disseminate to the general public. That being said, aerosol transmission of a weaponized (manufactured) form of the virus has been demonstrated and would represent the most likely route of mass infection if terrorists were able to produce large amounts of aerosolized virus.4,9 Other characteristics of the Alphaviruses that lend themselves to weaponization include the ability to inexpensively produce large amounts of stable virus and the potential for genetic manipulation of native viruses.7 One possible clue to an Alphavirus attack is a large number of sick or dying equine animals in the vicinity,9 thus arthropod vector control and vaccinating equine reservoirs may help to prevent the spread of encephalitis during an outbreak.4

PITFALLS • Failure to notify appropriate public health officials of a diagnosis of viral encephalitis • Failure to prepare local emergency departments and clinics to respond appropriately in case of an outbreak

662 VIRAL AGENTS

• Failure to disseminate medical instructions and training for local communities, as appropriate • Failure to recognize that reports of sick or dying equine animals in the area may be related to a vectorborne disease

CASE PRESENTATION The last few weeks have been hot and rainy, and there has been a moderate increase in the number of otherwise healthy individuals presenting to emergency departments with vague “viral syndrome” complaints. There are also news reports of a large number of equine illnesses in nearby communities. Many patients who were originally sent home with supportive care have returned with worsening mental status, lethargy, and seizures. An elderly patient, who has had a seizure, presents to the emergency department. He was reportedly seen at another hospital 3 days ago for nausea, vomiting, fatigue, low-grade fever, confusion, and headache. Since then his symptoms have become worse, with an inability to tolerate fluids by mouth and increasing agitation and confusion. He has a fever of 101˚F, with mild tachycardia and a stable blood pressure.

REFERENCES 1. Markhoff L. Alphaviruses. In: Mandell GL, Bennett JE, Dolin R, eds. Principles and Practice of Infectious Diseases. 5th ed. Philadelphia: Churchill Livingstone; 2000. 2. US Centers for Disease Control and Prevention, Division of VectorBorne Infectious Diseases. Arboviral Encephalitides. Available at: http://www.cdc.gov/ncidod/dvbid/arbor/index.htm. 3. Katona P. Bioterrorism preparedness: a generic blueprint for health departments, hospitals, and physicians. Infect Dis Clin Pract. 2002;11(3):115-22. 4. Rajagopalan S. Deadly viruses. Top Emerg Med. 2002;24(3):44-55. 5. Cherry CL, Kainer MA, Ruff TA. Biological weapons preparedness: the role of physicians. Intern Med J. 2003;33:242-53. 6. Harwood-Nuss A. The Clinical Practice of Emergency Medicine. 3rd ed. Philadelphia: Lippincott Williams & Wilkins; 2001. 7. Franz DR, Jarhling PB, Friedlander AM, et al. Clinical recognition and management of patients exposed to biological warfare agents. JAMA. 1997;278:399-411. 8. de Assis Aquino Gondim F, Oliveira G,Thomas FP. Viral Encephalitis. eMedicine.Available at: http://www.emedicine.com/. 9. Sardesai AM, Brown NM, Menon DK. Deliberate release of biological agents. Anesthesia. 2002;57(11):1067-82.

chapter 119

Tick-Borne Encephalitis Virus Attack Vittorio J. Raho

DESCRIPTION OF EVENT Tick-borne encephalitis (TBE) is classically caused by infection with one of two flaviviruses: Russian springsummer encephalitis virus (RSSEV) or Central European encephalitis virus (CEEV).1 However, the TBE virus-complex is sometimes extended to include other entities such as Omsk hemorrhagic fever and Kyasanur Forest disease, which are closely related viruses with associated tick vectors.2 The geographic distribution of TBE includes the former Soviet Union, Central and Eastern Europe, and Asia. TBE viruses are associated with hardbodied Ixodid ticks, such as Ixodes persulcatus, which act as reservoirs for the virus as well as vectors when they infect their hosts, usually small woodland mammals. Humans are accidental hosts and do not participate in the virus’s normal reproductive cycle. In Russia, 5000 to 10,000 cases of TBE are reported annually, with fatalities in the low hundreds.3 When comparing the two closest subtypes of TBE viruses, RSSEV has a much more virulent clinical course, with reported mortality rates between 20% to 30%.4,5 RSSEV is sometimes referred to as Far Eastern encephalitis. A recent report of a severe hemorrhagic syndrome not previously described has now been associated with TBE infections in Russia, suggesting that more virulent strains may yet be discovered.3 Natural outbreaks of TBE coincide with the well-defined periods of tick activity, usually from April to October. Cases have also been documented from human ingestion of raw milk from infected goats.2,5 TBE infection manifests clinically across a spectrum of severity, from mild aseptic meningitis to florid meningoencephalitis. After a 1- to 2-week incubation period, patients may experience a biphasic illness with initial symptoms of fever, malaise, myalgia, headaches, nausea, and vomiting that last around 2 to 4 days. After a brief remission of symptoms, between one fourth and one third of patients will develop the manifestations of severe meningoencephalitis, with symptoms of central nervous system dysfunction, including severe headache and meningismus, confusion, lethargy, delirium, convulsions, paralysis, coma, and death.6 Survivors have a significant rate of neurologic sequelae, including limb paralysis and cognitive deficits.7 A more rapid and severe course of illness is associated with RSSEV.

Nonspecific laboratory data include leukopenia, thrombocytopenia, and elevated liver function tests and sedimentation rate. During the meningoencephalitis phase, cerebrospinal fluid studies will show lymphocytosis and an elevated protein level.8 Magnetic resonance imaging has been shown to be superior to computed tomography in identifying tissue inflammation in other forms of viral encephalitis.9

PREINCIDENT ACTIONS Surveillance systems, which acquire data from government sources, hospital emergency room discharge summaries, and state public health networks, can effectively identify unusual clusters of viral syndromes in certain geographic distributions. Epidemiologic analysis may be the only way to detect such an attack, especially since symptoms are so nonspecific and may resemble a myriad of other domestic illnesses.

POSTINCIDENT ACTIONS Laboratory diagnosis of TBE is usually made using serologic testing, such as IgM enzyme-linked immunosorbent assay or reverse transcriptase PCR (polymerase chain reaction), for detection of viral ribonucleic acid. Laboratory workers should take biosafety precautions to prevent exposure to infectious aerosols.10 Fortunately, no person-to-person transmission of TBE has been reported. If the attack is via the natural tick-borne route, vector control using repellents such as permethrin may be the most efficient way to thwart an attack once it has been identified. Reports indicate that the TBE virus is neutralized by common disinfectants such as 1% sodium hypochlorite and formaldehyde.7

MEDICAL TREATMENT OF CASUALTIES No specific medical treatment is available for any of these viruses. The management of such patients is dictated by their neurologic and cardiovascular sequelae 663

and may include respiratory support including mechanical ventilation, hemodynamic monitoring, treatment of secondary bacterial infections such as pneumonia, or possible steroid administration to suppress cerebral or spinal edema. A formalin-inactivated vaccine was introduced in Austria in the late 1970s that confers some degree of immunity to TBE viruses, although it is not currently licensed in the United States.11 However, researchers have shown promise with naked-DNA (deoxyribonucleic acid) vaccine trials in mice that confer immunity to both the CEEV and RSSEV strains.12 Postexposure prophylaxis should be considered in high-risk groups.

UNIQUE CONSIDERATIONS Flaviviruses are a large group of heterogeneous viruses known for their ability to infect humans through various arthropod vectors. Yellow fever, Japanese encephalitis, and dengue hemorrhagic fever, among others, are well known to the international medical community. TBE has become a significant public health problem in many parts of Europe, as civilization encroaches on wilderness and people engage in more recreational activity in rural areas. TBE may not be as internationally recognized as other flaviviruses and therefore not screened for as often, making it more desirable as a bioweapon. The ability of TBE to infect humans through ingestion is also of concern.

PITFALLS • Failure to consider viral encephalitis as a potential cause of acute, febrile illness during such an outbreak • Failure to properly isolate and inspect patients who may have infected ticks on their body • Failure to collect blood, cerebrospinal fluid, or tick specimens and send appropriate samples to state public health laboratories • Failure to take proper respiratory precautions when handling body fluid samples from suspected cases • Failure to report suspected cases to the state department of public health or affiliated authority for appropriate Centers for Disease Control and Prevention notification and proper serologic testing • Failure to alert local and state agencies to a suspected biologic attack when presented with a cluster of unusual and uncommon illnesses REFERENCES 1. Gresikova M, Sekeyova M. Antigenic variation of the viruses belonging to the tick-borne encephalitis complex as revealed by human convalescent serum and monoclonal antibodies. Acta Virol. 1987;31:152-7.

664 VIRAL AGENTS

CASE PRESENTATION A 46-year-old man with no significant past medical history and up-to-date vaccinations presents to the emergency department with fevers, chills, myalgia, nausea, and vomiting of 3 days duration. He has had no recent exposures to sick persons, no insect bites, no recent travel, and owns no pets. Other than a fever of 101˚F, his vital signs are within normal limits. His physical examination is unremarkable, including a supple neck, clear lungs, and a normal neurologic examination. He is treated with acetaminophen and ibuprofen, tolerates oral fluids, and is sent home with a presumptive viral syndrome. After remaining afebrile and feeling better for several days, his fever recurs to 104˚F, and he develops a severe headache, neck stiffness, confusion, and vertigo. He is brought back to the emergency department by ambulance and is noted to be severely lethargic and confused, and he experiences a generalized tonic-clonic seizure. He is given antibiotics for presumed meningitis, and cerebrospinal fluid studies show a lymphocytic pleocytosis and a negative Gram stain. Herpesvirus tests, meningococcus serologies, and blood smears for malaria are negative, and computed tomography of the brain shows no bleeding or abscess. The patient remains unresponsive and intubated in the intensive care unit several days later. Records indicate that in the last month, 142 cases of severe acute viral syndromes of unclear etiology have been reported, with an associated mortality approaching 10%.

2. US Centers for Disease Control and Prevention. Tick-borne Encephalitis. Available at: http://www.cdc.gov/ncidod/dvrd/ spb/mnpages/dispages/TBE.htm. 3. Ternovoi VA, Kurzhukov GP, Sokolov YV, et al. Tick-borne encephalitis with hemorrhagic syndrome, Novosibirsk Region, Russia, 1999. Emerg Infect Dis. 2003;9(6):743-6. 4. Dumpis U, Crook D, Oksi J. Tick-borne encephalitis. Clin Infect Dis. 1999;28(4):882-90 (review). 5. Fauci AS, Braunwald E, Isselbacher KJ, et al. Harrison’s Principles of Internal Medicine. 14th ed. New York: McGraw-Hill; 1998:1136-9. 6. Monath TP, Heinz FX. Flaviviruses. In: Fields BN, et al. Fields Virology. 3rd ed. Philadelphia: Lippincott-Raven; 1996:961-1034. 7. World Health Organization. Technical Report Series 889, WHO Expert Committee on Biological Standardization, 48th Report. Geneva:World Health Organization; 1999. 8. Kaiser R, Holzmann H. Laboratory findings in tick-borne encephalitis. Correlation with clinical outcome. Infection. 2000;28:78-84. 9. Sampathkumar P. West Nile virus: epidemiology, clinical presentation,diagnosis,and prevention. Mayo Clinic Proc. 2003;78:1137-43. 10. US Centers for Disease Control, Office of Biosafety. Classification of Etiologic Agents on the Basis of Hazard. 4th ed. Atlanta: US Department of Health, Education and Welfare, Public Health Service, US Centers for Disease Control, Office of Biosafety; 1974. 11. Kunz C, Heinz FX, Hoffmann H. Immunogenicity and reactogenicity of a highly purified vaccine against tick-borne encephalitis. J Med Virol. 1980;6:103-9. 12. Schmaljohn C,Vanderzanden L, Bray M, et al. Naked DNA vaccines expressing the prM and E genes of Russian spring summer encephalitis virus and Central European encephalitis virus protect mice from homologous and heterologous challenge. J Virol. 1997;71:9563-9.

chapter 120

Viral Hemorrhagic Fever Virus Attack—Arenaviruses Sandra S. Yoon

DESCRIPTION OF EVENT The arenaviruses that cause viral hemorrhagic fevers (VHFs) include the Lassa, Junin, Machupo, Guanarito, and Sabia viruses. The latter four are also known as the New World arenaviruses. They are enveloped, single-stranded ribonucleic acid (RNA) viruses, whose natural host reservoir is the rodent. The rodent species has been identified for each virus except for the Sabia virus. Although its reservoir is unknown, it has caused several natural and laboratory infections. Because these viruses are highly species specific, they determine their endemic geographic distribution—West Africa, Argentina, Bolivia, Venezuela, and Brazil, respectively. Naturally occurring cases are transmitted by infected rodent blood, urine, or feces via aerosol, direct contact, or food contamination. Person-to-person transmission then may occur by direct contact with infected bodily fluids. The arenaviruses have been classified as category A biologic agents by the Centers for Disease Control and Prevention (CDC).1 A mortality rate as high as 30%, the relative ease of obtaining and propagating the viruses in cell culture, potential for transmission via the respiratory system, demonstrated person-to-person transmission, and the potential for inducing widespread panic in an affected population all contribute to this classification. Furthermore, these viruses have been produced in large quantities by other countries in the past. Even though person-to-person transmission via the aerosol route has not been proven, it has been suspected in several cases of nosocomial outbreaks involving the Lassa and Machupo viruses.2 After initial exposure, the incubation period is typically 3 to 19 days, but it may be as short as 2 to 6 days after parenteral exposure. There have not been any reports of disease transmission during the incubation period. The clinical syndrome of arenavirus hemorrhagic fevers may be difficult, if not impossible, to distinguish from other hemorrhagic fevers or even viral syndromes. The severity of the disease and prognosis are related to the degree of viremia. The virus, in addition to infecting endothelial cells, is thought to induce the release of inflammatory mediators from macrophages, contributing to capillary

leak, the hallmark of the disease. Typically, fever, headache, malaise, and myalgia are not sudden in onset as they are for other VHFs. Relative bradycardia and hyperesthesia of the skin may be clues to the diagnosis. Lassa fever is characterized by the gradual onset of fever, nausea, abdominal pain, severe sore throat, cough, conjunctivitis, ulcerations of buccal mucosa, exudative pharyngitis, and cervical lymphadenopathy, followed by severe swelling of the head and neck, pleural and pericardial effusions, hypotension, and shock. Additional symptoms include retrosternal chest pain, back pain, vomiting, diarrhea, and proteinuria. Deafness may occur, usually in the second to third week of illness.2–4 The New World hemorrhagic fevers are characterized by gradual onset of fever, myalgia, nausea, abdominal pain, conjunctivitis, flushing of the face and trunk, generalized lymphadenopathy, hypotension, and shock. Epigastric pain, retro-orbital pain, dizziness, photophobia, constipation, and proteinuria may also be present. Hemorrhagic manifestations, such as petechiae, especially in the axilla, and mucous membrane hemorrhages, as well as central nervous system manifestations, such as dysarthria, hyporeflexia, tremors, myoclonic movements, and seizures, are more common than in Lassa fever.2,3,5,6 Severe manifestations of the disease usually occur during the second week of illness. Routine laboratory analysis is typically unhelpful in making the diagnosis of VHFs. Laboratory studies may reveal leukopenia, thrombocytopenia, and hemoconcentration. Renal function is generally preserved until late in the course, although proteinuria is commonly present. Liver enzymes may be elevated, and in Lassa fever, aspartate transaminase levels greater than 150 IU/L are associated with higher mortality.3 Definitive diagnosis requires specialized laboratory studies available at the CDC or the U.S. Army Medical Research Institute of Infectious Diseases (USAMRIID) and include antigen detection by reverse transcriptase polymerase chain reaction (PCR) or enzyme-linked immunosorbent assays (ELISA), IgM and IgG antibody detection by ELISA, and viral isolation. Viral isolation requires a Biosafety Level 4 laboratory and may take several days.7 The presence of IgM antibody or a four-fold rise in IgG antibody titers is diagnostic; 665

however, antibodies may not be present until the second week of illness.

PREINCIDENT ACTIONS Hospitals should have disaster plans in place and should exercise them frequently. The plans should include methods for coordinating with local, state, and federal authorities and emergency medical services and a method to protect the hospital environment from contamination. Given the constellation of vague symptoms and the challenge of making a diagnosis of VHF, healthcare workers must maintain a high index of suspicion and consider this diagnosis in appropriate patients. Particular attention should be given to patients who have traveled to an endemic region, who have had direct contact with blood or other bodily fluids of a known infected person, or who work in a laboratory that handles the specific viruses.7 In the event of a bioterrorism attack, these risk factors would be absent. However, one would expect multiple victims with similar symptoms presenting within days of each other.

POSTINCIDENT ACTIONS As with any suspected biologic attack, the appropriate local and state public health authorities should be notified.8 The state authorities are then required to notify the Federal Bureau of Investigation, local law enforcement authorities, and the CDC. Decontamination of patients may be necessary, although this is unlikely in the case of VHFs because symptom presentation lags days to weeks after exposure. Person-to-person transmission via infected bodily fluids is a common and known method of transmission; therefore, specific barrier precautions should be instituted immediately. These include handwashing; double gloving; and the use of gowns, face shields, eye protection, and leg and shoe coverings. Although person-to-person airborne transmission is rare, given the difficulty of differentiating the VHFs, the high mortality, the unknown consequences of massive inoculation that may occur during a bioterrorism attack, and the potential for possible high viral loads, airborne precautions should be instituted as well.5,7 These include the use of negative air pressure rooms and either an N95 mask or a powered air-purifying respirator. The hospital’s clinical laboratory should be notified as a precaution before sending a potentially infectious specimen. These viruses must be handled in a Biosafety Level 3 laboratory with viral isolations attempts occurring only in Biosafety Level 4 laboratories.2 Specimens should be hand delivered, not placed in pneumatic tubes. Surfaces or objects contaminated with blood or other bodily fluids, including laboratory equipment, should be disinfected with either 1:100 dilution of household bleach or a U.S. Environmental Protection Agency–registered hospital disinfectant. Bulk bodily fluids can also be treated with bleach before disposal; however, this may damage septic tanks, and the virus is unlikely to survive standard sewage treatment. Linens should be autoclaved, inciner666 VIRAL AGENTS

ated, or may be washed in hot water with bleach. Laboratory samples of patients with known VHF virus should be pretreated with polyethylene glycol ptert-octylphenyl ether (Triton X-100) for 5 minutes to reduce the titers of hemorrhagic fever viruses in serum.6

MEDICAL TREATMENT OF CASUALTIES Medical management of VHF patients consists primarily of supportive care. The antiviral drug ribavirin and, in some cases, convalescent plasma, may be available as a treatment option via an investigational new drug (IND) protocol. Patients should have their fluid balance and electrolytes monitored and corrected, receive adequate analgesia, and have secondary infections aggressively treated. Indwelling lines should be kept to a minimum to prevent damage to already fragile vessels. Aspirin, nonsteroidal antiinflammatory, and other anticoagulant medications, as well as intramuscular injections, should be avoided. If a VHF is suspected, ribavirin should be given while waiting for diagnostic tests. The dose is 30 mg/kg intravenously once (maximum of 2 g) followed by 16 mg/kg intravenously (maximum 1 g per dose) every 6 hours for 4 days, then 8 mg/kg intravenously (maximum 500 mg per dose) every 8 hours for 6 days. In the event of mass casualties, oral ribavirin may be given at the dose of 2000 mg loading; this is followed for the next 10 days by 600 mg twice a day if the patient weighs more than 75 kg, or 400 mg in the morning and 600 mg in the evening if the patient weighs less than 75 kg. Follow the same dosing guidelines for children, with the exception that for mass casualty settings, oral ribavirin is given at 30 mg/kg loading, followed by 15mg/kg/day divided into twice-daily dosing for 10 days.2 Ribavirin may be effective in the treatment of Lassa, Junin, and Machupo infections, especially if given within 7 days of disease onset, and it has been suggested for Guanarito and Sabia viruses. The main toxicity of ribavirin therapy is doserelated anemia.9 Passive immunity using convalescent plasma has been used in the treatment of Junin and Machupo infections, and is suggested in Guanarito infection; however, there have been mixed clinical results.6 An effective live attenuated vaccine exists for the Junin virus and has been used in endemic regions of Argentina. Laboratory data suggest that this vaccine may also be effective for the Machupo virus.3 Postexposure prophylaxis with ribavirin has not been studied in humans. The current recommendations consist of medical surveillance, twice-daily temperature monitoring, and reporting of temperatures greater than 101˚F or any symptoms. This should continue for 21 days past the potential exposure.2

UNIQUE CONSIDERATIONS The arenavirus hemorrhagic fevers are difficult to diagnose. The diagnosis should be considered in patients with temperatures greater than 101˚F for less than 3 weeks, who present with severe illness, and who have

experienced at least two hemorrhagic manifestations without a known predisposition. If there is any suspicion, ribavirin therapy should be considered and the CDC should be consulted for IND protocol approval. The effect of massive exposure to aerosolized virus has not been studied. In the event of a mass casualty incident, airborne and universal precautions should be followed. Higher levels of viremia are likely to result in greater person-to-person transmission rates. Multiple patients presenting with possible VHF should be clustered in the same part of the hospital.

PITFALLS • Failure to have appropriate disaster plans in place • Failure to consider VHF in the differential of an acutely ill patient with vague complaints

CASE PRESENTATION A previously healthy 30-year-old man presents to an emergency department with a 6-day history of fever, headache, myalgia, epistaxis, and diarrhea. His examination is significant for a temperature of 102˚F, heart rate of 70, blood pressure of 110/80 mm Hg, dehydration, hyperemic conjunctivae, and an exudative pharyngitis. Laboratory results are significant only for leukopenia (white blood cell count of 4.0), thrombocytopenia (platelet count of 74), and 2+ proteinuria. On further questioning, the patient stated that he recently returned from Venezuela, where he remembered hearing that there was a problem with the growing rodent population.

• Failure to consider ribavirin therapy in a timely manner • Failure to notify the appropriate authorities and the laboratory • Failure to practice strict barrier and airborne precautions REFERENCES 1. US Centers for Disease Control and Prevention. Bioterrorism Agents/Diseases. Available at: http://www.bt.cdc.gov/Agent/ Agentlist.asp. 2. Borio L, Inglesby T, Peters CJ, et al. Hemorrhagic fever viruses as biological weapons: medical and public health management. JAMA. 2002;287(18):2391-2405. 3. Peters CJ. Arenaviridae. In: Mandell GL, Bennett JE, Dolin R, eds. Principles and Practice of Infectious Disease. 5th ed. Vol 2. Philadelphia: Churchill Livingstone; 2000:1855-62. 4. Isaacson M. Viral hemorrhagic fever hazards for travelers in Africa. Clin Infect Dis. 2001;33:1707-12. 5. Charrel RN, Lamballerie X. Arenaviruses other than Lassa virus. Antiviral Res. 2003;57:89-100. 6. Harrison LH, Halsey NA, McKee KT, et al. Clinical case definitions for Argentine hemorrhagic fever. Clin Infect Dis. 1999;28:1091-4. 7. US Centers for Disease Control and Prevention. Update: management of patients with suspected viral hemorrhagic fever—United States. Morb Mortal Wkly Rep. 1995;44(25):475-9. 8. Steinhauer R. Bioterrorism. RN. 2002;65(3):48-55. 9. Huggins JW. Prospects for treatment of viral hemorrhagic fevers with ribavirin, a broad-spectrum antiviral drug. Rev Infect Dis. 1989;11(Suppl 4):S750-61.

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chapter 121

Viral Hemorrhagic Fever Attack—Bunya Virus Sean Michael Siler

DESCRIPTION OF EVENT In general, the hemorrhagic fever viruses, which consist of four families—Filoviridae, Arenaviridae, Bunyaviridae, and Flaviviridae—are seen as emerging pathogens because of the continued intrusion of man into areas where these viruses have developed an ecologic niche. With the increase in international travel, outbreaks caused by these viruses are more widely spread, and it would not be unexpected to see infections in cities with international travelers. Only the Arenaviridae, which include the etiologic agents of the Argentine, Bolivian, and Venezuelan hemorrhagic fevers and Lassa fever, and the Filoviridae, which consist of the Ebola and Marburg viruses, are classified as Centers for Disease Control and Prevention (CDC) category A biologic agents.1 Crimean-Congo hemorrhagic fever (CCHF) and Rift Valley fever (RVF) are a subset of the Bunyaviridae viruses that cause hemorrhagic fevers, and although not technically classified as category A agents, they do have the potential to be weaponized and delivered as fine-particle biologic aerosols. Both are a single-stranded ribonucleic acid (RNA) virus, spherical in shape, range from 70 to 120 nm in diameter, and possess a lipid envelope. Bunyaviridae are distributed endemically throughout the world, including Crimea, much of Africa, Iraq, Pakistan, Egypt, Korea, Eastern Europe, Russia, and Scandinavia.2 CCHF virus is spread by the species of Ixodid ticks, primarily the tick Hyalomma marginatum, and occurs widely across Africa, southeastern Europe, the Middle East, and Asia. CCHF also represents a growing threat as bioterrorists seek to weaponize natural pathogens for delivery in populated areas outside the pathogens’ endemic regions. The CCHF virus possesses some characteristics that a bioterrorist might find desirable, including the potential for aerosolization and human-to-human transmission; however, it has proven difficult to weaponize.2 In aerosol form, CCHF is highly contagious, and as technology improves, this agent may become a greater threat. Mortality for Korean and Seoul subspecies is around 15%, and mortality from the Crimean-Congo subspecies ranges from 13% to 50%. Both the young and the old are 668

at increased risk, as are those who have increased opportunity for exposure in the workplace, such as workers in healthcare and agriculture.2,3 RVF virus is mosquito-borne illness that causes an acute-onset illness in livestock and wild animals as well as in humans, with an incubation period of 2 to 6 days.3 Despite high levels of viremia, there have been no reported person-to-person transmissions of RVF. Humans are infected by the bite of an infected mosquito or by direct specimen exposure. Livestock are readily infected and produce high viral titers, which provides a reservoir for mosquitoes to infect humans.3 RVF has the potential to be used as a bioweapon; it was studied by the U.S. Army in the 1960s but was never weaponized.3 Mortality is 1%, and there is no sex predilection. Highrisk patients include the young and old, farm workers, travelers to endemic areas, and exposure to sick animals or people in the last 21 days. Healthcare workers who treat infected patients are at risk from bodily fluid exposure. Infections from percutaneous exposures have the shortest incubation times and the greatest mortality.3 In general, Bunya viruses damage the vascular beds throughout the body, causing increased permeability. CCHF is an influenza-like virus that has a 2- to 12-day incubation period. Initial symptoms include an abrupt onset of fever and chills, headache, myalgia, abdominal pain, nausea, and vomiting. Facial flushing and conjunctival injection are also prominent. A petechial rash starting on the back may extend over the trunk and then to the rest of the body. A hemorrhagic exanthem may begin on the soft palate and uvula. As many as 75% of patients will have hemorrhagic symptoms that begin between days 3 and 7 and include ecchymosis, bleeding from the gums, nose, mouth, uterus, gastrointestinal tract, pulmonary tract, and venipuncture sites. One-half of patients will have hepatomegaly and central nervous system involvement, such as agitation, depression, nuchal rigidity, or coma; central nervous system involvement is associated with a poor prognosis. Multiple organ system failure, severe hemorrhage, and shock can develop, and secondary infections often lead to concomitant sepsis. Death usually occurs between days 5 and 14.1–6

RVF leads to the destruction of the infected cell, and patients will have varying degrees of vasculitis and hepatic necrosis. Reduced levels of anticoagulation factors are seen also secondary to disseminated intravascular coagulation (DIC) and hepatic dysfunction. Symptoms include fever, headache, jaundice, retro-orbital pain, and photophobia. RVF may cause retinitis in as many as 10% of individuals, with a rate of blindness of approximately 1%. Fewer than 1% of patients will develop hemorrhagic fever or encephalitis, but the mortality rate is as high as 50% in patients who do.3,7 Patients will often have leukopenia and thrombocytopenia, which result in focal inflammatory reactions that produce thrombocytosis. Partial thromboplastin times may be prolonged, but prothrombin times are relatively unaffected. A common pathway for the systemic effects of CCHF is DIC.8 Transaminase levels are elevated, and hepatic damage is common. Aspartate aminotransferase (AST) is usually raised, and virtually all VHFs distinguish themselves from viral hepatitis because the AST is disproportionately high compared with alanine aminotransferase (ALT). Ratios of AST to ALT may be as high as 11 to 1; the higher the ratio of AST/ALT, the poorer the prognosis. Patients are rarely jaundiced (except in yellow fever), and the bilirubin level is usually normal.5 An enzyme-linked immunosorbent assay is available to identify IgM, IgG, or viral antigens in the serum of acutely ill patients. Immunofluorescence assay, complement fixation, and neutralization assays may also be used. These tests are not widely available and often require sending samples to reference laboratory facilities. Isolation and identification often require 3 to 10 days. Electron microscopy of infected tissue also may be helpful in identification. Specimens should be transported only after consultation with the CDC or U.S. Army Medical Research Institute of Infectious Diseases and under very specific biosafety precautions.6

PREINCIDENT ACTIONS Hospitals should have disaster plans in place and run routine drills. The plans should include coordination of local and state authorities and emergency medical services and a method to protect the hospital environment from contamination and exposure to others.

POSTINCIDENT ACTIONS Report all suspected or confirmed cases to your hospital infection control personnel; laboratory personnel; your public health agency; and, if appropriate, law enforcement personnel. Patients may present as an isolated case or in clusters to one or more hospitals. The clinical situation will dictate when to initiate decontamination procedures. Persons with known or suspected exposures to CCHF or RVF should take a soap-and-water shower and irrigate any potentially exposed mucous membranes. Extreme heat, detergents, chlorine, formalin, or ultraviolet radiation, including prolonged sunlight, can inactivate viruses. Equipment may be decontaminated with

an Environmental Protection Agency–registered hospital disinfectant, or a dilution of household bleach. Care should be taken to ensure solutions are freshly made and correctly applied to allow the disinfectant to completely sterilize the area.5 Potentially exposed persons should be instructed to check themselves for fever twice daily and to report any temperature of 101°F (38.3°C) or greater or any new symptoms to their physician or public health authority. Surveillance should continue for 21 days, and ribavirin therapy should be considered if either a fever of more than 101°F (38.3°C) or appropriate symptoms are noted. Consultation with the CDC is required since ribavirin would have to be administered under an investigational new drug (IND) protocol.

MEDICAL TREATMENT OF CASUALTIES Treatment of most viral hemorrhagic fevers is supportive. Patients should be admitted or transferred to facilities capable of providing intensive care for patients in isolation. The early use of vasopressors is often necessary with the goal of minimizing end-organ dysfunction. The most commonly affected areas include the hematologic, pulmonary, and neurologic systems. Extreme care should be used when replacing fluids because the increased vascular permeability often leads to third spacing of fluids.3 Pulmonary edema is common after aggressive fluid replacement, and patients may require mechanical ventilation. Massive electrolyte shifts are common with aggressive fluid replacement and will need to be closely monitored. Blood component transfusions may be required. Pain and anxiety are also common and should be aggressively managed. Intramuscular injections, venipuncture, and central line placement should be minimized; they carry the same risks as when used with a massively anticoagulated patient. Secondary infections are common, and aggressive antibiotic therapy is often required. Antibiotic selection and dosing should be directed toward the source of the infection, with special consideration being given to any end-organ dysfunction.3 Ribavirin is an inhibitor of viral RNA and deoxyribonucleic acid synthesis, and it has been shown to benefit CCHF infections in vitro, in animal studies, and in human case reports.9,10 The Food and Drug Administration, however, has not officially approved the use of ribavirin for use in viral hemorrhagic fevers, and any use should be administered under an IND protocol. The CDC has recommended the use of ribavirin in suspected or confirmed cases of arenavirus or bunyavirus infection. The initial loading dose is 30 mg/kg (maximum 2 g) IV, followed by 16 mg/kg (maximum 1 g/dose) IV every 6 hours for 4 days, followed by 8 mg/kg intravenously (maximum 500 mg/dose) every 8 hours for 6 days. In a mass casualty setting the CDC recommends a loading dose of 2000 mg orally. This is followed by a 10-day treatment with 600 mg orally twice a day for patients with a body weight greater than 75 kg, or 400 mg every morning and 600 mg every evening for patients with a body weight less than 75 kg. Ribavirin is a category X VIRAL HEMORRHAGIC FEVER ATTACK—BUNYA VIRUS 669

drug for pregnant women, but the treatment benefit for the mother may outweigh any risk to the fetus.3 Dosing in pregnancy is the same as for adults. For mass casualty settings, the pediatric dosing recommendations are a loading dose of 30 mg/kg orally, followed by 15 mg/kg per day in two divided doses for 10 days. A pediatric syrup is available for use under an IND application from the manufacturer, Schering-Plough Corp.3 Steroids have not been shown to improve outcomes.11 Both live and attenuated vaccines for RFV are under investigation, but none has been approved.7 Interferon-alpha given before or just after exposure to RVF has been shown to protect monkeys from viremia and hepatocellular damage, but no human trials have been published to date.3 After aggressive and early supportive care, most patients will do well and recover, although convalescence may be prolonged.

UNIQUE CONSIDERATIONS Diagnosis of RVF and CCHF may be quite challenging. The differential diagnosis is quite broad and may include malaria, typhoid fever, leptospirosis, rickettsial infections, relapsing fever, fulminant hepatitis, shigellosis, and meningococcemia. Other noninfectious conditions include acute leukemia, lupus erythematosus, idiopathic or thrombotic thrombocytopenic purpura, hemolytic uremic syndrome, and the multiple causes of DIC. Treatment of RVF and CCHF is largely supportive, but if either is strongly suspected, ribavirin therapy should be considered.

PITFALLS • Failure to prevent nosocomial spread of infectious material due to a lack of adequate safety precautions or procedures • Failure to recognize a patient with symptoms consistent with CCHF or RVF with known travel to an endemic area or exposure to persons who have recently traveled to such an area • Failure to consider the use of a VHF agent in an attack when multiple patients present with symptoms of VHF • Failure to aggressively treat hypotension with vasopressors • Failure to use caution with fluid replacement, resulting in third spacing of fluids

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• Failure to notify public health and law enforcement officials of suspected or confirmed cases of CCHF or VHF

CASE PRESENTATION A 39-year-old man presents to an emergency department with 2 days of malaise, nausea, and vomiting and an abrupt onset of fever and chills the previous day. This morning he had two episodes of epistaxis that resolved with direct pressure. The patient also noticed a petechial rash that started this morning. He has a frontal headache and photophobia. He denies any recent illnesses or travel, but notes that several animals in the neighborhood have fallen ill over the past week. On admission and further evaluation, the patient is noted to be in massive hepatic failure. Meanwhile, local surveillance in the emergency department throughout the day notes an increased incidence of patients presenting with “viral syndrome,” with several others also commenting that pets and livestock were “not acting right.”

REFERENCES 1. Darling R, Catlett C, Huebner K, et al. Threats in bioterrorism I: CDC category A agents. Emerg Med Clin North Am. 2002;20(2):273-309. 2. Alai N, Saemi A, Saemi A. Viral Hemorrhagic Fevers. Available at: http://www.emedicine.com/derm/topic880.htm. 3. Borio L, Inglesby T, Peters CJ, et al. Hemorrhagic fever viruses as biological weapons: medical and public health management. JAMA. 2002;287(18):2391-2405. 4. Mayers D. Exotic virus infections of military significance: hemorrhagic fever viruses and pox virus infections. Dermatol Clin. 1999;17(1):29-41. 5. McCormick J. Viral hemorrhagic fevers. In: Cohen J, Powderly WG, eds. Infectious Diseases. 2nd ed. St. Louis: Mosby; 2004:1675-8. 6. Artenstein A. Bioterrorism and biodefense. Infect Dis Clin North Am. 2001;15(4):99-106. 7. Tsai T, Khan A, McJunkin J: Rift Valley fever. In: Long SS, ed. Principles and Practice of Pediatric Infectious Diseases. 2nd ed. Philadelphia: Churchill Livingstone; 2003:1115. 8. Swanepoel R, Gill DE, Shepherd AJ, et al. The clinical pathology of Crimean-Congo hemorrhagic fever. J Infect Dis. 1989;11(Suppl 4): S794-800. 9. Tignor GH, Hanham CA. Ribavirin efficacy in an in vivo model of Crimean-Congo hemorrhagic fever virus (CCHF) infection. Antiviral Res. 1993;22(4):309-25. 10. Watts DM, Ussery MA, Nash D, et al. Inhibition of Crimean-Congo hemorrhagic fever viral infectivity yields in vitro by ribavirin. Am J Trop Med Hyg. 1989;41(5):581-5. 11. Jahrling P:Viral hemorrhagic fevers. Textbook of Military Medicine. Vol 1. Falls Church,Va: Office of the Surgeon General; 1989.

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Viral Hemorrhagic Fever Attack—Filo Viruses William Porcaro

DESCRIPTION OF EVENT The Ebola and Marburg viruses are members of the Filoviridae family of viral hemorrhagic fevers, which have the ability to produce a high degree of morbidity and mortality, making them enticing candidates to be used as biologic weapons. The Centers for Disease Control and Prevention (CDC) has classified filoviruses as category A biologic agents because of their high degree of virulence, demonstrated aerosol infectivity, and ability to instill fear and anxiety in the population.1 Concern exists about terrorist groups obtaining samples of filoviruses from existing laboratory stocks, rogue government agents, or from natural outbreaks. Some researchers have suggested that the Japanese cult group Aum Shinri Kyo, which was responsible for the Sarin subway attack in Tokyo in 1995, sent members to Zaire in the 1990s to obtain samples of the Ebola virus.2 Viral hemorrhagic fevers are clinical syndromes characterized by acute onset of fevers and generalized symptoms such as malaise, headache, myalgia, and diarrhea. In the majority of victims the syndrome progresses to a bleeding diathesis, septic shock, and multiple organ failure. Russia and the former Soviet Union have produced and stockpiled large quantities of weaponized Marburg and possibly Ebola as recently as the 1990s.3 Marburg virus was first discovered in 1967 in Germany and Yugoslavia. African green monkeys, originating from Uganda, were determined to be the source animals that infected laboratory workers. Thirty-two cases were reported, with a 23% mortality rate. The Ebola virus, whose genome is remarkably homologous with the Marburg virus, was first identified in 1976 in Zaire and Sudan when simultaneous outbreaks occurred. In part, because of poor infection control practices, the human impact was devastating, with rapid spread to patients, family members, and healthcare workers. The Ebola-Zaire outbreak involved 318 patients with an 88% mortality rate,and the Ebola-Sudan outbreak affected 284 people with a 53% mortality rate.4 During the past quarter of a century, there have been numerous outbreaks of Ebola. Different strains of the virus have been identified, and several have been named according to the location of the outbreak.

The filoviruses are enveloped, negative-sense ribonucleic acid (RNA) viruses. They are generally grouped into “Marburg-like” or “Ebola-like” families. Several strains have been characterized in the Ebola family, including Ebola-Zaire, Ebola-Sudan, Ebola-Reston, and Ebola-Cote d’Ivoire. Microscopically, these viruses appear as thread-like filaments that have linear, circular, and U-shaped forms. Each of the viral genomes encodes nine protein products. Some demonstrate immunomodulatory properties, and others cause vascular cell toxicity.5 To date, the natural reservoirs for the filoviruses have not been discovered. Both Ebola and Marburg viruses produce similar clinical syndromes. Current epidemiologic evidence suggests that these viruses are spread through direct contact with blood, secretions, or infected tissues. The viruses may also be transmitted via mucosal contact; thus, there is risk of human finger-to-mouth or conjunctiva spread. Although there is no conclusive documented evidence, several human and animal cases have raised some concern for airborne spread of the virus via droplet nuclei.3,6 Of note, Ebola and Marburg are relatively stable and may retain infectivity for some time at room temperature when exposed to the environment. Previous biologic weapons programs have also succeeded in aerosolizing these viruses and proving aerosol transmission in animal models.4 The incubation periods are 2 to 21 days for Ebola and 3 to 10 days for Marburg. Because of the possibly prolonged asymptomatic incubation period,the danger of delayed recognition and possible continued dissemination of disease exists. Initial clinical symptoms may include myalgia and arthralgia,fever,nausea and vomiting, abdominal pain, and a rash (petechiae, purpura, and ecchymosis) spreading from the trunk distally. As the hemorrhagic fever progresses, oliguria, hematemesis, melena, pericarditis, encephalitis, acute renal failure, and shock may occur. In severe cases the victim succumbs to disseminated intravascular coagulation.3,4,7 The classic dermatologic manifestations are quite common since patients generally exhibit a maculopapular rash within 5 days of illness. Although petechiae may be initially apparent, larger patchy lesions generally form and progress to confluent regions. Desquamation may occur 671

and may be the first skin lesion noted in non-Caucasian individuals. Victims may also complain of burning and paresthesias over areas of their skin. The other classic manifestation of viral hemorrhagic fever is bleeding. More than 70% of infected, symptomatic patients suffer from bleeding diatheses. Bleeding may be pronounced and present as melena, epistaxis, hematemesis, hemoptysis,bleeding gums,or puncture sites. The rate of bleeding complication does not appear to differ between survivors and nonsurvivors.4 Individuals who survive acute viral hemorrhagic fever may be left with long-term sequelae, including arthralgia, uveitis, orchitis, and hearing loss. The virus has been isolated from the urine and seminal fluid of patients who were recovering from the disease up to 3 months after the onset of acute disease.8 Specific polymerase chain reaction (PCR) or antibody studies are required to identify infection. These tests are generally only available at specialized laboratories. Reverse transcription-PCR (RT-PCR) has been demonstrated to be effective in the rapid diagnosis of the Ebola virus. Studies have also shown a correlation between disease severity and higher RNA copy levels.9 The PCR technique has also been used with success in field settings using TaqMan-RT-PCR on a portable SmartCycler during African Ebola outbreaks.10 The techniques of viral growth in tissue culture followed by electron microscopy and enzyme-linked immunosorbent assay (ELISA) testing have also been used to identify filovirus infection.11 Immunohistochemical staining of skin biopsies may also prove to be an effective method for identifying infection.12

PREINCIDENT ACTIONS As with any disaster or possible bioterrorism attack, hospitals and emergency departments should have preexisting disaster plans in place that are rehearsed before an event. In suspected cases of filovirus infection/terrorist attack, coordination of local, state, and federal agencies would be required to diagnose and manage the incident. Notably, state departments of public health, the CDC, and the U.S. Army Medical Research Institute of Infectious Diseases (USAMRIID) would need to be involved early in the process of identification and treatment. As always, universal precautions must be practiced. A high level of vigilance must be maintained by healthcare workers when patients present in clusters with febrile illnesses. This vigilance must be even greater if the patient reports recent travel to an area endemic with viral hemorrhagic fever or if there is a report of a recent outbreak. In the event of suspected cases of filovirus infection, facilities must be prepared for proper isolation of the patient, bodily fluids, and specimens. Protective gowns, gloves, high efficiency particulate air (HEPA) face masks, and eye protection should be used by clinical and laboratory personnel because of the theoretical risk of aerosol transmission.

POSTINCIDENT ACTIONS Level of suspicion for filovirus infection should be high when patients present with the aforementioned signs and 672 VIRAL AGENTS

symptoms, particularly once there are reports of recent cases or a terrorist attack with viral agents. When there is a high level of suspicion of a filovirus terrorist attack, as previously mentioned, state and federal authorities must be rapidly notified. If there are a limited number of patients, consideration should be given to transferring patients to dedicated Biosafety Level 4 facilities, namely the CDC in Atlanta or the USAMRIID in Fort Detrick, Md. In cases of suspected Ebola or Marburg infection, blood and bodily fluid samples must be handled with extreme caution. No material should be forwarded to the CDC or USAMRIID without prior consultation and arrangement. If a filovirus aerosol attack occurred, victims would begin presenting with illness about 1 week later; at this point, virtually no infectious virus should remain viable in the environment. Patients or staff contaminated with liquids or materials possibly containing a filovirus should be decontaminated via a vigorous hot shower with soap and water. Surfaces or items that may be contaminated should be sterilized with a dilute bleach solution or standard hospital quaternary ammonium or phenol disinfectants. Steam serialization, where applicable, is the most effective method for inactivating filoviruses.11

MEDICAL TREATMENT OF CASUALTIES Unfortunately, treatment for victims of filovirus hemorrhagic fever is largely supportive. As victims progress to disseminated intravascular coagulation and septic shock, usual treatment with blood, clotting products, and vasopressor medications should be instituted. Conventional antiviral agents such as ribavirin have not been shown to have any significant clinical benefit in either in vitro or in vivo studies. Interferon-alpha (INF-a) has shown some success in suppressing filovirus replication in cell culture and some promise in protecting Ebola-infected mice from the illness.11 Attempts have been made to treat patients by passive immunization through the use of the convalescent blood and serum from recovered filovirus patients. After the transfer of IgG Ebola antibodies to infected patients, a lower mortality rate was observed. However, there were a small number of patients in these studies and questions have arisen about other confounders in their care.13 Purified IgG from horses hyperimmunized with Ebola-Zaire was shown to protect baboons and guinea pigs from disease when given to them shortly after virus challenge.14 A concerted effort to develop an Ebola vaccine is under way. Ebola-related deoxyribonucleic acid, liposome-encapsulated irradiated Ebola virus, and Ebola protein segments are all being studied for possible use as vaccines. Ebola virus-like particles, when injected into mice, allowed the animals to develop Ebola-specific antibodies and conferred protection from the lethal virus.15

UNIQUE CONSIDERATIONS The filoviruses have the potential to be used as devastating biologic weapons. Their high level of virulence and

equally impressive mortality rate make them a tempting target for any terrorist organization wishing to obtain a weapon of mass destruction. Initial identification of a viral hemorrhagic fever attack will be difficult given the week-long incubation period and nonspecific signs and symptoms in the initial phase of disease. The high risk of transmission to healthcare providers is another factor that makes this threat even more ominous.

PITFALLS • Failure of healthcare personnel to recognize the nonspecific signs and symptoms of viral hemorrhagic fever and delayed institution of containment procedures • Delayed reporting of possible cases of viral hemorrhagic fever to state and federal officials, leading to delay in appropriate diagnostic procedures and isolation of materials and patients • Failure to practice simple universal precautions, leading to uncontrolled spread of the viral agent • General public fear and reaction over release of information regarding possible cases of viral hemorrhagic fever

CASE PRESENTATION A 25-year-old man presents to a suburban emergency department because he “does not look well.” He is febrile, tachycardic, hypotensive, and minimally responsive. Small amounts of blood are noted in his nares and on his gums, and he is still bleeding from several venipuncture sites. His fiancée states that he has been generally unwell for the past few days with low-grade fevers, body aches, and diarrhea. On further questioning, she reports that he returned from a trip to Europe 10 days ago. Given the patient’s history, examination findings, and symptoms, the health department is contacted because of the concern for viral hemorrhagic fever. You learn from the health officials that several similar cases have also just been reported in the region.

REFERENCES 1. Rotz LD, Khan AS, Lillibridge SR, et al. Public health assessment of potential biological terrorism agents. Emerg Infect Dis. 2002;8:(2):225-30. 2. Kaplan D. Aum Shinrikyo. In: Tucker J, ed. Toxic Terror: Assessing Terrorist Use of Chemical and Biological Weapons. Cambridge, MA: MIT Press 2000; 207-26. 3. Borio L, Inglesby T, Peters CJ, et al. Hemorrhagic fever viruses as biological weapons: medical and public health management. JAMA. 2002;287(18):2391-2405. 4. Salvaggio MR, Baddley JW. Other viral bioweapons: Ebola and Marburg hemorrhagic fever. Dermatol Clin. 2004;22(3):291-302, vi (review). 5. Takada A, Kawaoka Y. The pathogenesis of Ebola hemorrhagic fever. Trends Microbiol. 2001;9(10):506-11. 6. Francesconi P, Yoti Z, Declich S, et al. Ebola hemorrhagic fever transmission and risk factors of contacts, Uganda. Emerg Infect Dis. 2003;9(11):1430-7. 7. Easter A. Ebola. Am J Nurs. 2002;102(12):49-52. 8. Rowe AK, Bertolli J, Khan AS, et al. Clinical, virologic, and immunologic follow-up of convalescent Ebola hemorrhagic fever patients and their household contacts, Kikwit, Democratic Republic of Congo. J Infect Dis. 1999;179(Suppl 1):S28-35. 9. Towner JS, Rollin PE, Bausch DG, et al. Rapid diagnosis of Ebola hemorrhagic fever by reverse transcription-PCR in an outbreak setting and assessment of patient viral load as a predictor of outcome. J Virol. 2004;78(8):4330-41. 10. Weidmann M, Muhlberger E, Hufert FT. Rapid detection protocol for filoviruses. J Clin Virol. 2004;30:94-9. 11. Bray M. Defense against filoviruses used as biological weapons. Antiviral Res. 2003;57(1-2):53-60 (review). 12. Zaki SR, Shieh WJ, Greer PW, et al. A novel immunohistochemical assay for the detection of Ebola virus in skin: implications for diagnosis, spread, and surveillance of Ebola hemorrhagic fever. J Infect Dis. 1999;179(Suppl 1):S36-47. 13. Mupapa K, Massamba M, Kibadi K, et al. Treatment of Ebola hemorrhagic fever with blood transfusions from convalescent patients. J Infect Dis. 1999;179(Suppl 1):S18-23. 14. Jahrling PB, Geisbert J, Swearengen JR, et al. Passive immunization of Ebola virus-infected cynomolgus monkeys with immunoglobulin from hyperimmune horses. Arch Virol Suppl. 1996;11:135-40. 15. Warfield KL, Bosio CM,Welcher BC, et al. Ebola virus-like particles protect from lethal Ebola virus infection. Proc Natl Acad Sci USA. 2003;100(26):15889-94.

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Viral Hemorrhagic Fever Attack—Flaviviruses John D. Cahill and James McKinnell

DESCRIPTION OF EVENT Flaviviruses belong to the family of arboviruses. More than 60 of these viruses are known to exist throughout the world. These viruses share some common features. Most are 40 to 50 nm in diameter and are enveloped, positive-sense, single-stranded ribonucleic acid (RNA) viruses that are transmitted from arthropods, particularly mosquitoes and ticks.1 Clinically these viruses can cause hemorrhagic fevers and encephalitis. This chapter focuses on those causing hemorrhagic fever: yellow fever, Kyasanur Forest disease, Omsk hemorrhagic fever, and dengue fever. There is at least the potential for these viruses to be manufactured into biologic weapons. It should be appreciated that in the natural setting, these infections have a wide spectrum of presentation: from mild to severe. From a clinical standpoint, these viruses can present in a similar fashion with findings that may include fever, often biphasic; relative bradycardia; hypotension; bleeding diathesis; petechiae; epistaxis; hemoptysis; hematemesis; melena; hematochezia; and hematuria. Laboratory findings may include leukopenia, thrombocytopenia, hemoconcentration, elevated liver function tests, and prolonged bleeding or prothrombin or activated partial thromboplastin times. Death in infected patients is often secondary to bleeding, shock, and organ failure. The differential diagnosis of these infections is broad and includes influenza, viral hepatitis, gram-negative sepsis, meningococcemia, toxic shock syndrome, rickettsial infections, leptospirosis, typhoid fever, Q fever, malaria, other viral hemorrhagic fevers, collagen vascular diseases, acute leukemia, and platelet disorders. Yellow fever, Omsk hemorrhagic fever, and Kyasanur Forest disease have been considered by the Working Group on Civilian Biodefense as having some key features that characterize biologic agents that pose particularly serious risks if used as biologic weapons against civilian populations: (1) high morbidity and mortality; (2) potential for person-to-person transmission; (3) low infective dose and highly infectious by aerosol dissemination, with a commensurate ability to cause large outbreaks; (4) effective vaccine unavailable or available only in limited supply; (5) potential to cause panic in the 674

affected population; (6) availability of pathogen or toxin; (7) feasibility of large-scale production; (8) environmental stability; and (9) prior research and development as a biologic weapon.2 Dengue fever is not considered in this group since initial infection rarely causes hemorrhagic fever and it is not transmissible by small-particle aerosol.3 Yellow fever was weaponized by the United States offensive biologic weapons program until its cessation in 1969, but it may have been weaponized by North Korea.3 The incubation period of yellow fever is usually 3 to 6 days, then symptoms of fever, malaise, headache, photophobia, nausea, vomiting, and irritability may occur. Physical examination at symptom onset reveals a patient who is febrile; toxic in appearance; and who has hyperemic skin, injected conjunctiva, coated tongue, and epigastric or hepatic tenderness. Faget’s sign, a relative bradycardia with a fever, may be present. After 3 to 5 days, either the patient recovers or enters the next stage of fulminate disease, in which there is extensive hepatic injury with jaundice (hence the name “yellow fever”). Renal failure is not uncommon. A hemorrhagic diathesis may occur, causing epistaxis, oozing at the gums, petechiae, ecchymosis, hematemesis often described as “black vomit,” melena, hematuria, thrombocytopenia, and disseminated intravascular coagulation. Myocarditis, encephalopathy, and shock may also ensue. The case fatality rate is 20% to 50%. If one survives, a full recovery can be expected. The diagnosis of yellow fever may be very difficult in isolated cases; when epidemics occur, physicians are vigilant and the diagnosis is more obvious. In the tropics, the diagnosis is often clinical. A liver biopsy may be performed in an effort to identify the characteristic pathologic changes, such as Councilman bodies and midzonal necrosis. However, the biopsy findings are not absolute and do not exclude the possible diagnosis. Moreover,liver biopsies in yellow fever can be associated with massive hemorrhage. Developed nations have specialized laboratories that can assist in the diagnosis. In such facilities the diagnosis can be made by viral cultures, polymerase chain reaction (PCR), or preferably from enzyme-linked immunosorbent assay (ELISA) tests looking for the IgM rise during acute infection, or IgG later on.4

In patients with Kyasanur Forest disease, after an incubation period of 3 to 12 days, a severe febrile illness may ensue that may be biphasic in nature. The patient may complain of the acute onset of headache, photophobia, myalgia, upper respiratory symptoms, vomiting, and diarrhea. Physical examination may reveal a febrile patient with a relative bradycardia; hypotension; facial erythema; conjunctivitis; palatal vesicles; lymphadenopathy; hepatosplenomegaly; and manifestations of a bleeding diathesis, including petechiae, epistaxis, hematemesis, hemoptysis, melena, and hematochezia. Patients may develop hemorrhagic pulmonary edema, which is the most common cause of death. The mortality rate may approach 8%.5 Renal or hepatic organ failure may occur. Between 20% and 50% of individuals will progress to the second stage of the illness after several days of apparent improvement. During this stage, symptoms of encephalitis may appear.6 The complete blood count may show leukopenia, hemoconcentration, and thrombocytopenia. Elevation of liver and renal function tests may also be seen. The virus can be directly isolated from blood during the first 12 days of illness. Appropriate laboratory precautions should be taken when handling these samples. Serologic studies are available for IgM and IgG. In the natural setting, Omsk hemorrhagic fever is, fortunately, a self-limited acute infection with only a small minority of patients developing hemorrhagic complications. The mortality rate is 0.5% to 3%. Clinically there is an incubation period of 3 to 7 days and the patient has a presentation similar to that seen in patients with Kyasanur Forest disease; however, there is generally no central nervous system involvement. Diagnosis is made by detecting viral RNA by PCR or by serodiagnosis using ELISA IgM and IgG. Dengue fever has a global distribution throughout the tropics. The frequency of dengue viral infections has been on the rise since the mid-1950s. Historically, dengue viruses caused sporadic and infrequent epidemics. However, during the last half century, dengue infections have grown to pandemic proportions and patients appear to be presenting with more severe clinical disease. By 1998, 1.5 million cases of dengue fever and dengue hemorrhagic fever from 56 countries marked the first worldwide pandemic. The pandemic in 1998 was followed 3 years later by another worldwide outbreak in 2001. During a span of 50 years, the incidence of dengue viral infection increased approximately 30-fold, affecting approximately 51 million people worldwide per year. In Puerto Rico alone more than $250 million has been spent during the last 10 years in an attempt to deal with the consequences of this disease.7 The dramatic change in disease epidemiology has been attributed to the population shift from rural to urban centers and the rise in international travel and commerce that characterized the 20th century. There are four serotypes of dengue virus: DEN-1, DEN-2, DEN-3, and DEN-4. All cause clinical dengue fever. Dengue can be separated from other tropical infectious diseases in that the immunologic response to viral infection is relatively unique. Resolution of the primary infection is thought to produce lifelong immunity to the infecting serotype but only brief protection from the

other serotypes. After the transient period of relative immunity, exposed patients become susceptible to secondary infections with other DEN serotypes. It is principally secondary infections,particularly with DEN-2,that are more likely to result in severe disease and dengue hemorrhagic fever.8 It has been convincingly argued that an antibody-dependent enhancement of secondary infections is responsible for increased viremia and the development of dengue hemorrhagic fever. Patients with initial infections often present with dengue fever symptoms, whereas those with secondary infections with a different serotype may present with dengue hemorrhagic fever. The incubation period of dengue fever is 2 to 15 days. The classic presentation of dengue fever, or “break bone fever,” is a syndrome associated with fever, frontal headache, retro-orbital pain, severe myalgia, and severe arthralgia. Conjunctival injection,pharyngeal irritation,nausea,vomiting,and a fine maculopapular rash that spreads centrifugally may accompany the syndrome. Initially, the fever rises rapidly for 2 to 7 days and may then drop, only to reoccur 24 hours later (hence the name “saddleback fever”). Hepatic transaminase level elevations have been reported in more than 80% of cases, with some reports of fulminant hepatic failure. Transcytopenia can be seen 4 to 5 days into infection, although this is not a universal finding. Although dengue fever is usually a self-limited infection, it can be accompanied by bleeding complications. Severe bleeding, particularly gastrointestinal losses, can be a fatal complication of dengue fever.9–11 Dengue hemorrhagic fever is differentiated from dengue fever on the basis of increased capillary leakage of plasma with associated hemoconcentration (hematocrit increase greater than 20%) and thrombocytopenia. Pleural effusions and ascites are possible complications of the microvascular leakage. Sudden extravasation of plasma, typically concomitant with defervescence, is responsible for the circulatory compromise associated with the dengue shock syndrome. The exact pathologic cascade behind microvascular leakage in dengue hemorrhagic fever is unclear but appears to be related to high viral titers causing complement activation and cytokine release, which in turn cause endothelial dysfunction and resulting plasma leakage.12 Mortality rates may be as high as 50%. Diagnosis is made serologically. The tourniquet test can be used, but it is not disease specific.

PREINCIDENT ACTIONS Healthcare providers must maintain a high index of suspicion for these diseases since they are sometimes difficult to diagnosis and since some of these agents may be used as biologic weapons. A clinician’s level of suspicion should be increased particularly if a large number of individuals present with a “viral syndrome” or coagulation and bleeding problems. Providers should be familiar with the clinical presentation of these illnesses and the resources available to diagnose and manage infected patients. It should be anticipated that blood products will be in great demand if a large number of patients become infected with these viruses and present for care. VIRAL HEMORRHAGIC FEVER ATTACK—FLAVIVIRUSES 675

From a public health standpoint, rapid diagnosis would be of utmost importance, since an outbreak of Ebola would be handled very differently from a yellow fever outbreak. Institutions and public health officials should also be prepared to handle mass panic and a large number of psychologic casualties that overwhelm the healthcare system. The availability of yellow fever vaccine and a plan for mass vaccination should be anticipated.

POSTINCIDENT ACTIONS Since there is no publicly known experience of these viruses being used as biologic weapons, it is not completely clear how infected individuals would present. Standard isolation precautions should be taken by healthcare personnel. Potentially exposed contacts should be placed under medical surveillance for several weeks, looking for evidence of fever and signs of viral hemorrhagic fever. Fortunately, in the natural setting, human-to-human transmission has not been reported. If the virus identified is vaccine-preventable, mass vaccination should begin as soon as possible. If viral hemorrhagic fever is suspected, local health officials must be notified to facilitate identification of the agent as well as access to vaccines, in coordination with state and federal health officials.

MEDICAL TREATMENT OF CASUALTIES Treatment of all viral hemorrhagic fevers due to flavivirus infection is largely supportive and may include intravenous fluids, vasopressor support, blood products, vitamin K, avoiding nonsteroidal antiinflammatory medications and anticoagulants, and correcting electrolyte imbalances. Although the data are limited, ribavirin has not been shown to be effective in the treatment of flavivirus infection. Beyond the provision of supportive care to infected patients, management of a yellow fever epidemic involves the institution of preventive measures, including vector control, surveillance, and immunization. A yellow fever vaccination is available. It is a live, attenuated vaccine and has several contraindications, including children younger than 9 months old, pregnancy, and immunosuppression. The vaccine can only be administered at a designated yellow fever center. The vaccination dose is 0.5 mL given subcutaneously in the upper arm. Immunity appears to last at least 10 years after a single dose. Treatment for Kyasanur Forest disease and Omsk hemorrhagic fever is supportive. In endemic areas, patients should avoid ticks. A formalin inactivated vaccine is available in endemic regions for Kyasanur Forest disease.13 No vaccine is available for Omsk hemorrhagic fever; however, the tick-borne encephalitis vaccine may offer some cross-protection.14 Treatment is of dengue hemorrhagic fever is also supportive. Preventive measures include eradication of mosquito breeding sites and personal protective measures. No vaccine is available; however, several vaccine trials are currently under way. 676 BIOLOGIC EVENTS

UNIQUE CONSIDERATIONS To date, there is no specific treatment for flaviviral hemorrhagic fevers. Treatment is supportive, although with development of antiviral medications, there may be a role for their use in the future. Several of these diseases are vaccine-preventable, and vaccine trials are under way for dengue fever. Fortunately, unlike some of the other hemorrhagic fevers, the flaviviruses are not known to spread person to person.

PITFALLS • Failure to obtain a detailed clinical history, which could result in these illnesses being mistaken for a “flu” or simple viral syndrome • Failure to obtain careful travel history, including geographic locations, length of trip, activities undertaken, and exposure to mosquitoes or ticks • Failure to determine the time of onset of symptoms and time of return from travel, since many of these illnesses have a specific incubation period • Failure to obtain a past medical history that includes previous vaccines • Failure to maintain clinical suspicion for these viruses when multiple individuals present with similar symptoms outlined in this chapter • Failure to report suspected hemorrhagic fever cases to the public health officer or department of health

CASE PRESENTATION The staff physicians at an urban hospital have been overwhelmed by an unusually early onset of the flu this season. The strain seems especially virulent, since several patients have died and the census in the emergency department has increased by 25%. As the week progresses, many of the patients admitted with the “flu” develop gastrointestinal bleeding, necessitating blood transfusions and intensive care unit support. Presenting symptoms of one such 30-year-old male patient include a fever to 101˚F, a heart rate of 80, and a blood pressure of 90/50 mm Hg. He has petechiae, is complaining of intermittent epistaxis, and has bloody stools. Laboratory findings include low white blood cell and platelet counts, an elevated hematocrit level, and elevated liver function tests. His bleeding time is prolonged as well.

REFERENCES 1. International Committee on Taxonomy of Viruses. Seventh Report of the International Committee on Taxonomy of Viruses. San Diego, Calif:Academic Press; 2000. 2. Borio L, Inglesby T, Peters CJ, et al. Hemorrhagic fever viruses as biological weapons: medical and public health management, JAMA. 2002;287(18):2391-2405.

3. Peters CJ, Jahrling PB, Khan AS. Patients infected with high-hazard viruses. Arch Virol Suppl. 1996;11:141-68. 4. Monath TP. Yellow fever. In: Guerrant RL, Walker DH, Weller PF, eds. Tropical Infectious Diseases. Philadelphia: Churchill Livingstone; 1999:1262. 5. Monath TP. Kyasanur Forest disease. In: Monath TP, ed. The Arboviruses: Epidemiology and Ecology. Vol 3. Boca Raton, Fla: CRC Press; 1998. 6. Pavri K. Clinical, clinicopathological and hematological features of Kyasanur Forest disease. Rev Infect Dis. 1989;11(Suppl 4):S854-9. 7. Clark G, et al. Dengue fever. In: CDC Yellow Book. Atlanta: Centers for Disease Control and Prevention; 2003. 8. Vaughn DW, et al. Dengue viremia titer, antibody response pattern, and virus serotype correlate with disease severity. J Infect Dis. 2000;181:2-9.

9. Kautner I, et al. Dengue virus infection: epidemiology, pathogenesis, clinical presentation, diagnosis, and prevention. J Pediatr. 1997;131:516-24. 10. Hayes EB, et al. Dengue and dengue hemorrhagic fever. Pediatr Infect Dis J. 1992;11:311-17. 11. Kalayanarooj S, et al. Early clinical and laboratory indicators of acute dengue illness. J Infect Dis. 1997;176:313-21. 12. Lei HY, et al. Immunopathogenesis of dengue virus infection. J Biomed Sci. 2001;8:377-88. 13. Broom AK, et al. Kyasanur Forest disease. In: Cook GC, Zumla A, eds. Manson’s Tropical Diseases. 21st ed. Philadelphia: Saunders; 2003:748-9. 14. Broom AK, et al. Omsk hemorrhagic fever. In Cook GC, Zumla A, eds. Manson’s Tropical Diseases. 21st ed. Philadelphia: Saunders; 2003:751.

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Chikungunya Virus Attack Heather Long

DESCRIPTION OF EVENT The chikungunya virus (CHIK) is an alphavirus borne by Aedes mosquitoes. The virus is endemic to many tropical and subtropical regions throughout the world, including sub-Saharan Africa, southeast Asia, India, and the western Pacific. The CHIK virus was first isolated from human serum and Aedes aegypti mosquitoes in 1953 after an epidemic in Tanzania.1 Even though the most common route of transmission is human-mosquito-human, the CHIK virus may also be aerosolized.2 It is highly infectious, and many laboratory workers have been infected while working with the virus.3–5 As an agent of biologic terrorism, it would most likely be dispersed as an aerosol or by release of infected mosquitoes.6 No person-to-person transmission has been documented. To date, there have been no confirmed reports of terrorist acquisition or planned use of this agent. In the event of a CHIK virus attack, a large percentage of the exposed population would be expected to become ill after an incubation period of 2 to 10 days.2 Illness associated with the CHIK virus is generally selflimited and short-lived; however, it may be temporarily debilitating, and a large number of affected patients would be expected to seek care for fever and severe joint pain. Hospitals with few isolation areas appropriate for screening patients with these presenting complaints may be overwhelmed. Infection with the CHIK virus is characterized by the triad of fever, maculopapular rash, and arthralgia.7 Nausea, headache, vomiting, and myalgia are also common. Sudden onset of fever is characteristically the first symptom to appear after an incubation period of 2 to 10 days.2 Arthralgia is the most prominent symptom, and the word chikungunya, translated from Swahili as “that which bends up,” refers to this joint pain.8 Severity ranges from mild weakness and stiffness to excruciating pain. The pain is typically symmetric and involves multiple joints. Previously injured joints and the fingers, wrists, elbows, toes, ankles, and knees are most commonly affected.6 Joints appear swollen and are tender to palpation. Frequency and severity of symptoms are generally less in children. Complete resolution of all symptoms occurs in most patients after 2 to 5 days; however, about 12% of patients will have a persistent arthropathy 678

that may last months to years.5 Persistent arthropathy is associated with high titers of CHIK virus antibodies.5 Although not classified as a hemorrhagic virus, hemorrhagic forms of the disease that mimic dengue fever and yellow fever have been reported.9,10 In some outbreaks of CHIK virus infection, up to 10% of patients were noted to have mild hemorrhage, including petechia, epistaxis, and bleeding gums. Cases of myocarditis and cardiomyopathy after CHIK virus infection have been reported.11,12 Rare deaths among the elderly and children have been associated with CHIK outbreaks, and the CHIK virus was isolated from one Sri Lankan child who died.13,14 Diagnosis of CHIK virus infection in a patient without history of either travel to an endemic area or laboratory exposure to the virus would require a high degree of clinical suspicion. Results from routine laboratory tests are nonspecific. Laboratory confirmation via polymerase chain reaction (PCR) or enzyme-linked immunoabsorbent assay (ELISA) requires submission of serum to either the Centers for Disease Control and Prevention (CDC) or the U.S.Army Medical Research Institute of Infectious Disease (USAMRIID), and results take 2 to 5 days.6

PREINCIDENT ACTIONS Prehospital services, hospitals, and local and state health departments should have implemented preparedness programs for bioterrorism and mass casualty events. Recognition of a CHIK virus event would require familiarity with the agent as well as a high degree of clinical suspicion. Maintaining a high level of alertness to abnormal patterns is critical to the recognition of any covert bioterrorist attack.

POSTINCIDENT ACTIONS All suspected cases of CHIK virus infection should be reported to local and state health departments, who would then notify the CDC. Infection control professionals and laboratory personnel should be notified immediately. Biosafety Level 3 practices should be maintained in handling specimens. If CHIK virus infection is

suspected, 10 to 12 mL of serum from the affected patient(s) should be shipped cold or on dry ice in a plastic tube. Public health authorities, in conjunction with the CDC, should aid clinicians in preparing specimens for transport to a reference laboratory. (See “Packaging Protocols for Biological Agents/Diseases” at http://www. bt.cdc.gov/Agent/VHF/VHF.asp.) Laboratory personnel must be alerted to the possibility of small-particle aerosol generation to minimize their risk of infection. With prior notice, the CDC can offer a preliminary laboratory diagnosis after approximately 1 working day.15 In its natural state, the CHIK virus is not environmentally stable for long periods. Environmental Protection Agency–registered hospital disinfectants, moist heat, and drying all kill the virus. However, decisions regarding the need for decontamination after an attack should be made after expert analysis of the contaminated environment,the agent used, and the means of distribution. Similarly, contact and respiratory isolation of exposed and infected patients is not believed to be necessary, but specific recommendations should be made after expert analysis. Given that laboratory confirmation may take several days, stricter infection control practices may be warranted until an agent with person-to-person transmission is ruled out. Universal precautions should be taken with all patients.

MEDICAL TREATMENT OF CASUALTIES The mainstay of treatment of CHIK virus infection is supportive care. Fluid and electrolyte balance should be closely monitored. Nonsteroidal antiinflammatory agents are the first-line therapy for fever and pain. Antiemetics may be required in cases of persistent nausea and vomiting. Antiviral agents,including ribavirin,6-azauridine,interferon-alpha2b, and glycyrrhizin, alone and in combination, have demonstrated in vitro anti-CHIK activity.16 Whether any of these agents would be effective in postexposure prophylaxis or treatment remains unstudied. There is currently no U.S. Food and Drug Administration indication for the use of ribavirin after CHIK virus infection. Given the low morbidity and exceedingly rare mortality associated with CHIK virus infection in its natural state, ribavirin should be administered only after expert analysis under an investigational new drug application.15 There is presently no vaccine for the CHIK virus,but development is on-going; results of a phase II safety and immunogenicity study of a live CHIK virus vaccine were published in 2000.17

UNIQUE CONSIDERATIONS The CHIK virus is highly infectious; a large percentage of people exposed to the agent would be expected to become ill. Illness with the CHIK virus is short-lived but temporarily debilitating and not considered lethal. Because there is no animal reservoir for the virus in Western countries and no person-to-person transmission, it is seen as a “clean” biologic weapon that may be a desirable agent for use against a civilian site.6

PITFALLS • Failure to consider a CHIK virus infection or attack in patients presenting with the nonspecific symptoms of fever, rash, and arthralgia • Failure to alert laboratory personnel to the possibility of small-particle aerosolization in suspected cases • Failure to notify local and/or state health departments of suspected cases

CASE PRESENTATION A 22-year-old woman with no significant past medical history complains of severe bilateral wrist, elbow, and knee pain since waking this morning. The patient had been in her usual state of health until 1 day before presentation when she had a sudden onset of fever and shaking chills while at work. The patient has no rhinorrhea, cough, or sore throat; she complains of headache and nausea but no vomiting or diarrhea. She has no chest or abdominal pain. She denies any sick contacts, trauma or falls, or recent travel.The only medication she takes is oral contraceptives. Vital signs are as follows: temperature is 39.5°C, heart rate is 120, blood pressure is 118/74 mm Hg, and respiratory rate is 16. The patient appears flushed and in obvious physical discomfort but in no respiratory distress. Her physical examination is remarkable for slight swelling of the knees bilaterally; pain is elicited with active and passive range of motion of the knees, wrists, and elbows bilaterally. There is no warmth or erythema of the joints. Routine laboratory results including white cell count with differential are normal. The erythrocyte sedimentation rate is 40. Aspiration of the left knee joint reveals clear fluid negative for crystals with a white cell count of 200 cells/high-powered field.

REFERENCES 1. Ross RW. The Newala epidemic. III. The virus: isolation, pathogenic properties and relationship to the epidemic. J Hyg (Lond). 1956;54:177-91. 2. Tesh RB. Arthritides caused by mosquito-borne viruses. Ann Rev Med. 1982;33:31-40. 3. Shah KV, Baron S. Laboratory infection with chikungunya virus: a case report. Indian J Med Res. 1965;53:610-13. 4. Banerjee K, Gupta NP, Goverdhan MK. Viral infections in laboratory personnel. Indian J Med Res. 1979;69:363-73. 5. Ramachandra RJ, Singh KRP, Pavri KM. Laboratory transmission of an Indian strain of chikungunya virus. Current Sci. 1964;33:235-6. 6. CBWInfo. Factsheets on chemical and biological warfare. Chikungunya fever: essential data. Available at: http://www.cbwinfo. com/Biological/Pathogens/CHIK.html. 7. Brighton SW, Prozesky OW, de la Harpe AL. Chikungunya virus infection. A retrospective study of 107 cases. S Afr Med J. 1983;63:313-15. 8. Pfeffer M, Linssen B, Parker MD, et al. Specific detection of chikungunya virus using a RT-PCR/nested PCR combination. J Vet Med. 2002;49:49-54. 9. Hammon WM, Rudnick A, Sather GE. Viruses associated with epidemic hemorrhagic fevers of the Philippines and Thailand. Science. 1960;131:1102-3. CHIKUNGUNYA VIRUS ATTACK 679

10. Sarkar JK, Chatterjee SN, Chakravarti SK, et al. Chikungunya virus infection with haemorrhagic manifestations. Indian J Med Res. 1965;53:921-5. 11. Maiti CR, Mukherjee AK, Bose B, et al. Myopericarditis following chikungunya virus infection. J Indian Med Assoc. 1978;70:256-8. 12. Obeyesekere I, Hermon Y. Myocarditis and cardiomyopathy after arbovirus infections (dengue and chikungunya fever.) Br Heart J. 1972;34:821-7. 13. Rao AR. An epidemic of fever in Madras—1964: a clinical study of 4,223 cases at the Infectious Diseases Hospital. Indian J Med Res. 1965;53:745-53. 14. Hermon YE. Virological investigations of arbovirus infections in Ceylon, with special reference to the recent chikungunya fever epidemic. Ceylon Med J. 1967;12:81-92.

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15. Borio L, Inglesby T, Peters CJ, et al. Hemorrhagic fever viruses as biological weapons: medical and public health management. JAMA. 2002;287:2391-2405. 16. Briolant S, Garin D, Scaramozzino N, et al. In vitro inhibition of Chikungunya and Semliki Forest viruses replication by antiviral compounds: synergistic effect of interferon-alpha and ribavirin combination. Antiviral Res. 2004;61:111-7. 17. Edelman R, Tacket CO, Wasserman SS, et al. Phase II safety and immunogenicity study of live chikungunya virus vaccine TSIGSD-218. Am J Trop Med Hyg. 2000;62:681-5.

chapter 125

Variola Major Virus (Smallpox) Attack Robert G. Darling

DESCRIPTION OF EVENT Smallpox may be responsible for more human deaths throughout history than any other known disease, with estimates that it has killed more than 100 million people since the beginning of recorded history.1 Smallpox was declared eradicated in 1980 by the World Health Organization, and there have been no cases of smallpox anywhere in the world since 1978. By treaty there are only two official repositories of smallpox in the world today: one repository is at the Russian State Research Center of Virology and Biotechnology in Novosibirsk, Russia, and the other is at the Centers for Disease Control and Prevention (CDC) in Atlanta, Ga. A single case of smallpox should be presumed to be intentional unless it can be shown to be the result of a laboratory accident. Terrorist use of variola as a biologic weapon could occur under one of several different scenarios. The simplest method might involve obtaining an illicit sample of the virus from a clandestine stock and then exposing a number of unsuspecting victims. These unfortunate individuals would then go about their daily business and serve as vectors for further spread of the disease once they become contagious. This might not be the most efficient manner to spread the infection since most victims become quite ill as symptoms develop and are unlikely to remain ambulatory. The most efficient manner to infect a large number of people would involve the deliberate spread of a weaponized aerosol of the virus. The incubation period of smallpox averages 12 days, with a range of 7 to 17 days after exposure. Clinical manifestations begin acutely with malaise, fever, rigors, vomiting, headache, and backache; 15% of patients develop delirium. Approximately 10% of light-skinned patients exhibit an erythematous rash during this phase. Two to three days later,an enanthem appears concomitantly with a discrete rash about the face, hands, and forearms. After eruptions on the lower extremities,the rash spreads centrally to the trunk over the next week. Lesions quickly progress from macules to papules and eventually to pustular vesicles. Lesions are more abundant on the extremities and face, and this centrifugal distribution is an important diagnostic feature. In distinct contrast to varicella,lesions on various segments of the body remain generally synchronous in their stages of development. From 8 to 14 days after onset,

the pustules form scabs that leave depressed depigmented scars upon healing. Although variola concentrations in the throat, conjunctiva, and urine diminish with time, the virus can be readily recovered from scabs throughout convalescence. Therefore, patients should be isolated and considered infectious until all scabs separate. For the past century, two distinct types of smallpox were recognized. Variola minor was distinguished by milder systemic toxicity and more diminutive pox lesions; it caused 1% mortality in unvaccinated victims. However, the prototypical disease, variola major, caused mortality of 3% and 30% in the vaccinated and unvaccinated, respectively.2 Smallpox must be distinguished from other vesicular exanthems, such as chickenpox, erythema multiforme with bullae, or allergic contact dermatitis. Particularly problematic to infection control measures would be the failure to recognize relatively mild cases of smallpox in persons with partial immunity. An additional threat to effective quarantine is the fact that exposed persons may shed virus from the oropharynx without ever manifesting disease. Therefore, quarantine and initiation of medical countermeasures should be promptly followed by an accurate diagnosis to avert panic. The usual method of diagnosis is demonstration of characteristic virions on electron microscopy of vesicular scrapings. Under light microscopy, aggregations of variola virus particles, called Guarnieri bodies, are found. Another rapid but relatively insensitive test for Guarnieri bodies in vesicular scrapings is Gispen’s modified silver stain, in which cytoplasmic inclusions appear black. None of the aforementioned laboratory tests is capable of discriminating variola from vaccinia, Monkeypox, or cowpox. This differentiation has classically required isolation of the virus and characterization of its growth on chorioallantoic membrane. The development of polymerase chain reaction diagnostic techniques promises a more accurate and less cumbersome method of discriminating between variola and other orthopoxviruses.3

PREINCIDENT ACTIONS Pre-event preparations should focus on first responder, medical, and public health personnel education. This is 681

particularly important for healthcare providers since an astute clinician will be far more likely to diagnose a first case of smallpox before any surveillance system would lead public health authorities to suspect there is an epidemic in the community. Rapid identification and vaccination of contacts will be the keys to controlling an outbreak of smallpox. Ideally, all first responders and medical and public health personnel will be vaccinated against smallpox before an outbreak and will have extensively drilled their local smallpox response plans. However, efforts by the CDC in 2003 to vaccinate up to 500,000 volunteers were unsuccessful, largely due to concerns about side effects of the vaccine and a general belief among the public that the threat of terrorist use of smallpox was low. To date the U.S. military has vaccinated more than 600,000 of its personnel with a relatively low rate of complications.4 A well-developed, integrated “all-hazards” hospital disaster response plan should be in place and tested regularly. It should include provisions to care for a rapid influx of large numbers of contagious patients. The local plan should be linked to other regional, state, and federal disaster plans.

POSTINCIDENT ACTIONS A single case of smallpox should be treated as an international public health emergency. Hospital infection control and laboratory personnel; law enforcement authorities, including the Federal Bureau of Investigation; and local, state, and federal public health authorities, including the CDC, must be notified immediately. An epidemiologic investigation to identify all of those potentially exposed must be initiated so that a postexposure vaccination effort can commence. With a mortality rate of 30% and high morbidity, the vaccination risk-benefit ratio shifts markedly in favor of vaccination, even for patients with contraindications to receiving the vaccine. Patients who have been exposed to a smallpox patient should be vaccinated as soon as possible, even up to 5 to 7 days after exposure since the disease may either be prevented or ameliorated.5 The smallpox vaccine, using vaccinia virus, is most often administered by intradermal inoculation with a bifurcated needle. The current smallpox vaccine is the Wyeth DryVax, which is a licensed product derived from calf lymph. Future smallpox vaccines will be grown on human cell cultures.6 Primary vaccinees receive three punctures with the needle; repeat vaccinees receive 15. A vesicle typically appears at the vaccination site 5 to 7 days after inoculation, with associated erythema and induration. The lesion forms a scab and gradually heals over the next 1 to 2 weeks; the evolution of the lesion may be more rapid, with less severe symptoms in those with previous immunity. Side effects include a low-grade fever and axillary lymphadenopathy. The attendant erythema and induration of the vaccination vesicle is commonly misdiagnosed as bacterial superinfection. More severe vaccine reactions include inadvertent inoculation of the face,eyelid,or other parts of the body;generalized vaccinia;and transient,acute 682 BIOLOGIC EVENTS

myopericarditis. Rare, but often fatal, adverse reactions include eczema vaccinatum (generalized cutaneous spread of vaccinia in patients with eczema), progressive vaccinia (systemic spread of vaccinia in immunocompromised individuals), and postvaccinia encephalitis.7 Vaccination is contraindicated in the following conditions: immunosuppression; HIV infection; history or evidence of eczema; other active severe skin disorders; during pregnancy; or current household, sexual, or other close physical contact with individuals possessing one of these conditions. In addition, vaccination should not be performed in breast-feeding mothers, in individuals with serious cardiovascular disease or with three risk factors for cardiovascular disease, or individuals who are using topical steroid eye medications or who have had recent eye surgery. Despite these caveats, most authorities state that, with the exception of significant impairment of systemic immunity, there are no absolute contraindications to postexposure vaccination of a person with a confirmed exposure to variola. However, concomitant vaccine immune globulin (VIG) administration is recommended for pregnant and eczematous persons in such circumstances.8 VIG is indicated for treating some complications of the smallpox vaccine, including generalized vaccinia with systemic illness,ocular vaccinia without keratitis,eczema vaccinatum, and progressive vaccinia, and should be available when administering vaccine. The dose for prophylaxis or treatment is 100 mg/kg for the intravenous formulation (first line), or 0.6 mL/kg for the intramuscular preparation (second line). Due to the large volume of the intramuscular formulation (42 mL in a 70-kg person), the dose would be given in multiple sites over 24 to 36 hours. If VIG is not available, cidofovir may be of use for treating vaccinia adverse events. Limited data suggest that VIG may also be of value in postexposure prophylaxis of smallpox when given within the first week after exposure, and concurrently with vaccination. Vaccination alone is recommended for those without contraindications to the vaccine. If more than 1 week has elapsed after exposure, administration of both products, if available, is reasonable.9 In the event of a large-scale smallpox outbreak, the controversial issue of quarantine must be considered. Historically, imposition of quarantine was a key element in the eventual control of a smallpox outbreak, but it has been more than 50 years since any such measure has been taken in the United States.

MEDICAL TREATMENT OF CASUALTIES People who have been exposed to known cases of smallpox should be monitored for a minimum of 17 days from exposure, regardless of their vaccination status; such individuals should be immediately isolated using droplet and airborne precautions at the onset of fever. Strict quarantine of asymptomatic contacts may prove to be impractical and impossible to enforce. A reasonable alternative would be to require contacts to remain at home and to check their temperatures daily.10 Any fever

greater than 38˚C (101˚F) during the 17 days after exposure to a confirmed case would suggest the development of smallpox. The contact should then be isolated immediately, preferably at home, until smallpox is either confirmed or ruled out and remain in isolation until all scabs separate. Immediate vaccination or revaccination should also be undertaken for all personnel exposed to a clinical case of smallpox. Caregivers should be vaccinated and continue to wear appropriate personal protective equipment regardless of vaccination status. Vaccination with a verified clinical “take,” defined as vesicle with scar formation, within the past 3 years is considered to render a person immune to smallpox. Antivirals for use against smallpox are under investigation. Cidofovir has had significant in vitro and in vivo activity in animal studies.11 Whether it would offer benefit superior to immediate postexposure vaccination in humans has not been determined. Even though cidofovir is a licensed drug,its use for treating smallpox is “off-label,” and thus it should be administered as an investigational new drug. Topical antivirals such as trifluridine or idoxuridine may be useful for treating smallpox ocular disease. Supportive care is imperative for successful management of smallpox victims; measures include maintenance of hydration and nutrition, pain control, and management of secondary infections.

UNIQUE CONSIDERATIONS Smallpox (variola major) is categorized as a category A critical biologic agent by the CDC because of its transmissibility, high morbidity and mortality, ability to cause panic in afflicted populations, and the extraordinary public health measures that would be required to contain an epidemic.12 Of particular concern with smallpox is evidence that it can be transmitted person-to-person via airborne droplet nuclei. This has been seen among some smallpox patients who have prominent respiratory symptoms.13 Significant progress has been made in acquiring enough licensed smallpox vaccine for every American, and work continues on the development of a safer smallpox vaccine with fewer side effects.6 Recently,Australian researchers have demonstrated an interleukin-2 modified poxvirus that was able to defeat the current smallpox vaccine in an animal model.14 Research likewise continues on antiviral drugs that could be used to treat smallpox patients, and the drug cidofovir offers some promise.

PITFALLS • Failure to recognize a case of smallpox on clinical grounds • Failure to immediately institute airborne and droplet precautions among patients and hospital staff • Failure to notify hospital laboratory personnel that clinical specimens may be from a smallpox patient

• Failure to immediately notify law enforcement and public health authorities of a suspected case of smallpox

CASE PRESENTATION An 18-year-old male presents with a fever of 104˚F, severe cough, a sore throat, a severe backache, and an erythematous maculopapular rash. He has a pulse of 120 that is regular, a respiratory rate of 18, and a blood pressure of 126/88 mm Hg. He appears quite ill. The cutaneous lesions appear all over the patient’s body but may be slightly more prominent on the face and arms than on the trunk or lower extremities. The lesions on the face consist mostly of red papules; on the arms they are mostly reddish macules. The lesions all appear about the same stage of development.

REFERENCES 1. Fenner F, Henderson DA, Arita I, Jezek Z, Ladnyi ID. Smallpox and its eradication. Geneva:World Health Organization; 1988. 2. Dumbell DR, Huq F. The virology of variola minor: correlation of laboratory tests with the geographic distribution and human virulence of variola isolates. Am J Epidemiol. 1986;123:403-15. 3. Ibrahim M, Lofts R, Jahrling P, et al. Real-time microchip PCR for detecting single-base differences in viral and human DNA. Anal Chem. 1998;70:2013-17. 4. Grabenstein J,Winkenwerder W. US military smallpox vaccination program experience. JAMA. 2003;289:3278-82. 5. Wharton M, Strikas R, Harpaz R, et al. Recommendations for using smallpox vaccine in a pre-event vaccination program. Supplemental recommendations of the Advisory Committee on Immunization Practices (ACIP) and the Healthcare Infection Control Practices Advisory Committee (HICPAC). MMWR Recomm Rep. 2003;52:1-16. 6. Bicknell W, James K. The new cell culture smallpox vaccine should be offered to the general population. Rev Med Virol. 2003;13:5-15. 7. Frey S, Couch R,Tacket C, et al. Clinical responses to undiluted and diluted smallpox vaccine. New Engl J Med. 2002;346:1265-74. 8. Suarez V, Hankins G. Smallpox and pregnancy: from eradicated disease to bioterrorist threat. Obstet Gynecol. 2002;100:87-93. 9. Jahrling PB, Zaucha GM, Huggins JW. Countermeasures to the reemergence of smallpox virus as an agent of bioterrorism. In: Scheld WM, Craig WA, Hughes JM, eds. Emerging Infections 4. Washington, DC:ASM Press; 2000. 10. Henderson D, Inglesby T, Bartlett J, et al. Smallpox as a biological weapon: medical and public health management. Working Group on Civilian Biodefense. JAMA. 1999;281:2127-37. 11. De Clercq E. Cidofovir in the therapy and short-term prophylaxis of poxvirus infections. Trends Pharmacol Sci. 2002;23:456. 12. US Centers for Disease Control and Prevention. Bioterrorism Agents/Diseases. Available at: http://www.bt.cdc.gov/agent/ agentlist.asp. 13. Wehrle PF, Posch J, Richter KH, Henderson DA. An airborne outbreak of smallpox in a German hospital and its significance with respect to other recent outbreaks in Europe. Bull World Health Organ. 1970;43:669-79. 14. Jackson R, Ramsay A, Christensen C, et al. Expression of mouse interleukin-4 by a recombinant ectromelia virus suppresses cytolytic lymphocyte responses and overcomes genetic resistance to mousepox. J Virol. 2001;75:1205-10.

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Influenza Virus Attack Anna I. Cheh

DESCRIPTION OF EVENT Influenza is an acute respiratory illness of viral etiology. The influenza virus is a member of the Orthomyxoviridae family. The genome of this enveloped virus contains eight segmented, single-stranded, negative sense RNA. There are three immunologic types:A, B, and C. Type A is the primary pathogen for human disease. Its two surface glycoproteins, hemagglutinin (H) and neuraminidase (N), determine host immunity and subtype designation. Unlike types B and C that reside only in humans, type A also infects birds, pigs, horses, and sea mammals. The gene’s segmented nature facilitates genetic reassortment during infection within this broad reservoir. Such genetic shifts (major) or drifts (minor) lead to the genetic diversity of type A.1 Major antigenic variations underlie the deadly worldwide pandemics, such as that of 1918 and 1957. New concerns regarding disease epidemiology surfaced in 1997 as direct disease transmission from animals to humans caused fatalities in Hong Kong. Influenza is not classified as a bioterrorism agent by the Centers for Disease Control and Prevention.2 Among immunocompetent individuals, influenza infection is largely self-limited with low mortality rates. However, several factors support the possible role of influenza in an urban attack. Influenza is highly contagious. Transmission can be via respiratory droplets or fomites.3 Aerosol transmission of influenza, the method likely used in an attack, takes 27,000 times fewer virion than that required in direct respiratory contact to induce equivalent disease.4 The incubation period is short, ranging from 18 to 72 hours. A person is contagious within a day after infection and can remain so for a week after becoming symptomatic. Also, the influenza virus is readily available, unlike many other agents that are more difficult to obtain. More worrisome are recent advances that allow infectious agents to be directly produced in the lab without a natural template.5 The classic presentation of influenza is the abrupt onset of fever, headache, myalgia, and extreme malaise. The virus targets and reproduces within the ciliated columnar epithelial cells of the respiratory tract.1 Therefore, signs of both upper and lower respiratory involvement can also be present. Constitutional symptoms are more pronounced during the acute phase 684

encompassing the first 3 to 5 days. The subsequent convalescence phase can last for weeks with lingering respiratory symptoms and malaise, often termed postinfluenza asthenia.6 Complicated influenza has a predilection for individuals with chronic underlying illnesses. High-risk groups include those with cardiovascular or pulmonary disease, diabetes mellitus, renal disease, or immunosuppression. Pneumonia is the complication most responsible for the excess fatalities associated with influenza outbreaks. Other less-common complications include myositis, myocarditis, rhabdomyolysis, and Reye’s syndrome. Central nervous system involvement such as encephalitis and aseptic meningitis has also been documented, although a direct relationship has been never clearly established. Viremia is rare. Diagnosis is often based on clinical presentation. This is especially appropriate within an epidemic. However, during a possible terrorist attack, distinguishing between different viral pathogens will be imperative. Tissue cultures can be obtained within 48 to 72 hours of inoculation.7 Increasingly, rapid viral diagnostic tests such as enzyme immunoassays (EIA) and PCR are also available for diagnosis. These newer methods, however, cannot be used to identify the responsible subtype strain. Although common, influenza can still be a formidable foe. Attack rates are between 10% and 20% in the general population but can exceed 50% during pandemics. Institutionalized and close-quartered populations are especially at increased risk. During non-pandemic years, approximately 20,000 annual deaths are attributed to influenza in the United States.8

PRE-INCIDENT ACTIONS Influenza is possibly the most tracked virus in the world. The CDC and the World Health Organization (WHO) Global Influenza Network has in place an extensive worldwide surveillance system (WHO Flunet) to monitor disease activity and identify viral isolates for the development of the annual vaccine. Influenza has the distinct advantage of having this developed immunization infrastructure. Two types of vaccine are currently approved for use in the United States. The trivalent inac-

tivated vaccine contains a killed virus and is safe to use during pregnancy and breastfeeding. The newer trivalent live-attenuated cold-adapted vaccine (LAIV) is administered intranasally. Effective surveillance and early detection of outbreaks is pivotal for agents such as influenza for which effective prophylaxis and immunization exist.8 Establishing population immunity to influenza will also aid in distinguishing it from the more deadly biological agents that have a similar initial prodrome.9 Therefore, increasing immunization rates should be part of a broader strategy against bioterrorism.

POST-INCIDENT ACTIONS Recognition of an emerging pandemic is aided by influenza’s classic presentation and clustering epidemiology. Initiation of a coordinated effort to expedite vaccine development and dissemination will be pivotal. During the initial period following a bioterrorist attack, antiviral agents are another key mechanism of containing morbidity and protecting exposed individuals.10 Public awareness campaigns regarding measures to reduce transmission and seeking early medical intervention should be quickly instituted to blunt the mortality of an outbreak.8,11

ens were slaughtered to prevent further transmission of the Hong Kong avian influenza virus in 1997. Influenza is a virus that impacts certain segments of the population disproportionately. As the population ages and a greater segment live with higher risk morbidities, the impact of a pandemic will also escalate.

PITFALLS • Failure to consider terrorism during the early phase of a pandemic because of influenza’s natural existence. • Failure to diagnose accurately. The broad spectrum of influenza symptoms often overlaps with many other possible bioterrorism agents. Clinicians should be educated for greater utilization of confirmatory tests and reporting positive cases to a central tracking database. • Failure to institute mechanisms to ensure adequate supply of antiviral medications, currently unlikely to be able to meet prolonged demand. • Failure of existing vaccine infrastructure to respond quickly to a novel virulent strain. Currently, a vaccine is almost a year out of date by time of administration. • Failure to update immunization strategy to better address the unique threats of terrorism. • Failure to anticipate the social and economic impact of a pandemic outbreak.

MEDICAL TREATMENT OF CASUALTIES Treatment of influenza is largely supportive. Specific antiviral agents such as amantadine and rimantadine are approved for both the treatment and prophylaxis for influenza A. Newer agents such as oseltamivir and zanamivir are effective for both types A and B. Although not proven to be any more efficacious, these agents are associated with fewer central side effects. Optimal efficacy of all drugs depends on starting the regimen within 48 hours after symptom onset. During possible acute outbreaks, these agents can provide effective chemophylaxis until vaccine-induced immunity can be established in target populations.10 Constraints on existing medical systems could reach critical levels, pending the extent of the attack.

UNIQUE CONSIDERATIONS The potential advantage of influenza as a bioterrorism agent is its genetic variation. A variant strain from which wide human immunity does not exist could hold devastating potency.12 Some experts estimate that a virus of comparable virulence to the 1918 strain could result in 100 million deaths today.13 Although the self-limiting course of influenza would fail to produce the dramatic and immediate effects that are the aim of terrorist acts, the real impact of an influenza outbreak will be its indirect costs. Modern influenza pandemics have evolved into economic disasters even as medical advances help to avert direct fatalities.14 For example, 3 million chick-

CASE PRESENTATION In a large metropolitan city, public health officials are baffled by a surge of influenza cases earlier in the winter season than expected. CDC and WHO work overtime to identify the responsible strain, ultimately found to be a novel subtype different than any previously recorded. Nursing homes are virtually emptying out as residents are admitted to hospitals for pneumonia. Even the local colleges are feeling the effects as the school clinics are inundated with students complaining of debilitating myalgia and malaise. Parents pull children from school to avoid exposure. Doctors are flooded by calls from patients frustrated with being unable to fill their amantadine prescription at their local pharmacies. Antiviral medications are being depleted as people wait for the new vaccine to arrive, which is announced to be available in 8 months. Public health officials predict one of the worst influenza seasons ever in economic costs as more people are calling in sick, productivity is lost, tourism shuts down, and hospital resources are stretched to the breaking point.

REFERENCES 1. Schoch-Spana M. Implications of pandemic influenza for bioterrorism response. Clin Infect Dis. 2000;31: 1409-13. 2. Centers for Disease Control and Prevention. Bioterrorism Agents/Diseases. Available at: http://www.bt.cdc.gov/agent/ agentlist-category.asp. 3. Rao BL. Epidemiology and control of influenza. Nat Med J India. 2003;16:143-8.

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4. Madjid M, Lillibridge S, Mirhaji P, et al. Influenza as a bioweapon. J R Soc Med. 2003;96:345-6. 5. Cello J, Paul AV,Wimmer E. Chemical synthesis of poliovirus cDNA: generation of infectious virus in the absence of natural template. Science. 2002;297:1016-8. 6. Harrison’s Internal Medicine On-Line (Chap 190). Available at: www.accessmedicine.com. 7. Covalciuc KA, Webb KH, Carlson CA. Comparison of four clinical specimen types for detection of influenza A and B viruses by optical immunoassay (FLU OIA Test) and cell culture methods. J Clin Microbiol. 1999;37:3971. 8. Lutz BD, Bronze MS, Greenfield RA. Influenza virus: natural disease and bioterrorism threat. J Okla State Med Assoc. 2003;96:27-8. 9. Irvin CB, Nouhan PP, Rice K. Syndromic analysis of computerized emergency department patients’ chief complaints: an opportunity for bioterrorism and influenza surveillance. Ann Emerg Med. 2003;41:447-52.

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10. Simberkoff MS. Vaccines for adults in an age of terrorism. J Assoc Acad Min Phys. 2002;13:19-20. 11. Krug RM. The potential use of influenza virus as an agent for bioterrorism. Antiviral Res. 2003;57:147-50. 12. Owens SR. Being prepared: preparations for a pandemic of influenza. EMBO Reports. 2001;21:1061-3. 13. Webster RG, Shortridge KF, Kawaoka Y. Influenza: interspecies transmission and emergence of new pandemics. FEMS Immun Med Microbiol. 1997;18:275-9. 14. Longini IM, Halloran ME, Nizam A, et al. Containing pandemic influenza with antiviral agents. Am J Epidemiol. 2002;159:623-3. 15. Ferguson NM, Fraser C, Donnelly CA, et al. Public health risk from the Avial H5N1 influenza epidemic. Science. 2004;304:968-9. 16. O’Brien KK, Higdon ML, Halverson JJ. Recognition and management of bioterrorism infections. Am Fam Phys. 2003;67:1927-34.

chapter 127

Monkeypox Attack John D. Malone

DESCRIPTION OF EVENT Monkeypox is an orthopox virus, recognized in 1958 in laboratory monkeys. The natural host may be an African squirrel, but the virus can also infect rodents and rabbits. Monkeypox is in the same genus as smallpox (Variola major and minor), Molluscum contagiosum, cowpox, and the vaccinia virus. Other non–human associated animal orthopox infections include volepox, skunkpox, raccoonpox, camelpox, and buffalopox. Monkeypox has been endemic in Ghana and Zaire and is associated with the hunting and consumption of infected monkeys and rodents.1 In April 2003,six infected African rodents,Gambian giant rats, were imported into the United States. They transferred the monkeypox virus to prairie dog rodents housed in adjacent cages. Within 2 months, human cases were reported in individuals who had been bitten or scratched by the infected prairie dogs.2 In the outbreak, there were 71 suspected cases and 37 confirmed cases.3 There was no laboratory-confirmed human-to-human transmission. The patients presented with fever greater than 38˚ C and skin lesions. Skin manifestations ranged from nodular swellings in the wound margins to satellite and disseminated lesions. Papules progressed to vesicles and pustules. Significant symptoms include severe chills and sore throat. Lymphadenopathy and tonsillar hypertrophy were present. Along with an intimate rodent animal exposure history, adenopathy is a helpful sign for emergency physicians to differentiate monkeypox from a “flu syndrome” in those with minimal or subtle skin lesions and similar headache, fever, sweats, chills, and cough. Four of the initial eleven cases were hospitalized. The clinical course was self-limited with some central scarring of larger lesions. With close cooperation of the Centers for Disease Control and Prevention (CDC) and multiple Midwestern state health authorities, the outbreak was controlled through an emergency embargo and quarantine orders against the “importation, sale, distribution, or display of prairie dogs or any mammals that had been in contact with prairie dogs after April 1, 2003.”4 Appropriate and aggressive animal control measures prevented the establishment of monkeypox in the North American rodent population; a vast improvement compared with the his-

tory of the plague bacillus, Yersinia pestis, that entered the Southwestern U.S. desert rodent population after a 1900 epidemic in San Francisco.5 The skin lesions for monkeypox are identical to those for smallpox: morbilliform, hard and pea sized on an erythematous base, and classically described as dew drops on a rose petal. The rash begins as maculopapular lesions 2 to 5 mm in diameter, progressing through papular, vesicular, pustular, and crust phases over a 14-day period.6 The lesions are initially located on cooler body parts, particularly the extremities including the palms and soles,and the face. Over the initial days, the lesions spread to the trunk. The initial papules become umbilicated vesicles, with all of the lesions in the same stage at the same time. The skin vesicles are a product of bloodborne viral seeding of the terminal capillaries in the initial viremia. The initial viremia is manifested by the sudden onset of fever, malaise, headache, and severe back pain, and manifested less often with abdominal pain and vomiting.7 As for the differential diagnosis of monkeypox, herpes viruses are much more likely to be an etiology of similar skin lesions. The Varicella Zoster Virus (VZV) produces varicella “chickenpox”vesicles that begin centrally on the trunk. The multiple lesions exist in different stages of maturation. VZV may also cause disseminated herpes zoster in an immunocompromised host. A varicella virus direct fluorescent antibody (DFA) test should be available in major emergency departments and initially performed to diagnose this infection. Coxsackievirus commonly occurs in children under 10 years of age in the autumn season. Secondary syphilis (syphilis serology should be positive), erythema multiforme, and drug eruptions can produce less typical vesicular rashes on the palm and soles. Rocky Mountain Spotted Fever, a rickettsial illness, is associated with a spring/summer tick exposure in the Southeastern United States. Meningococcal infection is characterized by rapid progression to shock. Molluscum infection occurs in healthy children and HIV-infected adults; the painless lesions do not cause fever. Definitive laboratory diagnosis of monkeypox infection is required to ensure that smallpox is not present and for an appropriate public health response. Electron microscopy of vesicular scrapings will identify orthopox viruses by the appearance of an exceedingly large box with rounded corners. Polymerase chain reactions definitively 687

identify the specific species. Tissue from lymph nodes and blood specimens can also be evaluated. Specimen collection instructions are detailed by the CDC.8 It is not known whether the monkeypox virus was ever weaponized. However, the process would probably be similar to the method used to weaponize the smallpox virus. Scientists from the former Soviet Union accomplished this. Like smallpox, monkeypox is contagious but less so. If a stable, infectious monkeypox biological aerosol was produced and delivered as a fine particle aerosol under ideal atmospheric conditions over a targeted population, one would expect to see large numbers of casualties presenting at about the same time to local hospitals and doctor’s offices with signs and symptoms as described here. The ensuing epidemic and secondary cases would probably not be as severe as one would expect to see if a smallpox weapon was used, since the monkeypox virus is not nearly as contagious as the smallpox virus. Of course, with the genetic engineering techniques that are available today, novel characteristics could be created and infectivity of the virus could be enhanced. There is no evidence to date that this has been attempted.

PRE-INCIDENT ACTIONS Emergency departments should have well-rehearsed standard operating procedures to evaluate potentially contagious infectious disease patients using airborne transmission precautions (protective gowns, gloves, HEPA face masks). A small cadre of smallpox-vaccinated healthcare workers should be available to initially evaluate and care for patients with suspected orthopox infection. Along with concerns for patient transmissible bioterrorism agents, such as smallpox, pneumonic plague, and viral hemorrhagic fevers, clinical suspicion is necessary for the more common agents of SARS and rubeola virus in our highly mobile global society.

POST-INCIDENT ACTIONS When presented with an initial case of monkeypox, great concerns about the possibility of smallpox are appropriate in this age of ongoing terrorist threats. In contrast to smallpox, monkeypox would be a poor agent for bioterrorism because of a very low mortality rate and respiratory transmission by large droplets that requires direct and prolonged face-to-face contact. Monkeypox is highly unlikely to be able to sustain itself in human communities. However, if suspected, appropriate local and state health authorities must be notified early to assist with agent identification.

MEDICAL TREATMENT OF CASUALTIES Supportive therapy with antipyretics and fluids are indicated. Monkeypox has a low lethality (1.5% in a 1996 Democratic Republic of the Congo outbreak) and requires close family contact for transmission. Accumulating expe688 BIOLOGIC EVENTS

rience in the United States suggests a relatively low risk of person-to-person transmission. According to the CDC, all healthcare settings such as hospitals, emergency departments, and physician offices should have the capacity to care for monkeypox-infected patients and protect health care workers and other patients from exposure.9 A combination of standard, contact, and droplet precautions, which include gowns, gloves, eye shields, and surgical masks, should be applied in all healthcare settings when concerns for monkeypox exist. Because of a theoretical risk of airborne infection, airborne precautions using N95rated respirator masks are recommended when possible. A negative pressure room should be used if available. Viremic individuals spread the disease through large respiratory droplets, most likely with the symptoms of cough, pharyngitis, and fever.

Unique Considerations Smallpox vaccination with the vaccinia virus (Dryvax) is protective against monkeypox infection. The vaccinia virus likely evolved through a reassortment of the cowpox virus and the smallpox virus. During the 2003 monkeypox outbreak, CDC guidelines for vaccination included public health and animal control investigators, healthcare workers caring for monkeypox patients or those who may be asked to care for infected patients, or family members with close contact with someone who was symptomatic with monkeypox. Also included were veterinarians and their technicians who had direct physical exposure to an infected animal. Vaccination up to 14 days after exposure will attenuate or prevent monkeypox illness. Extensive data from the Department of Defense exist over the safety and efficacy of the “Dryvax” smallpox vaccination.10 As of July 2005, more than 830,000 individuals have been vaccinated. A causal relationship to one death from a lupus-like illness after both anthrax and smallpox vaccinations has resulted along with 99 cases of myopericarditis with documented complete recovery in 64 cases. Among 27,700 smallpox vaccinated healthcare workers, there were no cases of transmission of vaccinia to a patient. Other investigators have also shown the risk of inadvertent vaccinia transmission from vaccination sites covered by occlusive dressings to be quite low.11 Fear and panic are major issues for monkeypox viral infection. Commonality in name with smallpox raises anxieties and misperceptions in the public, patients, and healthcare providers. Significant psychological and economic impacts result. Preliminary knowledge of monkeypox, personal protective equipment, and effective leadership of the healthcare team will ensure appropriate patient care and avoid crisis and closure of emergency departments.

PITFALLS • The skin lesions of monkeypox and smallpox are identical. • Lymphadenopathy, tonsillar hypertrophy, and intimate rodent exposure will assist in differentiating monkeypox from a “flu syndrome.”

• Monkeypox has relatively low risk of person-to-person transmission; however, airborne precautions (N95 mask) are recommended. • A high clinical suspicion and well-rehearsed standard operating procedures are needed to safely evaluate potentially contagious patients. • Emergency departments should have a cadre of smallpox-vaccinated healthcare workers.

CASE PRESENTATION The right index finger of a child has a lesion with a raised border and necrotic center 14 days after a prairie dog bite and 11 days after a febrile illness.12 Secondary lesions also present on the dorsum of the left hand. The pustules are raised, firm, several millimeters in diameter, and with erythematous flares. One day previously, her mother developed fever, sweats, malaise, and sore throat. The mother has smaller disseminated umbilicated vesicles. The family has multiple animals, including cats, dogs, horses, goats, and donkeys.

3. Cunha BE. Monkeypox in the United States: an occupational health look at the first cases. AAOHN J. 2004;52:164-8. 4. CDC. Multistate Outbreak of Monkeypox–Illinois, Indiana, Wisconsin, 2003. MMWR Morb Mortal Wkly Rep. 2003;52:537-40. 5. Smith G. Plague on Us. New York: The Common Wealth Fund; 1941. 6. DiGiulo DB, Eckburg PB. Human monkeypox: an emerging zoonosis. Lancet Infect Dis. 2004;4:15-25. (Review article) 7. Jezek Z, Szczeniowski M, Paluku KM, et al. Human monkeypox: clinical features of 282 patients. J Infect Dis. 1987;156:293-8. 8. Centers for Disease Control and Prevention. Interim guidance for collection of diagnostic specimens from persons with suspected monkeypox, June 23, 2003. Available at http://www.cdc.gov/ncidod/monkeypox/diagspecimens.htm. 9. Centers for Disease Control and Prevention. Updated interim infection control and exposure and exposure management guidance in the health care and community setting for patients with possible monkeypox virus infection. Available at: http:// www.cdc.gov/ncidod/monkeypox/infectioncontrol.htm. 10. Department of Defense. Smallpox vaccination program (updated September 20, 2005). Available at http://www. smallpox.mil 11. Talbot TR, Ziel E, Doersam JK, et al. Risk of vaccinia transfer to hands of vaccinated persons after smallpox immunization. Clin Infect Dis. 2004;38:536-41. 12. Reed KD, Melski J, Stratman E. Index case and family infection of monkey pox from prairie dogs diagnosed in Marshfield, WI, Marshfield Clinic May-June 2003. Available at: http://www. research.marshfieldclinic.org/crc/monkeypox.asp.

REFERENCES 1. Huntin YJF, Williams RJ, Malfait P, et al. Outbreak of human monkeypox, Democratic Republic of Congo, 1996 to 1997. Emerg Infect Dis. 2001;7:434-8. 2. Reed KD, Melski JW, Graham MB, et al. The detection of monkeypox in humans in the western hemisphere. N Engl J Med. 2004;350:342-50.

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chapter 128

Hantavirus Pulmonary Syndrome Attack Bonnie H. Hartstein and Curtis J. Hunter

DESCRIPTION OF EVENT Hantavirus pulmonary syndrome (HPS) is characterized by rapidly developing non-cardiogenic pulmonary edema, which develops after infection with rodentborne Hantavirus. Early recognition of HPS is essential as the initial flu-like symptoms of malaise, fever, and muscle aches can progress to shock and complete respiratory failure within a few days.1 Although hantavirus has not been weaponized or used for bioterrorism to date, it is recognized by the Centers for Disease Control and Prevention (CDC) as a category C agent, an emerging pathogen that could be engineered for mass exposure in the future because of its presumed ease of production and dissemination, and potential for high morbidity and mortality.2 A genus of the family Bunyaviridae, Hantavirus was first isolated in Korea in 1978 as the culpable agent in the Old World disease known as hemorrhagic fever with renal syndrome (HFRS), an acute prostrating febrile illness with renal failure and shock.3,4 In 1993 a mysterious clinical entity causing fever, rapid respiratory failure, and cardiopulmonary dysfunction killed 29 people in the southwestern United States.5 Linked by genetic sequencing to a previously unknown Hantavirus species but lacking the renal and hemorrhagic manifestations, the disease was named hantavirus pulmonary syndrome and changed the recognized spectrum of hantavirus disease. Over 20 different sero/genotypes of Hantavirus have been identified, each maintained in nature by a single unique rodent species. Human infection occurs through inhalation of aerosolized virus shed in rodent saliva, urine, and feces, or by direct inoculation via rodent bites.4 The primary causative agent of the largest outbreak in the United States, the Sin Nombre virus, is carried by the deer mouse, Peromyscus maniculatas. Other hantaviruses know to cause HPS in the United States include the New York, Black Canal, and Bayou viruses hosted by the white-footed mouse (Peromyscus leucopus), the cotton rat (Sigmodon hipidus), and the rice rat (Oryzomys palustris). The rodent reservoir of the Seoul virus, Rattus norvegicus, thought to have been brought by cargo ship to the Western Hemisphere from Europe, has caused the only cases of HFRS documented in the United States.6 Nearly all of the United States falls within 690

range of one or more hantavirus-carrying rodent species, all of which cause HPS. The incubation period for human hantavirus infections is documented from 4 to 42 days, with an average range of 12 to 16 days.7 HPS progresses through four clinical phases: prodrome, pulmonary edema and shock, diuresis, and convalescence.8 The initial prodrome lasts for 3 to 6 days and is characterized by malaise, myalgia, fever, tachypnea, and gastrointestinal symptoms such as nausea, vomiting, diarrhea, or abdominal pain. In 10% of cases the abdominal pain is reported to be severe enough as to mimic appendicitis.1 Presenting symptoms may overlap with more common viral infections, challenging early recognition by healthcare workers. One study attempting to quantify a clinically distinct constellation of symptoms suggests excluding patients with rapid Influenza A proven infection from consideration and that the presence of sore throat or nasal symptoms and the finding of an injected pharynx are less likely to be associated with HPS.9 The subsequent cardiopulmonary phase is heralded by the acute onset of non-cardiogenic pulmonary edema.10 Clinically, patients have progressive cough and shortness of breath. On the cellular level, significant capillary leak in pulmonary endothelial cells occurs.7,10 The time interval from the development of dyspnea to the need for ventilator support is reported to be within 1 to 6 hours, underscoring the extremely rapid progression of respiratory collapse.1,8 Other signs include hypoxia and copious amber-colored non-purulent secretions with secretion protein/serum protein ratio greater than 80%.5,11 Specific laboratory and radiographic findings that are suggestive of HPS assist in diagnosis and should raise clinical suspicion. A peripheral blood smear triad of thrombocytopenia, leukocytosis with left shift, and circulating immunoblasts are unique to HPS in North America.11 Elevated lactate levels, and hemoconcentration up to 77% that corrects to anemic levels after fluid resuscitation, are observed.12 Radiographically HPS is distinguished by the central location of infiltrates rather than the peripheral pattern typically seen in ARDS and the lack of focal consolidation common in most pneumonias.9 The sepsis syndrome observed in HPS features a diminished cardiac index and normal or elevated systemic vascular resistance, which is the opposite of that

typically seen in sepsis.13 Hypotension, which may be seen initially, is a result of low cardiac stroke volume resulting from inadequate left ventricular preload exacerbated by myocardial depression and is usually marked by hemoconcentration. Death rates range between 50% and 70% with cardiogenic shock and pulseless electrical activity as the proximate cause.5 Survivors of the cardiopulmonary phase recover quickly with a spontaneous diuresis occurring 2 to 5 days after the onset of pulmonary edema, usually facilitating extubation within 1 week of initiating ventilator support. Convalescence ensues with minor residual respiratory impairment.8 Identification of the virus is achieved through serologic testing in the acutely ill for IgG and IgM antibodies to viral nucleocapsid proteins.1 ELISA assays are available at most state public health laboratories or by state health department referral at CDC.6 Because of the time delay before results are obtained, a recombinant immunoblot assay in the form of a test strip is being evaluated.1

PRE-INCIDENT ACTIONS Exposure of individuals or groups to hantavirus might occur naturally as a result of increased exposure caused by an environmental change such as increased rodent food production or decreased rodent predator population, or because of a planned bioterrorist attack. Similar to the epidemic that heralded the discovery of HPS in the southwestern United States in 1993, individuals or groups of people can be exposed through contact with contaminated material. Increased rodent population or high-risk activities such as cleaning enclosed rodentinfested areas can lead to infection. Disaster scenarios, either naturally occurring or as a result of terrorism, that displace populations, disrupt the sanitation infrastructure, or create living conditions where people are forced to reside in makeshift structures or sleep on the ground significantly increase the risk of hantavirus exposure. Risk reduction suggestions published by the CDC serve as a useful guide to mitigate risks. Actions to reduce exposure to rodents involve securing food and trash in rodent-proof containers; keeping items that attract rodents such as garbage cans, woodpiles, and bird feeders far from human dwellings; and using raised cement foundations in new construction of outbuildings or shelters.14 Hantavirus is recognized as an emerging pathogen for bioterrorism because of its relative ease of transmission and high mortality. Dissemination would most likely occur via aerosolization of infectious particles released over populated areas. Bioterrorists might use low-flying aircraft, munitions, or indoor contamination through air ducts to initiate exposure.

POST-INCIDENT ACTIONS Suspicious patterns of disease presentation would be the first clue that an HPS outbreak had occurred at the hands

of bioterrorists. An understanding of the demographic distribution of naturally occurring hantavirus infection allows the healthcare professional to recognize unusual variations and to suspect bioterrorist activity. Infection caused by hantavirus and rodent hosts not recognized in the United States, an infectious disease consistent with HFRS in the New World, and disease in nonendemic areas or in patients with no travel history should all raise suspicion of an unnatural or deliberate infection. Virus isolation, genotyping, and comparison to known national and world prevalence data could unveil irregular geographic incidence patterns. Cases of natural hantavirus have generally occurred in young adults and previously healthy persons because exposure occurred during activities like farming, cleaning, or camping.5 An attack generated by terrorism with infectious particles in high concentration on the ground or in soil in densely populated areas might affect children, who are smaller and shorter, in greater proportion than observed naturally. Also, an increase in disease incidence without a rise in the endemic rodent population or in persons not exposed to rodents should raise suspicion. Universal precautions and respiratory isolation of affected individuals is recommended. Although personto-person transmission is generally not recognized, during one hantavirus outbreak in Argentina, five health care workers involved in treating HPS patients may have contracted disease without known exposure to rodents.3

MEDICAL TREATMENT OF CASUALTIES Supportive care is the mainstay of treatment for HPS. Volume replacement must be cautious and conservative because of the potential for significant pulmonary capillary leak. Pulmonary artery occlusive pressures higher than 10-12 mmHg are associated with significant pulmonary edema. Classic to HPS is a shock state characterized by decreased cardiac output and increased systemic vascular resistance, although frank hypotension is also observed. Use of inotropic agents such as dobutamine should usually be accompanied by judicious volume resuscitation. Despite the presence of severe pulmonary edema, adequate oxygenation can usually be maintained with mechanical ventilation and high levels of positive end-expiratory pressure.1 Further studies on the treatment of HPS are needed to assess the role of immunologic therapy and inflammatory mediators on vascular function, as well as the use of antiviral agents such as ribavirin, which has been shown to reduce mortality in HFRS.6 It is also conceivable that some added benefit could be achieved by applying the principles of early goal-directed therapy, which is showing some promise among patients with sepsis.

UNIQUE CONSIDERATIONS The importance of rapid recognition of HPS and the need for widespread dissemination of information HANTAVIRUS PULMONARY SYNDROME ATTACK 691

between other health care institutions and health departments is the key to effective management. Since nearly all infected patients become ventilator dependent, the prospect of a mass casualty situation caused by HPS could prove catastrophic unless adequate intensive care unit capabilities were mobilized and appropriately staffed to augment local healthcare facilities.

• Failure to recognize respiratory failure and initiate appropriate ventilatory support • Failure to prepare for significant numbers of patients requiring ventilator support • Failure to judiciously manage fluid balance and cardiovascular status REFERENCES

PITFALLS • Failure to rapidly recognize the symptoms of HPS and to disseminate information to other health care institutions and health departments

CASE PRESENTATION A 24-year-old male presents to the emergency department of a small community hospital with a chief complaint of flu-like symptoms and cough. He states that 3 days ago he awoke with a headache, general malaise, vomiting, diarrhea, and crampy abdominal pain, which he initially attributed to a hangover and food poisoning. Over the following days the symptoms persisted and worsened. Most concerning to him is a dry cough with amber-colored sputum that started last night, kept him from sleep, and prevented him from his normal routine of running in the morning. He states he just returned from a trip to White Sands Proving Ground,Arizona where he participated in a commemorative marathon honoring military troops killed in combat. He states that two of his close friends who also participated in the event are developing the same symptoms. His vital signs are pulse 86, respiratory rate 22, blood pressure 112/78, temperature 101.4˚F, and pulse oximetry 99% on room air. A chest radiograph reveals early interstitial edema with Kerley B lines and peribronchial cuffing. The patient begins to complain of dyspnea and the pulse oximetry continues to decline despite switching to a non-rebreather mask with high flow oxygen. A portable chest radiograph reveals significantly worsening pulmonary edema and the patient is electively sedated and intubated for respiratory failure.

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1. Simpson SQ. Hantavirus pulmonary syndrome. Heart Lung. 1998;27:51-7. 2. Moran GJ. Threats in bioterrorism II: CDC category B and C agents. Emerg Med Clin North Am. 2002;20:311-30. 3. McCaughey C, Hart CA. Hantaviruses. J Med Microbiol. 2000; 49:587-99. 4. Chapman LE, Khabbaz RF. Etiology and epidemiology of the Four Corners hantavirus outbreak. Infect Agents Dis. 1994;3:234-44. 5. Levy H, Simpson SQ. Hantavirus pulmonary syndrome. Am J Respir Crit Care Med. 1994;149:1710-3. 6. Doyle TJ, Bryan RT, Peters CJ. Viral hemorrhagic fevers and hantavirus infections in the Americas. Infect Dis Clin North Am. 1998;12:95-110. 7. Butler JC, Peters CJ. Hantaviruses and hantavirus pulmonary syndrome. Clin Infect Dis. 1994;19:387-95. 8. Jenison S, Koster F. Hantavirus pulmonary syndrome: clinical, diagnostic, and virologic aspects. Semin Respir Infect. 1995; 10:259-69. 9. Moolenaar RL, Dalton C, Lipman HB, et al. Clinical features that differentiate hantavirus pulmonary syndrome from three other respiratory illnesses. Clin Infect Dis. 1995;21:643-9. 10. Graziano KL. Hantavirus pulmonary syndrome: a zebra worth knowing. Am Fam Physician. 2002;66:6. 11. Duchin JS, Koster FT, Peters CJ, et al. Hantavirus pulmonary syndrome: a clinical description of 17 patients with a newly recognized disease. N Engl J Med. 1994;330:949-55. 12. Zakik SR, Greer PW, Coffield LM, et al. Hantavirus pulmonary syndrome, pathogenesis of an emerging infectious disease. Am J Pathol. 1995;146:552-79. 13. Hallin GW, Simpson SQ, Crowell RE, et al. Cardiopulmonary manifestations of hantavirus pulmonary syndrome. Crit Care Med. 1996;24:252-8. 14. Mills JN, Corneli A, Young JC, et al. Hantavirus pulmonary syndrome—United States: updated recommendations for risk reduction. MMWR 2002;51:RR-9.

chapter 129

Hendra and Nipah Virus Attack (Hendra Virus Disease and Nipah Virus Encephalitis) Kelly J. Corrigan

DESCRIPTION OF EVENT Both the Hendra virus and the Nipah virus belong to the same subfamily, Paramyxoviridae. They have both been identified in various zoonotic disease outbreaks in Southeast Asia and Australia within the past 10 years. Formerly known as the equine Morbillivirus, Hendra virus was the first to be identified and has been implicated in three separate disease outbreaks in Queensland,Australia between 1994 and 1999. It was first isolated in 1994 following an outbreak of severe respiratory disease in both horses and humans in Brisbane, Queensland, Australia.1-3 Out of 21 horses infected in the first outbreak, 14 died. Three human infections resulting in two deaths have been reported as a result of the Hendra virus. These individuals reportedly had severe flu-like symptoms and others have presented with severe, often fatal, pneumonia. Encephalitis-like clinical signs have also been reported. The primary source of the Hendra virus appears to be the black fruit bat, with birds having been implicated as carriers of the deadly virus as well.4,5 The Nipah virus is genotypically similar to the Hendra virus, and they both belong to a new genus within the family Paramyxoviridae.6 Nipah has been implicated in outbreaks of encephalitis in Malaysia in 1998 and 1999. Investigations of these outbreaks concluded that the pigs and humans were likely infected with Nipah via the respiratory route. In April 1999, 100 fatal encephalitis cases were reported in Malaysia.7 Nipah was identified as the cause, and pigs were the primary source. However, Nipah does not appear to be transmitted from person to person. Nipah-infected patients present with fever, headache, dizziness, vomiting, and altered mental status.8 Autonomic instability is also a common sequelae of infection that suggests brain stem involvement. Some patients who have undergone magnetic resonance imaging demonstrate widespread microinfarctions of the CNS, which are presumably the result of small vessel disease.8 This is supported by direct evidence from human autopsies that have revealed systemic CNS thrombotic occlusions and microinfarctions in victims of Nipah virus infection.9 The Centers for Disease Control and Prevention (CDC) has conclusively identified both of these viruses and has

developed serologic tests to detect both IgG and IgM antibodies to Hendra and Nipah.6 Both IgG and IgM antibodies can be detected in blood and cerebrospinal fluids.10

PRE-INCIDENT ACTIONS In preparation for potential chemical and biological terrorist attacks, the Committee on Research and Development to Improve Civilian Medical Response recommends that major hospitals conduct mass-casualty planning and training; designate isolation rooms available for infectious diseases, create decontamination capacity, and be fully supplied with drugs, ventilators, and personal protective equipment.11 The committee also encourages the CDC to keep medical care providers up to date on current dangerous biologic materials and promotes advance notice from law enforcement agencies regarding potential terrorist incidents. The CDC must maintain a containment level 4 laboratory in order to run the appropriate tests that identify Nipah and Hendra, without risking further human infection.

POST-INCIDENT ACTIONS Suspicion of an outbreak of Hendra or Nipah virus infection should be reported to the proper authorities (local public health and CDC) immediately so that appropriate diagnostic and response measures can be taken. Isolation of the viruses, as previously mentioned, should only be done in a biosafety level 4 containment laboratory located at either The United States Army Medical Research Institute for Infectious Diseases (USAMRIID) or the CDC.6 Humanto-human transmission is not known. Infected patients should be treated by following standard precautions. Infected animals apparently excrete the Hendra virus through their urine, therefore, in order to prevent further transmission of Hendra virus, it is recommended that horse stables follow strict hygiene guidelines.4 Nipah outbreak control has been accomplished in Malaysia through the mass culling of hundreds of thousands of potentially infected pigs and by banning the importation 693

of pigs into the country. Other efforts include educational programs directed at farmers and a national surveillance program to monitor for outbreaks of disease.1

MEDICAL TREATMENT OF CASUALTIES Supportive therapy should be initiated as appropriate, including airway management and ventilatory support. Previous work has demonstrated the drug ribavirin to be effective against both Hendra and Nipah viruses in vitro.2 A trial of ribavirin in 140 patients infected with Nipah virus, with 54 of these patients serving as the control, showed 32% mortality in the ribavirin group compared with 54% mortality in the control group.12 Given the low side effect profile of ribavirin in the acute treatment setting, ribavirin should be seriously considered in Nipah virus victims as well as Hendra virus infections, since they are similar sub-types. The dosing of ribavirin is 30 mg/kg IV once (maximum of 2 g) followed by 16 mg/kg IV (maximum 1 g/dose) every 6 hours for 4 days, then 8 mg/kg IV (maximum 500 mg/dose) every 8 hours for 6 days. In the event of mass casualties, oral ribavirin may be given at the dose of 2000 mg loading, followed by 600 mg twice a day if greater than 75 kg, and 400 mg in AM, 600 mg in PM if less than 75 kg for 10 days. Children follow the same dosing guidelines, with the exception that oral ribavirin is given at 30 mg/kg loading, followed by 15 mg/kg/day divided into twice-daily dosing for 10 days.6 Research continues on the development of vaccine against Nipah virus infection.3

UNIQUE CONSIDERATIONS Since Hendra virus infection may resemble severe influenza and since Nipah-infected patients present with symptoms similar to meningitis and encephalitis, suspicion for infection with these organisms will largely be based on an appropriate history. Hendra virus has been diagnosed only in humans who were exposed to secretions and bodily fluids of infected horses. Human Nipah infections were identified mostly in humans exposed to infected pigs; however, the World Health Organization has received recent reports of infections among children in Bangladesh who had no known exposure to swine.5 The fruit bat is suspected as the primary source in these cases, but the specific mode of transmission remains to be identified. No human-to-human transmission has been reported. Both Hendra and Nipah virus have short incubation periods and high mortality.

PITFALLS • Failure to suspect Hendra or Nipah when the history suggests these as a possible etiology.

694 BIOLOGIC EVENTS

• Failure to immediately report suspicious cases to the CDC for definitive diagnostic studies in a level 4 biocontainment laboratory. • Failure to consider treatment with ribavirin in the acute setting.

CASE PRESENTATION A 41-year-old male presents to the emergency department with a 5-day history of flu-like symptoms, fever, cough, and now shortness of breath. He denies headache, rash, nausea, vomiting, diarrhea, or abdominal pain. He has no known medical problems and no HIV risk factors. He cleans horse stables for a living and a new shipment of horses came in 2 weeks ago from Australia. A co-worker has been complaining of some of the same symptoms since yesterday. His vital signs are: temperature 102.1˚F, heart rate 110, blood pressure 123/79, respiratory rate 24, and room air oxygen saturation of 93%. His chest radiograph shows a small right lower lobe infiltrate.

REFERENCES 1. CDC: Morbidity and Mortality Weekly Report. Update: Outbreak of Nipah Virus: Malaysia and Singapore, 1999. April 30, 1999. 2. CDC: Hendra virus disease and Nipah virus encephalitis. November 26, 2003. 3. Guillaume V, Contamin H. Loth P, et al. Nipah virus: vaccination and passive protection studies in a hamster model. J Virol. 2004;78(2):834-40. 4. Chong HT, Kunjapan SR. Nipah encephalitis outbreak in Malaysia, clinical features in patients from Seremban. Can J Neurol Sci. 2002;29(1):83-7. 5. Das P. Infectious disease surveillance update. Lancet Infect Dis. 2004;4(4):657. 6. Brown D, Lloyd G. Zoonotic viruses. In: Cohen and Powderly: Infectious Diseases. Philadelphia: Elsevier; 2004, pp 2095-109. 7. Moran GJ. Threats in bioterrorism II: CDC category B and C agents. Emerg Clin North Am. 2002;20(2):311-30. 8. Nipah Virus. In: Gershon. Krugman’s Infectious Diseases of Children, ed 11. St Louis: Mosby; 2004. 9. Wong KT. A golden hamster model for human acute Nipah virus infection. Am J Pathol. 2003;163(5):2127-37. 10. Hendra and Hendra-Like (Nipah) Viruses. In: Mandell. Principles and Practice of Infectious Diseases, ed 5. London: Churchill Livingstone; 2000. 11. Institute of Medicine, Committee on Research and Development Needs for Improving Civilian Medical Response to Chemical and Biological Terrorism Incidents. Pre-Incident Communication and Intelligence and Medical Communities. In: Chemical and Biological Terrorism. National Academy Press, 1999, pp 29-34. 12. Chong HT, Kamarulzaman A, Tan CT, et al. Treatment of acute Nipah encephalitis with ribavirin. Ann Neurol. 2001;49(6):810-3.

chapter 130

SARS-CoV Attack (Severe Acute Respiratory Syndrome) Suzanne M. Shepherd, Stephen O. Cunnion, and William H. Shoff

DESCRIPTION OF EVENT The events unfolding between November 2002 and June 2003, which heralded the advent of severe acute respiratory syndrome (SARS), effectively demonstrated one significant downside of globalization and air travel: the ability to rapidly disseminate lethal respiratory infections worldwide. Although SARS was a natural biologic pandemic, it tested the global medical community’s ability to recognize and rapidly respond to a potential covert biologic weapon attack. Dispersion of a previously unknown biologic agent produced illness after a relatively short incubation period, when victims had already dispersed to five continents. Effective medical response depended upon the ability of astute clinicians, not sophisticated electronic surveillance, to identify the case cluster announcing the presence of a new illness. Although many details regarding SARS-CoV, its origin, spreading mechanisms, full extent of illness, and effective management remain to be elucidated, much has already been determined. SARS-CoV, a novel Coronavirus species, produces a rapidly progressive atypical pneumonia. Coronaviruses are a family of enveloped, singlestranded RNA viruses that produce disease in several animal species, including humans. Seroepidemiologic data suggest that SARS-CoV originated as an animal virus, with live game animal markets hypothesized to be the potential site of recent interspecies transmission.1-3 Isolation of SARS-CoV from several species, including the palm civet (Paguma larvata), suggests a wide range of host hiding places for SARS between human epidemics. SARS-CoV is the cause of SARS, as it satisfied all four of Koch’s postulates. Reverse transcriptase polymerase chain reaction (RT-PCR) and virus isolation demonstrated virus from lung biopsy specimens, feces, urine, and respiratory secretions in SARS patients, but not controls. Seroconversion to SARS-CoV was shown in ill patients. Experimental cynomolgus macaque infection with SARS-CoV produced pneumonia pathologically similar to SARS in humans.4-9 No vector has been identified. Several SARS-CoV characteristics make it an interesting bioweapon candidate. Its unique RNA-dependent

RNA polymerase allows for ready mutation and potential adaptation. It shows moderate transmission, with two to four secondary cases, and occasional “super-spreader” events, involving transmission to multiple individuals. Within months, more than 8000 individuals were infected and 774 individuals died in 26 countries on five continents. SARS-CoV has an incubation period of 2 to 10 days (median 4-7 days; range 2-14 days). Although mild and asymptomatic cases have been documented, they are uncommon and do not appear to contribute to infection spread. SARS-CoV is stable, surviving for many days in feces and for 1 or more days on hard surfaces. The primary mode of transmission is via direct or indirect mucous membrane contact with infectious respiratory droplets or fomites.10 Fecal-oral transmission may be an important secondary means, as virus is found in large quantities in stool and profuse, watery diarrhea is not uncommon.5,11,12 Transmission is not described before clinical illness onset,which corresponds with peak viral load at day 12 to 14 of symptoms. As such, early patient isolation may facilitate transmission prevention.11 Transmission occurs with close patient contact, with passage to casual contacts being unusual. Transmission is facilitated by aerosol-generating procedures in medical settings. Seasonality is suspected but remains to be elucidated. SARS affects individuals of all age groups and immune status, although children appeared less severely affected in the 2003 epidemic. Infected individuals initially experience fever, myalgias, and chills. Cough is common early, but tachypnea and shortness of breath are more prominent later in the illness. The elderly may not present with fever but may manifest decreased appetite and malaise.13 Upper respiratory symptoms are uncommon, perhaps serving as one clinical clue differentiating a cluster of epidemiologically linked SARS patients from those with other atypical pneumonias. Pulmonary findings, such as rales, occurred in less than one third of SARS cases, and often did not correlate clinically with chest radiography (CXR) findings.7,14 Twenty percent of patients had prominent gastrointestinal symptoms, including watery diarrhea. CXR findings appear to correlate with the rapidity at which patients require 695

hospitalization. The most common initial findings on CXR are ground-glass opacifications or focal consolidations of the peripheral, subpleural lower lung fields. In 67% of patients with an initially normal CXR, findings appear on subsequent high-resolution chest tomography (HRCT). Pleural effusions, mediastinal lymphadenopathy, and cavitation are rare.16 One third of SARs patients showed improvement, with defervescence and radiographic resolution over several weeks. In the remainder, fever persisted and progressive shortness of breath, hypoxia, tachypnea, increasing auscultative findings, and often diarrhea were noted. Serial radiography, or HDCT, revealed progression to multifocal unilateral or bilateral air-space consolidation, and often non-iatrogenic pneumomediastinum. Approximately 20% to 30% of patients require intensive care. Death is usually due to respiratory failure and/or multiple organ failure, sepsis, or accompanying cardiac decompensation. Later lung findings include diffuse alveolar damage, edema, hyaline membrane formation, pneumocyte desquamation, giant cells, a high viral load, and an inflammatory infiltrate.6,14,17 Mortality risk factors, determined by multivariate regression analysis, include advanced age, co-morbid cardiovascular disease and diabetes, and high neutrophil and lactate dehydrogenase levels on presentation.17,18 Between 6% and 20% of recovered patients have some residual respiratory impairment.3 Clinical manifestations are nonspecific. In one study, the WHO case definition was shown to be 96% specific but only 26% sensitive.3 Laboratory data are nondiagnostic; however, lymphocytopenia is common and thrombocytopenia may be noted. Alanine aminotransferase, lactate dehydrogenase, and creatine kinase levels may be elevated. Although RT-PCR has been shown to be diagnostic in respiratory and fecal specimens, and viral RNA is detectable in serum and urine, the CDC and WHO do not deem RT-PCR currently reliable to rule out SARS infection.19 Lower respiratory tract specimens are the most useful but place healthcare providers at the most risk of transmission via aerosol generation.20 Seroconversion 21 to 28 days after symptom onset (wholevirus immunoassay via IFA or ELISA) remains the gold standard to confirm SARS infection.21

PRE-INCIDENT ACTIONS Pre-incident actions focus on preparedness, healthcare provider education, and surveillance. Active syndromic surveillance for fever and respiratory symptom clusters should occur. Research focuses on improving testing sensitivity earlier in illness and on finding effective antiviral and immunomodulating agents.21 Emergency department, hospital, and outpatient facilities should have disaster plans in place that address bioterrorist attack/major infectious disease outbreaks, and they should regularly conduct mock attacks. The importance of incorporating travel, immigration, and contacts into routine history-taking must be reinforced. Facilities should upgrade isolation and ventilation systems, using increased air flow in clustered negative pressure rooms. Strict staff universal precautions, frequent 696 BIOLOGIC EVENTS

and thorough hand-washing, and the use of properly fitting N95 respiratory masks must be stressed.22 Measures should be delineated for changing triage guidelines to accommodate rapid increases in patient census; isolating patients; and safely holding large numbers of ill and infectious patients in the likely advent of hospital overloading. These plans, developed in coordination with those of local, state, and federal EMS, public health and government agencies should specify leadership and decisionmaking roles.23 Policies regarding restricted public gatherings, contact quarantine, and prepared quarantine facilities, if individuals will not maintain home quarantine, should be in place.24,25 The possibility of contracting SARS-CoV by particle inhalation from laboratory culture is significant, and negative pressure measures and BSL-3 procedures within laboratories should be used.26

POST-INCIDENT ACTIONS Healthcare providers entertaining a high level of suspicion for a possible SARS-CoV attack should notify hospital infection control, the administrator on duty, and the local public health officer. Appropriate local, state, and federal public health and law enforcement authorities should be involved. In the healthcare area, provision of adequate supplies and reinforcement of patient isolation, mask placement, and thorough hand-washing precautions should be enforced immediately and strictly. Healthcare provider use of N-95 mask, eye protection, gown, shoe covers, and gloves must be enforced; adequate equipment ensured; and clearly marked biohazardous waste receptacles placed to facilitate use and disposal. Rooms, materials, and surfaces possibly contaminated by SARS-CoV patients should be disinfected appropriately with hypochlorite solution. Aerosol-generating procedures, such as intubation and bronchoscopy, if necessary, should be performed by highly experienced staff under the most strict infection control precautions. Exclusion from duty should be considered for exposed unprotected healthcare workers, with temperature and symptom monitoring. Visitors should be excluded from contact with suspected SARS-CoV patients and their close contacts.25

MEDICAL TREATMENT OF CASUALTIES Treatment of SARS-CoV patients focuses on emergency management of life-threatening complications and ventilatory support. Interventions to manage profound hypoxemia should be instituted, including intubation, sedation, paralysis, lung recruitment maneuvers, and high-frequency, low–tidal volume and inflation pressure ventilator management.28 To date, no efficacious antiviral or antiinflammatory drugs are identified.3,27 Current research focuses on candidate antiviral agents and vaccine development. If patients are not sick enough to warrant admission, they should be sent home, with strict guidelines regarding activity restriction and hospital return if symptoms worsen.12,25

UNIQUE CONSIDERATIONS SARS-CoV has several potential advantages over other respiratory biologic weapons because of its clinical similarity to other common atypical pneumonias, its relative stability, and its spread potential by large droplets, stool, and on fomites. Its unique RNA-dependent RNA polymerase allows for mutation and adaptation to adverse conditions. SARS-CoV release into a community could produce a large number of casualties in a relatively short period and allow widespread dispersion of infected individuals before symptoms manifest. Potential disadvantages of SARS-CoV use include the lack of transmission before clinical illness onset, suggesting that early patient isolation may facilitate transmission prevention and its apparent uncommon transmission to casual contacts. An aerosolized SARS-CoV attack would most likely occur in a large urban setting transportation hub, allowing significant spread over large population areas globally. Identification of SARS-CoV as the cause, without the obvious epidemiologic clue of an outbreak in another country, would be delayed because of its clinical similarity to other atypical pneumonias during respiratory virus season.

PITFALLS • Failure to prepare, and frequently test, a system’s ability to respond to potential terrorist attacks in advance • Failure to notify appropriate public health agencies when an outbreak of atypical lower respiratory illness is suspected • Failure to ask an appropriate travel, immigration, and exposure history • Failure to adequately isolate patients suspected of having SARS • Failure of medical staff to use appropriate respiratory and contact precautions

CASE PRESENTATION A 25-year-old student presents with fever and malaise for 2 days and increasing cough today and has right-sided rales on pulmonary examination. The patient is requesting a chest radiograph and a prescription for azithromycin, which has “worked in the past.” A travel history discovers that she just returned 8 days ago from visiting her cousin in Singapore. She states that her cousin is proud of his job, testing antiviral agents against SARS-CoV, and she toured the facility and was introduced to his co-workers.

REFERENCES 1. Enserlink M. Clues to the animal origins of SARS. Science 2003;300:1351-5. 2. Wenzel RP, Edmond MB. Listening to SARS: Lessons for infection control. Ann Int Med. 2003;139(7):592-3.

3. Peiris JSM,Yuen KY, Osterhaus ADME, et al. Current concepts:The severe acute respiratory syndrome. N Engl J Med. 2003; 349(25):2431-41. 4. Peiris JS, Lai ST, Poon LL, et al. Coronavirus as a possible cause of severe acute respiratory syndrome. Lancet 2003;361:1319-25. 5. Drosten C, Gunther S, Preiser W, et al. Identification of a novel coronavirus in patients with severe acute respiratory syndrome. N Engl J Med. 2003;348:1967-76. 6. Ksiazek TG, Erdman D, Goldsmith CS, et al. A novel coronavirus associated with severe acute respiratory syndrome. N Engl J Med. 2003;348:1953-66. 7. Poutanen SM, Low DE, Henry B, et al. Identification of severe acute respiratory syndrome in Canada. N Engl J Med. 2003;348:19952005. 8. Rota PA, Oberste MS, Monroe SS, et al. Characterization of a novel coronavirus associated with severe acute respiratory syndrome. Science 2003;300:1394-7. 9. Marra AM, Jones SJ, Astell CR, et al. The genome sequence of the SARS-associated coronavirus. Available at: http://www.cdc.gov/ ncidod/sars/factsheetcc.htm. 10. Peiris JSM, Chu CM, Cheng VCC, et al. Clinical progression and viral load in a community outbreak of coronavirus-associated SARS pneumonia: a prospective study. Lancet 2003;361:1767-72. 11. Cheng PKC, Wong DA,Tong LKL, et al. Viral shedding patterns of coronavirus in patients with probable severe acute respiratory syndrome. Lancet 2004;363:1699-700. 12. Masur H, Emmanuel E, Lane HC, Severe acute respiratory syndrome: providing care in the face of uncertainty. JAMA 2003;289(21):2861-3. 13. Li G, Zhao Z, Chen L, et al. Mild severe acute respiratory syndrome. EID 2003;9(9):360-4. 14. Lee N, Hui D, Wu A, et al. A major outbreak of severe acute respiratory syndrome in Hong Kong. N Engl J Med. 2003;348:1986-94. 15. Hsueh PR, Cheng HH, Shiou Hwei Y, et al. Microbiologic characteristics, serologic responses, and clinical manifestations in severe acute respiratory syndrome,Taiwan. EID 2003;9(9):367-70. 16. Nicolaou S, Al Nakshabandi NA, Muller NL. Radiologic manifestations of severe acute respiratory syndrome. N Engl J Med. 2003; 348:2000-1. 17. Lew TWK, Kwek T-K, Tai D, et al. Acute respiratory distress syndrome in critically ill patients with severe acute respiratory syndrome. JAMA 2003;290:374-80. 18. Chan JW, Ng CK, Chan YH, et al. Short term outcome and risk factors for adverse clinical outcomes in adults with severe acute respiratory syndrome (SARS). Thorax 2003;58:686-9. 19. Centers for Disease Control and Prevention. Severe acute respiratory syndrome and coronavirus testing-United States, 2003. Available at: http://www.cdc.gov/mmwr/preview/mmwrhtml/ mm5214a1.htm. 20. Cheng P, Tsang OT, Chau NT, et al. Coronavirus-positive nasopharyngeal aspirates as predictor for severe acute respiratory syndrome. EID 2003;9:1381-7. 21. Hui DSC, Sung JJY. Severe acute respiratory syndrome. Chest 2003;124(1):12-5. 22. Seto WH, Tsang D, Yung RW, et al. Effectiveness of precautions against droplets and contact in prevention of nosocomial transmission of severe acute respiratory syndrome (SARS). Lancet 2003;361:1519-20. 23. Inglesby TV, Grossman R, and O’Toole T. A plague on your city: observations from TOPOFF. Clin Infect Dis. 2001;32:436-45. 24. Mitka M. SARS thrusts quarantine into the limelight. JAMA 2003;290:1696-8. 25. Centers for Disease Control and Prevention. Interim guidance on infection control procedures for patients with suspected severe acute respiratory syndrome (SARS) and close contacts in households. Available at: http://www.cdc.gov/ncidod/sars/factsheetcc.htm. 26. Heymann DL,Aylward RB,Wolff C. Dangerous pathogens from the laboratory: From smallpox to today’s SARS setbacks and tomorrows polio free world. Lancet 2004;363:1566-7. 27. Rubenfeld GD. Is SARS just ARDS. JAMA 2003;290(3):397-9. 28. Mazulli T, Farcas GA, Poutanen SM, et al. Severe acute respiratory syndrome-associated coronavirus in lung tissue. EID 2004;10:20-30.

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S E C T I O N

T E N

( P A R T

T H R E E )

Toxins

chapter 131

Staphylococcal Enterotoxin B Attack Robert G. Darling

DESCRIPTION OF EVENT Staphylococcus aureus produces a number of exotoxins including staphylococcal enterotoxin B (SEB). Such toxins are referred to as exotoxins because they are excreted from the organism that synthesizes them. Because they normally exert their pathologic effects on the gastrointestinal tract,they are also called enterotoxins. SEB causes a markedly different clinical syndrome when inhaled than it characteristically produces when ingested. Significant morbidity is produced in persons who are exposed to this toxin by either portal of entry to the body. SEB is one of the most common causes of food poisoning. It is a pyrogenic toxin that commonly causes food poisoning in humans when improperly handled foodstuffs are contaminated with S. aureus, which in turn produces and releases SEB into the food that is subsequently ingested, causing illness. Often these outbreaks occur in a setting such as a picnic or other community event due to common source exposure in which contaminated food is consumed. Although an aerosolized SEB toxin weapon would not likely produce significant mortality, it could render a significant percentage of an exposed population clinically ill for 1 to 2 weeks.1 The demand on the medical and logistical systems could be overwhelming. For these reasons, SEB was one of several biologic agents stockpiled by the United States during its biologic weapons program, which was terminated in 1969.2 Staphylococcal enterotoxins are proteins produced by coagulase-positive staphylococci. Up to 50% of clinical isolates of S. aureus produce exotoxins. They are produced in culture media and also in foods when there is overgrowth of the organism. SEB is one of at least seven antigenically distinct, moderately stable enterotoxins that have been identified. SEB causes symptoms in humans when inhaled at doses at least 100 times less than the lethal dose that would be sufficient to incapacitate 50% of those exposed.1 This toxin could also be used to sabotage food or small-volume water supplies. Staphylococcal enterotoxins belong to a class of potent immune stimulants known as bacterial superantigens.3 Superantigens bind to monocytes at major histocompatibility complex type II receptors rather than the usual antigen-binding receptors. This leads to the direct stimulation of large populations of T-helper lymphocytes while bypass698

ing the usual antigen processing and presentation pathway. This induces a brisk cascade of proinflammatory cytokines (such as tumor necrosis factor, interferon, interleukin-1, and interleukin-2), with recruitment of other immune effector cells and relatively deficient activation of counter-regulatory immune inhibitory mechanisms. This results in an intense inflammatory response that injures host tissues. Released cytokines are thought to mediate many of the toxic effects of SEB.4 Symptoms of SEB intoxication begin after a latent period of 3 to 12 hours after inhalation,or 4 to 10 hours after ingestion. Symptoms include nonspecific flu-like symptoms (e.g., fever, chills, headache, myalgias) and specific clinical features dependent on the route of exposure. Oral exposure results in predominantly gastrointestinal symptoms: nausea, vomiting, and diarrhea. Inhalation exposures produce predominantly respiratory symptoms: nonproductive cough, retrosternal chest pain, and dyspnea. Gastrointestinal symptoms may accompany respiratory exposure due to inadvertent swallowing of the toxin after normal mucociliary clearance of toxin-containing secretions from the respiratory tract. Respiratory pathology is due to the activation of proinflammatory cytokine cascades in the lungs, leading to pulmonary capillary leak and pulmonary edema. Severe cases may result in acute pulmonary edema and respiratory failure.5 Fever may last up to 5 days and range from 103˚ to 106˚F, with variable degrees of chills and prostration. The cough may persist up to 4 weeks, and patients may not fully recover for 2 weeks. Physical examination in patients with SEB intoxication is often unremarkable. Conjunctival injection may be present, and postural hypotension may develop due to fluid losses. Chest examination yields unremarkable results except in the unusual case in which pulmonary edema develops, when rales may be heard on auscultation. The chest x-ray also generally has normal results, but in severe cases increased interstitial markings, atelectasis, and possibly overt pulmonary edema or adult respiratory distress syndrome may occur.

PREINCIDENT ACTIONS It is essential that hospitals have a well-developed emergency response plan that is regularly exercised by hospi-

tal staff and is well integrated into community, state, and federal emergency response plans. There should be robust plans in place to expand patient care facilities to accommodate large numbers of sick patients who selfrefer or who arrive by ambulance. At the present time, there is no vaccine available for human use to protect against aerosol exposure to SEB; however, studies in animals are promising, and human trials may begin soon.6

POSTINCIDENT ACTIONS Identifying aerosolized SEB as the cause of a mass-casualty event will be difficult unless the healthcare provider considers exposure to this toxin early in the course of the event. One must maintain a high index of suspicion. The differential diagnosis for patients presenting with a febrile respiratory illness is quite large and involves most respiratory pathogens including many bacteria and viruses. Diagnosis of SEB intoxication is based on clinical and epidemiologic features. The symptoms of SEB intoxication may be similar to several respiratory pathogens such as influenza, adenovirus, and mycoplasma. Persons experiencing any of these symptoms might present with fever, nonproductive cough, myalgias, and headache. The epidemiologic pattern of the illness outbreak is an important clue for determining the causative agent of, as well as the circumstances leading to, the epidemic (i.e., a naturally occurring or biologic attack). SEB attack would cause cases to present in large numbers over a very short period of time, probably within a single 24-hour period. Naturally occurring pneumonias or influenza would involve patients presenting over a more prolonged interval of time. Persons with naturally occurring staphylococcal food-poisoning would not exhibit pulmonary symptoms. Because it is not an infection, SEB intoxication tends to plateau rapidly to a fairly stable clinical state, whereas inhalational anthrax, tularemia pneumonia, or pneumonic plague would all continue to progress if left untreated. Tularemia and plague, as well as Q fever, would be associated with infiltrates on chest radiographs. Other diseases, including hantavirus pulmonary syndrome, Chlamydia pneumonia infection, and chemical warfare agent inhalation (e.g., mustard and phosgene) should also be considered. Laboratory confirmation of SEB intoxication includes antigen detection enzyme-linked immunosorbent assay) and electrochemiluminescence on environmental and clinical samples and gene amplification techniques (polymerase chain reaction to detect staphylococcal genes) on environmental samples.7 SEB may not be detectable in the serum by the time symptoms occur; regardless, a serum specimen should be drawn as early as possible after exposure. SEB accumulates in the urine and can be detected for several hours after exposure. Therefore, urine samples should also be obtained and tested for SEB. Respiratory secretions and nasal swabs may demonstrate the toxin early (within 24 hours of exposure). Because most patients will develop a significant antibody response to the toxin, acute and convales-

cent sera should be drawn for retrospective diagnosis. Nonspecific findings include a neutrophilic leukocytosis, an elevated erythrocyte sedimentation rate, and chest x-ray abnormalities consistent with pulmonary edema. Once a mass-casualty situation is recognized as a possible bioterrorism event, the hospital’s emergency plan should be activated. Simultaneously, public health and law enforcement officials should be notified. An epidemiologic investigation should begin immediately. Standard precautions are sufficient because SEB intoxication is not contagious and secondary aerosol production is unlikely. Decontamination with soap and water is sufficient.

MEDICAL TREATMENT OF CASUALTIES Supportive care is the current mainstay of treatment. Attention to oxygenation and hydration is essential. Most patients’ conditions will quickly stabilize after the acute phase of the illness; rarely, some patients may develop acute pulmonary edema requiring intubation and mechanical ventilation.

CASE PRESENTATION Thirteen patients suddenly present to your emergency department after attending a major football bowl game earlier in the day. There was national interest in the game, and the press covered the event heavily on both radio and television. The national terrorism threat level had not changed from “elevated” prior to the game, and there was no unusual terrorist “chatter” being reported by the Department of Homeland Security. Most of the patients presenting for care are young college students. All attended the bowl game that afternoon. Several are in acute respiratory distress. All have fever and cough. You immediately suspect some sort of toxic exposure. As you begin administration of supplemental oxygen and monitoring of several of the sicker patients, you begin to consider the differential diagnosis. You attempt to gather additional history and learn that nothing out of the ordinary occurred during the game. One of the students tells you there was an “awesome” halftime show involving a flight demonstration by a number of small airplanes that flew over the stadium performing aerobatics. One plane appeared to be producing more smoke than the others, and for a moment some thought the plane might be experiencing an engine malfunction, but when it continued to fly normally, this idea was dismissed. Suddenly the phone rings. You are told by your local emergency medical systems director that hundreds of patients are requesting ambulance transport to your facility.

UNIQUE CONSIDERATIONS SEB toxin is one of the most ubiquitous toxins in nature and, in its natural state, is one of the most common STAPHYLOCOCCAL ENTEROTOXIN B ATTACK 699

causes of food poisoning. However, respiratory disease caused by exposure to an SEB aerosol is never a natural event and will almost certainly be due to either a laboratory accident or bioterrorism. The U.S. government weaponized SEB in the 1960s and investigated its use on the battlefield as an incapacitating agent.2 The toxin was especially attractive because of the extremely small doses required to cause incapacitating illness in soldiers. The incapacitating dose, or effective dose to produce 50% casualties (ED50), was found to be 0.0004 μg/kg; the lethal dose (LD50) was estimated to be 0.02 μg/kg. Both measurements were taken in terms of the inhalational route.2 Ingestion of SEB toxin causes classic food poisoning: nausea, vomiting, and diarrhea without fever. Aerosol exposure produces a far different clinical picture consisting of fever, headache, severe respiratory distress, and sometimes nausea, vomiting, and diarrhea. The gastrointestinal symptoms seen after aerosol exposure are most likely due to the swallowing of toxin from respiratory tract secretions and are not likely to be as severe as those seen in primary gastrointestinal SEB exposure. Prophylactic administration of an investigational vaccine protects laboratory animals against aerosol exposure and is nearing transition for study in humans.6 However, it is not currently available for clinical use.

PITFALLS Several potential pitfalls in response to an SEB attack exist. These include the following: • Failure to consider aerosolized SEB as the potential cause for large numbers of patients presenting with an acute febrile respiratory illness

700 TOXINS

• Failure to notify laboratory personnel of a suspected case of SEB intoxication and failure to collect appropriate clinical specimens to aid in the diagnosis, including nasal swabs and urine • Failure to notify appropriate law enforcement and public health authorities in the event of a suspected biologic attack REFERENCES 1. Hursh S, McNally R, Fanzone J Jr, Meshon M. Staphylococcal Enterotoxin B Battlefield Challenge Modeling with Medical and Non-Medical Countermeasures. Technical Report MBDRP-95-2. Joppa, Md: Science Applications International Corp; 1995. 2. Textbook of Military Medicine. Part I: Medical Aspects of Chemical and Biological Warfare. Available at: http://www.nbc-med.org/Site Content/HomePage/WhatsNew/MedAspects/Ch-31electrv699.pdf. 3. Ulrich RG, Bavari S, Olson M. Bacterial superantigens in human diseases: structure, function and diversity. Trends Microbiol. 1995; 3:463-8. 4. Stiles BG, Bavari S, Krakauer T, et al. Toxicity of staphylococcal enterotoxins potentiated by lipopolysaccharide: major histocompatibility complex class II molecule dependency and cytokine release. Infect Immun. 1993;61:5333-8. 5. Mattix ME, Hunt RE,Wilhelmsen CL, et al. Aerosolized staphylococcal enterotoxin B–induced pulmonary lesions in rhesus monkeys (Macaca mulatta). Toxicol Pathol. 1995;23:262-8. 6. Coffman JD, Zhu J, Roach JM, et al. Production and purification of a recombinant staphylococcal enterotoxin B vaccine candidate expressed in Escherichia coli. Protein Expr Purif. 2002;24:302-12. 7. USAMRIID’s Medical Management of Biological Casualties Handbook. 5th ed. August 2004. Fort Detrick, Md. Available at: http://www.usamriid.army.mil/education/bluebook.htm.

chapter 132

Clostridium botulinum Toxin (Botulism) Attack Gary M. Vilke

DESCRIPTION OF EVENT Botulinum toxin has been used by terrorists as a bioweapon, although unsuccessfully, on several occasions. Clostridium botulinum was obtained from soil and cultivated, and the toxin was then collected. The attacks likely failed due to faulty microbiologic techniques, deficient aerosol-generating equipment, or internal sabotage.1 As with many biologic agents, it is not likely that a terrorist attack using botulinum toxin will be reported or even noticed at the time it occurs. There is a variable delay before the effects of botulinum toxin poisoning become clinically apparent, depending on the route of exposure, with as little as 2 hours before onset of symptoms and up to a week or more after ingestion. Patients will initially present with prominent bulbar palsies including blurred vision, mydriasis, diplopia, ptosis, and photophobia. Dysarthria, dysphonia, and dysphagia also tend to present early in the clinical course. Patients will be afebrile with a clear sensorium and, as symptoms progress, will develop progressive, symmetrical, descending skeletal muscle paralysis to the point of respiratory failure when muscles of respiration become involved.

PREINCIDENT ACTIONS Background knowledge of C. botulinum, the bacterium that produces botulinum toxin, is critical if diagnosis and treatment are to be rendered in a timely manner to prevent significant casualties from an exposure, either accidental or intentional. Botulinum toxins compose a family of neurotoxic proteins produced and secreted by the anaerobic bacteria C. botulinum. There are seven serotypes, A through G, that are produced by different strains of the bacteria, all acting by similar mechanisms and with slight variations in their effects. Although technical factors would make such dissemination difficult, a single gram of crystalline toxin effectively weaponized and aerosolized would kill more than 1 million people.1 These toxins are the most poisonous substances known

with an oral dose lethal to 50% of an exposed population (LD50) estimated to be 1 ng/kg.2 This lethality is consistent in laboratory animals whether the toxin is given by the subcutaneous, intravenous, or intraperitoneal route. The inhalational route appears to have less toxicity, with the human LD50 for inhalation estimated at 3 ng/kg.3 Botulinum toxin’s site of action is within the presynaptic nerve terminal of the neuromuscular junction and cholinergic autonomic synapses. Botulinum toxin is a simple dichain polypeptide that consists of a 100-kd “heavy” chain joined by a single disulfide bond to a 50-kd “light” chain. The toxin’s light chain is a Zn++-containing endopeptidase that cleaves one or more fusion proteins, which blocks acetylcholine-containing vesicles from fusing with the terminal membrane of motor neurons, thereby preventing the presynaptic release of acetylcholine.4 This disrupts cholinergic neurotransmission, generating the clinical findings of bulbar palsies, skeletal muscle weakness, and paralysis. Inhibition of acetylcholine release also causes dry mucous membranes, as is seen in anticholinergic poisoning. Although nerve agent poisoning also causes muscular paralysis, the cholinergic finding of copious secretions typically differentiates it from botulism. If an intentional exposure threat is identified by intelligence, botulinum toxin vaccines can be considered for use. The vaccine is developed by treating the toxin with formalin, destroying its toxicity, but maintaining its antigenic properties. The toxoid protects against serotypes A through E and is administered at 0, 2, and 12 weeks, followed by annual booster doses. Eighty percent of patients receiving the vaccine will develop protective titers at 14 weeks, but almost all will not have any measurable titer just before receiving the first booster dose.5 The 1-year booster dose will result in a robust response in almost all patients. Clinical experience with the vaccine in many persons, mostly military personnel, reflects that it is safe and effective. A recombinant vaccine is also in developmental stages.6 It is also important to identify the local source of any botulinum antitoxin that can be required so that it can be located quickly if it is needed. 701

POSTINCIDENT ACTIONS Postincident actions include early diagnosis and initiation of treatment. With the presentation of a single patient, the diagnosis can be challenging. The classic presentation is an acute, symmetric, descending flaccid paralysis with bulbar musculature involvement in an afebrile patient. Multiple cranial nerve palsies are always associated with symptomatic botulism exposures. However, the clinical presentation is often confused early with other neuromuscular disorders, such as myasthenia gravis, Guillain-Barré syndrome, or tick paralysis.7 In the evaluation of such a patient, the edrophonium (Tensilon) test for myasthenia gravis may have transiently positive results for botulism. Electromyelography testing characteristically shows normal nerve conduction velocity and sensory nerve function, small amplitude motor potentials, and an incremental response (facilitation) to repetitive stimulation. The cerebral spinal fluid analysis in patients with botulism is normal. Laboratory testing is of little utility in the clinical diagnosis of botulism. Diagnosis is confirmed with a mouse bioassay neutralization test, which demonstrates botulinum toxin in bodily fluids or blood. This test is available at the Centers for Disease Control and Prevention (CDC) and a number of state and municipal public health laboratories. Samples used for this assay can include serum, stool, gastric aspirate, vomitus, and suspected contaminated foods. Serotyping of the botulinum toxin is by neutralization of the bioassay with the appropriate botulinum antisera (serotypes A through G). Because a terrorist attack is a criminal event, it is important to treat all laboratory samples collected as evidence, maintaining an appropriate chain of custody between collection and delivery to the testing agency. Serum samples must be obtained before therapy with antitoxin because it nullifies the diagnostic mouse bioassay. The mouse bioassay can detect as little as 0.03 ng of botulinum toxin and usually yields results in 1 to 2 days.8 Fecal and gastric specimens can also be anaerobically cultured, with results typically available in 7 to 10 days. Toxin production by culture isolates is then confirmed by the mouse bioassay. If a respiratory route of exposure is suspected,then persons in the area where the patient was exposed should wear full-face respirators to protect themselves from residual aerosolized toxin. Environmental persistence of botulinum toxin is difficult to determine after an initial release. Conditions such as weaponization techniques, humidity, temperature, wind, and size of aerosol particles will determine the rate of atmospheric dissipation. The toxin does not penetrate intact skin, so special protective clothing is not necessary for caregivers. Botulism is not contagious and is not transmitted person to person. Local and state health authorities must be notified quickly for several reasons. They assist in obtaining botulinum antitoxin to treat current patients and to arrange for assay tests to confirm the toxin. Additionally, health authorities assess the route of exposure and initiate tracking of other potential victims who may benefit from early intervention. If a terrorist attack is suspected, local, state, and federal law enforcement and emergency 702 TOXINS

management agencies must be notified as early as possible. This will facilitate criminal investigations and initiate activation of federal response assets, such as the Strategic National Stockpile, if needed. The toxin is heat sensitive; therefore decontamination of equipment can be accomplished by heating to 85°C for 10 minutes or using a 0.1% hypochlorite bleach solution.

MEDICAL TREATMENT OF CASUALTIES The two main treatment modalities available for managing botulism patients are supportive therapy and antitoxin treatments. Treatment of botulism is largely supportive, including ventilatory support if respiratory failure develops. Some patients may be mildly affected, whereas others may become completely paralyzed, appear comatose, and require months of ventilatory support. The rapidity of onset and the severity of paralysis depend on the amount of toxin absorbed into the circulation. Symptoms of foodborne botulism may begin as early as 2 hours or as long as 8 days after ingestion of toxin.8 The time to onset of inhalational botulism in humans was approximately 72 hours after exposure in the three known cases reported of inhalational botulism from small amounts of reaerosolized toxin.9 Supportive therapy involves mechanical ventilation when appropriate, and often long-term enteral feeding is necessary. In patients who do not require mechanical ventilation but have some degree of respiratory insufficiency, reverse Trendelenburg’s position of 20 to 25 degrees with cervical stabilization on a rigid mattress is reported to potentially improve ventilation and respiratory excursion by reducing entry of oral secretions into the airway and by suspending more of the weight of the abdominal viscera from the diaphragm.1 Up to 20% of patients involved in foodborne outbreaks require mechanical ventilation, and more than 60% of children suffering infant botulism require ventilation.10,11 Repeated bedside spirometry is used to assess diaphragmatic function. Indication for intubation is a vital capacity less than 12 to 15 mL/kg. Antibiotics have no role in most cases of acute botulism; however, it is often recommended that patients suffering from wound botulism be treated with penicillin to eliminate the source of the toxin.12 Patients with botulism are prone to secondary infections, particularly pneumonia. If antibiotics are required for secondary infections, aminoglycosides and clindamycin are contraindicated because they can exacerbate neuromuscular blockade.13,14 Activated charcoal has no reported effect in foodborne botulism. Unlike nerve agent exposures that involve excess acetylcholine at the neuromuscular junction due to inhibition of acetylcholinesterase, botulism is caused by a lack of acetylcholine in the synapse. Therefore, pharmacologic treatments such as atropine are relatively contraindicated and could worsen the symptoms. Beyond supportive therapy, the mainstay of treatment rests with the early use of botulinum antitoxin. Early administration of passive neutralizing antibody is critical,

so that the agent might bind with circulating toxin before it becomes tissue bound. Antitoxin will minimize subsequent nerve damage and severity of disease but will not reverse existent paralysis.15 Antitoxin should be administered to patients with neurologic signs of botulism as soon as possible and must not be delayed for laboratory confirmatory testing. In the United States, botulinum antitoxin is available from the CDC via state and local health departments. There are three forms of the vaccine available. The licensed trivalent equine antitoxin contains neutralizing antibodies against botulinum toxin types A, B, and E, which are the most common causes of naturally occurring human botulism. It is provided in a single 10-mL vial that provides 5500 to 8500 IU of each type of specific antitoxin, is diluted at a ratio of 1:10 in normal saline, and is given as a slow intravenous infusion. This product has all of the side effects of any equine serum product, including anaphylaxis and serum sickness. An investigational heptavalent (ABCDEFG) antitoxin held by the U.S. Army could be used to cover for additional serotypes.16 Although it is said to be despeciated by cleaving the Fc fragments from the horse immunoglobulin G molecules, approximately 4% of equine antigens still remain. A monovalent human type A antitoxin is available for infant botulism from the State of California Department of Health Services. Use of the equine antitoxin requires skin testing for horse serum sensitivity prior to use. This is performed by injecting 0.1 mL of a 1:10 sterile dilution of antitoxin intradermally and observing for 20 minutes. The skin test result is considered positive if there is any of the following: fever or chills; hypotension with a drop of 20 mm Hg in the systolic and diastolic blood pressures; hyperemic skin induration > 0.5 cm; nausea and vomiting; shortness of breath or wheezing; or skin rash or generalized itching. If any of these reactions occur, desensitization should be performed and allergy specialist consultation is advised. Even if the skin test result is negative, anaphylaxis may still occur unpredictably. If no allergic reactions occur, then the dose of 10 mL of antitoxin is given as a single intravenous dose in saline over 20 to 30 minutes. Pretreatment with intravenous diphenhydramine 50 mg and possibly an H2 blocker is recommended as well as having epinephrine immediately available in case an anaphylactic reaction does occur. Recovery results from new motor axon twigs that sprout to reinnervate paralyzed muscle fibers—a process that, in adults, may take weeks or months to complete.17

CASE PRESENTATION A patient presents with progressive bilateral symmetric descending flaccid paralysis that was preceded by ptosis and disconjugate gaze. The patient is afebrile, with unremarkable vital signs and a normal sensorium. There was no noted inciting event. No previous medical or neurologic history is present. The evaluation reflects a normal laboratory evaluation, including normal cerebrospinal fluid study results from lumbar puncture.

UNIQUE CONSIDERATIONS Four routes of exposure to botulism exist. Intestinal and wound botulism result from the production of botulinum toxin in devitalized tissue in a wound or the intestine. Neither is usually considered to be from an act of bioterrorism. However, foodborne botulism can be either natural or intentional, and the aerosolized route is highly likely to be intentional. No cases of waterborne botulism have ever been reported.18 The rapidity with which patients present largely depends on the route of exposure and the dose absorbed. Symptoms may not appear for several days if the toxin is inhaled at lower concentrations, but they may appear earlier if inhaled at higher concentrations or if absorbed by ingestion. With ingestion, the course from onset of symptoms to respiratory failure has progressed in less than 24 hours. There is no indication that treatment of children, pregnant women, and immunocompromised persons with botulism should differ from standard therapy.1 Children and pregnant women have received equine antitoxin without apparent short-term adverse effects; however, the risks to fetuses of exposure to equine antitoxin are unknown.19-22 A human-derived neutralizing antibody, Botulism Immune Globulin, decreases the risk of allergic reactions that are associated with equine botulinum antitoxin, but use of this investigational product is limited to suspected cases of infant botulism.23

PITFALLS Several potential pitfalls in response to a botulism attack exist. These include the following: • Failure to consider the diagnosis of botulism in a patient presenting with descending paralysis • Failure to notify local and state health authorities as soon as possible to access botulism antitoxin in an expedited fashion • Failure to make the clinical diagnosis of botulism if multiple patients present with bulbar and cranial nerve palsies and a descending paralysis • Exacerbation and prolongation of neuromuscular blockade with use of aminoglycosides and clindamycin in patients with botulism

REFERENCES 1. Arnon SS, Schechter R, Inglesby TV, et al. Working Group on Civilian Biodefense. Botulinum toxin as a biological weapon: medical and public health management. JAMA 2001;285:1059-70. 2. Gill DM. Bacterial toxins: a table of lethal amounts. Microbiol Rev. 1985;21:654-5. 3. McNally RE, Morrison MB, Berndt JE, et al. Effectiveness of medical defense interventions against predicted battlefield levels of botulinum toxin A. Vol 1. Joppa, Md: Science Applications International Corporation; 1994:3. 4. Montecucco C, ed. Clostridial neurotoxins: the molecular pathogenesis of tetanus and botulism. Curr Top Microbiol Immunol. 1995;195:1-278. CLOSTRIDIUM BOTULINUM TOXIN (BOTULISM) ATTACK 703

5. Middlebrook JL. Contributions of the U.S. Army to botulinum toxin research. In: Das Grupa B, ed. Botulinum and Tetanus Neurotoxins and Biomedical Aspects. New York: Plenum Press; 1993:515-9. 6. Byrne MP, Smith LA. Development of vaccines for prevention of botulism. Biochimie 2000;82:955-66. 7. Schantz EJ, Johnson EA. Properties and use of botulinum toxin and other microbial neurotoxins in medicine. Microbiol Rev. 1992;56: 80-99. 8. Terranova W, Breman JG, Locey RP, et al. Botulism type B: epidemiological aspects of an extensive outbreak. Am J Epidemiol. 1978;108:150-6. 9. Holzer VE. Botulism from inhalation. Med Klinik. 1962;57:1735-8. 10. St Louis ME, Peck SH, Bowering D, et al. Botulism from chopped garlic: delayed recognition of a major outbreak. Ann Intern Med. 1988;108:363-8. 11. Schreiner MS, Field E, Ruddy R. Infant botulism: a review of 12 years’ experience at the Children’s Hospital of Philadelphia. Pediatrics. 1991;87:159-65. 12. Bleck TP. Clostridium botulinum (botulism). In: Mandell GL, Bennett JE, Dolin R, eds. Mandell, Douglas and Bennett’s Principles and Practice of Infectious Diseases. 6th ed. Philadelphia: Churchill Livingstone; 2005:2822-8. 13. Santos JI, Swensen P, Glasgow LA. Potentiation of Clostridium botulinum toxin by aminoglycoside antibiotics: clinical and laboratory observations. Pediatrics 1981;68:50-4.

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14. Schulze J,Toepfer M, Schroff KC, et al. Clindamycin and nicotinic neuromuscular transmission. Lancet 1999;354:1792-3. 15. Tacket CO, Shandera WX, Mann JM, et al. Equine antitoxin use and other factors that predict outcome in type A foodborne botulism. Am J Med. 1984;76:794-8. 16. Hibbs RG,Weber JT, Corwin A, et al. Experience with the use of an investigational F(ab’)2 heptavalent botulism immune globulin of equine origin during an outbreak of type E botulism in Egypt. Clin Infect Dis. 1996;23:337-40. 17. Duchen LW. Motor nerve growth induced by botulinum toxin as a regenerative phenomenon. Proc R Soc Med. 1972;65:196-7. 18. Centers for Disease Control and Prevention. Botulism in the United States 1899-1996: Handbook for Epidemiologists, Clinicians, and Laboratory Workers. Atlanta, Ga: Centers for Disease Control and Prevention; 1998. 19. Weber JT, Goodpasture HC,Alexander H, et al. Wound botulism in a patient with a tooth abscess: case report and literature review. Clin Infect Dis. 1993;16:635-9. 20. Keller MA, Miller VH, Berkowitz CD, et al. Wound botulism in pediatrics. Am J Dis Child. 1982;136:320-2. 21. Robin L, Herman D, Redett R. Botulism in a pregnant woman. N Engl J Med. 1996;335:823-4. 22. St Clair EH, DiLiberti JH, O’Brien ML. Observations of an infant born to a mother with botulism. J Pediatr. 1975;87:658. 23. Krishna S, Puri V. Infant botulism: case reports and review. J Ky Med Assoc. 2001;99:143-6.

chapter 133

Clostridium perfringens Toxin (Epsilon Toxin) Attack Lynne Barkley Burnett

DESCRIPTION OF EVENT Because of their relative ease of manufacture, capability to be deployed without a sophisticated delivery system, and capacity to kill or injure significant numbers of people, biologic weapons have been termed the “poor man’s nuclear bomb.”1 As the former head of a secret bioweapons research program said,“A small container of pathogens could kill a million people. It’s hard enough to secure fissile materials, which are large and easy to detect. How do you begin to control a substance that looks like nothing more than sugar?”2 Bioterrorists may use microorganisms that produce one or more toxins, biologically active proteins that are antigenic but do not grow or reproduce. In the case of a toxin bioweapon, it is the poison produced, rather than the microorganism that produced it, that is weaponized and is harmful.3 Epsilon toxin is one of numerous toxins produced by bacteria of the genus Clostridium that cause pathologic medical conditions including botulism, tetanus,4 “gas gangrene,” and food poisoning.5,6 Clostridia are gram-positive, nonencapsulated, spore-forming, fermentative, catalase-negative bacilli.7 Of approximately 90 species, fewer than 20 are known to be associated with clinical illness in humans.6 Clostridium perfringens, which may well be the most common bacterial pathogen,6 has five strains designated types A through E,5 elaborating more than 20 toxins.8 In humans, type A is notorious for producing alpha-toxin and causing clostridial myositis and myonecrosis, also known as gas gangrene. During World War II, at the infamous Unit 731, the Japanese tested the intentional contamination of shrapnel or fléchettes with C. perfringens to increase the likelihood of wound infection9—something modern-day terrorists might find attractive if explosive devices were used. Epsilon toxin, the most potent clostridial toxin after botulinum and tetanus neurotoxins,4 is a permease enzyme made by C. perfringens types B and D.5 These are commensal organisms whose primary host is sheep, although they are occasionally isolated from other herbi-

vores such as goats and cattle10 and, rarely, humans.11 In a natural infection in herbivores, a large dose of epsilon toxin results in increased intestinal permeability, facilitating entry of C. perfringens from the gut into the blood with hematogenous spread to all organs.12 As a biologic weapon, epsilon toxin could be manufactured via fermentation of C. perfringens or genetically combined with a producer microorganism that could express the cloned gene for the toxin.13-15 Indeed, the gene producing epsilon toxin has been cloned16 and genetically combined with Escherichia coli.2 After freeze-drying, it was placed into a sealed glass cylinder, inserted into a toothpaste tube along with a few grams of cooling gel to ensure a stable temperature, and transported into the United States. This was done to provide proof to government officials of a top secret project carried out by South Africa to develop bioweapons, such as anthrax, plague, salmonella, botulinum, and epsilon toxin, that have been genetically altered to make them harder to detect and to treat. The literature is bereft of reports of human illness caused by this toxin,10 but a brief examination of its natural history readily demonstrates why epsilon toxin is designated a category B biologic agent by the U.S. Centers for Disease Control and Prevention (CDC).17 Epsilon toxin is not taken up into cells and does not appear to have any intracellular activity.12 Its putative mechanism of action is cell membrane pore formation, producing wide, nonselective diffusion channels permeable to hydrophilic solutes, including potassium, sodium, and other ions.10,12 This disrupts the vascular endothelium, causing widespread osmotic alterations with extravasation of serum proteins and red blood cells and massive edema18 involving the brain,19 kidneys, lungs,18 and liver.20 Subserous and subendocardial hemorrhages are also often seen.21 At a cellular level, formation of membrane pore complexes22 causes ion loss from cells, with a rapid decrease in intracellular potassium, a rapid increase in intracellular chloride and sodium, and a slower increase in intracellular calcium.12 The efflux of intracellular potassium causes plasma membrane blebbing, cell swelling, lysis,10 and cell death.12 705

In animal studies, epsilon toxin administered intravenously accumulates preferentially in the brain, where pathologic changes are characterized by focal-to-diffuse4 liquefactive necrosis and, secondary to damage of vascular endothelial intercellular junctions,7 perivascular proteinaceous edema in the internal capsule, thalamus, cerebellar white matter19 and meninges.7 It appears likely that, at high doses, the neurotoxicity of epsilon toxin is due to stimulation of neurotransmitter release from glutamatergic and dopaminergic neurons.4 It is thought that the toxin binds to presynaptic glutamatergic nerve fibers, inducing excessive release of glutamate, resulting in postsynaptic dendritic damage and pyramidal cell death. Epsilon toxin also accumulates in the kidney,18 where necrosis of the renal cortex (“pulpy kidney disease”) may occur.7,21 These pathologic effects in animals manifest clinically as cerebral edema,19 pulmonary edema,5 pericardial fluid collections,10 and diarrhea, with severe abdominal cramping and abdominal distention.13 Onset of neurologic signs19—including ataxia, trembling,20 nervousness, opisthotonos, seizures, agonal struggling,10 and hyperesthesia—may be observed within 2 to 60 minutes after intravenous injection in calves.19 Surviving animals can have residual neurologic deficits resulting from focal symmetric encephalomalacia.20 Epsilon-toxin toxicity results in hyperglycemia and glycosuria21 due to altered hepatic metabolism of glycogen20 and a stress response caused by cerebral edema that initiates catecholamine release and activation of adenylate cyclase.21 The anticipated primary routes for mass dissemination of epsilon toxin would be as an aerosol10 or in foodstuffs or water. Epsilon toxin is taken up from the gut in naturally occurring disease in animals; thus, food contamination might be the most natural avenue for a terrorist attempt to cause human disease. In an aerosol toxin attack, the presumption is that the agent cloud retains its harmful potential for 8 hours.3 To use epsilon toxin as an effective aerosolized biologic weapon, terrorists would need to manufacture a respirable aerosol of the purified toxin,23 with particles ranging from 0.5 to 5 microns— the “ideal” droplet size for absorption into the circulatory system via the inhalational route. Particles within this size range remain airborne for a prolonged period of time and are optimal for being carried to the distal airways, where retention and absorption of a toxin biologic weapon is maximized. Similarly, aerosolized infectious biologic agents (e.g., anthrax spores) achieve their highest rates of infection in the distal airways.3 However, unlike the spores of Bacillus anthracis, there is no evidence that spores of clostridia can be aerosolized to produce disease. Studies in sheep, goats, and mice5 suggest the most likely effects on humans following inhalation could be damage to pulmonary vascular endothelial cells, resulting in high-permeability pulmonary edema, with hematogenous spread and damage to the kidneys, heart, and central nervous system.10 Although such spread results in pulmonary edema, renal failure, shock, and multisystem organ failure,5 the central nervous system is the primary target of epsilon toxin.4 Further speculation on the clinical presentation in humans might include central nervous system manifesta706 TOXINS

tions such as weakness, dizziness, ataxia, and neurologic dysfunction.24 Pulmonary manifestations include respiratory irritation, cough, bronchospasm, dyspnea,19 adult respiratory distress syndrome, and respiratory failure.24 Cardiovascular abnormalities include tachycardia,hypotension, or hypertension.11 Gastrointestinal distress including nausea, vomiting, and diarrhea may also be seen.24 Pancytopenia is a late complication resulting in bleeding, increased susceptibility to bruises, and immunosuppression. Initial laboratory studies might reveal anemia caused by intravascular hemolysis, thrombocytopenia, elevation of serum aminotransferase levels, and hypoxia.25 The estimated lethal dose via inhalation is 1 μg/kg.10 Onset of illness is anticipated to be within 1 to 12 hours of exposure.13,24 Death can occur within 30 to 60 minutes of symptom onset in affected animals20; thus, the abrupt onset of clinical illness could eventuate rapidly in death.10 Clinical acumen, tempered by an appreciation of the context of the presentation, facilitates appropriate reporting, definitive diagnosis, and response to a biologic weapon attack using epsilon toxin.26 Diagnosis of an epsilon-toxin attack would have to be based on clinical and epidemiologic grounds, possible confirmation by growth of C. perfringens in culture (only true if the actual organism [C. perfringens] were used in the attack; if the attacker used epsilon toxin, there is nothing to culture because it is a poison, not a live infectious organism), or identification of toxin via polymerase chain reaction genotyping5 or immunoassay.23 Swabs of the nasal mucosa,23 acute serum, and possibly tissue samples should be collected as soon as possible27 in cooperation with the local or state health department or the CDC and sent to an appropriate reference facility25,27 via the laboratory response network. They must be properly packaged to preserve their biologic structure and/or activity. Because these samples are also evidence of a crime, they must be transported in a manner that maintains an appropriate chain of custody.

PREINCIDENT ACTIONS Terrorist attacks are unpredictable, may vary in size, occur in multiple sites simultaneously or be conducted sequentially, and will likely overtax resources at every level of response: local, state, and national.1 Thus, while there are no preincident steps to be taken insofar as epsilon toxin is specifically concerned, it is essential that emergency medical response (EMS) agencies, hospitals, and healthcare professionals proactively plan, organize, train, and obtain the supplies necessary for responding to terrorist incidents involving biologic agents.

POSTINCIDENT ACTIONS It may be unclear whether the initial cases of an infectious disease outbreak are the result of a natural occurrence or an act of hostility. Thus, all apparent infectious disease outbreaks should be approached as possible

bioterrorist attacks until proven otherwise. Implications of such a posture for clinical practitioners include the immediate reporting of suspicious or clustered syndromes to local, state, or federal public health officials for investigation; immediate implementation of respiratory protection and/or body fluid precautions for all responders; and recognition that biologic samples and other materials (e.g., clothing), as well as laboratory results, have potential forensic, as well as clinical, relevance. Therefore, appropriate steps must be taken to preserve their evidentiary value.26 Toxins are easier to remove by decontamination than are live organisms.3 Use of soap and water is the recommended approach.13,23 There is no known person-to-person spread of epsilon toxin by air.5 Direct contamination of consumables, such as water, food,19,24 or medications,3 is a possible route of dissemination and would be difficult to detect prior to the onset of illness because it is unlikely that appearance, taste, or smell would be significantly affected. Epsilon toxin is dermonecrotic8 and can be transmitted via contaminated wound discharge24; thus, body fluid precautions should be observed.

MEDICAL TREATMENT OF CASUALTIES The biggest challenge faced by EMS, emergency department, and community medical practitioners after a terrorist attack may well be the psychological trauma that may affect most of the population.1 Insofar as epsilon toxin is concerned, there are no vaccines, antitoxins,5 antidotes,24 or specific treatment25 for humans, although C. perfringens epsilon toxoid has been prepared for use in animals.28,29 Supportive medical care, including airway management24 and fluid replacement, with particular attention paid to electrolyte status because of potassium loss, would be the mainstay of therapy.13 Critical care in an intensive care unit setting, including mechanical ventilation and vasopressors, may be needed for the treatment of multisystem organ failure and shock.5 If weaponized and aerosolized C. perfringens were the biologic agent disseminated (as opposed to weaponized purified epsilon toxin), high-dose penicillin might be indicated, although a primary role for antibiotic therapy has not been established.5 A study of guinea pigs with gas gangrene (caused by clostridial alpha toxin) showed that protein synthesis inhibitors were more effective inhibitors of cell wall–active toxins than were antimicrobial agents with a different mechanism of action,6 with penicillin plus clindamycin considerably more efficacious than penicillin alone. There are also reports that rifampin stopped the lethal intoxication of the toxin microcystin in animal models when administered within 15 to 30 minutes of exposure to the agent.14 Adjunctive hyperbaric oxygen therapy for gas gangrene is based on blocking production of alpha toxin at a partial pressure of oxygen level of more than 250 mm Hg.29 However, use of hyperbaric oxygen and its effect on the production of epsilon toxin have not been reported.

UNIQUE CONSIDERATIONS Children who have been infected with epsilon toxin are more likely to decompensate if not monitored carefully and treated appropriately and are at greater risk from many bioterrorism agents. For example, aerosolized agents create special risks for pediatric patients. Compared with adults, their larger minute ventilation volume may result in the inhalation of a larger relative dose of an aerosolized agent and a more rapid onset of illness. Furthermore, children may absorb more of a given substance before its clearance from the respiratory tract. In addition, the breathing zone of children is closer to the ground, where many heavier-than-air aerosols may settle. Children are also at greater risk from agents that cause vomiting and diarrhea because they dehydrate easily and possess less physiologic reserve than adults. Thus, agents that cause minor symptoms in adults may precipitate hypovolemic shock in an infant.1

PITFALLS Several potential pitfalls in response to an epsilon toxin attack exist. These include the following: • Absence of familiarity with weapons of mass destruction on the part of medical personnel, public health officials, and disaster planners is a pitfall.1 All healthcare providers are essential to community preparedness for a terrorist incident.26 • Failure to recognize a bioterror incident early in its presentation may compromise the removal or decontamination of the agent, the appropriate medical care of casualties, and the criminal investigation to apprehend those responsible.26 • Failure to consider C. perfringens epsilon toxin in the differential diagnosis of an outbreak of a gastrointestinal or neurologic syndrome can also lead to a less-thanoptimal response. REFERENCES 1. Redlener I, Markenson D. Disaster and terrorism preparedness: what pediatricians need to know. Disease-A-Month. 2004;50:6-40. 2. Warrick J, Mintz J. Lethal legacy: bioweapons for sale. Washington Post. April 20, 2003:A01. Available at: http://www.washingtonpost.com. 3. Biological Weapons. Chapter 4 in: The Medical NBC Battlebook. The U.S. Army Center for Health Promotion and Preventive Medicine. USACHPPM Tech Guide 244; 2000:4-1-40. 4. Miyamoto O, Minami J, Toyoshima T, et al. Neurotoxicity of Clostridium perfringens epsilon-toxin for the rat hippocampus via the glutamatergic system. Infect Immunol. 1998;66:2501-8. 5. Lucey DR. A guide to the diagnosis and management of 17 CDC category B bioterrorism agents (“Beware of Germs”). Washington Hospital Center.April 10, 2003.Available at: http://bepast.org/docs/ posters/BEWARE%20OF%20GERMS%20Category%20B%20page% 201%2023-04-03.pdf. 6. Lorber B. Gas gangrene and other Clostridium-associated diseases. In: Mandell GL, Bennett JE, Dolin R, eds. Principles and Practice of Infectious Disease. 5th ed. London: Churchill Livingstone, Inc.; 2000:2549-61. 7. Anaerobic infections. Veterinary Pathobiology 331 Lectures. College of Veterinary Medicine, University of Illinois at UrbanaCLOSTRIDIUM PERFRINGENS TOXIN (EPSILON TOXIN) ATTACK 707

CASE PRESENTATION The speed of the patient’s decompensation had impressed everyone. A 28-year-old man, whose personal papers identified him as a foreign national, had been found alone, having apparently collapsed on his kitchen floor. His landlady had called 9-1-1 when she heard a loud sound, as if something heavy hit the floor, and there was no answer to her ringing of his doorbell or her telephone calls. Police arrived on the scene at approximately 7:31 AM. The landlady reported the patient and his roommate had been making noise all night, something unusual for them. Initially, she said, her impression was that they were “making something...or cleaning,” given the repeated sounds of objects being moved, water running, etc. Then, as the sounds of movement subsided, she noticed a lot of coughing—she wasn’t sure whether it was one or both of them—with the coughing increasing in frequency and intensity as daylight approached. She further informed the police that the patient shares the apartment with a male roommate of approximately the same age. Both are from the same country, and both work at the convention center, a venue that will be packed with 50,000 people for tonight’s collegiate basketball championship. On entering the apartment the police officer found, in addition to the patient, several empty boxes and multiple plastic containers—some empty, some partially filled. The officer assessed the patient, found him to be alive, and summoned paramedics, who arrived at 7:38 AM. Because of fluid on the floor, possibly used in an attempt to clean up some kind of spill, emergency personnel had to be careful they didn’t slip as they worked in the kitchen. A fan was blowing, and the mist created by the fan was making them wet. Although it was cool in the apartment, they opted to keep the fan on because it helped dissipate the odors of vomitus, urine, and feces emanating from the patient. Examination revealed a male with snoring respirations, mild bilateral wheezing, and rales on auscultation of the lungs; sinus tachycardia at a rate of 126 per electrocardiogram; blood pressure 144/82; Glasgow Coma Scale score of 6 (E1V1M4); pupils that were equal and reactive bilaterally at 4 mm; and pale, cool, wet skin. Paramedics intubated

8.

9. 10. 11.

12.

13.

Champaign. Available at: http://www.cvm.uiuc.edu/courses/ vp331/AnaerobesandAnaerobiosis/. Songer G. Clostridia causing enteric disease. Lecture notes: Pathogenic bacteriology. Veterinary Science and Microbiology,The University of Arizona. Available at: http://microvet.arizona. edu:16080/courses/mic420/classnotes.html. Mangold T, Goldberg J. Plague Wars: The Terrifying Reality of Biological Warfare. New York: St. Martin’s Griffin; 1999:14-28. Greenfield RA, Brown BR, Hutchins JB, et al. Microbiological, biological, and chemical weapons of warfare and terrorism. Am J Med Sci. 2002;323:326-40. Structural studies on epsilon toxin from Clostridium perfringens. Research in the School of Crystallography. Birkbeck College, The University of London. Available at: http://people.cryst.bbk.ac.uk/ ~bcole04/epsilontoxin.html. Petit L, Maier E, Gibert M, et al. Clostridium perfringens epsilon toxin induces a rapid change of cell membrane permeability to ions and forms channels in artificial lipid bilayers. J Biol Chem. 2001;276:15736-40. Clostridium perfringens epsilon toxins: essential data. CBWInfo.com. Available at: http://www.cbwinfo.com/Biological/ Toxins/Cper.html.

708 TOXINS

the patient, confirmed correct tube position, and ventilated him with 100% oxygen. They also inserted a large-bore intravenous tube and administered glucose and naloxone, without effect. His wet, soiled clothes were removed and he was covered with a blanket before being taken to the ambulance. The patient arrived at the emergency department at 8:05 AM, his clinical condition having markedly deteriorated since first assessed by paramedics 27 minutes earlier. The patient was in clinically obvious pulmonary edema, and he was hypotensive with muffled heart sounds. The patient was placed on a ventilator and a second intravenous tube was inserted. A bedside ultrasound revealed pericardial fluid. While preparations were being made to perform a pericardiocentesis, the patient’s cardiac rhythm changed to pulseless electrical activity. Resuscitation efforts lasting approximately 30 minutes, including pericardial decompression, were unsuccessful and the patient died. Lines and tubes were left in situ, the patient’s body was moved to a holding room, and a call was placed to the medical examiner’s office. Because of the patient’s atypical presentation and rapid death, you agreed with the emergency department nurse who suggested that local public health officials be notified as well. The medicolegal death investigator is the first to respond 3 hours after the patient’s death. He indicates that he needs to interview you and also asks that you have the paramedics and police return to the hospital, so that all the interviews can take place in one location. You respond that you will have a nurse call the paramedics’ dispatch center, as well as the police. However, at that very moment, you happen to see both paramedics walking through the emergency department doors. The difference in their appearance from that observed earlier, when bringing the patient to the emergency department, is striking. Both paramedics appear ill, have obvious wet coughs, and one paramedic seems to have an unsteady gate you had not previously noticed. On seeing you, the other paramedic says,“Doc, something’s got to be going on here!”

14. Franz DR. Defense against toxin weapons. In Sidell FR, Takafuji ET, Franz DR, eds. Medical Aspects of Chemical and Biological Warfare. Washington, DC: Office of the Surgeon General at TMM Publications, Department of the Army, United States of America; 1997:608, 616. 15. Takafuji ET, Johnson-Winegar A, Zajtchuk R. Medical challenges in chemical and biological defense for the 21st century. In Sidell FR, Takafuji ET, Franz DR, eds. Medical Aspects of Chemical and Biological Warfare. Washington, DC: Office of the Surgeon General at TMM Publications, Department of the Army, United States of America; 1997:682. 16. Minami J, Katayama S, Matshushita C, et al. Lambda-toxin of Clostridium perfringens activates the precursor of epsilon-toxin by releasing its N- and C-terminal peptides. Microbiol Immunol. 1997;41:527-35. 17. Agrawal AM, O’Grady NP. Biological agents and syndromes. In: Farmer JC, Jiminez EJ, Talmor DS, et al, eds. Fundamentals of Disaster Management. Des Plaines, Ill: Society of Critical Care Medicine; 2003:72. 18. Structural studies on the epsilon toxin from Clostridium perfringens. Birkbeck College, The University of London. Available at: http://people.cryst.bbk.ac.uk/~toxin/cproj/eps.html.

19. Epsilon toxin of Clostridium perfringens. Ames, Ia: Center for Food Security and Public Health, Iowa State University College of Veterinary Medicine; 2003. Available at: http://www.scav.org/ Epsilon-toxin%20Fact%20Sheet.htm. 20. Williamson L. Clostridium perfringens type D: young ruminant diarrhea. LAMS 5350 Large animal digestive system. Available at: http://goatconnection.com/articles/publish/article_38.shtml. 21. Kit for the detection of Clostridium perfringens epsilon toxin in biological fluids or culture supernatants. Available at: http://64.233.161.104/search?q=cache:6Nd61xZ_t4MJ:www. biox.com/Epsilon.htm+kit+for+the+detection+of+clostridium+ perfringens+epsilon+toxin+in+biological+fluids+or+culture+ supernatants&hl=en. 22. The channel-forming ε-toxin family. Transport Classification Database. University of California San Diego. Available at: http://tcdb.ucsd.edu/tcdb/tcfamilybrowse.php?tcname=1.C.5. 23. Franz DR. Defense Against Toxin Weapons. Fort Detrick, Md: US Army Medical Research Institute of Infectious Diseases; 1997. 24. Clostridium perfringens toxins. Bioterrorism Treatment Guidelines. Illinois Department of Public Health. Available at: http://www.idph. state.il.us/Bioterrorism/pdf/bioterrorismcards.pdf.

25. Clostridium perfringens toxins. NATO Handbook on the Medical Aspects of NBC Defense. Virtual Naval Hospital: FM8-9. Available at: http://www.vnh.org/MedAspNBCDef/2appb.htm. 26. Bogucki S, Weir S. Pulmonary manifestations of intentionally released chemical and biological agents. Clin Chest Med. 2002;23:777-94. 27. Clostridium perfringens. USAF pamphlet on the medical defense against biological weapons. Available at: http://www.gulflink. osd.mil/declassdocs/ af/19970211/970207_aadcn_015.html. 28. Titball R, Mainil J, Duchesnes C, et al, eds. Protein toxins of the genus Clostridium and vaccination. In: Genus Clostridium. Concerted Action QLK2-CT2001-01267. Liege, Belgium: Presse de las faculte de Medecine Veterinaire de l’Universite de Liege; 2003. Available at: http://www.genusclostridium.net/scbooklet2.pdf. 29. Van Unnik AJM. Inhibition of toxin production in Clostridium perfringens in vitro by hyperbaric oxygen. Antonie Leeuwenhoek Microbiol. 1965;31:18;181-6.

CLOSTRIDIUM PERFRINGENS TOXIN (EPSILON TOXIN) ATTACK 709

chapter 134

Marine Toxin Attack Wende R. Reenstra

DESCRIPTION OF EVENT Marine toxins are poisons of biologic origin that may be used as chemical weapons. These toxins are produced by a variety of organisms ranging from small microbes to fish and snails. These toxins are not infectious. Exposure to the toxins either by invenomation, ingestion, or inhalation may lead to a death through paralysis of cardiac or respiratory muscles. Several marine toxins discussed here are further classified as neurotoxins. These toxins can interfere with the transmission of the nerve impulse by blocking specific ion channels. The neurotoxins vary in mechanism of action. The concentration of the exposure to the toxin is not indicative of its effects. Several toxins can cause seizures or paralysis in nanomolar concentrations, others may cause gastrointestinal upset or blindness in much larger concentrations. Three of the marine toxins classified as neurotoxins are saxitoxin, conotoxin, and tetrodotoxin. The fourth toxin—palytoxin—exerts its effects on all cell membranes and is not classified as a neurotoxin.

PREINCIDENT ACTIONS As in other toxin attacks a robust public healthcare system is of most benefit in the preincident phase. Hospitals should have disaster plans that would be adaptable to a toxin attack and the subsequent surge of patients demonstrating the characteristic symptoms of the marine toxins. Adequate resuscitation equipment, including mechanical ventilators, should be part of the preparation of such an attack.

POSTINCIDENT ACTIONS Emergency medical providers should recognize a rise in the number of patients exhibiting the characteristic parasthesias and progressive paralysis seen in marine toxin exposure. Once a trend is recognized, notification should be made to local and regional public health departments and adequate supplies to handle large numbers of symptomatic patients should be gathered. Rising 710

numbers of symptomatic patients should be an indicator of a potential terrorist attack using a marine toxin agent, especially in areas where such toxins are not commonly seen (e.g., inland regions). Once an attack is suspected, notification of law enforcement on the local and federal level should follow.

MEDICAL TREATMENTS OF CASUALTIES Saxitoxin Saxitoxin is one of the family of neurotoxins that cause paralytic shell fish poisoning (PSP).This toxin is soluble in water and stabile at high temperatures.1 The toxin is made by small organisms called dinoflagellates, which contaminate shellfish (clams, scallops, oysters). The toxin is also produced by blue green algae. The algae may grow rapidly, producing blooms called “red tides.” Human ingestion of filter-feeding crabs and lobsters or shellfish results in an intoxication.1–4 Saxitoxin binds to voltage-gated sodium channels on nerve fibers and muscle cells. The binding of the toxin blocks conduction of the nerve impulse. General symptoms of saxitoxin poisoning are neurologic and respiratory paralysis.1–3 Clinical Features General: There is an initial latent period varying from 30 minutes to several hours following ingestion, before the onset of neurological symptoms. Cardiovascular: There are no specific cardiovascular effects although in laboratory animals, saxitoxin caused hypotension and conduction defects. Respiratory: Respiratory distress from muscular paralysis may occur up to 12 hours after intoxication. The respiratory paralysis may lead to death.1,5 Gastrointestinal: Gastrointestinal symptoms may appear hours to days after ingestion. These symptoms may include nausea, vomiting, abdominal pain, and diarrhea.1,5 Other: A tingling and burning sensation, initially occurring around the mouth and lips, is usually the first symptom. The numbness may be on the hands and spread

over the chest and abdomen.1,5 These symptoms may progress, with difficulty walking and arm and leg weakness.1,5 Involuntary movements and tremors may occur.1 There are no specific antidotes for saxitoxin poisoning.1 Treatment is symptomatic. If oral ingestion is suspected, emptying the stomach via emetic or gastric lavage is recommended. Intubation and mechanical ventilation with monitoring to support respiration may be necessary.1 Routine laboratory studies are not helpful. Diagnosis is confirmed by detection of the toxin in food, water, or environmental samples.5,6 Saxitoxin is water soluble and therefore can be easily aerosolized. It is toxic by both inhalation and ingestion.1

The toxin is named from the pufferfish family (Tetraodontidae), where it has been found to be concentrated in the liver and other organs.9,10 The toxin can also be found in the Blue Ringed Octopus, Parrot fish, crabs, newts, and algae.2,5,9–11 The toxin is made by a bacterium that forms a symbiotic relationship with the animals.5,12 Tetrodotoxin is a neurotoxin that interferes with transmission of the nerve impulse at the nerve-muscle junction.5,12 The toxin is heat stable and can be soluablized in acetic solutions.5,12 This toxin specifically blocks sodium channels on the nerve cell and inhibits transmission of the impulse.2,5,12 The target molecular channels are thought to be very similar to saxitoxin.9

Conotoxin

Clinical Features

The venom of the cone snail is composed of small substances termed conotoxins. There are more than 2000 peptides identified7 that lead to a complex set of symptoms. The toxins are heat stable but are inactivated by the disinfectants glutaraldehyde and formaldehyde.7 The conotoxins mechanism of action can be divided into pre- and post-synaptic pathways. The presynaptic conotoxin blocks the release of acetylcholine.5,8 The postsynaptic conotoxin inhibits sodium, potassium, and calcium channels and blocks muscular contraction.5 The toxicity of the venom is thought to result from the additive effects and not the concentration of the toxin.

General: The onset of symptoms is almost immediate upon injection. Common symptoms include localized pain, swelling, numbness, and ischemia at the injection site.5,7 The numbness, swelling, and tingling may spread rapidly from the injection site to involve the entire body.5,7 Cardiovascular: No specific cardiac effects are seen. Respiratory: Progressive weakness, droopy eyelids, headache, abdominal pain, and difficulty breathing, may occur. Death results from respiratory paralysis.5,7 Gastrointestinal: Stomach cramps and nausea are common effects. Other: The clinical course is characterized by rapid onset and deterioration for the first 6 to 8 hours.7 This is followed by improvement, and complete recovery may take 4-6 weeks.5,7 Diagnosis is by clinical signs and symptoms, and there are no laboratory tests available. Treatment is to immobilize the limb or site of envenomation. Pressure dressings should be applied and pain medication and tetanus prevention provided.7 Intubation and mechanical ventilation may be necessary to support breathing.5,7 Conotoxins are very small, stable toxins that theoretically may be weaponized and disseminated as aerosols. A search of the open scientific literature regarding their inhalation toxicity found no publications.7 They are poisonous by injection.

General: The first symptom is increasing numbness and tingling in the face and around the mouth.12 These may extend to the extremities or become generalized.5,12 Cardiovascular: Hypotension and cardiac arrhythmias may occur.5,12 Respiratory: There is increasing respiratory distress. The victim usually exhibits difficulty breathing and cyanosis. Paralysis increases and convulsions, mental impairment, and cardiac arrhythmia may occur.5,12 Gastrointestinal: Autonomic effects such as headache, diaphoresis, and chest pain may occur and gastrointestinal symptoms such as nausea, diarrhea, and/or vomiting may develop.5,12 Other: A coagulation disturbance, which is an occasional complication, may lead to bleeding into the skin and mucosa, formation of blood blisters, and peeling of the skin. The neurologic involvement may start as muscular twitching and proceed to complete skeletal muscle paralysis, interfering with speech and swallow.10,12 The pupils, after initially constricting, may become fixed and dilated.12 The victim may be completely paralyzed but conscious. Untreated, the death rate is 50–60% in some studies.5,12 Death usually occurs within 4 to 6 hours, with a known range of about 20 minutes to 8 hours.10,12 Management is supportive and standard management of poison ingestion should be employed if intoxication is by the oral route. These include gastric lavage or emetics, particularly after control of the airway has been obtained. Intubation and mechanical ventilation may be required in severe intoxication.5,12 After weakness has become apparent, the treatment is symptomatic (e.g., maintenance of respirations, monitoring of vital signs and electrolytes).5,10,12 Because of the likelihood of consciousness being maintained with complete paralysis, periodic administration of a tranquillizer is recommended along with continuous reassurance.10,12 Relatively little is known about TTX as a possible toxin weapon. A company in Japan is known to produce the toxin.12 It is not known to be made in large quantities that could be used in weapons, and little or nothing has been published about its inhalational toxicity.12

Tetrodotoxin

Palytoxin

Tetrodotoxin is one of the best characterized marine toxins because of its involvement in fatal food poisoning.

Palytoxin is one of most potent marine toxins known. It was isolated first from corals located in the South

Clinical Features

MARINE TOXIN ATTACK 711

Pacific.13,14 Originally it was thought that the toxin was made by the corals; now, however, it is known that the toxin is made by a dinoflagellate (a small single-celled organism) and the corals concentrate the toxin.2,8,13 It is estimated that the lethal dose for a human is less than 5 μg.3,10,13,14 Palytoxins are stable in seawater and alcohols. Extensive pharmacological research has determined that palytoxin is not a neurotoxin.13,15 It instead acts at the cellular membranes to make them porous to charged molecules such as sodium, potassium, and calcium.13,15 Without the gradients of these ions, the cells are unable to function or maintain the cell shape.14,15

General: Symptoms are rapid, with death occurring within minutes.13 Cardiovascular: Initial symptom may be chest pain from constriction of the cardiac blood vessels. This may lead to cardiac ischemia and death of cardiac tissue. This may be seen on the EKG as peaked T waves or ST segment elevation.13 The next symptom may be the loss of consciousness as unstable blood pressure, particularly episodes of low blood pressure, reduce blood flow to the brain.13 Respiratory: There may be difficulty breathing, with symptoms of wheezing. This again may be due in part to constriction of blood vessels in the lungs. Gastrointestinal: There are no specific gastrointestinal effects. Other: Hemolysis (breakdown of blood cells) may occur as the cell membranes become permeable to various ions,the red blood cells swell and the membranes rupture. This results in decreased oxygen carrying capacity. Death is thought to result from decreased oxygenation.13 There are no known therapeutics for Palytoxin poisoning. Relatively is little is known about Palytoxin as a possible toxin weapon. It is not known to be made in large quantities that could be used in weapons and little or nothing has been published about its inhalational toxicity.13 In summary these toxins act on a variety of sites. Table 134-1 summarizes their specific effects.

TABLE 134-1 SPECIFIC EFFECTS OF MARINE TOXINS TOXIN

ORIGIN

EFFECT

Conotoxin

Marine snail

Blocks voltage-sensitive calcium channels; blocks voltage-sensitive sodium channels; blocks ACh receptors Activates sodium channels, ATPase Blocks voltage-sensitive sodium channels Blocks sodium channels

Soft coral

Saxitoxin

Dinoflagellate

Tetrodotoxin

Puffer fish

ACh, acetylcholine; ATPase, adenosine triphosphatase.

712 TOXINS

Marine toxins should be considered when a number of patients present with the characteristic parasthesias and paralysis. It is highly unusual to have large numbers of such patients, particularly in non-coastal regions, and therefore a terrorist attack should be suspected when this is seen. Early intervention with supportive care, including mechanical ventilation if needed, can be lifesaving.

PITFALLS

Clinical Features

Palytoxin

UNIQUE CONSIDERATION

Several potential pitfalls in response to a marine toxin attack exist. These include the following: • Failure to prepare adequate systems to respond to possible terrorist attacks before an attack occurs • Failure to consider marine toxins as the cause for paralysis in patients • Failure to consider a marine toxin attack in the setting of a large number of otherwise healthy people presenting over several hours with acute paralysis • Failure to rapidly support the respiratory system with urgent intubation and mechanical ventilation • Failure to notify appropriate public health and law enforcement agencies when marine toxin exposure is suspected or confirmed among persons with no aquatic environment exposure or seafood ingestion

CASE PRESENTATION As an emergency physician in a small hospital outside of Chicago, you begin to see several patients during the first hours of your shift complaining of numbness and tingling in their face and mouth. During the next 3 hours you have four more patients present with the same symptoms while your original patients begin showing signs of respiratory distress. After intubating the patients in respiratory distress, you begin to suspect there may be more than just a coincidence occurring. You pick up the phone to make a call to your local Department of Public Health, only to find out a hospital 20 miles away is also seeing a surge in patients with similar symptoms.

REFERENCES 1. Saxitoxin: essential date. Available at: http://www.cbwinfo.com/ Biological/Toxins/Saxitoxin.html. 2. Yasumoto T, Murata M. Marine toxins. Chem Rev. 1993;93:1897-909. 3. Tu A, ed. Handbook of Natural Toxins: Marine Toxins and Venoms. Marcel Dekker, 1988. 4. Mines DM, Stahmer S, Shepherd S. Poisonings: Food, Fish, Shellfish. Emerg Med Clin North Am 1997;15:157-77. 5. Edmonds C. In: Dangerous Marine Creatures: a Field Guide for Medical Treatment. Best Publishing; 1995. 6. Edmonds C, Lowry C, Pennefather J, eds. Diving and Subaquatic Medicine, ed 3. Butterworth-Heinemann; 1997.

7. Conotoxins: essential data. Available at: http://www.cbwinfo. com/Biological/Toxins/Conotox.html. 8. Halstead BW. In: Poisonous and Venomous Marine Animals of the World, rev ed 2. Darwin Publications; 1988. 9. Kao C, Levinson SR, eds. Tetrodotoxin, Saxitoxin and the Molecular Biology of the Sodium Channel. New York: The New York Academy of Sciences; 1986. 10. Hall S, Strichartz G, eds. Marine Toxins, ACS Symposium series. Washington DC: American Chemical Society; 1990. 11. Underman AE, Leedom JM. Fish and shellfish poisoning. Curr Clin Top Inf Dis. 1993;13:203-25. 12. Tetrodoxin: essential data. Available at: http://www.cbwinfo.com/ Biological/Toxins/TTX.html. 13. Palytoxin: essential data. Available at: http://www.cbwinfo.com/ Biological/Toxins/Palytoxin.html. 14. Moore RE, Scheuer PJ. Palytoxin: a new marine toxin from a coelenterate. Science 1971;172(982):495.

15. Haberman E. Palytoxin acts through Na+,K+-ATPase. Toxicon 1989;27:1171-87.

FURTHER RECOMMENDED READING 1. Velez P, Sierralta J, Alcagaga C, et al. A functional assay for paralytic shellfish toxins that uses recombinant sodium channels. Toxicon 2001;39:929-35. 2. Benton BJ, Rivera VR, Hewetson JF, Chang FC. Reversal of saxitoxin-induced cardiorespiratory failure by a burro-raised alpha-STX antibody and oxygen therapy. Toxicol Appl Pharmacol. 1994; 124:39-51. 3. Bove A, ed. Bove and Davis’ Diving Medicine. WB Saunders; 2004.

MARINE TOXIN ATTACK 713

chapter 135

T-2 Toxin (Trichothecene Mycotoxins) Attack Frederick Fung

DESCRIPTION OF EVENT The 1972 Biological and Toxin Weapons Convention is a major international treaty to control biologic and chemical warfare that prohibits state parties from developing, producing, and testing biologic and toxic weapons.1,2 However, with the expansion of terrorism, the possibility of using mycotoxins as a chemical weapon exists. In reality, there are three likely attack scenarios using T-2 mycotoxin as an agent of terrorism: 1. Product tampering: substantial human and economic damages caused by product tampering, such as the cyanide contamination of Tylenol in 1984, could happen. Use of T-2 mycotoxin to contaminate premade consumer products may be the most plausible attack scenario. 2. A second scenario is the use of T-2 mycotoxin as part of state-sponsored bioterrorism against a discrete population, group, or region. 3. The third scenario is related to food industry contamination: food, especially in the dairy industry (e.g., milk transported by tanker truck) is vulnerable to biologic and chemical attack. An attack on the food industry could cause local outbreaks of disease within hours or days, as well as enormous economic damage. Trichothecenes (Fig. 135-1) are a large group of sesquiterpenoid chemicals characterized by a tetracyclic 12,13-epoxy ring commonly known as the 12,13epoxytrichothecene and are classified into four groups. Group A includes T-2 toxin and diacetoxyscirpenol. Group B includes 4-deoxynivalenol and nivalenol. Many Fusarium species produce group A and B trichothecenes. Baccharis megapotamica produces the group C trichothecene baccharin. Group D mycotoxins include roridins produced by Myrothecium roridum, verrucarin produced by Myrothecium verrucaria, and satratoxins produced by Stachybotrys atra.3 It is important to point out that the more common and potent trichothecenes are produced by Fusarium species. There are nearly 150 toxins produced by fusaria and related fungi. They infect wheat and other grains that are important as sources of human food. 714

They are highly resistant to heat. T-2 toxin has been the most extensively studied. All trichothecenes are mycotoxins, whereas some mycotoxins belong to other chemical groups and are not trichothecenes. T-2 is rapidly absorbed from the gastrointestinal (GI) tract. Although there are no human data on absorption through inhalational or dermal exposure, in vitro and animal studies have shown that trichothecenes are poorly absorbed through intact skin.4 Trichothecenes undergo deepoxidation and glucuronidation, resulting in less toxic metabolites. The elimination half-life is estimated at 1.6 ± 0.5 hours after intravenous injection of the toxin in a canine model.5 Another model using swine and cattle showed a half-life of 13 and 17 minutes, respectively.6 T-2 does not require metabolic activation to exert its toxicity. The presence of the reactive electrophilic 12,13-epoxide moiety accounts for a rapid onset of its toxicity. The mechanism of toxicity involves inhibition of protein and DNA synthesis.7 They also produce general cytotoxicity by inhibiting the mitochondrial electron transport system.8 The 12,13-epoxide of the trichothecenes is essential for the toxicologic activity. The deepoxidation of T-2 in mammalian systems results in loss of toxicity.9 The dose of trichothecene needed to cause symptoms in humans is unknown. There is great variability in the toxicity of these compounds in animal studies. The dose of trichothecenes that will be fatal to 50% of an exposed population ranges from 0.5 to 300 mg/kg, depending on the route of administration and animal model used.10 T-2 is a potent blistering agent. Purified trichothecenes have been investigated because of their potential use in chemical warfare. T-2 toxin was implicated in the “yellow rain” attacks in Southeast Asia. However, further investigations have been inconclusive.11 Acute pulmonary hemorrhage in infants was purportedly associated with residential exposure to Stachybotrys chartarum and other toxigenic fungi. A detailed analysis of this report was conducted by the Centers for Disease Control and Prevention, which found methodologic shortcomings and concluded that the association was not confirmed.12

H H3C 9

10

8

O

O

6

CH2

2

5 CH2

CH3

tus associated with trichothecene exposure is a complete blood count (CBC) with white blood cell differential.

H

3 O 12 4

OH

OH

R1

O

CH CH3

13

7

C H3C

11

H O 1

O

C CH3

FIGURE 135–1. Structure of T-2 and HT-2. Trichothecenes:T-2 (R1 = OAc) and its metabolite HT-2 (R1 = OH).

An early report indicates that direct contact with trichothecenes produced irritant contact dermatitis after skin exposure.13 Mild to moderate abdominal pain has been reported to develop within 15 minutes to 1 hour after ingestion of foods contaminated with significant levels of trichothecenes. Throat irritation and diarrhea have also been frequently described after ingestion. GI tract symptoms usually resolve within 12 hours.14,15 After a presumed T-2 attack, four clinical stages have been suggested.16 The first stage includes irritation and inflammation of the GI mucosa, leading to abdominal pain, vomiting, and diarrhea, which may last 3 to 9 days. The second stage occurs on days 10 to 14 after exposure and is a latent period; symptoms are not prominent, but progressive anemia, thrombocytopenia, and leukopenia with relative lymphocytosis develop. The third stage occurs over the ensuing 3 to 4 weeks. Clinically, patients may show petechial hemorrhages on their skin and mucous membranes, and a hemorrhagic diathesis from mucous surfaces occurs. Varying degrees of necrotic lesions may develop in the GI tract or larynx, and generalized lymphadenopathy may appear. Blood abnormalities become more severe, and the erythrocyte sedimentation rate is elevated. Infections and sepsis during this stage are usually fatal. The fourth is the convalescence stage, when there is a rebound in the white blood count, the necrotic lesions of the mucous membranes resolve, and the patient recovers completely. The current weight of scientific evidence does not support a causal relationship between purported inhalation exposure to fungi capable of producing trichothecenes in the indoor environment and specific health effects.17 High-performance liquid chromatography, gas chromatography, and liquid chromatography mass spectrometry18,19 have been used for trichothecene analysis in human blood and urine. However, these methods have not been validated by or used in sound epidemiologic studies. Serologic testing for antibodies specific to toxigenic fungi does not provide accurate information on exposure to trichothecenes or mycotoxins because the immunoglobulin is directed toward fungal antigens, not mycotoxins. Concerns on cross-reactivity in laboratory assays exist between S. chartarum antigens and fungi that are commonly found in outdoor environments.20 Abnormalities in lymphocyte subset analysis have been reported in some studies, but consistent and specific findings have not been identified. The most appropriate diagnostic test to evaluate hematologic and immune sta-

PREINCIDENT ACTIONS Hospital, emergency department, and ambulatory care facilities should have general disaster plans in place in the event of mycotoxin attack. The plan should be well thought out, should include an “all-hazards” approach, should be robust enough to respond to large numbers of victims, and should be tested by periodic and realistic exercises involving all essential personnel. The early detection of illness outbreaks requires surveillance systems that are capable of finding and validating the diagnosis and providing a means of communication between clinicians and health departments.21 This would require coordination of local, state, and federal public health and safety resources. In the event of a large number of patients seeking medical care in a short timeframe, emergency medical services, hospital, and ambulatory care facilities need to be mobilized in a coordinated and expeditious fashion. Isolation and decontamination procedures should be in place and triage and decontamination personnel trained well before an attack occurs. Since most physicians and healthcare providers, as well as first responders, may not be familiar with mycotoxin attack, close contact with local poison control center or local health department may be important to identify and treat the initial cases.

POSTINCIDENT ACTIONS Medical providers should maintain a high level of suspicion for possible mycotoxin attack should there be a sudden increase in the number of patients with similar symptoms and histories. Appropriate local, state, and federal public health and law enforcement authorities will need to be notified. Materials (e.g., clothing), bodily fluids, and surfaces possibly contaminated by mycotoxins should be decontaminated with 10% bleach (sodium hypochlorite) solution. Proper environmental sampling may be necessary for mycotoxin identification and documentation. Further epidemiologic investigations in collaboration with state or local health authorities may be necessary. CBC and liver function tests are recommended. Analysis of blood or urine samples may provide information concerning the metabolites of the mycotoxin. All samples should be stored and shipped using strict chain of custody procedures to preserve their evidentiary value.

MEDICAL TREATMENT OF CASUALTIES There are no specific antidotes for trichothecene or T-2 poisoning. Standard supportive care is indicated for symptomatic cases after removal from the exposure and decontamination. These measures should include management of the airways, breathing, and circulation. T-2 TOXIN (TRICHOTHECENE MYCOTOXINS) ATTACK 715

Supplemental oxygen can be given, if indicated. Contaminated clothing should be removed before skin decontamination occurs. The skin can be effectively decontaminated within minutes after T-2 exposure through washing with an aqueous soap solution. Polyethylene glycol 300 (PEG 300) is also effective at removing large doses of T-2 toxin from the skin.22 An animal model has shown dexamethasone may improve survival after low- and high-dose exposure to T-2 toxin.23 T-2 toxin is tightly adsorbed onto activated charcoal and has been associated with improved survival when administered with oral or parenteral doses of T-2 toxin in a mouse model.24 These findings suggest that activated charcoal may decrease toxin absorption from the GI tract and may possibly enhance elimination of toxin via enterohepatic circulation. Although human data are lacking, a single dose of activated charcoal is probably warranted after acute trichothecene ingestion. Laboratory testing should include serial CBC and differential evaluations for thrombocytopenia, anemia, and effects on the various white blood cell lines. The development of significant immune suppression, including pancytopenia, warrants neutropenic precautions and antibiotic coverage for fevers. After ingestion, careful examination of the oral mucous membranes and GI tract is warranted to evaluate for the presence of petechial, necrotic, or ulcerative lesions. In cases of airway compromise due to blistering effects of inhaled T-2 mycotoxin, patients should be monitored in a critical care setting with aggressive airway management readily available.

CASE PRESENTATION A previously healthy man comes to the emergency department complaining of blisters on his hands and the exposed skin of his neck and face that began to appear after he went jogging through a park a day prior. He also complains of nausea, vomiting, diarrhea, and abdominal pain but denies fever or chills. He also reports weakness, severe dizziness, and shortness of breath. Blood tests reveal that his white blood cell count is normal, but his lymphocyte count appears to be on the low side. On examination, there is evidence of extreme redness to his eyes, nose, and throat. There are a few hemorrhagic petechia noted on his trunk, arms, face, and oral mucosa. A general blood chemistry panel shows normal liver and kidney function. Due to his severe vomiting and diarrhea, he is hospitalized and treated with intravenous fluids. The next day, the local news media reports that an additional 50 people had been hospitalized or treated in local emergency departments for similar symptoms.

UNIQUE CONSIDERATIONS Although skin blistering may be produced by dermal exposure to T-2, T-2 is most toxic when ingested. An attack using an aerosolized T-2 weapon is unlikely to produce sufficient inhalational dosages to cause significant 716 TOXINS

morbidity or mortality.25 The most probable sign that a T-2 toxin or related mycotoxins attack has occurred may be the presentation of a large number of previously healthy persons over a course of hours to days with nonspecific and systemic symptoms.

PITFALLS Several potential pitfalls in response to a mycotoxin attack exist. These include the following: • Failure to prepare adequate plans, to perform realistic training exercises, and to develop emergency response systems to respond to a possible terrorist attack before the incident occurs • Failure to consider mycotoxin as the cause for nonspecific, as well as systemic, symptoms in previously healthy patients • Failure to consider mycotoxin attack in the setting of a large number of otherwise healthy people presenting over hours to days with a similar range of general as well as specific complaints • Failure to notify appropriate public health, safety, and law enforcement authorities when a possible biochemical agent attack is suspected, especially when animals are affected along with people • Failure to provide basic supportive medical care when a patient is suspected to have undergone exposure to a biochemical warfare agent

REFERENCES 1. Zilinskas RA. Verifying compliance to the biological and toxin weapons convention. Crit Rev Microbiol. 1998;24:195-218. 2. Zilinskas RA. Terrorism and biological weapons: inevitable alliance? Perspect Biol Med. 1990;34:44-72. 3. Fung F, Clark RF. Health effects of mycotoxins: a toxicological overview. J Tox Clin Tox. 2004;42:1-18. 4. Kemppainen BW, Riley RT. Penetration of [H]T-2 toxin through excised human and guinea pig skin during exposure to [H]T-2 toxin adsorbed to corn dust. Food Chem Toxicol. 1984;22:893-6. 5. Barel S,Yagen B, Bialer M. Pharmacokinetics of the trichothecenes mycotoxin verrucarol in dogs. J Pharm Sci. 1990;79:548-51. 6. Beasley VR, Swanson SP, Corley RA, et al. Pharmacokinetics of the trichothecene mycotoxin, T-2 toxin, in swine and cattle. Toxicon 1986;24:13-23. 7. Ueno Y. Mode of action of trichothecenes. Ann Nutr Aliment. 1977;31(4-6):885-900. 8. Khachatourians GG. Metabolic effects of trichothecene T2 toxin. Can J Physiol Pharmacol. 1989;68:1004-8. 9. Yoshizawa T, Sakamoto T, Kuwamura K. Structure of deepoxytrichothecene metabolites from 3-hydroxy HT-1 toxin and T-2 tetraol in rats. Appl Environ Microbiol 1985;50:67-9. 10. World Health Organization. WHO Environmental Health Criteria 105. Selected Mycotoxins: Ochratoxins, Trichothecenes, Ergot. Geneva:World Health Organization; 1990. 11. Marshall E. Yellow rain: filling in the gaps. Science 1982;217:31-4. 12. Update: Pulmonary hemorrhage/hemosiderosis among infants— Cleveland, Ohio, 1993-1996. Morb Mort Wkly Rep. 2000;49:180-4. 13. Drobotko VG. Stachybotryotoxicosis: a new disease of horses and humans. Am Rev Soviet Med. 1945;2:238-42. 14. Wang ZG, Feng JN,Tong Z. Human toxicosis caused by moldy rice contaminated with Fusarium and T-2 toxin. Biomed Environ Sci. 1993;6:65-70. 15. Bhat RV, Beedu SR, Ramakrishna Y, et al. Outbreak of trichothecene mycotoxicosis associated with consumption of mould-damaged

16. 17. 18. 19. 20.

wheat production in Kashmir Valley, India. Lancet 1989; 1(8628):35-7. Stahl CJ, Green CC, Farnum JB. The incident at Tuol Chrey: pathologic and toxicologic examinations of a casualty after chemical attack. J Forensic Sci. 1985;30:317-37. Hardin BD, Kelman BJ, Saxon A. Adverse human health effects associated with molds in the indoor environment. ACOEM evidencebased statement. J Occup Environ Med. 2003;45:470-8. Gilbert J. Recent advances in analytical methods for mycotoxins. Food Additive Contam. 1993;10(1):37-48. Yagen B, Sintov A. New sensitive thin-layer chromatographic-highperformance liquid chromatographic method for detection of trichothecene mycotoxins. J Chromatogr. 1986;356:195-201. Halsey J. Performance of a Stachybotrys chartarum serology panel. Abstract of presentation at the Western Society of Allergy, Asthma and Immunology Annual Meeting. Allerg Asthma Proc. 2000;21:174-5.

21. Buehler JW, Hopkins RS, Overhage JM, et al. Framework for evaluating public health surveillance systems for early detection of outbreaks. MMWR 2004;53(RR05):1-11. 22. Fairhurst S, Maxwell SA, Scawin JW, et al. Skin effects of trichothecenes and their amelioration by decontamination. Toxicology. 1987;46:307-19. 23. Fricke RF, Jorge J. Beneficial effect of dexamethasone in decreasing the lethality of acute T-2 toxicosis. Gen Pharmacol. 1991; 22:1087-91. 24. Fricke RF, Jorge J. Assessment of efficacy of activated charcoal for treatment of acute T-2 toxin poisoning. J Toxicol Clin Toxicol. 1990;28:421-31. 25. Ciegler A. Mycotoxins: A New Class of Chemical Weapons. Department of Defense, Washington DC: NBC Defense and Technology International; 1986:52-7.

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chapter 136

Ricin Toxin from Ricinus communis (Castor Beans) Attack Angela C. Anderson

DESCRIPTION OF EVENT Ricin is a potent biologic toxin derived from the castor bean plant Ricinus communis. After pressing for castor bean oil, 1% to 5% of the bean’s dry weight is comprised of ricin.1,2 It is three to five times more toxic than the nerve agent VX. Although ricin is thought to be 1000fold less toxic than botulinum toxin, it remains an important consideration as a potential terrorist weapon because it is stable in ambient conditions, readily available, and easily produced in mass quantities.2 Ricin is technically difficult to disseminate in concentrations high enough to be an effective weapon of mass destruction. However,its potential use in smaller-scale terrorist attacks cannot be ignored. Ricin is classified by the Centers for Disease Control and Prevention (CDC) as a category B agent (i.e., an agent that is moderately easy to disseminate and causes moderate morbidity and low mortality). R. communis is indigenous to Africa but can be found worldwide and can be purchased via the Internet. It grows wild in the southwestern United States and other parts of the world. The plant is cultivated commercially for the production of castor oil, which is used as an industrial lubricant, as a medical purgative and laxative, and as an additive in paints, shampoos, and cosmetics. Major producers include India, China, and Brazil. Castor oil contains no ricin because of the extraction process. Extraction of ricin toxin from the oil is a relatively simple procedure that involves using hexane or carbon tetrachloride and the process of chromatography. During the extraction, the ricin-rich resin portion of the plant is separated from the non–ricin-containing oil portion. Any ricin remaining in commercially produced oil is heat inactivated. The ricin-rich resin that remains is known as castor meal or “waste mash” and contains 5% to 10% (dry weight) ricin. The maximum amount of ricin that can be extracted from a single bean is approximately 10 mg.3 Active ricin toxin can be produced in the form of a liquid, a crystal, or a dry powder. Ricin exerts its effects by inhibiting protein synthesis. It belongs to a group of poisons known as A-B toxins.These toxins have a moiety (the B chain) that binds to cell surfaces and another moiety (the A chain) that enters the cell 718

and promotes catalytic activities that result in cell death. Bacterial toxins in this group include Shiga’s toxin, diphtheria toxin, pseudomonas exotoxin A, and cholera toxin. Similar plant toxins are abrin, modeccin, and viscumin (from mistletoe).4,5 The ricin B chain binds to cell-surface glycoproteins and glycolipids that have a terminal galactose residue.4,6 Reticuloendothelial cells are particularly susceptible because they bear surface receptors to which ricin can bind. Once bound, ricin uses the cell’s intracellular transport pathways to travel to ribosomes in the cytosol.4,7 The ricin A chain then removes a specific adenine residue from ribosomal ribonucleic acid (rRNA): the 28s rRNA subunit.6,8 Inactivation of the 28s ribosomal subunit blocks protein synthesis, which leads to cell death. Damage to endothelial cells results in extravascular fluid and protein leakage and tissue edema, which is known as vascular leak syndrome. Clinical ricin poisoning requires ingestion, inhalation, or injection of a sufficient amount of the toxin. A summary of human clinical presentations is listed in Table 136-1. Contamination of food or water supplies or commercial products would be likely methods by which oral ricin poisoning would occur. Ingestion is the least toxic route because gastrointestinal absorption of ricin is poor and it is partially deactivated by passage through the stomach. Ricin toxin is complexed within the matrix of the castor bean, and intact beans pass through the gastrointestinal tract with little or no toxic effect. To cause significant toxicity by the oral route, the beans must be chewed or crushed to facilitate ricin release. Lethal oral doses vary greatly between animal species. The dose of ricin that will be fatal to 50% of an exposed population (LD50) in laboratory mice is 20 mg/kg with a time to death of 85 hours after intragastric administration.2 The National Institute for Occupational Safety and Health Registry of Toxic Effects of Chemical Substances lists 2 mg/kg as the lowest published oral lethal dose in humans.9 Symptoms of mild ricin poisoning by ingestion include nausea, vomiting, abdominal pain/cramping, and diarrhea (often bloody), typically within 10 hours of ingestion. Moderate to severe toxicity causes significant fluid loss due to vomiting, diarrhea, hemorrhage, and third spacing of fluids into the tissues of the gastrointestinal tract with

TABLE 136-1 SUMMARY OF HUMAN CLINICAL PRESENTATIONS EXPOSURE ROUTE

SYMPTOMS

Mild ingestions

Nausea, vomiting, abdominal pain and cramping Extravascular fluid extravasation with resultant tachycardia, hypotension and mental status change, renal and hepatic failure Allergic symptoms including conjunctival irritation, rhinitis and bronchospasm. Cough dyspnea, chest tightness, and arthralgias Flu-like symptoms and extravascular fluid extravasation leading to pulmonary edema, hypotension, and renal insufficiency Local necrosis, weakness, myalgias, nausea, hepatorenal failure, cardiorespiratory failure

Moderate to severe ingestions

Inhalational exposure

Intravenous exposure

Intramuscular/Subcutaneous injections

resultant tachycardia, hypotension, oliguria, and possibly mental status change. Renal failure and hepatic failure have also been reported. Fatality rates from ricin ingestion are low, ranging from 2% to 6%. Ingestion of fatal doses of ricin results in rapid onset of symptoms (less than a few hours). In these cases, death usually occurs within 36 to 72 hours of exposure. Autopsy findings include multifocal mucosal ulcerations and hemorrhages of the stomach and small intestine, mesenteric lymph node necrosis, hepatic necrosis, splenic inflammation, and nephritis.10 The ability to deliver ricin via the inhalational route is limited by two variables: (1) the estimated amount of ricin required to kill 50% of the people in a 100 km2 area is significant: 8 metric tons11; and (2) to cause significant ricin inhalation, one must succeed at the technically difficult task of aerosolizing the toxin into particles less than 5 μm.10 With these facts in mind, the toxic dose of ricin by inhalation is significantly less than that required for ingestion: 3 mcg/kg (in mice).2 The only human data regarding ricin inhalation come from reports of workers occupationally exposed to castor bean dust, which can be a potent allergen. Susceptible patients present with conjunctival irritation, rhinitis, urticaria, and possible bronchospasm.3 Human studies regarding inhalation of aerosolized ricin are sparse. In the 1940s, unintentional sublethal exposures led to fever, chest tightness, cough, dyspnea, diaphoresis, and arthralgias.10 Symptoms appeared within 4 to 8 hours of exposure and did not progress to severe illness or death. Mice exposed to the aerosol LD50 of ricin (14 mcg/kg) developed an alveolar influx of inflammatory cells (predominantly neutrophils), pulmonary edema, type 2 pneumocyte hyperplasia, and peribronchovascular fibroplasias.12 Bronchoalveolar lavage (BAL) revealed pulmonary inflammation with an increase in BAL protein.12 Rats exposed to lethal ricin concentrations developed necrotizing interstitial and alveolar inflammation and edema, as well as fibropurulent pneumonia.2,13 These changes were delayed 8 or

more hours after exposure.2,12 Immunohistochemical evaluation revealed that ricin binds to bronchiolar cilia, alveolar macrophages, and alveolar lining cells.2,12 Death occurred 36 to 48 hours after exposure. It is likely that dose, duration of exposure, and particle size will affect clinical presentation and symptom progression. Much of the information regarding intravenous ricin exposures is derived from persons with cancer who are treated with ricin as a means of targeting and killing tumor cells. Research evaluating the use of ricin as a chemotherapeutic agent evolved from the concept of replacing the binding moiety of ricin (the B chain) with a moiety that could recognize and bind cancer cell surface proteins (such as an antibody directed against cancer antigens). Administration of intravenous ricin immunotoxin in cancer patients at low doses (18 to 20 mcg/kg) has caused a flu-like illness (i.e., nausea, vomiting, fatigue, and muscular pain).14 Intravenous ricin immunotoxin at a dose of 30 mg/kg/day for 7 days caused fatal vascular leak syndrome.14,15 In fact, the doselimiting adverse effect in ricin antitumor immunotherapy appears to be the development of the vascular leak syndrome.16,17 This syndrome is characterized by hypoalbuminemia, pulmonary edema, renal insufficiency, cardiac failure, and hypotension.17 Intramuscular and subcutaneous injections of ricin can cause local necrosis, weakness, myalgias, nausea, dizziness, hepatorenal failure, cardiorespiratory failure, and death. The lowest published lethal dose from subcutaneous injection in a human is 43 mcg/kg.9 Dermal ricin exposures are unlikely to cause significant toxicity if the skin is intact. It is unknown whether the addition of a solvent will increase dermal absorption. Ocular exposure of ricin in rabbits has caused severe inflammation and pseudomembranous conjunctivitis.18

PREINCIDENT ACTIONS Currently there is no approved immunization or prophylactic agent against ricin. Most studies involve mice exposed to aerosolized ricin after immunization by various routes. Poli and colleagues19 found that treating mice with aerosolized specific anti-ricin immunoglobulin (Ig) G 1 hour prior to aerosolized ricin exposure improved survival and greatly reduced the lung pathology. Yan and others20 demonstrated that intranasally administered microsphere-encapsulated ricin toxoid protected mice against lethal doses of aerosolized ricin. Oral administration of microencapsulated ricin toxoid induced IgG and IgA antibodies within 7 weeks and provided complete protection against death from aerosolized ricin exposure.21 Smallshaw and colleagues22 experimented with a recombinant intramuscular vaccine; they induced a single mutation of the ricin A chain at the site thought to cause vascular leak syndrome. These vaccines protected mice against 10 times the LD50 of ricin without the toxicity associated with the vascular leak syndrome. Parenteral administration of ricin toxoid improves survival but is only

RICIN TOXIN FROM RICINUS COMMUNIS (CASTOR BEANS) ATTACK 719

partially protective against lung damage caused by aerosolized ricin.19 The U.S. Department of Defense has submitted an investigational new drug application to the Food and Drug Administration (FDA) for the purpose of conducting ricin vaccine trials in humans. The administration of vaccine may prove to be protective; however, with the exception of the aerosolized vaccine by Poli and colleagues,19 most animal studies thus far have found that vaccination must take place weeks before ricin exposure to be effective.

POSTINCIDENT ACTIONS The regional poison control center (1-888-222-1222), local health and law enforcement agencies, and federal authorities should be notified if ricin use is suspected. Ambulances, environmental surfaces, and equipment should be cleaned with 0.1% sodium hypochlorite solution (i.e., household bleach) or soap and water. Contaminated articles should be disposed of in a sealed plastic bag placed inside another sealed plastic bag.

MEDICAL TREATMENT OF CASUALTIES Currently, there is no antidote for ricin poisoning. Additionally, there are few evidence-based data to direct the management of ricin-exposed casualties. Mouse studies evaluating the use of a monoclonal antibody to neutralize ricin toxicity are promising but have yet to obtain FDA approval.23 Consequently, management options must be extrapolated from animal studies and previous experience with similar toxins. The course of medical management is partially determined by the route of ricin exposure. All healthcare providers, regardless of the exposure route encountered by the patient, should use standard universal precautions including a disposable gown, disposable nitrile gloves, and respiratory and eye protection.

Ricin Ingestion Gastric decontamination will likely be unsuccessful and unnecessary if intact, unchewed beans have been ingested. A single dose (adults, 50 g; children, 1 g/kg) of activated charcoal should be administered if the airway is protected. Fluid losses and cardiovascular instability should be treated with fluid resuscitation and vasopressors. Electrolytes, liver and renal function, hematocrit count, and white blood cell count should be monitored. Gastrointestinal blood losses should be treated with follow-up stool guaiacs, hemoglobin and hematocrit measurements, and blood transfusions as necessary. Ricin is a large (66-kDa) globular protein that is not dialyzable, therefore there is no role for hemodialysis in ricin poisoning except in the setting of renal failure.

720 TOXINS

Exposure to Aerosolized Ricin Contaminated clothing and jewelry should be removed; this can potentially reduce additional patient contamination by as much as 90%10 and may prevent contamination of the emergency department, its staff, and other patients. Pulmonary effects, such as airway edema and necrosis and noncardiogenic pulmonary edema, should be treated supportively and aggressively. Continuous positive airway pressure or endotracheal intubation and ventilation may be necessary to manage pulmonary edema. Fluid and electrolyte abnormalities should be treated with intravenous fluid resuscitation and repletion of electrolytes. Allergic reactions should be treated with beta-2 adrenergic agonists, steroids, and antihistamines.

Parenteral Exposure Routine burn and wound care can be used to treat local necrosis. Analgesia should be provided as necessary, as should replacement of fluids and electrolytes. Healthcare providers should watch for signs of systemic toxicity such as hepatic and renal failure. Cardiopulmonary collapse can be treated with vasopressors and ventilatory support.

Dermal/Ocular Exposure If ricin has been dispersed in a powder form, skin decontamination at the scene is preferable. Contaminated clothing and jewelry should be removed, and skin should be washed with soap and water. It is unlikely that ricin will be absorbed to any significant extent through intact skin; however, it is prudent to decontaminate patients to prevent secondary contamination of healthcare providers and equipment. The eyes of patients with ocular exposures should be irrigated with tepid water for at least 15 minutes.

CASE PRESENTATION Over the course of a few days, 10 patients present to local emergency departments complaining of nausea, vomiting, and bloody diarrhea. Within hours of presentation, patients experience severe fluid losses with associated tachycardia and hypotension requiring significant fluid resuscitation. Two days after presentation, many patients develop evidence of hepatic and renal failure. Routine stool and blood cultures all have negative results. All but two patients recover completely with supportive therapy. Further investigation revealed that all 10 patients had been at a small company picnic where they had ingested the same beverage. The beverage was sent to a laboratory response network, which found evidence of the ricin by fluorescence immunoassay.The presence of ricin was confirmed by the CDC. The amount of ricin ingested by each person, based on personal accounts of the patients before death, was approximately 2 mg/kg or greater.

UNIQUE CONSIDERATIONS Ricin is stable at ambient temperatures. It can be detoxified by exposing it to temperatures of 176°F (80°C) for 10 minutes or 122°F (50°C) for 1 hour.24 In 1999, the CDC established the Laboratory Response Network (LRN) to test for substances that could potentially be used in a terrorist event. Each of the 50 states has a state department of health laboratory called the public health laboratory. There are also other national, military, hospital-based, and state-based laboratories within this network. Suspicious samples of potentially toxic agents should be sent to an LRN reference laboratory. These laboratories currently can test for ricin by either of two methods: (1) time-resolved fluorescence immunoassay in which antibodies that bind to ricin are used; and (2) polymerase chain reaction, which searches for DNA of the gene that produces ricin protein. If a sample is found to contain ricin by a LRN reference laboratory, the sample is then sent to the CDC for additional testing, archiving, or storage. (Information on shipping procedures can be found at http://www.bt. cdc.gov/labissues/index.asp.) At present, testing can only document or confirm exposure. Testing results are not immediately available; therefore, its use as a diagnostic tool to aid in clinical decision-making is limited. Ricinine is an alkaloid derived from the leaves and seeds of the castor bean plant. Recently, Darby and colleagues25 developed a method using matrix-assisted laser desorption/ionization time-of-flight mass spectrometry and electrospray liquid chromatography/mass spectrometry to screen for and identify ricinine in samples.Thus far, tests for ricinine are not available for clinical use. Ricin is very immunogenic. Circulating antibodies develop 2 weeks after exposure. Therefore, patients surviving at least 2 weeks after exposure can be tested for a humoral immune response. Further information can be obtained from the following sources: the CDC Public Response hotline (1-888246-2675); and the CDC Emergency Preparedness and Response Web site (http://www.bt.cdc.gov); the Agency for Toxic Substances and Disease Registry (1-888-4228738); and the CDC’s “Chemical Agents: Facts About Personal Cleaning and Disposal of Contaminated Clothing” (http://www.bt.cdc.gov/planning/personalcleaning facts.asp).

PITFALLS Several potential pitfalls in response to a ricin attack exist. These include the following: • Exposure may mimic gastroenteritis or the flu. • Ingestion can cause symptoms easily confused with iron, arsenic, or colchicine poisoning. • Clinical presentation can mimic ingestion of bacterial pathogens such as salmonella and shigella.

• Inhalational ricin exposure may mimic infectious agents including community-acquired pneumonia, influenza, anthrax, Q fever, and pneumonic plague. • Ricin inhalation may mimic inhalation of other toxins such as products of combustion from burning Teflon and Kevlar, nitrogen oxides, and phosgene. • Patients may be exposed to more than one toxin, making the constellation of clinical symptoms confusing. REFERENCES 1. Savino D. CDI Factsheet: Ricin. Washington DC: Center for Defense Information; 2003. 2. Franz D, Jaax N. Ricin toxin. In Zajtchuk R. ed. Medical Aspects of Chemical and Biological Warfare. Falls Church, Va: Office of the Surgeon General, Department of the Army; 1997:631-42. Available at: http://www.bordeninstitute.army.mil/cwbw/default_index.htm. 3. Bradberry S, Dickers KJ, Rice P, et al. Ricin poisoning. Toxicol Rev. 2003;22:65-70. 4. Sandvig K, Grimmer S, Lauvrak SU, et al. Pathways followed by ricin and Shiga toxin into cells. Histochem Cell Biol. 2002;117: 131-41. 5. Doan L. Ricin: mechanism of toxicity, clinical manifestations, and vaccine development. A review. J Toxicol Clin Toxicol. 2004;42: 201-8. 6. Olsnes S, Kozlov J. Ricin. Toxicon 2001;39:1723-8. 7. Poli MA, Rivera VA, et al. Aerosolized specific antibody protects mice from lung injury associated with aerosolized ricin exposure. Toxicon 1996 Sep;34(9):1037-44. 8. Kende M,Yan C, et al. Oral immunization of mice with ricin toxoid vaccine encapsulated in polymeric microspheres against aerosol challenge. Vaccine 2002 Feb 22;20(11-12):1681-91. 9. Ricin TRECS#:VJ2625000. Washington DC: National Institute for Occupational Safety and Health: Registry of Toxic Effects of Chemical Substances; 2002. 10. Daniels K, Schier J. Recognition, management and surveillance of ricin-associated illnesses. Public Health Practice Program Office, Webcast WC 0-0-4-8. Atlanta, Ga: Centers for Disease Control and Prevention; December 30, 2003. Available at: http://www. phppo.cdc.gov/phtn/webcast/ricin/RicinScript.rev.07-14-04.htm. 11. Shea D, Gottron F. Ricin: Technical Background and Potential Role in Terrorism. Washington DC: Congressional Research Service. Library of Congress; 2004. 12. DaSilva L, Cote D, Roy C, et al. Pulmonary gene expression profiling inhaled ricin. Toxicon 2003;41:813-22. 13. Darby SM, Miller ML, et al. Forensic determination of ricin and the alkaloid matter is ricinine from castor bean extracts. J Forensic Sci. 2001 Sep; 46(5):1033-42. 14. Fodstad O, Kvalheim G, Godal A, et al. Phase I study of the plant protein ricin. Cancer Res. 1984;44:862-5. 15. Fidias P, Grossbard M, Lynch TJ Jr. A phase II study of the immunotoxin N901-blocked ricin in small-cell lung cancer. Clin Lung Cancer. 2002;3:219-22. 16. Baluna R, Coleman E, Jones C, et al.The effect of a monoclonal antibody coupled to ricin A chain-derived peptides on endothelial cells in vitro: insights into toxin-mediated vascular damage. Exp Cell Res. 2000;258:417-24. 17. Baluna R, Sausville EA, Stone MJ, et al. Decreases in levels of serum fibronectin predict the severity of vascular leak syndrome in patients treated with ricin A chain-containing immunotoxins. Clin Cancer Res. 1996;2:1705-12. 18. Grant E, ed. Toxicology of the Eye. 3rd ed. Springfield, Ill: Charles C. Thomas; 1986.

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chapter 137

Aflatoxin Attack (Aspergillus Species) Frederick Fung

DESCRIPTION OF EVENT Aflatoxins are metabolites produced by certain strains of the fungi Aspergillus flavus and Aspergillus parasiticus. They were discovered during a disease epidemic in Great Britain that wiped out more than 100,000 turkeys in 1960. The source of the illness was traced to aflatoxin-contaminated turkey feed made of moldy Brazilian peanuts. Eventually it was discovered that all crops and foodstuffs, including corn, rice, wheat, barley, and nuts, can contain naturally occurring mycotoxins.1 There are several aflatoxins and their metabolites (such as AFB1,AFG1,AFM1) that are capable of producing human disease.2 Aflatoxins are named by their fluorescence under ultraviolet light as blue (AFB) or green (AFG) as well as other analytic characteristics. Aflatoxins M (AFM), where M denotes milk or mammalian metabolites, are secreted in the milk of animals exposed to aflatoxins. There are two broad categories of aflatoxins according to their structures: aflatoxins B1 and M1 are within the difurocoumarocyclopentenone series (Fig. 137-1), and aflatoxin G1 is of the difurocoumarolactone series (Fig. 137-2). Exposure to aflatoxins is typically via ingestion of contaminated foodstuff. Dermal exposure results in slow and insignificant absorption.3 Inhalational exposure in humans has not been studied. In vitro metabolism studies have shown the following metabolic reactions for AFB1:reduction produces aflatoxicol (AFL); hydroxylation produces AFM1; hydration produces AFB2a; and epoxidation produces AFB12,3-epoxide. The epoxide is the most reactive metabolite and is thought to be responsible for both the acute and chronic toxicity of AFB.4 In an Indian report, ingestion of an estimated 2 to 6 mg/kg/day of aflatoxin over 1 month produced hepatitis, with some fatalities.5 However, a suicide attempt by acute ingestion of 1.5 mg/kg of pure aflatoxin resulted only in nausea, headache, and rash.6 The liver is the primary target of toxicity and may lead to hepatic failure. Early symptoms of hepatic injury from acute poisoning include abdominal pain, anorexia, malaise, and low-grade fever.7 Icterus and jaundice develop within several days, followed by abdominal distention, vomiting, ascites, and edema.8 Mortality rates from acute aflatoxicosis range from 10% to 76%.7 The chronic effects of aflatoxins are primarily carcinogenesis resulting in hepatocellular carcinoma. Laboratory tests of liver 722

function confirm the extent of hepatic injury in acute aflatoxicosis. Elevated aspartate and alanine aminotransferase levels frequently exceed 5000 IU/liter. Bilirubin levels are also increased. Acute jaundice and death have been recently reported in an outbreak of aflatoxin poisoning in Kenya.9 In cases of liver failure, elevation of the prothrombin time, metabolic acidosis, and hypoglycemia are the characteristic signs.10 Pathologically, there is extensive centrilobular necrosis in the perivenular zone (zone 3) extending to periportal zones (zone 1) with giant cell infiltration and cholestasis.11 The 1972 Biological and Toxin Weapons Convention is a major international treaty seeking to control biologic warfare. It prohibits state parties from developing, producing, stockpiling, and testing biologic and toxic weapons.12,13 However, with the expansion of terrorism, the use of mycotoxins as weapons is a real threat. Possible attack scenarios include the following: 1. Product tampering: Substantial human and economic damage could result from consumer product tampering such as the cyanide poisoning of Tylenol in 1984.13 Tampering by spiking premade consumer products with mycotoxins may be the most plausible attack scenario. 2. Chemical weaponry: A second scenario is large-scale terrorism using aflatoxins as chemical weapons against a population group or region, such as the Anfal Operations against the Kurds of Northern Iraq. 3. Food tampering: Another scenario is an attack on food industries. The dairy industry is especially vulnerable to biochemical agents, probably because of the nature of manufacturing process and the reliance of animal feeds that could be contaminated with biochemical (mycotoxins) agents.13 Such an attack would cause local outbreaks of disease within hours or days. In September 2004, the Hungarian government pulled paprika off the market due to excessive levels of aflatoxin detected in much of their product.14

PREINCIDENT ACTIONS Hospitals, emergency departments, and ambulatory care facilities should have general disaster plans in place to

sional may be necessary for aflatoxin identification and evidence documentation. Further epidemiologic investigations in collaboration with state or local health services may be necessary. Complete blood count and liver function tests are recommended. Analysis of blood or urine samples may provide information concerning the metabolites of the mycotoxin.

O

O

O R

O

O

OCH3

AF

R

AFB1

H

AFM1

OH

MEDICAL TREATMENT OF CASUALTIES

FIGURE 137–1. Structures of AFB1 and AFM1 (see text). O

O

O

O

O

O

OCH3

FIGURE 137–2. Structure of AFG1.

respond to a biochemical (mycotoxin) attack. Early detection of a biologic or chemical weapon attack requires a surveillance system that is capable of finding and confirming the diagnosis and serving as a means of communicating this information between clinicians and health departments in a timely fashion.15 Current syndromic surveillance appears to be directed more toward respiratory and flu-like illness, although several monitor gastrointestinal illness.16 Efforts should be made to include hepatitis syndromes in such monitoring efforts. This would require coordination of local, state, and federal public health and safety resources. In the event of an attack, emergency medical services, hospitals, and ambulatory care facilities need to be mobilized to care for potentially large numbers of patients seeking medical care in a short timeframe. Decontamination and triage procedures should be in place, and personnel properly trained, before an attack occurs. Since most physicians, healthcare providers, and first responders are not likely to be familiar with the characteristics of an aflatoxin terrorist attack, close contact with the local poison control center or local health department may be important in identifying the initial cases.

POSTINCIDENT ACTIONS Medical providers should include aflatoxin toxicity in the differential of acute hepatitis. Appropriate local, state, and federal public health agencies and law enforcement authorities need to be notified. Aflatoxin-contaminated materials, body fluids, and surfaces should be decontaminated with a 10% bleach (sodium hypochlorite) solution. Bleach should not be used to decontaminate patients. Proper sampling by a qualified industrial hygiene profes-

Treatment of acute aflatoxin exposure requires identification of and removal from the source of exposure. Activated charcoal is recommended in cases of recent ingestion. Aggressive supportive management, especially for acute liver failure, is indicated in all suspected cases. Hemodialysis and hemoperfusion are not expected to enhance elimination. Although there is no known antidote, N-acetylcysteine (NAC) may have a protective effect against aflatoxin carcinogenesis by increasing intracellular glutathione levels.17 An animal model18 found reduced hepatic injury when NAC was coadministered with high daily doses of AFB1; however, efficacy in humans has not been demonstrated.

CASE PRESENTATION There are several reports from Asia and Africa that suggest acute poisonings secondary to aflatoxins resulting from ingestion of a large amount of toxin over a short period of time. A typical presentation is as follows: Two young children are taken to the local hospital emergency department from the neighborhood village. Patient’s family members inform the emergency department physician that they have all consumed corn from a local farmers market. Over the last 5 days, the children developed swelling of their lower extremities, abdominal pain, vomiting, and diarrhea, but no fever. Further history reveals that the adults experienced similar but milder symptoms. On examination, the patients are lethargic. Also present is slight jaundice with an enlarged liver that is tender to palpation. The next day, it is reported in the news media that an additional 30 children have been admitted to surrounding hospitals and more than 100 adults and children have been seen in local ambulatory care clinics for similar but milder symptoms. They all report eating corn and fruits purchased from a local farmers’ market. Laboratory testing of the initial two young children reveals elevated liver aminotransferase levels, low blood glucose, and elevated blood ammonia levels. These two patients fully recover after 1 week of supportive care and intravenous fluids.

UNIQUE CONSIDERATIONS Diseases caused by mycotoxins such as aflatoxins are most effective when they are ingested. Aflatoxin attack using an aerosolized mechanism is unlikely to produce sufficient levels to cause significant morbidity or mortality.19 AFLATOXIN ATTACK (ASPERGILLUS SPECIES) 723

PITFALLS Several potential pitfalls in response to an aflatoxin attack exist. These include the following: • Failure to prepare adequate systems to respond to possible terrorist attacks before an incident occurs • Failure to consider aflatoxin as the cause for nonspecific as well as systemic symptoms of acute hepatitis • Failure to consider aflatoxin attack in the setting of a large number of otherwise healthy people presenting over hours and days with a wide range of general and specific complaints • Failure to notify appropriate public health, safety, and law enforcement authorities when a biochemical agent attack is suspected, especially when animals fall sick along with people • Failure to collect specimens for identification of aflatoxins • Failure to provide basic supportive care when a patient is suspected to have been exposed to a biochemical warfare agent REFERENCES 1. Pitt JI, Basilico JC, Abarca ML, et al. Mycotoxins and toxigenic fungi. Med Mycol. 2000;38(suppl 1):41-6. 2. Fung F, Clark RF. Health effects of mycotoxins: a toxicological overview. J Tox Clin Tox. 2004;42:1-18. 3. Riley RT, Kemppainen BW, Norred WP. Penetration of aflatoxins through isolated epidermis. J Toxicol Environ Health.1985;15:769-77. 4. Hsieh DPH, Wong JJ. Metabolism and toxicity of aflatoxins. Adv Exp Med Biol. 1982;126(B):847-63.

724 TOXINS

5. Patten RC. Aflatoxins and disease. Am J Trop Med Hyg. 1981;30:422-5. 6. Willis RM, Mulvihill JJ, Hoofnagle JH. Attempted suicide with purified aflatoxin. Lancet 1980;1(8179):1198-9. 7. Ngindu A, Johnson BK, Kenya PR, et al. Outbreak of acute hepatitis caused by aflatoxin poisoning in Kenya. Lancet 1982;1:1346-8. 8. Krishnamachari KA, Bhat RV, Nagarajan V, et al. Hepatitis due to aflatoxicosis: an outbreak in Western India. Lancet 1975;1:1061-3. 9. Nyikal J, Misore A, Nzioka C, et al. Outbreak of aflatoxin poisoning: Eastern and central provinces, Kenya, January–July, 2004. MMWR 2004;53(34):790-3. 10. Olson LC, Bourgeois CH Jr, Cotton RB, et al. Encephalopathy and fatty degeneration of the viscera in northeastern Thailand: clinical syndrome and epidemiology. Pediatrics 1971;47:707-16. 11. Chao TC, Maxwell SM, Wong SY. An outbreak of aflatoxicosis and boric acid poisoning in Malaysia: a clinicopathological study. J Pathol. 1991;164:225-33. 12. Zilinskas RA. Verifying compliance to the biological and toxin weapons convention. Crit Rev Microbiol. 1998;24(3):195-218. 13. Zilinskas RA. Terrorism and biological weapons: inevitable alliance? Perspect Biol Med. 1990;34:44-72. 14. Greenberg G. Hungarian government temporarily prohibits sale of paprika. November 3, 2004. Available at: http://list.mc.duke. edu/cgi-bin/wa?A2=ind0411&L=occ-env-med-l&F=&S=&P=2429. 15. Buehler JW, Hopkins RS, Overhage JM, et al. Framework for evaluating public health surveillance systems for early detection of outbreaks. MMWR 2004;53(RR05):1-11. 16. Bravata DM, McDonald KM, Smith WM, et al. Systemic review: surveillance systems for early detection of bioterrorism-related diseases. Ann Intern Med. 2004;140:910-22. 17. De Flora S, Bennicelli C, Camoirano A, et al. In vivo effects of Nacetylcysteine on glutathione metabolism and on the biotransformation of carcinogenic and/or mutagenic compounds. Carcinogenesis 1985;6:1735-45. 18. Valdivia AG, Martinez A, Damian FJ, et al. Efficacy of N-acetylcysteine to reduce the effects of aflatoxin B1 intoxication in broiler chickens. Poult Sci. 2001;80:727-34. 19. Ciegler A. Mycotoxins: A New Class of Chemical Weapons. 1986 NBC Defense and Technology International, Department of Defense,Washington DC:April 1986:52-7.

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Other Biologic Agents

chapter 138

Coccidioides immitis Attack (Coccidioidomycosis) James F. Martin and Jill A. Grant

DESCRIPTION OF EVENT Coccidioidomycosis is a specific disease, caused by the fungus Coccidioides immitis. It was first defined as a syndrome in 1892 and shown to be a fungal infection in 1900. This disease is known as San Joaquin Valley fever, or valley fever, due to its native location in the San Joaquin Valley of California,Arizona, New Mexico,Texas, and Utah, as well as in Mexico and portions of Central and South America. There are approximately 25,000 clinically significant cases defined per year in the United States, with 75 deaths per year attributed to the illness.1-3 In 2001, the Arizona Department of Health reported 43 cases per 100,000 population, representing an increase of 186% since 1995.3 Although there are endemic areas, with the majority of long-term residents demonstrating evidence of prior C. immitis infection, those areas often experience intermittent sharp seasonal increases in the number of cases, demonstrating the infectivity of the disease as well as its capability for mutation. C. immitis exists as both a saprophyte and a parasite at different times during its life cycle. It is in the saprophytic stage in which it grows in soil as a mold with septate hyphae. It is initially spread by airborne spores, with epidemics often occurring after large-scale soil disturbances such as earthquakes, excavations, or storms. Once disturbed, these hyphae are broken off, forming arthroconidia, which in turn become airborne. The parasitic phase occurs if an animal or human inhales the arthroconidia, which become lodged in the pulmonary alveoli. It is here that they grow into multinucleate spherules, producing thousands of uninucleate endospores, each of which can give rise to a new spherule. The endospores have been shown to spread in a suitable host within the lung or through the bloodstream. Dissemination through the bloodstream has been shown to lead to deposition in perihilar,peritracheal,and cervical lymph nodes. Multisystem involvement can include skin and soft tissue infection, joint and bone infection, and meningitis. The majority of symptoms are pulmonary. In the 40% of acutely exposed persons displaying symptoms, the most common are cough, shortness of breath, chest pain, and sputum production, along with systemic symptoms

of fever, sweating, anorexia, weakness, and arthalgias.1 These symptoms may last for several weeks, with spontaneous resolution. The average otherwise healthy person infected with C. immitis misses an average of 1 month of school or work.1 If the disease becomes disseminated, multiple sites can be affected.4 The most common extrapulmonary site is the skin, with superficial maculopapules, keratotic nodules, verrucous ulcers, and subcutaneous fluctuant abscesses being found.2 The pus may be described as “gel-like.” These lesions have a predilection for the nasolabial fold. Erythema multiforme and erythema nodosum may occur, more commonly in female patients. Erythema nodosum may be the initial presentation and reflects a heightened immune response. These patients rarely go on to disseminate.2 The triad of fever, erythema nodosum, and arthralgias is called desert rheumatism.2 Bone and joint infections may occur, in the company of dramatic effusions and synovial involvement, with dissemination. Joint lesions are unifocal in 90% of cases. The knee is the most commonly affected joint, followed by the ankle.1,2 Coccidioidal meningitis is the most life-threatening of manifestations, with mortality approaching 90% at 12 months if untreated.1,2 Usually the basilar meninges are involved, and presenting symptoms include fever, headache, vomiting, and altered mental status. Complications include hydrocephalus, cerebral vasculitis, and focal intracerebral coccidioidal abscesses.2 Neurosurgical consultation may be urgent, for shunting or incision and drainage. Diagnosis of coccidioidomycosis may be difficult and challenging, primarily due to a failure to consider the disease outside its endemic areas.5 A specific travel history is usually necessary in nonendemic areas to prompt suspicion of the diagnosis.6 Skin testing results become positive after the initial onset of symptoms in most patients with primary infections; anergy, however, is common in progressive disease.1 Routine laboratory tests are not specific, although the erythrocyte sedimentation rate is usually elevated and the eosinophil counts are often increased.7 Culture and serologic testing are the most commonly available tests, although direct microscopic examination of tissue samples is deemed safest. The mycelial form of 725

the fungus has minimal growth requirements, growing after 3 to 7 days on most mycologic or bacteriologic media under aerobic conditions and at most temperatures.1,2 Mature colonies can have a myriad of appearances and are very highly infectious to laboratory workers.1 In histopathology specimens, a mature spherule with endospores is pathognomonic of infection and is easily recognizable on wet mounts using potassium hydroxide or Calcofluor white.8 Spherules also can be easily seen with multiple staining techniques,1 particularly with periodic acid-Schiff. The organism can often be seen in, or grown from, pus, sputum, and body fluid aspirates.1 Serologic testing is almost entirely based on immunoglobulin (Ig) M and IgG antibodies. False-positive test results are rare.1 IgM is detected transiently in 75% of acutely infected persons 1 to 3 weeks after onset of symptoms due to primary infection and may last 3 to 4 months. Complement-fixing IgG appears later after the acute infection and disappears in 6 to 9 months if symptoms resolve.8 Persistently elevated IgG antibody is observed in disseminated disease. In the case of C. immitis meningitis, cerebrospinal fluid (CSF) cultures are usually negative in 85% of early cases.1 The CSF will show an elevated pressure, a marked mononuclear pleocytosis, low glucose level, and high protein level.1 A positive result of an IgG test of the CSF confirms the diagnosis.2 Imaging studies are nonspecific but can aid in the diagnosis. Chest radiology may delineate cavities and granulomas. Magnetic resonance imaging may be useful to examine the brain for signs of meningitis or abscesses.2 Radionuclide bone scanning may delineate bone lesions. Coccidioidomycosis would appear to make a poor biologic weapon. Most immunocompetent patients are asymptomatic, with only 40% of infected persons displaying any type of symptom. Among those who are symptomatic, the most common form is an upper or lower respiratory tract infection, which usually resolves without specific therapy and can last up to 3 or 4 weeks and still go undiagnosed. Extrapulmonary manifestations have much higher morbidity and mortality but occur in only 0.5% of cases, may take up to a year to develop, and occur in subpopulations of immunocompromised persons with defects in delayed hypersensitivity, pregnant women in their third trimester, infants, or patients of Filipino, African American,or Mexican descent who are genetically predisposed to disseminate the disease. The organism is almost entirely contained in the “Western Hemisphere,” with an estimated majority of those Americans who are living in the endemic areas already showing signs of prior exposure or infection. Thus, if the fungus were used as a weapon of mass destruction, a minority of the population would be symptomatic, with most symptoms resolving in a few weeks. In those few persons who do have life-threatening infections, it will usually occur in minority populations and could take up to a year to develop. There are, however, some facts that demonstrate the potential lethality of coccidioidomycosis if used as a biologic weapon. First, each year, 25,000 new cases are diagnosed, and 75 deaths occur annually. These deaths almost always occur in those persons suffering from disseminated disease. The most common dissemination is to the 726 OTHER BIOLOGIC AGENTS

skin, closely followed by the meninges. If meningitis occurs, the 12-month mortality is 90% if not treated. Even with appropriate treatment,mortality rates from fulminant infections remain high. It is estimated that, even with our most advanced treatment, neurologic involvement by coccidioidomycosis has a 70% to 80% death rate. Hence, there is a significant mortality of the disseminated disease. Second, the fungus has a very high virulence, with only a single C. immitis arthroconidium required to produce pulmonary infection.2 However, devastating outbreaks have been demonstrated when coccidioidomycosis has been specifically grown in the laboratory setting, such as in the case of hospital laboratory personnel attempting to diagnose a patient. This occurrence demonstrates the increased virulence of the spore form of the organism when being grown in the laboratory. Add to this fact the apparent capability to mutate, and a potentially devastating biologic weapon could be developed. Third, healthcare workers may not initially recognize a coccidioidomycosis attack. With the majority of patients asymptomatic, and those who are symptomatic displaying a nonspecific upper respiratory infection, initial cases may be ignored or diagnosed with a self-limited viral disease. Three to 4 weeks is the incubation period for the pulmonary manifestations, so a delay from the initial exposure may be present. For the sickest patients, an even longer incubation period of up to 1 year may be evident, further complicating the diagnosis and increasing the morbidity in the specific population of infected persons with the highest mortality. Although there has been no documented incidence of person-to-person spread through air droplets, the infectivity of these longincubation patients is unknown. Use of C. immitis as a weapon could therefore cause a subtle increase in the workload of the healthcare system over time. The most likely scenario of a C. immitis attack would consist of a large urban population with a large number of persons presenting over a few weeks with a nonspecific upper respiratory infection. Minority populations; pregnant women; infants; and immunocompromised patients, such as those with HIV, those having received organ transplant; and patients taking steroids would be the worst affected. An effective attack would require a large target population localized in a specific area that could be inoculated with airborne particles. Although evidence of prior infection may already be present in much of the population, a dramatic increase in clinical cases should alert healthcare workers, and once positive diagnoses are made, a biologic attack should be considered. The population should be followed up for as long as 1 year after the incident for evidence of chronic severe infection; this requirement in itself will increase the load on the healthcare system and could increase public fear, as those exposed would constantly worry that they might develop delayed and serious illness.

PREINCIDENT ACTIONS In endemic areas, coccidioidomycosis can only be prevented by occupationally preventing susceptible per-

sons from working in high-risk situations; therefore, in these specific areas, focused educational programs for construction and agricultural workers should be in place, as well as for students, military personnel, and healthcare workers. Documented cases of mass infection with C. immitis show occurrence in one of three ways: (1) recent visit to an endemic area; (2) reactivation of a prior infection; or (3) exposure to spores brought out of an endemic area. Hospitals, emergency departments, and outpatient facilities should each have a disaster response plan in place. Coordination of local, state, and national public health and public safety resources are required in the event of a mass-casualty situation such as biologic warfare. Both emergency medical services and hospital triage systems may need to be altered to account for the influx of patients with specific treatment requirements—in this case, respiratory ailments. Universal precautions should be in place, even though person-toperson transmission of coccidioidomycosis has never been documented.9 Diagnosis of the index case may be difficult, again, mainly due to a lack of suspicion for the agent in nonendemic areas. Special and specific care needs to be taken with the culturing of C. immitis: namely, specialized training for laboratory technicians, universal precautions, Biosafety Level 3 procedures, and negative pressure rooms. Cultures should be planted on slants rather than on culture slides. Physicians should be trained to highlight their suspicions for coccidioidomycosis when submitting culture specimens from suspect patients. A real coccidioidomycosis attack or a major natural outbreak is unlikely; however, healthcare providers need to be aware of the disease and keep it on the differential diagnosis list. The possibly long incubation period, nonspecific complaints, and multiple organ involvement may make initial diagnosis extremely difficult. Universal precautions need to be in place, as well as a surveillance system that can recognize a trend in patient syndromes. With documentation of trends over time, a specific index incident may be able to be identified.

POSTINCIDENT ACTIONS Healthcare providers with suspicion of, or a clear demonstrated case of, coccidioidomycosis need to contact specific public health officials because coccidioidomycosis became a nationally reportable disease in 1995.3 Also, any medical providers or disaster response teams that may come into contact with an infected party or a putative exposure location should be notified and screened. Such responders may include any hospital or clinic worker or physician who treated patients from a specific location, as well as emergency medical services, police, or fire personnel; clean-up crews; those working for the Red Cross and other relief organizations; and the military. Disinfection of surfaces possibly contaminated with arthroconidia should be carried out with standard disinfectants or antiseptic agents.

MEDICAL TREATMENT OF CASUALTIES Of the endemic fungal infections, coccidioidomycosis is the most resistant to therapy.10 The treatment and care of the primary respiratory infection is controversial, primarily due to the lack of controlled clinical trials.1,2 For the majority of patients, care should include symptomatic treatment and careful reexamination to ensure the resolution of symptoms. Follow-up radiology to monitor the resolution of pulmonary findings is also recommended. The goal of this approach is to monitor resolution in the event of not using antifungal therapy. Historically, initial pulmonary manifestations have a 95% spontaneous resolution rate. However, some authorities propose rapid and high-dose antifungal medications at the time of diagnosis for unusually severe infections or with comorbid conditions such as organ transplantation, HIV infection, diabetes,or steroid use. The severity of the disease should be estimated, with the following characteristics kept in mind: symptoms that persist longer than 2 months; weight loss greater than 10%; greater than 3 weeks of night sweats; infiltrates involving greater than 1 lung; development of anergy to skin tests; prominent or persistent hilar adenopathy; Filipino,African American, or Mexican ethnic background; pregnant female patients in their third trimester; or an antibody test result demonstrating antibody to C. immitis in a titer greater than 1:16.2 For persons with severe infections, the two treatment options consist of surgical debridement or chemotherapy. Surgery should be determined on a case-by-case basis and is an option in the case of extensive bone or skin involvement. The theory behind the use of debridement is that the spherule wall (1) is a strong stimulus for inflammation, (2) cannot be degraded by the body, and (3) cannot be cleared by macrophages.2 Thus, continued tissue damage can occur until the spherule is physically removed. Also, pulmonary cavities have been shown to react poorly to chemotherapy.1,2 In cases of disseminated disease, chemotherapy should always be initiated.1 Chemotherapy is achieved with either amphotericin B or antifungal azoles (ketoconazole, fluconazole, itraconazole).1,2,10,11 Although known for potent side effects, amphotericin B is preferred due to the more rapid onset when compared with the azoles. Also, whereas the azoles as a group are categorized as pregnancy class C, amphotericin B is a class B agent. Standard precautions and monitoring with the medications should be performed. Amphotericin B is administered for a total of 2 months, or until the disease becomes inactive. Although the azoles are taken orally, and thus better tolerated, they are currently not approved for this use by the U.S. Food and Drug Administration. Efficacy seems to be similar between the two classes of drugs, but frequent relapses have shown that therapy with the azoles needs to be continued for 6 months.1,2,10 Future treatment may involve novel azole agents (e.g., posaconazole, voriconazole), caspofungin (an echinocandin that inhibits glucan synthetase), or sordarin derivatives (drugs that specifically inhibit fungal protein synthesis).10 COCCIDIOIDES IMMITIS ATTACK (COCCIDIOIDOMYCOSIS) 727

CASE PRESENTATION You have a follow-up visit with a patient who was initially seen 1 week ago in the emergency department by one of your peers. He is an elderly diabetic man, and his initial complaints were fever, night sweats, and vague upper respiratory complaints of a productive cough, sputum production, and shortness of breath. He states he was in his usual state of health until this past week, with his only unusual activity being 4 weeks ago when he was a guest at an archaeologic dig in New Mexico. When an initial workup yielded negative results, he was treated for a viral respiratory infection and discharged home. The patient returns today with the continuation of his initial complaints, but now he complains of a rash over his entire body, pain and swelling in his right knee, difficulty concentrating, and a persistent irritating headache. While reviewing the charts of the emergency department, you notice that there have been at least 10 other patients with similar symptoms in the past week, with seemingly the worst affected being a pregnant woman and a renal transplant patient.

PITFALLS Several potential pitfalls in response to an attack exist. These include the following: • Failure to have a disaster response plan • Failure to consider coccidioidomycosis as a possible cause in patients with mild symptoms • Failure to adequately diagnose persons suspected of having the disease process • Failure to adequately treat patients with both surgical options as well as antifungal agents • Failure to have adequately prepared and trained laboratory capabilities • Failure to notify laboratory workers of a high suspicion for coccidioidomycosis in submitted specimens, so that they may take appropriate precautions to limit their own exposure • Failure to notify and screen possibly infected persons who were involved with the index incident • Failure to notify local, state, and federal agencies in the instance of a suspected case REFERENCES

UNIQUE CONSIDERATIONS Coccidioidomycosis is a fungal infection that usually causes self-limited upper respiratory or febrile illnesses, but which, when disseminated, can cause life-threatening extrapulmonary disease. Its manifestations are similar to many common nonspecific illnesses and thus may elude diagnosis when the diagnosis is not sought. Although it is considered a possible biologic weapon due to the high virulence of the arthroconidia and severe mortality of the disseminated disease, C. immitis would likely make a poor bioweapon due to the fact that it is not a virulent infection in normal hosts. Terrorists would need to either find a way to cause immune suppression in a normal population in advance of seeding the infection or target a compromised host population. More important are its very long incubation period, that 60% of infected persons are asymptomatic, and that the majority of patients spontaneously recover. The use of coccidioidomycosis as a biologic weapon would be ineffective, and the identification of infected persons would be extremely difficult; a natural outbreak is far more likely but poses similar diagnostic pitfalls. The main points to remember are to keep this organism in the differential diagnosis and remember that appropriate therapy requires a multidisciplinary approach, using symptomatic therapy, antifungal chemotherapy, and surgery to produce the best outcome.

728 OTHER BIOLOGIC AGENTS

1. Stevens D. Current concepts: coccidioidomycosis [review article]. N Engl J Med. 1995;332:1077-82. 2. Riauba L. Coccidioidomycosis. Emedicine Web site. July 15, 2002. Available at: http://www.emedicine.com/derm/topic742.htm. 3. Centers for Disease Control and Prevention. Leads from the Morbidity and Mortality Weekly Report, Atlanta, Ga: Increase in Coccidioidomycosis:Arizona, 1998-2001. JAMA 2003;289:1500-2. 4. Galgiani J. Coccidioidomycosis: a regional disease of national importance. Rethinking approaches for control. Ann Intern Med. 1999;130:293-300. 5. Arsura E, Kilgore W. Miliary coccidioidomycosis in the immunocompetent [case series]. Chest 2000;117:404-9. 6. Standaert SM, Schaffner W, Galgiania JN, et al. Coccidioidomycosis among visitors to a Coccidioidomycosis immitis–endemic area: an outbreak in a military reserve unit. J Infect Dis. 1995;171:1672-5. 7. Galgiani JN. Coccidioidomycosis. In: Remington JS, Swartz MN, eds. Current Clinical Topics in Infectious Diseases. Vol. 17. Malden, Mass: Blackwell Sciences; 1997:188-204. 8. Walsh TJ, Chanock SJ. Diagnosis of invasive fungal infections: advances in non-cultural systems. In: Remington JS, Swartz MN, eds. Current Clinical Topics in Infectious Diseases. Vol. 18. Malden, Mass: Blackwell Sciences; 1998:127-8. 9. Centers for Disease Control and Prevention. Leads from the Morbidity and Mortality Weekly Report, Atlanta, Ga: Coccidioidomycosis – United States, 1991-1992. JAMA 1993;269: 1098-9. 10. Deresinki S. Coccidioidomycosis: efficacy of new agents and future prospects [review article]. Curr Opin Infect Dis. 2001;14:693-6. 11. Galgiani JN, Catanzaro A, Cloud GA, et al. Comparison of oral fluconazole and itraconazole for progressive, non-meningeal coccidioidomycosis: a randomized, double-blind trial. Ann Intern Med. 2000;133:676-86.

chapter 139

Histoplasma capsulatum Attack (Histoplasmosis) Carol L. Venable and Elizabeth L. Mitchell

DESCRIPTION OF EVENT Histoplasma capsulatum, the organism responsible for histoplasmosis, is a dimorphic fungus that is endemic to many parts of the world, most notably the United States and Latin America. H. capsulatum spores are present in soil, especially soil that has been contaminated by bird or bat excrement.1 In the Americas, histoplasmosis is found primarily in the regions of the Ohio, St. Lawrence, Mississippi, and Rio Grande river systems.2 Humans come into contact with aerosolized spores of H. capsulatum when they engage in occupational or recreational activities in endemic areas. Construction or demolition work, bridge cleaning or repairs, farming, gardening, and exploring caves are all high-risk activities for infection.2 In the endemic region, skin testing demonstrates that a majority of the population has had prior infection with H. capsulatum, and up to 25% of patients with acquired immunodeficiency syndrome (AIDS) in these areas will have active disease.3 Histoplasmosis has numerous clinical manifestations. The majority of infected persons are asymptomatic, which complicates the identification of outbreaks of this disease. When present, symptoms usually begin within 1 or 2 weeks of exposure.2 The most common clinical form of disease from H. capsulatum is acute pulmonary histoplasmosis, which typically presents with fever, fatigue, dry cough, and headaches.1 Acute pulmonary histoplasmosis tends to be self-limited and often resolves on its own over the course of 2 to 3 weeks.4 The disease may be so mild that affected patients may not seek medical attention. More severe or prolonged cases may prompt patients to visit clinics or emergency departments. Less commonly, patients will present with severe respiratory failure and, in these cases, acute pulmonary histoplasmosis can be fatal if not rapidly diagnosed and treated.5 Other, more chronic forms of histoplasmosis exist, such as chronic lung disease from H. capsulatum in patients with preexisting emphysema, but these disease manifestations do not have relevance to acute outbreaks or attacks. In patients with AIDS, hematologic malignancies, transplants, or some other source of immunocompromise,

there is a much greater risk of developing disseminated histoplasmosis, the manifestation of H. capsulatum that affects almost every organ system and is also potentially fatal.5 Infants and elderly persons may manifest this form as well, even in the setting of an apparently healthy immune system.1 Disseminated disease may progress rapidly and may present as dysfunction of the reticuloendothelial system, shock, and multiorgan system failure.5 In immunocompetent patients who are not at the extremes of age, disseminated histoplasmosis is less common and more indolent. It may present as a fever of unknown origin without many other associated symptoms.5 Despite having some virulent disease manifestations, there is no evidence that H. capsulatum has ever been weaponized. Although its spore form might lead one to believe that it could be easily manipulated, in fact, there are several features of the organism that make it difficult to use as an intentional biologic weapon. First, in areas where H. capsulatum is endemic, a significant percentage of the population has at least partial immunity to histoplasmosis, having been previously exposed at some level.2 This lowers the likelihood that a biologic attack would cause widespread, severe disease in these areas. Second, the toxic exposure limits for H. capsulatum are not known, making it difficult for an aggressor to know what level of concentration to produce for use as a weapon.2 Finally, histoplasmosis causes a broad spectrum of disease, the majority of which is nonfatal, selflimited, and treatable. Even in AIDS patients with disseminated disease, antifungal therapy has reduced the mortality to less than 25%.4 One can hypothesize, however, a variation on an intentional disaster scenario in which H. capsulatum would inadvertently become a biologic weapon. If an explosive device detonated in an area with soil containing H. capsulatum, there is a high likelihood that histoplasmosis could be a secondary cause of morbidity and mortality in victims or rescue workers who inhale the spores. Again, the prior consideration of partial immunity would hold for people living in the endemic area. However, if the soil contained a high enough spore concentration and was dispersed widely enough by the explosion,large numbers of people might still be at risk for significant infections. 729

A far more likely disaster scenario would be a completely unintentional exposure. In the past, unintentional exposures and the subsequent outbreaks they have caused have originated from a number of different sources. In Acapulco, Mexico, in the spring of 2001, the source of H. capsulatum that infected hundreds of American travelers is thought to have been the soil in the utility shaft adjacent to a central stairway in a major tourist hotel.6 In Nicaragua in October 2003,several tourists were infected during a visit to a bat-infested cave.7 Outbreaks have been reported in Tennessee, Kentucky, Indiana, Michigan, and several other states in which people cleaned, constructed, or demolished bridges or buildings that were surrounded with soil contaminated by bat or bird excrement.3,8-10 Many of these outbreaks theoretically could have been predicted, and prevented, if the workers or their employers had considered the risks of manipulating potentially contaminated soil and either decontaminated the area first or used protective gear. Diagnosis of histoplasmosis requires having a high clinical suspicion and obtaining a thorough travel and occupational history. The differential diagnosis is extensive and includes atypical pneumonia, influenza, tuberculosis, sarcoidosis, and other fungal diseases. Physical examination may be unrevealing, although in disseminated disease, patients may have hepatosplenomegaly or lymphadenopathy. Routine laboratory test results are likely to be normal in cases of acute pulmonary histoplasmosis. Disseminated disease may be associated with pancytopenia, as well as elevated liver function test results. Chest radiographs in cases of acute pulmonary histoplasmosis may be normal or may show reticulonodular infiltrates, often with hilar or mediastinal lymphadenopathy. The majority of cases of disseminated disease yield abnormal chest radiographs, also with interstitial or reticulonodular infiltrates.5 Cultures, fungal stains, serologies, and antigen detection permit the laboratory diagnosis of H. capsulatum. Cultures can detect between 80% and 90% of cases of disseminated disease but have a much lower sensitivity for acute pulmonary histoplasmosis.11 In addition, they may take several weeks of growth before they turn positive.5 This makes culture suboptimal in an outbreak setting. Serologic tests can be performed either by immunodiffusion or complement fixation technology, of which the complement fixation is the more sensitive although less specific test.2 The serologic tests have a sensitivity of greater than 90% for acute pulmonary histoplasmosis, although their sensitivity for disseminated disease is lower.12 The difficulty with these tests is that up to 6 weeks may be required before the serology yields positive results. In addition, positive serologic test results may be due to prior infections or infections caused by other fungi.5 Despite these limitations, complement fixation is a viable option for detecting acute pulmonary histoplasmosis in outbreaks, especially in patients with severe disease, because the test has a much better sensitivity in highly symptomatic patients.12 Urine antigen testing is the test of choice in the majority of patients during an outbreak. It has a turnaround time of 1 to 2 days and has a sensitivity of approximately 90% in patients with disseminated disease and approxi730 OTHER BIOLOGIC AGENTS

mately 75% in patients with acute pulmonary histoplasmosis.12 Serum antigen testing can also be performed but is less sensitive than urine antigen testing. Like the serologic tests, antigen testing has the potential drawback of cross-reaction with other fungal agents.11 The only other test as rapid as antigen testing is tissue fungal stain, which can be used if tissue is obtained from a patient— for example, from a transbronchial or bone marrow biopsy. The accuracy of fungal stain results is dependent, however, on a given laboratory’s skills in distinguishing among different types of fungal organisms.5

PREINCIDENT ACTIONS Histoplasmosis has a wide range of disease severity. Patients are likely to present to clinics, urgent care centers, and emergency departments with this disease. Rapid identification of an outbreak, therefore, requires a preexisting system of coordination among ambulatory care centers, emergency departments, and state or national public health authorities. Healthcare providers, especially those in endemic areas, need education about possible presentations of outbreaks and specific instructions as to the best way of reporting any suspected cases. If there were any threat of an explosion of a building in an area endemic for histoplasmosis, steps could be taken to eradicate H. capsulatum as a secondary threat. For example, obvious targets such as skyscrapers, bridges, and major government buildings could have soil testing performed in the area surrounding them. Any soil with significant concentrations of H. capsulatum could then be treated with a 3% solution of formalin, which inactivates the spores. 13,14 This would eliminate at least the threat of an inadvertent biologic disaster in the unfortunate case of an explosion. A similar approach is recommended, and has been used in the past, in the setting of building construction, demolition, and cleaning.2

POSTINCIDENT ACTIONS Histoplasmosis is not transmitted from one human to another.2 Therefore, isolation of potentially infected patients is not necessary. The two critical postincident actions that need to be taken are as follows: (1) rapid identification of H. capsulatum as the cause of the outbreak and (2) decontamination of any remaining H. capsulatum spores. Diagnosis can be performed by any of the methods listed above, but, in general, serologic and urine antigen testing will be the most useful modalities in an outbreak. Soil testing around the presumed site of an outbreak, along with subsequent formaldehyde decontamination of any H. capsulatum–containing soil, is critical for preventing continued exposures and infections. Investigators involved in outbreaks need to wear appropriate protective gear when evaluating possible sites of exposure. In particular, powered, air-purifying respirators with full face piece are optimal. These should be used along with disposable clothes and shoe coverings.2

MEDICAL TREATMENT OF CASUALTIES Not all cases of histoplasmosis require treatment, and in a disaster setting, antifungal agents must be restricted to those patients most in need. In the setting of acute pulmonary histoplasmosis without acute respiratory failure, treatment should only be given to patients who fail to improve after experiencing symptoms for 1 month. Oral itraconazole at a dosage of 200 mg daily for 6 to 12 weeks can be used in this group. For immunocompetent patients with severe manifestations of acute pulmonary histoplasmosis (e.g., requiring a ventilator), the treatment of choice becomes amphotericin B administered at a dosage of 0.7 mg/kg/day. Prednisone (60 mg) taken daily for 2 weeks may be used in conjunction with amphotericin B in immunocompetent patients, although the data studying this are limited. After discharge from the hospital, the patient’s treatment can be maintained on itraconazole (200 mg) taken once or twice daily to complete a 12-week antifungal course.4 Patients with disseminated histoplasmosis are subdivided for treatment purposes into persons with AIDS and those without AIDS. Patients with AIDS undergo a total of 12 weeks of therapy with amphotericin B (0.7 mg/kg/day) followed by itraconazole (200 mg twice daily) on discharge home. Patients who never require hospitalization can be treated with itraconazole (200 mg) three times daily for 3 days followed by twice daily for a total of 12 weeks. After the initial 12 weeks, a life-

CASE PRESENTATION A 30-year-old male construction worker in Tennessee presents to his primary care physician (PCP) in December with the chief complaint of having had a dry cough for the past 2 weeks. He is an otherwise healthy man with no history of any lung disease. During a review of systems, he notes that he has had some headaches, mild fatigue, and low-grade, subjective fevers. He denies any exposure to tuberculosis or any risk factors for human immunodeficiency virus. He states that none of his family is sick but that several of his coworkers have had “the flu.” He says that a couple of them are actually in the hospital,but he does not have any further details. The results of his lung examination are unremarkable, but because of the duration of the cough, the PCP obtains a chest radiograph, which is notable for diffuse reticulonodular infiltrates bilaterally. On reinterviewing the patient and focusing on occupational history, the PCP learns that he and his coworkers have been tearing down an old building previously infested with bats. They started the demolition process about 3 or 4 weeks prior. There are approximately 100 workers at the site. The PCP then contacts the state health department with her concerns about a possible outbreak of histoplasmosis.The health department instructs her to obtain serologic and urine antigen testing for H. capsulatum at that visit. She instructs the patient to return for antifungal therapy if he has worsening symptoms at any point or still has his current symptoms in 2 more weeks.

long maintenance regimen of itraconazole (200 mg) once or twice daily is recommended.4 Patients with disseminated histoplasmosis who do not have AIDS are treated with amphotericin B (0.7 to 1.0 mg/kg/day) if they require hospitalization. The amphotericin B can be switched to oral itraconazole once the patient defervesces. Itraconazole (200 mg) once or twice daily can be continued for 6 to 18 months for completion of therapy. Duration of treatment can be determined by serial measurement of H. capsulatum antigen concentrations.4

UNIQUE CONSIDERATIONS Low mortality and a vast range of disease manifestations make outbreaks of H. capsulatum difficult to detect. In addition, histoplasmosis resembles many other pulmonary and infectious diseases. Patients may not be identified as part of an outbreak unless a careful occupational, recreational, and travel history is obtained. A history of close contacts, especially those who went on the same trip or participated in the same job, may also be extremely helpful in diagnosis.

PITFALLS Several potential pitfalls in response to a histoplasmosis attack exist. These include the following: • Failure to consider histoplasmosis as a possible cause of secondary morbidity and mortality in natural disasters or explosions in areas in which H. capsulatum is endemic • Failure to obtain a complete occupational and travel history in patients presenting with nonspecific pulmonary complaints • Failure to consider histoplasmosis as a possible diagnosis during influenza season or during known outbreaks of other pulmonary illnesses • Failure to consider decontamination or protective gear for H. capsulatum as a protective option when attempting to evaluate the site of a possible outbreak • Failure to consider in advance the importance of decontamination of soil containing H. capsulatum surrounding buildings, bridges, and other structures that could be threatened by explosions or that are scheduled for cleaning, construction, or demolition

REFERENCES 1. Cano MVC, Hajjeh RA. The epidemiology of histoplasmosis: a review. Semin Respir Infect. 2001;16:109-18. 2. Centers for Disease Control and Prevention. Histoplasmosis: protecting workers at risk, revised guidelines for preventing histoplasmosis. National Institute for Occupational Safety and Health; 1997;97-146. Available at: http://www.cdc.gov/niosh/97-146.html. 3. Wheat LJ. Histoplasmosis in Indianapolis. Clin Infect Dis. 1992;14(suppl 1):S91-9. 4. Wheat J, Sarosi G, McKinsey D, et al. Practice guidelines for the management of patients with histoplasmosis. Clin Infect Dis. 2000;30:688-95. HISTOPLASMA CAPSULATUM ATTACK (HISTOPLASMOSIS) 731

5. Wheat LJ, Kauffman CA. Histoplasmosis. Infect Dis Clin North Am. 2003;17:1-19. 6. Morgan J, Cano MV, Feikin DR, et al. A large outbreak of histoplasmosis among American travelers associated with a hotel in Acapulco, Mexico, Spring 2001. Am J Trop Med Hyg. 2003;69:663-9. 7. Weinberg M,Weeks J, Lance-Parker S, et al. Severe histoplasmosis in travelers to Nicaragua. Emerg Infect Dis. 2003;9:1322-5. 8. Jones TF, Swinger GL, Craig AS, et al. Acute pulmonary histoplasmosis in bridge workers: a persistent problem. Am J Med. 1999;106:480-2. 9. Centers for Disease Control and Prevention. Histoplasmosis— Kentucky, 1995. MMWR 1995;44:701-3. 10. Stobierski MG, Hospedales CJ, Hall WN, et al. Outbreak of histoplasmosis among employees in a paper factory: Michigan, 1993. J Clin Microbiol. 1996;34:1220-3.

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11. Williams B, Fojtasek M, Connolly-Stringfield P, et al. Diagnosis of histoplasmosis by antigen detection during an outbreak in Indianapolis, Ind. Arch Pathol Lab Med. 1994;118:1205-8. 12. Wheat LJ. Laboratory diagnosis of histoplasmosis: update 2000. Semin Respir Infect. 2001;16:131-40. 13. Tosh FE, Weeks RJ, Pfeiffer FR, et al. The use of formalin to kill Histoplasma capsulatum at an epidemic site. Am J Epidemiol. 1967;85:259-65. 14. Bartlett PC,Weeks RJ,Ajello L. Decontamination of a Histoplasma capsulatum–infested bird roost in Illinois. Arch Environ Health. 1982;37:221-3.

chapter 140

Cryptosporidium parvum Attack (Cryptosporidiosis) Miriam John and Carol Sulis

DESCRIPTION OF EVENT Human cryptosporidiosis is a disease caused by the protozoan cryptosporidium, an obligate intracellular parasite. Cryptosporidium parvum is the most common species in humans, but other species have been identified in immunocompromised hosts. The human pathogen C. parvum (genotype 1) and the bovine pathogen C. parvum (genotype 2) are the most important agents in human disease.1 Reservoirs for C. parvum include humans; domesticated animals such as cows, goats, and sheep; and wild animals, such as deer and elk. Tyzzer and Clarke discovered cryptosporidia in the stomach of a mouse in 1907. The first human case was reported in 1976 in a child with diarrhea. Since 1982, and the beginning of the AIDS epidemic, cryptosporidia have been increasingly recognized as a cause of diarrheal illness in both immunocompromised and immunocompetent human hosts. Cryptosporidiosis is the leading cause of diarrhea due to protozoal infections worldwide.2 C.parvum is classified by the Centers for Disease Control and Prevention (CDC) as a category B bioterrorism threat agent and, more specifically, as a water safety threat. Cryptosporidia are highly infectious enteric pathogens that are resistant to chlorine, are small and difficult to filter, and are ubiquitous in many animals, making them a persistent threat to the U.S. water supply.3 C. parvum is also a hardy organism that can survive for 18 months at 4˚C in surface water and for 2 to 6 months in groundwater.4 Oocysts have been found in 87% of untreated water samples tested in the United States and Canada.5 Cryptosporidia are resistant to common water disinfection techniques such as chlorination, treatment with sodium hypochlorite, and filtration (if the filter pore size is greater than 1 micron).1 A recent study of 66 water treatment plants in 14 states and one Canadian province showed that 27% of filtered water samples contained Cryptosporidium oocysts.4 Cryptosporidium infection occurs after ingestion of fecally contaminated food or water. Transmission can also occur directly from animal to person or person to person. The infectious form of C. parvum is the thick-walled 4- to 6-micron oocyst.1 The dose at which 50% of those

exposed become infected ranges from 10 to 300 oocysts.5 Ingested oocysts undergo excystation in the upper small intestine after being exposed to reducing conditions, proteolytic enzymes, and bile salts. Sporozoites invade the intestinal brush border epithelial cells and mature into merozoites, leading to inflammation, villous blunting, malabsorption, and diarrhea. Merozoites undergo sexual reproduction to produce thin-walled oocysts, which continue autoinfection in the host, or thick-walled oocysts, which are excreted and can then infect other hosts.3,5 Cryptosporidium infection can be found at rates of 2.2% to 6.1% in immunocompetent persons with diarrhea in industrialized and developing countries, respectively. HIV-positive persons with diarrhea showed Cryptosporidium infection in 14% to 24% of cases in industrialized and developing areas, respectively.3,6 There have been numerous well-documented outbreaks of cryptosporidiosis in the United States. Most are waterborne outbreaks due to contamination of drinking water or recreational water, such as swimming pools or wading pools. There were approximately one dozen documented outbreaks of cryptosporidiosis in the United States between 1993 and 1998. The largest waterborne outbreak in U.S. history occurred in March and April 1993 in Milwaukee,Wisc., and affected an estimated 403,000 persons. This constituted a 52% cryptosporidiosis attack rate among those served by the South Milwaukee water works plant. Person-to-person spread has also been documented in institutions such as daycare centers and hospitals and may be especially difficult to control because infectious oocysts may be excreted for up to 5 weeks after diarrheal illness ends.3,6 The clinical manifestations of C. parvum infection are largely host dependent. In an immunocompetent host, cryptosporidiosis is primarily an intestinal disorder with a 1- to 2-week incubation period followed by symptoms of watery diarrhea,abdominal cramps,anorexia,nausea,vomiting, and possibly a low-grade fever. The disease is selflimited, with an average duration of 9 to 12 days. The main risk is dehydration. In the immunocompromised host, cryptosporidiosis can be an acute dehydrating diarrheal syndrome or a chronic diarrheal and wasting 733

syndrome. Patients with CD4 counts greater than 180 cells/mm3 tend to have the self-limited syndrome. Cryptosporidium infection of biliary and pancreatic ducts leading to cholangitis or acalculous cholecystitis has been documented in patients with CD4 counts less than 50 cells/mm3.1,5 There are also infrequent reports of pulmonary and tracheal cryptosporidiosis in immunocompromised hosts, which manifests as cough with low-grade fever, usually accompanying severe intestinal illness.2 Diagnosis of C. parvum is made using modified acid-fast staining on unconcentrated fecal smears. However, cryptosporidiosis is likely underdiagnosed in industrialized countries because relatively few laboratories routinely process stool ova and parasite specimens for cryptosporidium or other acid-fast enteric pathogens. Direct fluorescence antibody (DFA), enzyme-linked immunosorbent assay, and polymerase chain reaction testing are more sensitive and less user dependent than routine acid-fast testing,but these are newer and less commonly available.1,5

PREINCIDENT ACTIONS Since cryptosporidia are ubiquitous and persistent in the environment and highly transmissible,these organisms are well suited to be used in a covert biologic attack. Mortality in a bioattack would be low, except among immunocompromised patients, but morbidity could be extremely high, especially since there can be person-toperson transmission of cryptosporidiosis. Physicians, particularly those working in emergency departments, must remain vigilant to distinguish cryptosporidiosis from routine viral gastroenteritis. Large numbers of persons can be affected in an outbreak and may seek medical attention because of the frequency of stools (average of 12 to 15 per day), prolonged course of diarrheal illness (average of 9 to 12 days), or severity of illness if the person is immunocompromised.5 Patients with suspected cryptosporidiosis should undergo laboratory analysis of stool samples including modified acid-fast staining or DFA to confirm the diagnosis. Examples of pre-event public health surveillance might include monitoring the volume of antidiarrheal medication sold, monitoring HMO and hospital logs of patient chief complaints, or monitoring the incidence of diarrhea in nursing homes or daycare centers.7 To protect against widespread outbreaks, the public water supply should be monitored closely. Water filtration and flocculation techniques that can eradicate oocysts are not routinely performed at many plants. Waterborne outbreaks have occurred even when the water supply met required turbidity levels. Methods such as reverse osmosis, membrane filtration, ozone treatment, or irradiation can eradicate infectious oocysts from the water supply but are not cost-effective. Ozone treatment is likely the most effective chemical means of inactivating Cryptosporidium oocysts.3

POSTINCIDENT ACTIONS Public health authorities should be notified when cryptosporidia are confirmed by laboratory analysis of a stool 734 OTHER BIOLOGIC AGENTS

sample. If an outbreak is suspected, an epidemiologic investigation involving appropriate public health authorities should be initiated promptly to identify the source of the outbreak and to rapidly institute corrective measures. In addition to standard precautions in hospitals, contact precautions should be instituted for diapered children and incontinent adults. Rigorous handwashing by hospital staff is necessary to prevent nosocomial spread. Public health authorities would likely issue a boil-water advisory if the public water supply were contaminated. Information and education about Cryptosporidium species should be provided to the general public and should include instructions specific to immunocompromised groups. Boiling water is the most certain method of eradicating Cryptosporidium oocysts. Use of microstraining water filters capable of removing particles less than or equal to 1 micron, or using sterile water, can also reduce the risk of cryptosporidiosis.7-9

MEDICAL TREATMENT OF CASUALTIES There is no definitive therapeutic agent that eradicates cryptosporidiosis. The disease is self-limited in immunocompetent hosts requiring only supportive care and monitoring hydration and volume status. The disease is often sufficiently severe in immunocompromised hosts to warrant specific therapy, even though currently available therapeutic options have limited efficacy. The most commonly used medications are paromomycin and azithromycin. Paromomycin, a poorly absorbed aminogly-

CASE PRESENTATION In late July, an urban emergency department in a major metropolitan city begins to see a large number of otherwise healthy small children with prolonged courses of diarrhea, abdominal cramps, and vomiting. An astute physician notes that all the children she has treated belong to the same daycare center. She notifies local public health authorities about these cases. Their investigation yields similar findings in numerous emergency departments in the city. The investigation also shows that numerous immunocompetent and immunocompromised adults are also experiencing this illness. Public health authorities request that stool samples be analyzed for cryptosporidia, in addition to routine ova and parasites. This testing yields many stool samples with a positive modified acid-fast stain for cryptosporidia. The CDC and Environmental Protection Agency also become involved in the epidemiologic investigation. Water sample analysis from water treatment plants yields a heavy Cryptosporidium oocyst concentration at a municipal water plant that serves the daycare center and many other regions of the city. As control measures to quell the cryptosporidiosis outbreak, public health authorities change residents in the affected area to an alternative water supply, issue a boil-water advisory, and continue water sample analysis. The hunt for the source of the water contamination continues.

coside, has been shown to decrease stool frequency and oocyst excretion at doses of 2 g/day. It is approved in liquid formulation for pediatric use. Nitazoxanide, a nitrothiazole benzamide compound,has been shown to reduce both diarrhea and oocyst shedding in controlled trials conducted in Mexico; however, it is not currently approved by the Food and Drug Administration for use in the United States. Immune reconstitution in HIV disease, using highly active antiretroviral therapy (HAART), results in decreased stool frequency, weight gain, and fecal oocyst clearance. However, there is rapid relapse after discontinuation of HAART, suggesting that cryptosporidial infection had been suppressed rather than cured.1

UNIQUE CONSIDERATIONS C. parvum is a small, highly infectious and transmissible protozoan. These features make it a possible bioweapon and water safety threat. Although there is low mortality, there is substantial morbidity associated with cryptosporidiosis. A Cryptosporidium attack will be extremely difficult to identify and distinguish from routine viral gastroenteritis due to the similarity of illness presentation and lack of routine laboratory stool testing for C. parvum. Therefore, healthcare providers must be vigilant while treating diarrheal illness, especially in immunocompromised patients. Without appropriate supportive care and institution of paromomycin treatment, cryptosporidiosis can lead to high mortality levels in immunocompromised populations.

• Failure to request specific laboratory analysis of stool samples for C. parvum • Failure to aggressively treat immunocompromised patients with diarrheal illness • Failure to notify public health authorities about suspected or confirmed cases of cryptosporidiosis • Failure to notify public health authorities about a suspected or confirmed cluster of patients with diarrheal illness REFERENCES 1. Kosek M, Alcantara C, Lima A, et al. Cryptosporidiosis: an update. Lancet Infect Dis. 2001;1:262-9. 2. Butt A,Aldridge K, Sanders C. Infections related to the ingestion of seafood. Part II: parasitic infections and food safety. Lancet Infect Dis. 2004;4:294-300. 3. Guerrant RL. Cryptosporidiosis: an emerging, highly infectious threat. Emerg Infect Dis. 1997; 3:51-7. 4. Balbus J, Lang M. Is the water safe for my baby? Pediatr Clin North Am. 2001;48:1129-52. 5. Katz D, Taylor D. Parasitic infections of the gastrointestinal tract. Gastroenterol Clin North Am. 2001;30:797-815. 6. Chen X, Keithly JS, Paya CV, et al. Cryptosporidiosis. N Engl J Med. 2002;346:1723-31. 7. Addiss D,Arrowood M, Bartlett M, et al. Assessing the public health threat associated with waterborne cryptosporidiosis: report of a workshop. MMWR 1995;44:1-19. 8. Bongard J, Savage R, Dern R, et al. Cryptosporidium infections associated with swimming pools—Dane County, Wisconsin. MMWR 1994;43:561-3. 9. Weber DJ, Rutala WA. Cryptosporidiosis. N Engl J Med. 2002; 347:1287.

PITFALLS Several potential pitfalls in response to a cryptosporidiosis attack exist. These include the following: • Failure to consider cryptosporidiosis as the cause of diarrheal illness

CRYPTOSPORIDIUM PARVUM ATTACK (CRYPTOSPORIDIOSIS) 735

S E C T I O N

E L E V E N

Events Resulting in Blast Injuries

chapter 141

Introduction of Explosions and Blasts Michael I. Greenberg and Dziwe W. Ntaba

DESCRIPTION OF EVENT Physics of Blast Injury Although the exact physical parameters of bomb explosions are typically not known at the time of a given event, a basic understanding of the effects of blast wave physics can allow an estimation of the respective spectrum of blasts.1 An explosive blast is essentially an intense exothermic reaction generated by triggering a rapid chemical conversion of a solid or a liquid into a gas.1–3 The resulting compressed energy release leads to detonation and a massive increase in local pressure.4 Conventional explosive devices are typically categorized into two broad categories: “ordinary explosives” and “high explosives.” Ordinary explosives include materials such as propellants (e.g., gunpowder) and are designed to release energy relatively slowly.2 High explosives (e.g., trinitrotoluene [TNT]) are designed to detonate very rapidly, typically within only a few microseconds.5 As a consequence of the phase transformation mentioned above, a “pressure pulse” rapidly expands into the surrounding medium at speeds exceeding the speed of sound.6 This expanding pressure pulse moves, as a blast wave, in all directions. The leading edge of this blast wave is known as the “blast front.”1,5 As the blast front spreads, it slows down and loses strength.7 The potential for a given explosive to cause injury is related to the concept of overpressure. Blast overpressure represents the increased pressure, in excess of atmospheric pressure, associated with a blast. It is a dynamic phenomenon wherein a highly pressurized cascade superheats air molecules with which it interacts, propelling the blast wave at supersonic speeds.6 When the blast front encounters an object, it causes a virtually instantaneous rise in the atmospheric pressure from an ambient static pressure to a peak overpressure.1,4,7 The duration of overpressure is typically less that 100 milliseconds (ms) for conventional explosive devices, but may exceed 100 ms for other events such as nuclear detonations.1 With continued expansion of gases from their point of origin, the ambient pressure at a fixed point subsequently and exponentially drops below predetonation levels, temporarily creating a relative vacuum known as 736

underpressure. Eventually, the blast wave deteriorates and forms acoustic waves.6 Substantial overpressure may impart a force of impact known as a “shock wave,” which possesses a characteristic termed brisance, or shattering effect.1,5 The magnitude of the shock wave at the blast front, known as positive phase impulse, is an important factor determining the severity of blast-related injury.5,7 Other factors include the duration of overpressure and the medium in which it is propagated.1 Underpressure associated with a particular explosion generates a “blast wind,” which may attain speeds in excess of 800 miles/hour.4,5 Whereas overpressure is the major force generating primary blast injury (PBI), underpressure forces are the principle mechanisms involved in producing secondary and tertiary blast injury. Specific characteristics of the environment in which an explosion occurs are important modulators of blast effect.1,6 Explosions occurring in an open space are associated with peak pressures and overpressure durations related to both the size and nature of the explosive charge, as well as to the distance from detonation.1,7 Explosions in confined spaces involve reflecting surfaces that cause an extended duration of overpressure and lead to very complex wave patterns.1 If a pressure wave is reflected from a solid object, the pressures generated from the reflecting surfaces may be more than 20 times that of the incident wave.5,7 Consequently, a blast wave capable of causing only minor blast injury in an open space may be lethal for victims in closed spaces.1,7 This explains the popularity of the terrorist use of explosive devices inside confined spaces such as buses. Water, due to its incompressible properties, generates a greater speed of wave propagation, and the incident wave in underwater explosions conserves energy over distance and time. The lethal radius around an explosion in water is approximately three times what it would be in air.5,7

Physiology of Blast Injury The clinical spectrum of blast injury is usually described as involving primary, secondary, tertiary, and quaternary or miscellaneous blast injury. Combinations of these may also occur. PBI is a direct result of blast overpressure forces.1,5,6,8 Overpressure forces tend to damage air-containing

organs or those made up of tissues with internal varying densities such as the ear, lungs, intestine, and brain.6 Experimental studies conducted in the early 1940s showed that PBI of internal organs involves direct conduction of forces derived from a blast wave coming in contact with external bodily surfaces.5 The mechanism of blast injury, or blast load, can be further subdivided to include concepts of irreversible work, inertial effects, spalling, and implosion.2,4,5 Irreversible work results when blast loading results in extreme pressure differentials. The resultant external force creates two forms of stress on the body known as a stress wave and a shear wave, both of which are propagated into underlying tissues.3–6,9 The potential for injury induced by the stress wave is directly related to the peak amplitude. Damage caused by the shear wave is related to velocity.10 Inertial effects may occur when two adjacent objects of different densities are acted on by the same force.7 The lighter object accelerates faster than the denser object, creating a shearing stress at the boundary between the two.4,5,11 Spalling is the tendency of a boundary between two media of different densities to disrupt when a compression wave in the denser medium is reflected at the interface.7,11 When the components of a blast wave interact with a fluid-filled organ, the velocity and potential for injury are intensified.4,5 Implosion is defined as the forceful compression of a gas bubble by a shock wave in a liquid medium resulting in the pressure within the bubble rising higher than the initial compressive pressure.7 This leads to a disruptive reexpansion of tissue.4,5,11 The cumulative damage of blast overpressure forces can be illustrated by examining pulmonary PBI. Blast waves tend to strike the torso in a manner similar to any form of blunt trauma.1 Inward displacement of the chest wall causes compression of air within the lung parenchyma at a rate that is slower than the compression of the hollow respiratory tracts (inertial effects).3,4 This leads to a contained system within the air sacs that can generate internal pressures that match or exceed the initial blast overpressures.5 Compression and reexpansion (implosion) of the alveoli causes a form of lung injury similar to adult respiratory distress syndrome (ARDS), which is then complicated by disruption of the alveolarcapillary membrane (spalling) and potential introduction of air emboli into the vascular space.3,4,12 Secondary blast injury results from so-called missile effects generated by an explosion and has the broadest potential range of injury with regard to distance from the detonation site. Objects accelerated by the energy of an explosion may cause blunt and/or penetrating injuries.5 Blast-related debris may include fragments originating from the casing of the charge (shrapnel) or secondary fragments such as pieces of glass, wood, stones, and other materials.1 Skin and clothing may offer protection from debris at long ranges. Tiny particles of dust may be embedded in the skin, producing a discoloration known as “dust-tattooing.”1 Tertiary blast injury results from deceleration forces after a victim’s body has been set in motion by the pressure and high winds of an explosion.1 Once a victim’s body is in motion, it is at risk of injuries sustained from

striking and/or being impaled with stationary objects.5 The following survivor’s recollection of an explosion in Northern Ireland presents a sobering account of body displacement: “… as I started to pull the door open, there was a terrific noise. It was a tremendous whoosh. It was a similar noise made by a pool of petrol being ignited, only much magnified. Accompanied by this, I was aware of a great deal of debris and glass flying about. I was thrown up sideways towards the southern wall of the bar. This was as if by a terrific amount of pressure, not unlike the forces rendered by a very large sea wave. I was thrown sideways for a distance of about 6 feet…”1

Quaternary, or miscellaneous, blast injury is a broad category of injury including thermal and chemical burns, inhalational exposure, and crush-related trauma. Flash burns may result from heat generated by the initial explosion.4 Conventional thermal burn injury may result from the release of hot gases, secondary fires in the surrounding environment, and contact with hot dust-laden air.1 Chemical exposures result from the release of chemicals in the surrounding environment along with the inhalation of dust, chemically complex smokes, and carbon monoxide.1,13 Crush injury may result in the event of structural collapse of a building after an explosion.

HISTORICAL CONTEXT Increasing Prevalence and Lethality of Explosive Devices An accident in the early twentieth century demonstrated to the world the potential for death and destruction from an explosive blast. In 1917 two ships, the Imo and the Mont Blanc,collided in Halifax Harbor,Nova Scotia. Their cumulative cargoes included 35 tons of benzene, 2300 tons of picric acid, 10 tons of gun cotton, 200 tons of TNT, and 300 rounds of ammunition.14 The collision resulted in the largest manmade, non-nuclear explosion in history. Casualties reportedly included over 2000 deaths and 9000 injuries. One of the ships was reportedly blown a mile into the air. Approximately 2.5 km of the city was leveled, and the blast shattered windows 100 km away.14 Current events suggest that we are in the midst of a growing epidemic of terrorist bombings worldwide. The first documented terrorist bombing was probably in 1587, in Antwerp, Belgium, where 7 tons of gunpowder was used to destroy a bridge on the River Schelt.14 There was a 10-fold increase in terrorist bombings around the world between 1968 and 1980, with 5075 events documented between 1973 and 1983.14 From 1980 to 1990, 12,216 bombings and suspicious explosions occurred in the United States alone.14

Prognostic Factors and Critical Mortality Rates An instructive terrorist explosive attack occurred in 1983 in Beirut, Lebanon, where the U.S. Marine Corps barracks was bombed using an ammonium nitrate–based explosive device with an equivalent of roughly 6 tons of INTRODUCTION OF EXPLOSIONS AND BLASTS 737

TNT. The blast resulted in the near complete collapse of a four-story building with 234 immediate deaths (68% of all victims).14 Several first responders were killed by sniper fire from waiting terrorists carrying out a “second hit” tactic. Most of the survivors had noncritical injuries; however, 19 survivors (17%) did suffer critical injuries, and seven of these initial survivors ultimately died. Six of the seven late deaths were among victims who were rescued and treated more than 6 hours after the blast.14 Conversely, among all initial survivors rescued within 4 hours (n = 65), only one died. The reported causes of mortality in this event included the following: (1) head trauma as the cause of immediate death (71%) and late death (57%); (2) chest trauma as the cause of overall death (29%) (rare among survivors); and (3) burns as the cause of overall death (29%).14 Analysis of this event provides important lessons regarding the medical response to explosive device detonation. Most striking is the effect of early and aggressive resuscitation as a key prognostic factor for long-term survival. However, expeditious evacuation and treatment must be balanced with the danger to personnel when terrorists make use of secondary devices meant to kill responder personnel.14 Other lessons include the clear impact of both explosive magnitude and building collapse on survival and the importance of anatomic site and nature of injury as prognostic factors. In an excellent review discussing the medical response to terrorist bombings, Frykberg14 proposed the use of a “critical mortality rate” (the death rate only among those critically injured) as an appropriate measure when calculating vital statistics for a terrorist event. Since overall mortality rates may be falsely diluted by the number of noncritical survivors, the critical mortality rate more accurately describes those victims actually at risk for death.

Triage Efficacy A major terrorist event in Buenos Aires, Argentina, occurred when the Argentine Israeli Mutual Association (AMIA) was bombed in 1994. This explosion involved the detonation of ammonium-nitrate material (430 lb TNT-equivalent), leading to the complete collapse of a seven-story building. There were 286 casualties reported, with 82 (29%) immediate deaths.14,15 In the immediate aftermath of the explosion, the closest hospital emergency department (ED) faced rapid overcrowding by ambulatory survivors and medical personnel offering to help. Of the 204 survivors, 40 were eventually hospitalized, 7% (n = 14) in critical condition, among whom 4 later died. These figures represent a 3.4% overall mortality rate and a 29% critical mortality rate.15 Among survivors, 58% (n = 50) of those who visited the ED suffered minor injuries, 12 of whom were admitted. Moderate injuries were reported among 19% (n = 16) of survivors presenting to the ED, with 13 ultimately admitted. Major injuries were reported among 21% (n = 18) of presenting patients, 12 of whom were sent directly to the operating room or intensive care unit; seven later died.15 A total of five survivors were extricated from rubble, two of whom later died. Only five patients underwent laparotomy, and hepatic lacera738 EVENTS RESULTING IN BLAST INJURIES

tions were found in two of these. Three patients were found to have pneumothorax, and two others showed bilateral infiltrates consistent with PBI of lung.15 The AMIA bombing demonstrated that hospitals in close proximity to a major explosion suffer rapid and early overcrowding of their EDs with patients who have sustained minor and moderate injuries. This illustrates the need for disaster management plans that emphasize appropriate and effective triage to be carried out both in the field and at the ED entrance. A retrospective analysis of triage efficiency in the AMIA bombing showed only one case of “under-triage” and four cases of “over-triage.”15 Frykberg14 has demonstrated a linear correlation between critical mortality and the rate of over-triage in a series of terrorist bombings. He concluded, “[I]n mass casualty settings, over-triage can be as deadly as under-triage.” Kluger10 has suggested that a designated triage physician “guide medical teams as to the appropriate evaluation algorithms, considering the type of explosion (closed space vs. open space), explosive, and [presence of] metal projectiles… [and] on the proper use of auxiliary diagnostic modalities and the proper sequence of transferring patients to the operating rooms.”

Building Collapse Another example of a terrorist explosion resulting in a building collapse was the bombing of the Alfred P. Murrah Federal Building in Oklahoma City, Oklahoma, in 1995. In this incident, an ammonium nitrate–based bomb exploded with the equivalent of two tons of TNT, causing 759 total casualties with a 21% immediate mortality rate (n = 162).16 Fourteen percent of survivors (n = 83) were hospitalized, of which 52 were critically injured. Five of these later died (representing a 9.6% critical mortality rate).16 As with the AMIA bombing, the highest mortality and most severe morbidity in Oklahoma City occurred among victims who were located in collapsed portions of buildings at the time of blast.16 There were 506 survivors of the Oklahoma City bombing. The injury pattern among survivors included 85% who suffered soft tissue injuries, including lacerations, abrasions, contusions, and puncture wounds.16 Among survivors, 210 (35%) were reported to have musculoskeletal injury, with 60 patients suffering from fractures and/or dislocations and the remainder suffering from various sprains and/or strains. Smaller numbers of patients had severe soft tissue or musculoskeletal injuries.16 Head injuries were reported in 80 survivors, with 44% of these hospitalized (n = 35).16 Severe head injury was reported in eight patients, with four open skull fractures, two subdural hemorrhages, and two depressed skull fractures. Of 59 reported ocular injuries, there were nine ruptured globes, four of which were accompanied by detached retina.16 Internal organ injuries included four patients with intra-abdominal injury (lacerated spleen, kidney, liver, and partial bowel transection), four patients with ARDS, six patients with pneumothorax (four closed, one open, one hemopneumothorax), and three patients with pulmonary contusions.16

Severe burns (up to 70% body surface area) were reported in nine survivors, seven of whom were hospitalized. Four of these patients were near the point of detonation at the time of the blast.16 Auditory damage was found in 35% of survivors by self-report (n = 210), but only 78 of these patients had a documented medical diagnosis of auditory damage. Tympanic membrane perforation (unilateral or bilateral) was reported in 22 patients. Tinnitus, vestibular injury, or otalgia was reported in 12 patients.16 The majority of survivors of the Oklahoma City bombing incurred injuries caused by flying glass, other debris, and collapsed ceilings. A review of this event by Mallonee and colleagues16 suggests that the role of building collapse and flying glass should be a consideration in future building designs and in retrofitting of existing buildings. In addition, the National Research Council has published recommendations on blast hardening technologies.17

Open Air versus Confined Space Another important variable affecting the pattern of injury involves the occurrence of blast within a confined space. Leibovici and colleagues18 compared open air (OA) versus confined space (CS) terrorist bombings in Israel. This was a review of 297 victims from four separate events—two OA bombings and two bus bombings. The explosive devices used and victim density in proximity to each bomb were similar in all four incidents. The authors compared PBI, significant penetrating trauma, and injury severity score between the OA group and the CS group. A higher incidence of mortality and a greater severity of morbidity was reported from CS explosions, compared with a higher total volume of injuries in the OA settings.18 In addition, a higher incidence of PBI was seen in the CS group. These findings may be due to unique blast wave behavior within the relatively small confined spaces of buses.18 The two OA explosions in this review occurred at a bus station and a marketplace. Of the 15 fatalities in the OA group, only one died after admission to hospital. The two CS explosions reviewed both happened on buses, and there were fewer total casualties but a significantly higher mortality rate (Table 141-1). Of the 46 fatalities in the CS group, five died after admission to the hospital, all from injuries that were secondary to pulmonary PBI.18 There was a similar incidence of mild injury in both the OA and CS groups, with an injury pattern that included psychological stress, auditory damage with intact tympanic membrane (TM), and minor penetrating/musculoskeletal trauma. However, among the

TABLE 141-1 SETTING OA (n = 209) CS (n = 93)

severely injured patients in both groups, the OA population had a lower overall injury severity and more favorable initial clinical presentation than those in the CS comparison group.18 Published reports of predominantly outdoor bombings tend to show consistent patterns of mostly noncritical injuries with relatively low immediate and late death rates. A review by Adler and others2 discussed terrorist bombings occurring between 1975 and 1979, in Jerusalem, Israel. Various locales included 19 OA (e.g., seashore, street, marketplace) and five CS settings (bus, other public transport). Of the total 511 casualties, 340 were evacuated to an ED with 272 hospital admissions, three of which later died of their injuries. Injury severity was recorded using an Abbreviated Injury Scale (AIS), with results showing 87% “light,” 3% “medium,” and 10% “severe” injuries at presentation in the ED.2 These reviews clearly describe an increased mortality for victims of CS bombings. Survivors of CS bombings suffer from more severe injuries, as well as burns with a larger surface area compared with survivors from OA bombings. CS victims have a higher incidence of PBI than OA victims, particularly pulmonary PBI. Leibovici and colleagues18 postulated that the mechanism of increased mortality and severity of injury among CS explosions was linked due to the relatively sustained and markedly increased amplitude of overpressure (generated by comparatively similar explosive charges) as a result of reflective phenomenon within the confined spaces. The more extensive and severe burns in the CS group were thought to be due to containment of an initial fireball generated on detonation within the closed space. Conversely, the OA group showed a larger number of total casualties because these explosions were not contained within a closed space, therefore bomb fragments and other shrapnel were ejected to a considerable distance, with a capacity to injure more people.18 Other important lessons included the observation that the AIS score established in the ED was a valid prognostic factor when used to triage patients. Specifically, ED use of AIS scores correlated very well with subsequent and more detailed injury severity score on follow-up.2

MEDICAL TREATMENT OF CASUALTIES The most common injury patterns seen among explosion survivors are due to secondary and tertiary blast injury.19 The incidence of PBI varies according to explosive charge, proximity of the victim to the blast, and the

CHARACTERISTICS OF OPEN AIR (OA) VERSUS CONFINED SPACE (CS) BOMBINGS MORTALITY RATE

PULMONARY PBI

AUDITORY PBI

GI PBI

VICTIMS ADMITTED TO HOSPITAL

BURNS: BSA AFFECTED

7.8% 49.5%

6.8% 57.6%

12.1% 40.4%

0% 3.8%

13.1% 59.6%

18.3% 31.4%

PBI, primary blast injury; GI, gastrointestinal; BSA, body surface area.

INTRODUCTION OF EXPLOSIONS AND BLASTS 739

environment in which it occurs.3,13 However, given the general lack of familiarity with the assessment and management of PBI among U.S. civilian medical personnel, the following discussion will emphasize PBI at the expense of the more commonly encountered mixture of secondary and tertiary blast injury. Anatomically, the structures at greatest risk for PBI are the auditory system, thorax, and abdomen.11,13,19,20 The greatest potential for avoiding preventable deaths due to PBI lies in the appropriate treatment of thoracic PBI. Although injuries to the central nervous system (CNS) and extremities may involve some contribution from PBI, most of the injury burden to these areas results from the secondary and tertiary forms of blast injury. Survivors of explosions that occur in confined spaces or underwater may manifest a higher incidence of PBI.3,18 Most severely injured survivors of blasts have multiple injuries.10

Primary Stabilization As with any trauma patient, initial management begins with conventional priorities outlined in the advanced trauma life support protocols, which have been well described elsewhere. There are, however, several important caveats unique to the stabilization of a patient with suspected PBI. These include the potentially harmful consequences of prehospital intubation and the need for cautious fluid resuscitation. The potential for prehospital pain relief to mask latent abdominal PBI may be a valid concern.21 Wherever possible, blast victims should be kept at rest because some reports describe an increase in mortality in victims undergoing strenuous activity after an explosion.7,13

Auditory Injury The ear is the organ most frequently injured by an explosion.9 However, auditory PBI is frequently overlooked in the context of more serious co-existing injuries during mass-casualty scenarios.6 The auditory system is uniquely predisposed to PBI because the TM acts as an efficient means for transmitting pressure waves to the middle and inner ear.3,7 Auditory PBI rarely requires emergent intervention, and the important considerations involve recognition and appropriate referral to reduce long-term morbidity.9 All survivors of blast should have an otologic assessment and audiometry at some time in their aftercare.3,6 Symptoms of auditory PBI include tinnitus, otalgia, and a feeling of aural fullness.9 Perforation of the TM is a hallmark of auditory PBI and is typically seen as multiple “punched out” lesions or radial lacerations.6 The pars tensa is usually involved.3,5,7 Other signs include hearing loss, blood and/or debris in the ear canal, and disruption of the ossicles.13 The presence of tinnitus and hearing loss may be initially profound; however, these findings are usually self-limited and both improve quickly.3 Prolonged duration of these symptoms may be seen in survivors of blast occurring in confined spaces.9 Vertigo is uncommonly due to auditory PBI, and its presence should prompt evaluation for neurologic 740 EVENTS RESULTING IN BLAST INJURIES

injury.6,13 The complication of perilymph fistula should be considered in a patient with vertigo and sensorineural hearing loss, particularly if these findings are fluctuating. This is the only component of auditory PBI requiring prompt surgical treatment (i.e., emergent tympanotomy and fistula repair).3 Cholesteatoma may be a late complication (12 to 48 months) of TM perforation.3,6,22 Eighty percent of TM perforations heal spontaneously, and nonoperative management is appropriate for most cases.3,6,9,13 Large perforations may warrant surgical repair, but elective tympanoplasty can safely be delayed for up to 12 months with good outcomes.3 Antibiotics are not indicated unless underlying infection is suspected.6 It is important to note that TM perforation correlates poorly with PBI involving other organ systems and should not be used as a marker of latent PBI elsewhere in the body.3 In a study of 647 survivors of explosion, 9.3% had blast lung in the absence of TM rupture.8 Furthermore, of those survivors with isolated TM rupture at initial presentation, none went on to develop PBI of the lungs or intestine.8 Current evidence suggests that patients presenting with TM perforations in the absence of clinical features of other blast injuries, and with a chest radiograph having a normal appearance, may be safely discharged after 6 hours of observation.8

Thoracic Injury PBI has been shown to be a major cause of death in patients who survive initial resuscitation from blast injury.4,12 PBI involving the respiratory system can lead to a constellation of findings known as “blast lung.”1,7,13 Blast lung injury (BLI) involves pulmonary hemorrhage, edema, and associated disruption of alveolar architecture leading to air embolism.3,11,12 Gross lesions can range from scattered or multifocal petechiae to large confluent hemorrhages involving an entire lung.3,6 Certain regions of the lung tend to be more severely affected, including lung parenchyma proximal to the mediastinum and in the costophrenic angles.4 Bruising of the intercostal spaces has also been observed and paradoxically called rib markings.3,6 Pleural and subpleural hemorrhages tend to be bilateral but are usually more extensive on the side facing the source of blast.5,6 Recent studies show that the prognosis from BLI is significantly improved with aggressive treatment.12,23 Victims of explosions within confined spaces are at considerably greater risk of BLI.12 The etiology of BLI may be associated with disruption of alveolar membranes and interalveolar septa via implosion and spalling caused by the blast wave leading to shearing of the lung parenchyma from vascular structures with subsequent hemorrhage into the distal branches of the respiratory tree.1,3-6,12,13 These changes cause a ventilation-perfusion mismatch and reduced compliance resulting in hypoxia and increased work of breathing.3,5,13 Traumatic alveolar-capillary fistulae may form, and air may be introduced into blood vessels leading to air embolism.3,12 Carotid artery doppler ultrasound studies have demonstrated showers of intravascular bubbles in

blast-injured animals for up to 30 minutes after exposure, suggesting that PBI can affect the CNS.7,20 Ultrastructural damage of type II epithelial cells may disrupt surfactant production and further exacerbate pulmonary injury.3,6 Progressive pulmonary insufficiency has been described in many patients with BLI and is thought to be due to the cumulative effect of several mechanisms including blast effects, inhalation injury, hypovolemic shock, sepsis, aspiration and/or aggressive fluid resuscitation.6 Clinically, the pulmonary function of patients with BLI resembles pulmonary contusion and ARDS with symptoms including dyspnea, difficulty completing sentences in one breath, cough, hemoptysis, and chest pain.3,5,7 Clinical findings associated with BLI include tachypnea with rapid, shallow breathing; poor chest wall movement (due to decreased compliance); dullness to percussion; decreased air movement; hemopneumothorax; subcutaneous emphysema; and retinal artery emboli.3,5,6,11,24 The diagnosis is suspected on clinical grounds and is subsequently confirmed with radiographs. Signs and symptoms usually develop within hours after an explosion but may be delayed as long as 24 to 48 hours.3,12 Chest radiography is required for all patients exposed to blast forces to gauge the initial severity of injury and to monitor progression. Diffuse pulmonary opacities may develop within a few hours and will become maximal within 24 to 48 hours. They typically occur in a “butterfly distribution” of bilateral patchy infiltrates.25 Any changes that develop after 48 hours will most likely be due to complications such as ARDS or pneumonia.13 Other radiologic findings may include hemopneumothorax, pneumomediastinum, subdiaphragmatic free air, subcutaneous emphysema, and foreign body impaction.13,25 Computed tomography (CT) of the chest is not currently part of the routine evaluation, but some authors suggest a role for it in select patients because CT has shown a higher sensitivity than x-ray in the detection of early parenchymal lesions in patients with non–blast-related pulmonary contusion. CT may be useful in predicting which patients will require mechanical ventilation.3 Although the general management of BLI is similar to that of pulmonary contusion and ARDS, the relatively higher risk of significant barotrauma (i.e., alveolar rupture, systemic air emboli, and pneumothorax) in patients incurring BLI is a critically important feature.3,12,23 Persistent observations show that the use of positive pressure ventilation, especially high levels of positive end-expiratory pressure, increases the risk of and/or the exacerbation of pulmonary barotrauma and should therefore be avoided whenever possible.6,13,23,26 Furthermore, patients with BLI may be at increased risk of pulmonary complication related to overly aggressive fluid resuscitation.3,6,26 Various strategies aimed at ameliorating these risks have shown some success, including (1) permissive hypercapnia with a reduction of tidal volume and peak inspiratory pressure, (2) use of intermittent mechanical ventilation and continuous positive airway pressure to facilitate reversion to spontaneous breathing as soon as possible, and (3) prophylactic insertion of chest tubes.3,6,12,13,18,23,26 Patients with unknown neurologic status pose a particular challenge for the use of permis-

sive hypercapnia because of concerns regarding increased intracranial pressure. Some authors recommend bilateral tube thoracostomy for pulmonary PBI patients requiring aeromedical evacuation.3,6 The use of dual-lumen endotracheal tubes (i.e., independent lung ventilation) or high-frequency jet ventilation is recommended for patients with bronchopleural fistulae.5,12 Case reports have shown that high-frequency jet ventilation provides adequate oxygenation, whereas superimposed low-frequency positive pressure ventilation can improve ventilation with the lowest possible airway pressures.12 Expeditious use of hyperbaric oxygen therapy has been shown to reduce mortality in animal models and has been recommended in humans with BLI, although convincing evidence supporting this practice in humans is lacking.6,13,26 Extracorporeal membrane oxygenation has been used, but this modality is controversial.3,18,23,26 A retrospective study of patients sustaining BLI from explosions on civilian buses in Israel established that the first 24 hours after injury constitute a critical period for effective management.12 These authors proposed that a BLI severity score (BLISS) may be useful in the initial stabilization phase to direct treatment and predict outcome. The BLISS is derived from objective signs of hypoxemia, chest radiograph findings, and the presence of bronchopleural fistula.12 Based on the initial BLISS, none of the patients in this study who were classified as mildly injured went on to develop any form of lung injury. Of those classified as moderately injured, 33% went on to develop ARDS. All those classified as severely injured either developed ARDS or later died.12 Most importantly, this study showed that aggressive and complex interventions, guided by stratification of BLI severity, can lead to dramatic improvements in outcome. A follow-up study showed that most patients who survive BLI will regain good lung function within 1 year, although most of the patients involved were relatively young and healthy.27

Cardiovascular Injury In addition to conventional causes of hemodynamic instability seen in trauma patients, there are special factors particular to the management of victims with suspected blast injury. Although there are numerous reports of changes in heart rate and blood pressure that are thought to be due to effects of PBI, much of what is known about the PBI of the cardiovascular system has been gleaned from experimental studies in animal models.5 Beginning in World War I, it was observed that “men subjected to the concussion of large shells often developed a condition of shock that was unrelated to obvious trauma since no external wounds were visible.”6 A World War II study of 200 casualties assessed immediately after blast exposure showed that more than 25% of them had heart rates of less than 60 bpm and that over 90% had heart rates of less than 80 bpm. This review also found that hypotension was nearly universal, with blood pressures of 80 to 90 mm Hg (systolic) and 40 to 50 mm Hg (diastolic) being common.28 The bradycardia observed after blast exposure has been consistently INTRODUCTION OF EXPLOSIONS AND BLASTS 741

reproduced in animal studies and may be a vagal effect as experiments have shown the bradycardia can be prevented with bilateral vagotomy.28,29 Irwin and colleagues29 proposed that vagally mediated cardiovascular changes in humans are initiated by the socalled pulmonary defensive reflex. This reflex acts when acute pulmonary congestion and edema lead to fluid shifts in the lung, stimulating pulmonary C-fibers and triggering increased cholinergic activity with consequent systemic effects. This mechanism is supported by the clinical observation of brief periods of apnea after blast exposure, followed by rapid shallow respirations.3,24 This phenomenon has been observed in experimental blast injury models using artificial stimulation of pulmonary C-fibers.29 The hypotension observed in the World War II study has also been reproduced in animal simulations. Several studies have reported a greater than 50% decrease in mean arterial pressure in animals immediately after blast exposure, with spontaneous resolution over time.6,11,30 Clinically, the contribution of these various mechanisms for cardiovascular PBI may be complicated by co-existing factors such as hemorrhage. Given the importance of judicious fluid administration (including blood products) for appropriate cardiorespiratory resuscitation, in the context of potentially exacerbating soft tissue injury with suboptimal fluid resuscitation, invasive monitoring to guide therapy is often necessary.2,3,13,26 Colloid solutions are generally the resuscitation fluid of choice. Various electrocardiographic changes have been observed immediately after blast and are also thought to be due to blunt thoracic trauma and/or coronary air emboli.6,29 These may include atrioventricular and bundle branch blocks, nonspecific ventricular ectopy, low-voltage QRS complexes, and T-wave and ST-segment abnormalities. Blast-induced electrocardiographic changes typically revert to normal sinus rhythm within a few minutes but may deteriorate into sustained dysrhythmias, including lethal ventricular arrhythmias. Ischemic changes may also occur due to complications of air emboli.6,29

Abdominal Injury Nonlethal abdominal PBI is almost exclusively found in gas-containing organs and is likely caused by forces including shearing, spalling, and implosion. Solid organ damage may present as subcapsular hematomas or lacerations of the liver, spleen, and kidney.3,6,7 These injuries are thought to be due to acceleration-deceleration caused by either the initial effects of the blast wave and/ or from secondary and tertiary mechanisms of injury.5,13 The incidence of intestinal PBI may be higher in victims of underwater or CS explosions. The classic lesions of intestinal PBI involve small, multifocal intramural hematomas. These are morphologically similar to those caused by blunt abdominal trauma.31 Initial bleeding in submucosal regions may range from scattered petechiae or large confluent hematomas.3,6 Partial- or full-thickness lacerations may occur and may lead to immediate or delayed perforation 742 EVENTS RESULTING IN BLAST INJURIES

of the bowel.5 Since the ileocecal region and colon are the most likely areas to contain gas, these areas are the most prone to perforation during blast exposure.2,6,7 Since it is relatively uncommon, intestinal PBI presents a particular diagnostic challenge. Signs and symptoms of intestinal PBI include abdominal or testicular pain, nausea, vomiting, tenderness, absence of bowel sounds, and other peritoneal signs. Initial evaluation may be complicated by the overall acuity of a multiply injured patient or prior administration of pain-control medication. Gastrointestinal injury may be delayed as long as 48 hours after initial blast exposure.6 However, this may be more often due to latent injury with delayed perforation as opposed to delayed diagnosis.21 No reliable clinical predictors exist to help clinicians determine which patients may progress to delayed perforation.6 Abdominal CT, ultrasound, and diagnostic peritoneal lavage have been shown to be useful modalities for the evaluation of intestinal PBI.5,12 Kluger10 reported that diagnostic peritoneal lavage is particularly useful when treating blast injuries involving abdominal wall penetration by multiple metal projectiles. Colonoscopy has been suggested for the surveillance of large bowel contusions. But given the potential for iatrogenic perforation, colonoscopy may be ill advised in the post-blast period.3 Indications for urgent laparotomy are similar to those established for blunt abdominal trauma.3

Musculoskeletal/Extremity Injury Most blast injuries involving the musculoskeletal system are due to secondary and tertiary blast injury. There are numerous reports of traumatic amputation in blast victims that are thought to be due to PBI, but these injuries are rare among survivors.3 Blast-related amputations often traverse the proximal third of the tibia but rarely traverse joints such as the ankle and knee. This anatomic distribution may reflect an initial disruption of soft tissue and bone by the incident shock wave, followed by completion of the amputation by other components of overpressure forces.32 In an extensive review, Covey33 discussed important considerations in the physical examination of blast injuries of the musculoskeletal system. He highlighted the following: “(1) fragments do not always travel in straight lines, (2) small tissue wounds may be associated with extensive internal injury, (3) entry wounds in the buttocks, thighs, or peritoneum can be associated with intra-abdominal injury, (4) a high degree of suspicion for compartment syndrome should be maintained, and (5) an entry wound in the groin, or hematoma elsewhere may mean major vascular injury.” The conventional military approach to small fragment wounds has involved treating penetrating wounds in an aggressive fashion with early exploration, debridement, and delayed primary closure.33,34 However, recent evidence suggests that a more conservative approach may be appropriate provided that bacterial colonization is prevented with appropriate antibiotic coverage.34 Bowyer34 reported success with a conservative approach when the following criteria were met: (1) involvement of soft tissue only with no breach of pleura or peritoneum

and no major vascular involvement and (2) an entry or exit wound of less than 2 cm in maximum dimension that was (3) not frankly infected and (4) not caused by a mine blast. Although successful in wartime, nonoperative treatment of fragment wounds remains controversial. Microbial threats to fragment wounds include Clostridium species and Pseudomonas species for severely contaminated and high-grade open fractures.33 Appropriate antimicrobial coverage should be administered and tetanus immunization addressed. Primary closure of blast wounds greatly increases the risk of infection; therefore delayed primary closure is performed once the wound is clean and granulation tissue has appeared.33

CNS Injury CNS injury from explosions is an important entity because secondary and tertiary injuries to the head are common and are leading causes of immediate (71%) and delayed mortality (52%).3,14 Arterial air emboli may cause secondary damage to the CNS and are important causes of immediate death among blast victims.6,13 Although PBI of the CNS is poorly understood, there is increasing evidence that this mechanism may be a factor. Anxiety and adjustment reactions are nearly universal among survivors of explosions. Posttraumatic stress disorder (PTSD) is to be expected in victims and their families as well as in the responders and medical providers who care for them. Signs and symptoms of CNS PBI include headache, vertigo, ataxia, seizures, altered mental status, retinal artery emboli, tongue blanching, and anterograde or retrograde amnesia.2 If any of these findings are present, immediate administration of adequate oxygen therapy is appropriate. Expeditious administration of hyperbaric oxygen may be helpful for suspected CNS PBI. Previous recommendations of placing the patient in Trendelenburg’s position to avoid complications of arterial air emboli should be abandoned; the left lateral decubitus position with the head down is instead recommended.13 There have been several reports of transient motor paralysis with sensory preservation that may be due to blast effects on peripheral nerves.20,29 PTSD may also have an organic basis linked to CNS PBI. Cernak and others35 have speculated that behavioral alterations observed in the posttraumatic period, in the absence of structural changes, may be due to a variety of chemical alterations in the CNS after blast exposure. They report a substantially increased incidence of PTSD in patients after blast exposure. Mental health referral for blast victims is indicated for general counseling and surveillance of serious postincident morbidity. Critical incident stress debriefing sessions for providers are recommended.

PITFALLS A variety of pitfalls may be encountered when evaluating and managing survivors of blast injury incidents.

Perhaps the most critical issue in mass-casualty scenarios involves meeting the requirement for precise and effective triage. Several scoring systems with proven effectiveness have been developed or adapted for use in evaluating blast injury patients (e.g., AIS and BLI scores).2,12 Physicians and emergency medical systems that traditionally err on the side of over-triage in everyday operations must understand the direct relationship between over-triage and increased mortality observed in terrorist events.14 Understanding the epidemiology of past explosion scenarios will help providers allocate resources appropriately. For example, survivors of CS explosions will present with a much higher incidence of PBI than survivors of OA explosions, who tend to have predominantly fragmentation injuries.3,12 Experience shows that auditory injuries are commonly underestimated or overlooked during initial evaluation. The possibility of missing latent gastrointestinal injuries with the potential for delayed perforation must be kept in mind. Patients who are exposed to a significant blast with subsequent depressed mental status or after taking narcotic analgesics are at increased risk of missed diagnoses. Some authors recommend that such patients be observed for at least 48 hours and undergo serial abdominal examinations.7,21 Providers should anticipate a high incidence of psychological stress after an explosion and should make appropriate management referrals to minimize long-term morbidity and loss of productivity among survivors. Overly aggressive fluid resuscitation, which may be complicated by failure to recognize transient PBIinduced cardiovascular changes (e.g., hypotension, bradycardia), is an important pitfall. However, concomitant soft tissue injuries and burns requiring intensive fluid resuscitation are common. Therefore, meticulous attention to fluid balance and judicious use of fluid infusions are of paramount importance. Invasive monitoring is considered the standard of care in patients with suspected pulmonary PBI who require fluid management. The use of positive pressure ventilation in suspected pulmonary PBI is a well-established hazard due to the risk of progressive respiratory failure and air embolism. Patients who have incurred BLI reportedly do not tolerate anesthesia well, so regional or spinal anesthesia should be considered whenever possible.7,13,26 Although oxygen administration is indicated in all patients with signs of respiratory distress or air embolism, oxygen toxicity may result. Dilation of the pulmonary vasculature in response to supplemental oxygen may exacerbate pulmonary hemorrhage.6 REFERENCES 1. Cooper G, Maynard R, Cross N, et al. Casualties from terrorist bombings. J Trauma. 1983;23:955-67. 2. Adler J, Golan E, Golan J, et al. Terrorist bombing experience during 1975-79: casualties admitted to the Sharre Zedek Medical Center. Israel J Med Sci. 1983;19:189-93. 3. Horrocks C. Blast injuries: biophysics, pathophysiology, and management principles. J R Army Med Corps. 2001;147:28-40. INTRODUCTION OF EXPLOSIONS AND BLASTS 743

4. Mellor S. The relationship between blast loading to death and injury from explosion. World J Surg. 1992;16:893-98. 5. Wightman J, Gladish S. Explosions and blast injuries. Ann Emerg Med. 2001;37:664-78. 6. Guy R, Glover M, Cripps N. The pathophysiology of primary blast injury and it’s implications for treatment. Part I: the thorax. J R Nav Med Serv. 1998;84:79-86. 7. Philips Y. Primary blast injuries. Ann Emerg Med. 1986; 15:12;1446-50. 8. Leibovici D, Gofrit O, Shapira S. Eardrum perforation in explosion survivors: is it a marker pf pulmonary blast injury? Ann Emerg Med. 1999;34:168-72. 9. Cohen J, Ziv G, Bloom J, et al. Blast injury of the ear in confined space explosion: auditory and vestibular evaluation. Israel Med Assoc J. 2002;4:559-62. 10. Kluger Y. Bomb explosions in acts of terrorism: detonation, wound ballistics, triage and medical concerns. Israel Med Assoc J. 2003;5:235-40. 11. Irwin R, Lerner M, Bealer J, et al. Cardiopulmonary physiology of primary blast injury. J Trauma. 1997;43:650-55. 12. Pizov R, Oppenheim-Eden A, Matot I, et al. Blast injuries from an explosion on a civilian bus. Chest 1999;115:165-72. 13. Argyros GJ. Management of primary blast injury. Toxicology. 1997;121:105-15. 14. Frykberg ER. Medical management of disasters and mass casualties from terrorist bombings: how can we cope? J Trauma. 2002;53:201-12. 15. Biancolini C. Argentine Jewish community institution bomb explosion. J Trauma. 1999;47:728-32. 16. Mallonee S, Shariat S, Stennies G, et al. Physical injuries and fatalities resulting from the Oklahoma City bombing. JAMA 1996; 276:382-7. 17. National Research Council. Protecting Buildings from Bomb Damage: Transfer of Blast Effects Mitigation Technologies from Military to Civilian Applications. Washington, DC: National Academy Press; 1995. 18. Leibovici D, Gofrit O, Stein M, et al. Blast injuries: bus versus openair bombings—a cooperative study of injuries in survivors of open-air versus confined-space explosions. J Trauma. 1996; 41:1030-35. 19. Hadden W, Rutherford W, Merrit J, et al. The injuries of terrorist bombing: a study of 1532 consecutive patients. Br J Surg. 1978;65:525-31.

744 EVENTS RESULTING IN BLAST INJURIES

20. Guy R, Glover M, Cripps N. The pathophysiology of primary blast injury and it’s implications for treatment. Part III: injury to the central nervous system and the limbs. J Roy Nav Med Serv. 2000;86:27-31. 21. Paran H, Neufeld D, Shwartz I, et al. Perforation of the terminal Ileum induced by blast injury: delayed diagnosis or delayed perforation? J Trauma. 1996;30:472-75. 22. Kronenberg J, Ben-Shoshan J, Wolf M. Perforated tympanic membrane after blast injury. Am J Otolaryngol. 1993;14:92-4. 23. Sorkine P, Szold O, Kluger Y, et al. Permissive hypercapnia ventilation in patients with severe pulmonary blast injury. J Trauma. 1998;45:35-8. 24. Cernak I, Savic J, Dragan I, et al. Blast injury from explosive munitions. J Trauma. 1999;47:96-103. 25. Shaham D, Sella T, Makori A, et al. The role of radiology in terror injuries. Isr Med Assoc J. 2002;4:564-7. 26. Weiler-Ravell D, Adatto R, Borman J, et al. Blast injury of the chest. Israel J Med Sci. 1975;11:268-74. 27. Hirshberg B, Oppenheimer-Eden A, Pizov R, et al. Recovery from blast lung injury: one year follow up. Chest 1999;116:1683-8. 28. Barrow DW, Rhoads HY. Blast concussion injury. JAMA 1944;125:900-2. 29. Irwin R, Lerner M, Bealer J, et al. Shock after blast wave injury is caused by vagally mediated reflex. J Trauma. 1999;47:105-10. 30. Guy R, Kirkman E, Watkins P, et al. Physiologic response to primary blast. J Trauma. 1998;45:983-87. 31. Cripps N, Glover M, Guy R. The pathophysiology of primary blast injury and it’s implications for treatment. Part II: the auditory structures and then abdomen. J Roy Nav Med Serv. 1999;85: 13-24. 32. Hull J. Traumatic amputation by explosive blast: pattern of injury in survivors. Br J Surg. 1992;79:1389-92. 33. Covey DC. Blast and fragment injuries of the musculoskeletal system. J Bone Joint Surg Am. 2002;84:1221-34. 34. Bowyer GW. Management of small fragment wounds: experience from the Afghan border. J Trauma. 1996;40(suppl 3):S170-2. 35. Cernak I, Savic J, Zunic G, et al. Involvement of the central nervous system in the general response to pulmonary blast injury. J Trauma. 1996;40:S100-4.

chapter 142

Explosions: Conventional Robert Partridge

DESCRIPTION OF EVENT Explosions occur when solid or liquid material is rapidly transformed into a gas with sudden energy release. High explosives, such as trinitrotoluene (TNT) or other nitrate compounds, detonate very rapidly and release large amounts of energy capable of causing blast injuries as well as severe structural damage. Conventional explosions and blasts occur as a result of unintentional civilian incidents (e.g., explosive detonation during ship or truck transport), intentional and unintentional detonation of military ordinance, and terrorist attacks. Powerful explosions have the potential to inflict many different types of traumatic injuries on humans, but such injuries can vary depending on the type and amount of explosive agent, the location of the victims (inside or outside), and whether the blast occurs on air or water. Conventional explosions cause physical trauma by three mechanisms. Primary blast injury (PBI) results from the damage to human tissue from the sudden change in atmospheric pressure that propagates from the explosion (i.e., blast wave). Secondary blast injury occurs as debris accelerated by the blast strikes the victim, causing blunt or penetrating trauma. Tertiary blast injury occurs as the body of the victim is thrown onto the ground or into fixed objects as a result of the blast. In addition, quaternary injury can occur from inhalation of smoke or hot gases, carbon monoxide poisoning, fire, or structural collapse. The damage caused by PBI is a type of barotrauma that primarily affects gas-containing organs—the lungs, ears, and gastrointestinal tract. The degree of tissue injury is directly related to the magnitude and duration of the maximum overpressure of the blast wave. Most victims of primary blast lung injury are killed immediately, often as a result of massive coronary or cerebral air embolism. Other immediate deaths are attributed to severe multisystem injury due to secondary and tertiary blast injury. The majority of survivors will experience trauma caused by secondary, tertiary, or quaternary blast injury. PBI must be considered in all victims exposed to an explosion, even if there are no external signs of injury. Severe pulmonary manifestations include hemorrhage, barotrauma, and arterial air embolism, and gastrointestinal manifestations would include hemorrhage and hollow viscous perforation. Of the small number of

survivors with lung PBI, deaths may occur by progressive pulmonary insufficiency. These lesions appear similar to pulmonary contusion, both radiographically and pathologically.1,2 Indoor detonations or explosions within a vehicle appear to cause more severe PBIs than open-air bombings because the blast wave is magnified rather than dissipated as it is reflected off the floor, walls, and ceiling.3,4 The type of explosion and victim location at the time of the blast must be considered when managing blast injury.

PREINCIDENT ACTIONS Conventional explosions can occur anywhere,at any time, with variable numbers of casualties. For these reasons, there is little a person can do to prepare for a conventional explosion. However, communities can be prepared for such an event. Other than safety and law enforcement measures designed to prevent an explosion, the most effective preincident actions involve establishing an effective security, rescue, and medical infrastructure. One of the major determinants of mortality from conventional bombings is the availability of medical resources at the disaster scene. Explosions occurring in or near major cities with established prehospital systems, emergency departments, and advanced trauma care would be expected to have lower mortality rates than remote areas or areas with less advanced medical systems and longer rescue and transport times. Medical management of blast victims is also enhanced if help is available beyond the community affected and if there is an ability to transfer victims to other medical facilities. In addition, the panic, chaos, and emotional trauma of large conventional explosions can worsen morbidity and mortality. A plan for prompt leadership; coordination of security, rescue, and medical agencies involved in the disaster; and a preexisting plan for rapid rescue, disposition, and treatment of casualties can reduce this risk.3,5–8

POSTINCIDENT ACTIONS Previous disasters involving conventional explosions have demonstrated that safety and protection of first responders and medical personnel is the most important 745

initial action. In both terrorist bombings and other nonmilitary explosions, scene safety is the first priority for all responders, because of the risk of being struck by falling or unstable debris or becoming victims of a secondary explosion.7 Keeping medical personnel away from the scene of an explosion reduces their risk of injury from such events. Because first responders are trained to rescue and help victims, any secondary explosion and incapacitation of these persons would greatly impair subsequent rescue efforts.9 Immediately after a blast, rescue, police, and emergency medical services (EMS) personnel will be the first to care for casualties. Responders should not enter the blast scene until the incident commander has declared the area safe. Most victims will have traumatic injuries resulting from secondary and tertiary blast injury. EMS personnel should observe standard trauma protocols for management of these injuries. EMS personnel should assess casualties for PBI. A careful assessment of the scene can give clues to the potential for PBI. The presence of a crater or a building collapse are indicators of high blast strength. An assessment of crater size and structural damage and the location and time of the explosion may be useful in estimating the number of casualties and the likelihood of PBI. Blast peak overpressures in unobstructed open-air explosions are directly related to the explosive force of the blast and inversely proportional to the distance from the explosion.10 The further away a person is from a blast, the less likely he or she is develop severe PBI. The location and position that victims were in at the time of the blast should be noted. Reflected blast waves are even more likely to cause PBI. Solid surfaces that can reflect blast waves create a zone of very highly pressurized air as the blast wave is reflected back on itself.11,12 Rigid shields between a person and an explosion may reduce the risk of secondary blast injury but may not prevent significant PBI.13,14 Victims in close proximity to an explosion may have PBI only, and may initially appear uninjured. Because physical activity after PBI can result in a poorer outcome, EMS personnel must ensure that these persons are not physically active until evaluation and observation for PBI is complete. Injuries sustained from underwater PBI are different than those in open-air blasts. Because blast waves are reflected back underwater from the water-air surface boundary and interact with direct blast waves, greater blast loads are transmitted to the more deeply submerged parts of the victim. If a victim is submerged in a vertical position, particular concern should be raised for the possibility of PBI in the lower segments of the lungs or gastrointestinal tract. PBI to the bowel, including acute or delayed presentations of bowel perforation in addition to lower gastrointestinal bleeding, may occur in partially submerged victims of underwater blasts.2,15

MEDICAL TREATMENT OF CASUALTIES Management of casualties after a blast event initially involves gathering as much information as possible to 746 EVENTS RESULTING IN BLAST INJURIES

assess the potential for PBI, including the force of the blast, victim location inside or outside, whether the blast took place in air or submerged underwater, and whether there was any postevent strenuous activity. A thorough trauma evaluation is mandatory for all victims of explosive blasts. Standard trauma management for secondary and tertiary injury will be familiar to prehospital personnel, emergency physicians, and traumatologists, so this section will focus on management of PBI and other injuries commonly occurring in blast victims. The most critically injured patients after an exposure to a conventional blast succumb to their injuries at the scene. For those patients killed immediately after an explosion, death results from head injuries, PBI of the lung, abdominal injuries, or chest injuries.16,17 Among survivors, non–life-threatening injuries including fractures, soft tissue injuries, and blast injuries to ears and eyes are common.1,5,7,16,18 Of those who survive a conventional explosion, only very few will have severe chest and abdominal injuries, including blast lung. These injuries should be recognized as prognostic markers of severity, and it is important to identify and treat them early because surviving patients with such injuries have a significantly increased mortality rate. Evaluation of prior blast injuries indicates certain patterns of morbidity and mortality from which conclusions about future events may be drawn. Immediate deaths appear to be related to the strength of the explosion, an associated building collapse, or a blast location that is indoors. The Beirut bombing in 1983 illustrates some important principles of medical management of casualties after an explosion. Most survivors had noncritical injuries, and for those critically injured, death occurred days to weeks later. Most of these deaths (86%) occurred in victims who were rescued and treated more than 6 hours after the blast event. A short interval between blast event and treatment and early aggressive resuscitation are good prognostic factors for survival.16,19 Pulmonary PBI may have an acute or delayed presentation. Patients with acute pulmonary PBI will present with chest pain, dyspnea, and tachypnea with rapid and shallow respirations, dry cough, wheezing, and hemoptysis. Breath sounds will be diminished on the affected side, making the diagnosis of PBI difficult unless pneumothorax, hemothorax, and pulmonary contusion have been excluded. Inspiratory rales, dullness to percussion, and poor chest wall expansion may also be present.1 A chest radiograph is mandatory for all patients with respiratory difficulty or suspected PBI or chest trauma. Computed tomography (CT) scans of the chest may be useful to detect small pneumothoraces or pulmonary contusions, both of which may not be well visualized on a plain radiograph of the chest. Massive hemoptysis resulting from PBI can be managed by preferentially intubating the unaffected lung with a cuffed endotracheal tube, thus protecting the function of that side. Patients with PBI of the lung may have concurrent pneumothorax, tension pneumothorax, or hemothorax. Emergent decompression with a tube or needle thoracostomy is indicated.20 Patients with pulmonary PBI who are not having ventilatory problems are

at risk for hypoxemia and should be managed with highflow oxygen through a non-rebreather mask or continuous positive airway pressure. Patients able to ventilate spontaneously reduce their risk for arterial gas embolism. It has been suggested that patients requiring mechanical ventilation should be managed with low ventilatory pressures and permissive hypercapnia to reduce the risk of air embolism.21,22 Air embolism resulting from PBI may cause coronary vessel occlusion with subsequent myocardial infarction or cerebral infarction with altered mental status or stroke symptoms. Other organ systems may also be affected. Coronary artery air embolism after PBI can be difficult to diagnose but should be suspected in any blast victim who has electrocardiographic evidence of a myocardial infarction or is in shock with all other likely reasons for shock excluded. A head CT scan is mandatory in any patient with altered mental status, seizures, or focal neurologic deficits. Air embolism should be managed with hyperbaric oxygen therapy. Transferring patients to hyperbaric chambers may be problematic, given the risks of worsening the condition during aeromedical transportation and patient deterioration due to worsening pulmonary PBI. The abdominal evaluation for PBI should focus on the search for perforation and the signs of lower gastrointestinal hemorrhage and shock. The presentation and diagnosis of these conditions as well as diagnosis may be delayed. Diagnostic peritoneal lavage (DPL) is indicated in hemodynamically unstable patients with abdominal findings. Ultrasonography of the abdomen may be considered in patients with suspected intra-abdominal trauma or hypotension and may be especially valuable in managing mass-casualty incidents. Abdominal CT scanning in stable patients to detect abdominal injury due to PBI may be useful in detecting small gastrointestinal perforations or hemorrhage. An abdominal CT scan performed after a DPL may have false-positive results because air and fluid will have been introduced into the peritoneum during the DPL procedure.1 Tympanic membrane (TM) rupture is a relatively common injury as a result of blast waves. Patients with TM rupture may have acute pulmonary PBI but are unlikely to have delayed-onset pulmonary PBI. The absence of TM rupture is important because such patients are unlikely to develop pulmonary PBI.23 Patients who appear stable but may be at risk for delayed PBI—including those in close proximity to the blast, knocked unconscious, or who felt the blast wave hit them—should be admitted for observation. Patients who have abdominal pain or tenderness, even if initial studies have normal results, may develop lifethreatening bowel complications and should also be admitted.20 Patients can be discharged home if they have no chest complaints, normal chest radiographs, and no evidence of hypoxia, provided they have been observed at least 6 hours. The risk of pulmonary PBI is low in these patients, and onset of any PBI-related complications in such patients should present slowly. These patients can safely return to the hospital for a secondary evaluation. Additionally, patients with TM rupture

only may also be discharged home because they do not appear to be at risk of delayed-onset pulmonary PBI.24 These patients should be given standard instructions on care of ear perforations and provided with otolaryngologic follow-up.

CASE PRESENTATION There are numerous historical examples of conventional explosions. There were over 12,000 explosive or bombing incidents in the United States between 1980 and 1990.25,26 You are working in the emergency department of a medium-sized port city. A fire aboard a cargo ship on a weekday afternoon results in a massive response by city and regional fire departments. A large crowd of curious onlookers forms, and a major police and security effort is made to cordon off the area. Suddenly, the ship’s load of ammonium nitrate fertilizer explodes, destroying the ship, collapsing two nearby buildings, igniting fires, and hurling debris for more than a mile. There are hundreds dead at the scene, including rescue and security personnel, and there are over 1000 survivors. As the rescue effort begins and victims begin to flood local and regional healthcare centers, the challenge for healthcare providers is to identify and manage those with PBI while also evaluating and managing a larger number with varying degrees of trauma resulting from secondary, tertiary, and quaternary blast injury.

UNIQUE CONSIDERATIONS Conventional blasts are unique because blast waves can cause PBI in persons physically separated from the epicenter of the explosion. Blast waves travel around walls and can be magnified traveling down corridors. Persons in enclosed spaces frequently have the highest incidence of PBI regardless of whether the explosion occurred within that space or outside it.14,21,27 The risk of PBI also increases as the volume of the enclosed space decreases. Persons located next to walls or in corners at the moment of the blast are also more likely to sustain PBI.12 Persons wearing body protection, such as Kevlar, at the time of the blast, may be protected against secondary blast injury from flying objects but are still at risk for PBI. These garments transmit and may even amplify blast waves, so it should not be assumed that a blast victim wearing body protection has no PBI even if he or she has no secondary blast injury.28 Persons protected from secondary blast injury, either by a physical structure, body armor, or water may have sustained PBI. Because their injuries are not as immediately apparent as those with external injuries from secondary blast injury, they may still be active and helping with the relief effort in the aftermath of the blast. Strenuous activity after PBI may result in poorer outcome. EMS and other medical personnel on the scene must ensure that apparently uninjured persons in close proximity to an explosion do not engage in physical activity. EXPLOSIONS: CONVENTIONAL 747

PITFALLS The most significant pitfall in the evaluation of blast victims is failing to consider PBI in a person exposed to an explosion, whether near or far from the blast, indoors or outdoors, or in air or water. REFERENCES 1. Argyros GJ. Management of primary blast injury. Toxicology 1997;121:105-15. 2. Huller J, Bazini Y. Blast injuries of the chest and abdomen. Arch Surg. 1970;100:24-30. 3. Cooper GJ, Maynard RL, Cross NL, et al. Casualties from terrorist bombings. J Trauma. 1983;23:955-67. 4. Leibovici D, Gofrit ON, Stein M, et al. Blast injuries: bus vs. openair-bombings—a comparative study of injuries in survivors of openair versus confined space explosions. J Trauma. 1996;41:1030-5. 5. Brismar B, Bergenwald L. The terrorist bomb explosion in Bologna, Italy, 1980: an analysis of the effects an injuries sustained. J Trauma. 1982;22:216-20. 6. Rignault DP, Deligny MC. The 1986 terrorist bombing experience in Paris. Ann Surg. 1989;209:368-73. 7. Mallonee S, Shariat S, Stennies G, et al. Physical injuries and fatalities resulting from the Oklahoma City bombing. JAMA 1996;276: 382-387. 8. Ammons MA, Moore EE, Pons PT, et al. The role of a regional trauma system in the management of a mass disaster: an analysis of the Keystone Colorado chairlift accident. J Trauma. 1988;28:1468-71. 9. Stein M, Hirshberg A. Medical consequences of terrorism: the conventional weapon threat. Surg Clin North Am. 1999;79:1537-52. 10. Stuhmiller JH, Phillips YY, Richmond DR. The physics and mechanisms of primary blast injury. In: Bellamy RF, Zajtchuk R, eds. Conventional Warfare: Ballistic, Blast and Burn Injuries. Washington, DC: Office of the Surgeon General of the US Army; 1991:241-70. 11. Iremonger MJ. Physics of detonations and blast-waves. In: Cooper GJ, Dudley HAF, Gann DS, et al, eds. Scientific Foundations of Trauma. Oxford, UK: Butterworth-Heinemann; 1997:189-99.

748 EVENTS RESULTING IN BLAST INJURIES

12. Yelverton JT. Blast biology. In: Cooper GJ, Dudley HAF, Gann DS, et al, eds. Scientific Foundations of Trauma. Oxford, UK: Butterworth-Heinemann; 1997:200-13. 13. Wiener SL, Barrett J. Explosions and explosive device-related injuries. In: Wiener SL, Barrett J, eds. Trauma Management for Civilian and Military Physicians. Philadelphia: Saunders; 1986:13-26. 14. Mellor SG. The pathogenesis of blast injury and its management. Br J Hosp Med. 1988;39:536-9. 15. Paran H, Neufeld D, Shwartz I, et al. Perforation of the terminal ileum induced by blast injury: delayed diagnosis or delayed perforation? J Trauma. 1996;40:472-5. 16. Frykberg ER,Teppas JJ,Alexander RH. The 1983 Beirut Airport terrorist bombing: injury patterns and implications for disaster management. Am Surg. 1989;55:134-41. 17. Pyper PC, Graham WJH. Analysis of terrorist injuries treated at Craigavon Area Hospital, Northern Ireland, 1972-1980. Injury. 1982;14:332-8. 18. Frykberg ER, Tepas JJ. Terrorist bombings: lessons learned from Belfast to Beirut. Ann Surg. 1988;208:569-76. 19. Rignault DP. Recent progress in surgery for the victims of disaster, terrorism and war. World J Surg. 1992;16:885-7. 20. Wightman JM, Gladish SL. Explosions and blast injuries. Ann Emerg Med. 2001;37:664-78. 21. Pizov R, Oppenheim-Eden A, Matot I, et al. Blast lung injury from an explosion on a civilian bus. Chest. 1999;115:165-72. 22. Sorkine P, Szold O, Kluger Y, et al. Permissive hypercapnia ventilation in patients with severe pulmonary blast injury. J Trauma. 1988;45:35-8. 23. Mellor SG. The relationship of blast loading to death and injury from explosion. World J Surg. 1992;16:893-8. 24. Leibovici D, Gofrit ON, Shapira SC. Eardrum perforation in explosion survivors: is it a marker of pulmonary blast injury? Ann Emerg Med. 1999;34:168-72. 25. Slater MS, Trunkey DD. Terrorism in America: an evolving threat. Arch Surg. 1997;132:1059-66. 26. Karmy-Jones R, Kissinger D, Golocovsky M, et al. Bomb-related injuries. Mil Med. 1994;159:536-9. 27. Katz E, Ofek B, Adler J, et al. Primary blast injury after a bomb explosion on a civilian bus. Ann Surg. 1989;209:484-8. 28. Cooper GJ,Townend DJ, Cater SR, et al. The role of stress waves in thoracic visceral injury from blast loading: modification of stress transmission by foams and high density materials. J Biomech. 1991;24:273-85.

chapter 143

Explosions: Fireworks Craig Sisson

DESCRIPTION OF EVENT This chapter will address the preparation for and response to an explosion involving fireworks. Most formal fireworks displays follow strict safety guidelines meant to predict and prevent major complications. According to the American Pyrotechnics Association, only 3% of all fireworks injuries are related to public fireworks displays. In contrast, it is hard to predict and control the behavior of persons associated with the production and distribution of fireworks. There are multiple reports of large-scale explosions in fireworks factories around the world. This scenario is the focus of the chapter. Carelessness around fireworks can lead to an explosive event. In Lima, Peru, on Dec. 29, 2001, more than 1100 tons of fireworks were concentrated in the Mesa Redonda shopping area. A fire then developed, resulting in close to 300 deaths and 357 injuries.1 Chen and colleagues2,3 analyzed retrospective data from 339 patients involved in fireworks factory explosions from January 1987 to December 1999. They report a 13% mortality rate among victims, a significant percentage when compared with other causes of burns during the same period. Black powder, the basic component of fireworks, has not changed much since its invention by the Chinese approximately 1000 years ago. Historically, it is composed of saltpeter, charcoal, sulfur, and small amounts of water.4 Black powder is considered a “low explosive” and burns by a process known as deflagration.5 Compared with high explosives (e.g., TNT), the chemical reaction is relatively slow and releases energy over a longer period of time. However, if the reaction is enclosed within a contained space, pressure can build rapidly, leading to an explosion. This property makes black powder very useful as a propellant, eventually giving it the nickname gunpowder. The current classification system for explosive materials was developed by the U.S. Department of Transportation. Fireworks are included in this classification system under divisions 1.3 and 1.4, which include large display fireworks and “common” publicly available fireworks, respectively.

PREINCIDENT ACTIONS Perry and Lindell6 describe four key steps that a community must take to prepare for a disaster involving a largescale fireworks explosion: vulnerability analysis, capability assessment, plan development, and coordinated training exercises. The most vulnerable population in a fireworks disaster are those persons working inside the factory or storage facility and those found in close proximity to it. How easily can rescue teams access the site? How much and what kind of material is stored at the site? Where are the nearest first responders located? How far is it to the closest medical facility? Where is the nearest burn center? Are the surrounding buildings residential, commercial, or industrial? Do the citizens, first responders, and medical community know about this facility? How advanced are the safety systems found at the facility? Are the materials being stored properly? Is a protocol in place so that any change at the site is adequately communicated to those who would respond to an event? All of these factors will affect vulnerability. The capabilities of the responding parties must be analyzed to determine whether the community is prepared to respond to an event. A hospital may be located close to the potential disaster site but lack personnel and equipment to deal with a large volume of burn victims. Airway control is very important, and responders experienced in recognition of airway compromise and definitive airway management should have priority on the scene and in patient transport. The planning stage requires the collaborative effort of the local government, fire department, police, emergency medical systems, medical community, citizens, and site owners. A network of communication must be built so that all parties will be informed of changes in both vulnerability and capability. Finally, organized exercises must be performed to maintain the proper level of preparedness.

POSTINCIDENT ACTIONS In the immediate aftermath of a fireworks incident, the appropriate medical facilities and response personnel 749

should be dispatched through predetermined communication pathways. This ensures that information and resources are distributed in the most organized and effective way. Medical facilities must be made aware of potential trauma and burn victims so that space may be allocated and appropriate equipment and personnel made available. In the Mesa Redonda fireworks disaster, the local hospitals lacked adequately experienced personnel and were quickly depleted of intravenous fluids, antibiotics, and analgesics.1 In 1999, the Jahn Foundry in Springfield, Mass, exploded and within 5 minutes the first victims arrived at Baystate Medical Center. The Baystate emergency department was full at the time, necessitating reorganization.7 The initial responders to a fireworks storage facility explosion should be cautious. One should assess the scene immediately for any potential further danger to the victims and rescuers.8 The American Pyrotechnics Association instructs that emergency responders should never attempt to fight a fire that involves a building used in the manufacture of fireworks.9 The main goal should be removal and treatment of victims and prevention of secondary fires away from the initial site. The surrounding community should be evacuated immediately and triage and treatment areas set up at a safe distance from the disaster site. All nonambulatory patients should be transported to triage areas for evaluation.

MEDICAL TREATMENT OF CASUALTIES The majority of reports in the medical literature on fireworks injuries involve individual use of class 1.4 fireworks. Reports of large-scale fireworks disasters and the wounds they cause are very rare. The mortality rate associated with fireworks factory explosions is variable and depends on many factors. A study by NavarroMonzonis and others10 reports a mortality of 47% in casualties of industrial gunpowder explosions. A 13-year retrospective study by Chen and colleagues2,3 demonstrates a 13% overall mortality rate with greater than 50% mortality in those with inhalation injury. The injuries seen in the survivors were a combination of burns, blast injuries, trauma, and inhalation injury.3 In comparison with other blast injury disasters, fireworks disasters have a higher incidence of thermal injury. The burns characteristically involve a large total body surface area, and the majority of the burns are deep dermal or full thickness.1–3,10 Wounds found in casualties close to the blast may be severely contaminated with gunpowder residue.3 The primary explosion of gunpowder in combination with smoke generated by secondary fires makes inhalation injury a common finding.1–3 For the initial treatment of burn victims, remove all of the patients’ clothing to prevent further thermal or chemical injury. Jewelry and watches should also be removed to prevent a tourniquet effect from tissue swelling. First responders must evaluate the ABCs (i.e., airway, breathing, circulation) of each victim, taking time only to perform interventions that are immediately required on salvageable patients.11,12 Airway is a very important aspect of 750 EVENTS RESULTING IN BLAST INJURIES

management given the high incidence of inhalation injury and risk of blast lung injury. Indications for immediate definitive airway management include voice hoarseness, brassy cough, and stridor.13 If a patient was in an enclosed space or has facial burns or carbonaceous sputum, early definitive airway management should be considered. Early tracheostomy is the preferred option for long-term management of ventilated patients.2 Intravenous access and aggressive intravenous hydration with normal saline or lactated Ringer’s solution should be a priority. These patients will require extensive fluid resuscitation given the frequency of deep dermal and full-thickness burns, large burn surface area, inhalation injury, and potential delays in treatment.13–17 The Parkland formula may underestimate the fluid requirement and should only be used as a starting point for resuscitation. A urine output of 0.5–1.0 mL/kg/hour, a heart rate of less than 120 and a clear sensorium can be used as end points for resuscitation in adults.14 For children, a goal urine output of 1.0 mL/kg/hour and ageappropriate heart rate should be maintained.13 To decrease the temperature of the burned skin, cool tap water or a water-soaked towel should be used.12 Ice should be avoided because it can cause decreased circulation to already damaged tissue. Nguyen and colleagues18,19 report that cooling the burn wounds helps prevent progression to deep partial-thickness or fullthickness burns and reduces future complications. Medical providers must use sterile dressings to cover the wounds and wrap blankets around the patient to keep them warm. The principle is to keep the wounds cool and the patient warm. Primary, secondary, and tertiary blast injuries can be found in fireworks disaster patients.3,10 However, there are limited data available on blast injury resulting from large-scale explosion of stored gunpowder. Therefore, many of the treatments recommended in this text will be inferred from similar large-scale events. Primary blast injury is more severe when the victim is exposed to the blast wave overpressurization while inside an enclosed space.20–24 Leibovici and others23 make a specific comparison between open-air and enclosed-space explosions, showing an increased incidence of primary blast injury, more severe injuries, and higher mortality rate in enclosed-space explosions. Intuitively, victims who are located in the collapsed portions of buildings are far more likely to die.25,26 Most fireworks today are still made by hand inside enclosed buildings. One can expect a high incidence of immediate death of victims in close proximity to the initial blast.23,24 A rapid and complete secondary survey of all patients will prevent missed associated injuries. Chen and colleagues2 report 10% of burn victims to have an associated injury. The most common in decreasing frequency were limb fracture, blast lung injury, fractured rib with hemopneumothorax, and tympanic membrane rupture. The incidence of associated injuries among those who survived versus those who died was 5% and 48%, respectively. Leibovici and colleagues23 report psychological stress, tinnitus, mild hearing loss, minor penetrating trauma, and simple fractures as associated injuries for patients not requiring hospital admission in open-air bombings.

Patients should be provided with adequate analgesia after initial stabilization, either in the prehospital setting or in the emergency department. Once a patient has reached the hospital, aggressive early debridement of devitalized tissue and topical antimicrobial treatment should begin as soon as possible.14,15 Foreign bodies, such as paper fireworks covers and shrapnel from the blast, can increase the risk of infection and should be removed.10 Chen and others show that 68% of victims required surgery with an average of 2.7 surgeries per patient.3 There is a high risk of barotrauma in blast lung injury patients requiring mechanical ventilation.22,24 They also show decreased mortality in patients undergoing early tracheostomy and subsequent mechanical ventilation.2 Sepsis, multiple organ failure, hypovolemic shock from inadequate resuscitation, and pulmonary infection were common causes of death in hospitalized patients.2 Long-term management of these patients requires an experienced intensive care specialist, preferably within a burn unit setting.

UNIQUE CONSIDERATIONS Fireworks contain various chemical compounds and elements for the purpose of producing colored spectacles. One of these chemicals is elemental phosphorus. Elemental phosphorus is used in the military in various weapons due to its unique chemical properties. There are three allotropic forms of phosphorus: white, red, and black.27 White phosphorus is sometimes included in the manufacture of fireworks. It burns spontaneously at 34˚C, producing a bright greenish light, copious

amounts of white fumes, and a garliclike odor. A wound that is smoking white and exuding a garliclike odor is characteristic of this substance. When placed in contact with oxygen, white phosphorus is oxidized to phosphorus pentoxide, which then combines with water to form phosphoric acid. This chemical sequence releases heat into the environment, causing burns. The phosphoric acid formed lowers the pH of tissues, causing chemical burns.28 This chemical reaction sequence will continue until all of the phosphorus has reacted or until the phosphorus is deprived of its oxygen fuel. When an explosion occurs with a device containing white phosphorus, immediate steps must be taken to stop the chemical reaction. Treatment should focus on wound irrigation, phosphorus neutralization, and wound debridement.29 The victim’s clothing should be removed immediately to prevent any retained phosphorus particles from burning through to the skin or igniting the clothing. Once the clothing has been removed, the wounds should be washed with large amounts of water. This will cut off the oxygen supply and cool the wound to below the ignition temperature, effectively stopping the reaction.27,29–31 Before transport, the wounds should be covered with saline–soaked gauze to prevent them from drying and spontaneously igniting again. Oily dressings should not be used because white phosphorus is lipid–soluble and may penetrate into tissues.28,29 Once at the hospital, prompt debridement of all wounds is necessary to remove retained phosphorus particles. A Wood’s lamp causes retained phosphorus to fluoresce, aiding in removal.31 A second option is to wash the wound with a 1% copper sulfate solution, which reacts with elemental phosphorus and covers the particles with dark-colored copper phosphate. This easily

CASE PRESENTATION On December 29, 2001, more than 1100 tons of fireworks were being stored in the Mesa Redonda market in Lima, Peru. The market was stocked for a busy sales season during the Christmas and New Year’s fireworks celebrations. The streets were coated with a film of gunpowder left from careless transport of packaged fireworks. At 6:30 PM, a vendor ignited a firework for demonstration that in turn ignited nearby displays, leading to a chain of explosions lasting 2 hours.1 Within minutes, five city blocks were consumed in flame and smoke; nearly 300 people were killed and over 300 more wounded. The majority of fireworks injuries involve young males. In Mesa Redonda, 70% of the victims were women and children. Many of the bodies were found in groups of 15 to 30, presumably clustering in areas thought to be safe. Gulati and colleagues1 described the collapse of a high-voltage electrical transformer that crushed 40 people and electrocuted 27 others. Local hospitals treated 357 patients, 263 were treated for burns with 143 admissions for thermal injury.1 Seventy percent of admitted burn patients had involvement of greater than 20% of their total body surface area. The majority of the burns were second and third degree, and stores of fluids, antibiotics, and analgesics were quickly depleted.1 Inadequate fluid resuscitation due to fluid shortages led to acute renal failure in a number of patients. The majority of victims suffered some degree of smoke inhalation, and 16% of admitted burn patients had inhalation injury requiring ventilation. It took 8 hours for firefighters and police officers to bring the blaze and surrounding chaos under control. The stores and houses were built close together and constructed of a highly flammable mix of straw and mud. Combined with the wind and the large amount of gunpowder present, the fire and smoke spread with devastating speed. The streets were very narrow, and many of the buildings lacked windows and emergency exits. The streets were packed with vendors and shoppers at the time of the disaster. Electrical wires were not protected and dangled over the streets, posing another threat to victims and rescue workers. The fire departments were poorly funded, and much of their equipment was old and in need of replacement. There were not enough ambulances available in the area and access to victims was difficult. Most local hospitals were at or near capacity when the disaster occurred. Additionally, patients began arriving at hospitals around 8:00 PM, during staff shift changes, which added to the confusion. The production, importation, and sale of fireworks was banned by the president of Peru after this disaster.1 EXPLOSIONS: FIREWORKS 751

identifies sites that need further debridement and theoretically may slow the oxidation process. One concern is that copper itself is toxic and has never been shown to improve wound healing over normal saline washes alone.28–30 As a result of phosphorus absorption, rapid changes in serum calcium and phosphorus levels can occur. Animal models have linked this to cardiac electrical abnormalities with increased risk of sudden death.32 Therefore, continuous telemetry should be initiated for the patient, and his or her serum calcium and phosphorus levels should be monitored. Phosphorus absorption may also damage the kidneys and liver and cause other systemic effects.27,33 Magnesium and aluminum powders and pellets are also used in the production of fireworks. The chemical reactions are similar, producing a brilliant white light, intense heat, and loud noise effects if ignited in the presence of oxygen. Magnesium has an ignition temperature of 623˚C and burns at roughly 3600˚C. Once the oxygen source is removed, the reaction will stop.34 Magnesium can react with oxygen, nitrogen, carbon dioxide, and water. The reaction with carbon dioxide produces magnesium oxide and carbon, and the reaction with water produces magnesium oxide and hydrogen gas. These reactions are important information for first responders. Applying water to a fire containing magnesium will increase the severity of the fire.35 Hydrogen gas will be liberated and ignite, with the potential for a secondary explosion. Metal-extinguishing powders, such as graphite powder, powdered talc, and powdered sodium chloride present in class D fire extinguishers must be used to fight these fires. All explosions can spread flaming debris, but fireworks are unique. Many class 1.4 fireworks are designed as self-propelled projectiles. Class 1.4 fireworks, although not at risk of initiating an explosive event, can spread fire throughout the storage facility and surrounding environment. They can also cause a projectile injury during the initial stages of a fire similar to secondary blast injuries but preceding an explosion. This may inhibit a person’s ability to evacuate the site and put that person at risk for more severe injury.

PITFALLS Several potential pitfalls in response to a fireworks disaster exist. These include the following: • Failure to stop the burning process • Not performing ABCs with early definitive airway management • Failure to complete secondary survey; other types of trauma can kill faster than burns • Failure to remember: fluids, fluids, fluids • Attempting to extinguish fire in a fireworks warehouse; instead, all persons should be evacuated • Inadequate pain management • Failure to establish triage areas a safe distance from primary event site

752 EVENTS RESULTING IN BLAST INJURIES

REFERENCES 1. Gulati S, Cruz R, Milner S. The fireworks tragedy of Peru. J Burns Surg Wound Care. December 11, 2003. Available at: http//www. journalofburnsandwounds.Com/volume02/volume02_article 22.pdf. 2. Chen X,Wang Y,Wang C, et al. Gunpowder explosion burns in fireworks factory: causes of death and management. Burns 2002; 28:655-8. 3. Chen X,Wang Y,Wang C, et al. Burns due to gunpowder explosions in fireworks factory: a 13-year retrospective study. Burns 2002; 28:245-9. 4. Russell M. The Chemistry of Fireworks. Cambridge, UK: Royal Society of Chemistry; 2000. 5. Bailey A, Murray SC. The explosion process: detonation shock effects. In: Explosives, Propellants, and Pyrotechnics. London: Brassey; 1989:21-47. 6. Perry R, Lindell M. Preparedness for emergency response: guidelines for the emergency planning process. Disasters. 2003; 27: 336-50. 7. Leslie CL, Cushman M, McDonald GS, et al. Management of multiple burn casualties in a high volume ED without a verified burn unit. Am J Emerg Med. 2001;19:469-73. 8. Delaney J, Drummond R. Mass casualties and triage at a sporting event. Br J Sports Med. 2002;36:85-8. 9. National Council on Fireworks Safety. Available at: http//www.fireworksafety.com/home.htm. 10. Navarro-Monzonis A, Benito-Ruiz J, Baena-Montilla P, et al. Gunpowder-related burns. Burns 1992;18:159-61. 11. Bar-Joseph G, Michaelson M, Halberthal M. Managing mass casualties. Curr Opin Anaesthesiol. 2003;16:193-9. 12. Allison K, Porter K. Consensus on the prehospital approach to burns patient management. Emerg Med. 2004;21:112-4. 13. Monafo W. Initial management of burns. N Engl J Med. 1996; 335:1581-6. 14. Tang H, Xia Z, Lui S, et al. The experience in the treatment of patients with extensive full-thickness burns. Burns 1999; 25:757-9. 15. Rose J, Herndon D. Advances in the treatment of burn patients. Burns 1997;23:S19-26. 16. Navar P, Saffle J, Warden G. Effect of inhalation injury on fluid resuscitation requirements after thermal injury. Am J Surg. 1985;150:716-20. 17. Cancio L, Chavez S, Alvarado-Ortega M, et al. Predicting increased fluid requirements during the resuscitation of thermally injured patients. J Trauma. 2004;56:404-14. 18. Nguyen N, Gun R, Sparnon A, et al. The importance of immediate cooling—a case series of childhood burns in Vietnam. Burns 2002;28:173-6. 19. Nguyen N, Gun R, Sparnon A, et al. The importance of initial management: a case series of childhood burns in Vietnam. Burns 2002;28:167-72. 20. Wrightman J, Gladish S. Explosions and blast injuries. Ann Emerg Med. 2001;37:664-78. 21. Frykberg E. Medical management of disasters and mass casualties from terrorist bombings: how can we cope? J Trauma. 2002; 53:201-12. 22. Gans L, Kennedy T. Management of unique clinical entities in disaster medicine. Disaster Med. 1996;14:301-26. 23. Leibovici D, Gofrit O, Stein M, et al. Blast injuries: bus versus openair bombings—a comparative study of injuries in survivors of open-air versus confined-space explosions. J Trauma. 1996; 41:1130-5. 24. Pizov R, Oppenheim-Eden A, Matot I, et al. Blast lung injury from an explosion on a civilian bus. Chest 1999;115:165-72. 25. Mallonee S, Shariat S, Stennies G, et al. Physical injuries and fatalities resulting from the Oklahoma City bombing. JAMA 1996; 276:382-7. 26. Biancolini C, Del Bosco C, Jorge M. Argentine Jewish community institution bomb explosion. J Trauma. 1999;47:728. 27. Chau T, Lee T, Chen S, et al. The management of white phosphorous burns. Burns 2001;27:492-7. 28. Summerlin W,Walder A, Moncrief J. White phosphorous burns and massive hemolysis. J Trauma. 1967;7:476-84.

29. Konjoyan T. White phosphorus burns: case report and literature review. Mil Med. 1983;148:881-4. 30. Eldad A, Simon G. The phosphorous burn: a preliminary comparative experimental study of various forms of treatment. Burns 1991;17:198-200. 31. Davis K. Acute management of white phosphorous burn. Mil Med. 2002;167:83-4. 32. Bowen T, Whelan T, Nelson T. Sudden death after phosphorus burns: experimental observations of hypocalcemia, hyperphosphatemia and electrocardiographic abnormalities following pro-

duction of a standard white phosphorus burn. Ann Surg. 1971;174:779-84. 33. Ben-Hur N, Giladi A, Neuman Z, et al. Phosphorus burns: a pathophysiological study. Br J Plast Surg. 1972;25:238-44. 34. Mendelson J. Some principles of protection against burns from flame and incendiary munitions. J Trauma. 1971;11:286-94. 35. Madrzykowski D, Stroup W. Magnesium Chip Fire Tests Utilizing Biodegradable, Environmentally Safe, Nontoxic, Liquid Fire Suppression Agents. Gaithersburg, Md: Underwriters Laboratories Inc; 1995.

EXPLOSIONS: FIREWORKS 753

chapter 144

Suicide Bomber Jeffry L. Kashuk and Shamai A. Grossman

DESCRIPTION OF EVENT An unprecedented wave of terror has captivated world attention for several years, increasing in magnitude with daily warnings.1,2 Not unlike other disease outbreaks in world history, this terror epidemic knows no borders and strikes innocent civilians during their most productive years of life. The objective of terrorists is to kill and maim as many citizens as possible; hence, dense population centers and locations where the public congregate are emphasized targets. Differences have been noted between bombs prepared by terrorists and those of traditional warfare. Operating on more limited budgets, terrorists have discovered methods of packing bombs with nails, metal bolts, and similar objects so as to inflict maximum injury. These bombs are created so as to be easily transportable, usually hidden on the body of the terrorist who carries out the suicide mission. Other bombs are prepared in small, contained, transportable packages or in automobiles. Blast injury patterns have classically been described based on wartime injuries, with limited survivors requiring medical care.1–4 In contrast, civilian urban bomb explosions result in many patients simultaneously arriving at the hospital alive despite the devastating nature of their injuries. These patients may present with an extraordinarily varied constellation of clinical patterns. Virtually all patients exposed to the blast front will incur primary blast injury. The immediate blast front is dissipated from the explosion center based on forces of spalling, acceleration, and implosion mechanisms. Primary blast injuries classically result in injuries to aircontaining structures.4 More than 50% of patients exposed to a blast of greater than 50 psi will suffer tympanic membrane perforation. This injury can be used as sign of blast exposure and may be a harbinger of coincident injuries. Primary blast lung injury may not be readily apparent and should be carefully considered in such a scenario. Delayed infiltrates in blast injury are common in primary blast lung injury and may be difficult to differentiate from lacerated lung resulting from secondary blast mechanisms. Primary blast head injury appears to have a higher mortality than other conventional head 754

injuries, most probably due to the tremendous force of the exposure and associated injuries. Blast lung versus lacerated lung represents another clinical challenge. Whereas lacerated lung may result from secondary blast injury due to penetrating sheer forces, blast lung injury serves as the classic injury pattern of bomb explosions. Although both mechanisms may commonly manifest as pneumothorax, hemothorax is less common in classic blast lung injury. Both may develop significant respiratory difficulties, with persistent air leaks requiring creative ventilator techniques. However, in the early phase of injury, fluid management may be quite different; blast lung injury requires restrictive management whereas lacerated lung injury requires resuscitative therapy. Repair of a lacerated lung may occasionally require operative therapy—most commonly, tractotomy or oversew for hemorrhage control. In contrast, blast lung injury treatment is physically nonoperative. The secondary blast effect results from flying shards of glass, metal, and other explosive objects that inflict injury are similar to classic penetrating patterns. Benignappearing skin wounds may signal underlying severe injury due to the penetration of metal bolts, pellets, and nails. Terrorists know that maximum death and injury can be accomplished by bringing the explosive content to closed spaces. There is a direct correlation between the location of a blast and survivability. Open, closed, and sealed spaces result in differential injury patterns based on the standard categories of blast injury.5 Mortality appears to be highest in super-closed spaces such as buses. Explosions on buses result most commonly in the highly lethal tertiary blast front (i.e., Mach stem effect), where the human body may be propelled via a supercharged blast front against stationary objects, resulting in immediate amputation or death. Such patients typically arrive at the hospital with agonal breathing and extensively burned, mangled extremities. Survival for these persons is rare. Quaternary blast injuries are burn injuries perpetrated by the highly flammable surrounding area of the explosions. These burn patterns may include all types of classical burn injuries, including inhalation, chemical, and contact burns.

PREINCIDENT ACTIONS The multidimensional injury pattern, a complex of injuries that occur simultaneously in the same patient, seems unique to bomb explosions.5–7 Patients now arrive at the hospital alive who, in previous war settings, would have died of their extensive blast injuries. Although well-established trauma protocols such as advanced trauma life support remain the gold standard against which one should gauge treatment plans, this injury pattern has resulted in new dilemmas that demand a reassessment of established techniques to improve preparedness, treatment, and survival. The management of mass-casualty events demands strict adherence to established protocols and superb coordination of available manpower and medical resources, which are commonly stressed to the maximum.5,6,8,9 Given recent world events, many protocols are in evolution with plans for a high level of preparedness. Despite this, the sheer volume of injured patients encountered in such events may challenge even the most experienced institution. In addition, refinements in protocols and improvements in techniques are always in evolution as greater experience is gained.8–10 Triage protocols for mass-casualty events are different from other trauma situations. Virtually all local and regional hospital facilities are recruited to handle the sheer volume of injured patients.

POSTINCIDENT ACTIONS Care for the sickest patients should begin immediately. The initial clinical issue in these events is the lack of diagnostic capabilities. Patients who are triaged to smaller facilities for stabilization may require transfer to a trauma center for more definitive care.

MEDICAL TREATMENT OF CASUALTIES As with all critically ill patients, emergency care of casualties of a suicide bombing begins with evaluation of the ABCs: airway, breathing, and circulation. Once an airway has been secured and breathing and circulation established, the primary and secondary physical examination should proceed. In evaluating the multidimensional injury pattern with associated abdominal visceral injury, certain patterns have been noted. There appear to be more diffuse and associated injuries necessitating meticulous abdominal exploration. This may be particularly difficult in the midst of a multicasualty event involving other injured patients who are waiting to enter the operating room.8,10,11 An intensive and persistent search for injury must be undertaken, with the underlying mechanisms of both blunt and penetrating injuries being kept in mind. Diagnostic peritoneal lavage (DPL), first described almost 40 years ago, has returned as the most important diagnostic tool in mass-casualty events.5,7 It can be rap-

idly performed at the bedside and provides immediate diagnostic information to accompany triage decisions in mass-casualty events. In the absence of other diagnostic maneuvers or bedside ultrasound, this minimally invasive technique is valuable in the acute evaluation of the injured, as well as for follow-up evaluation after the tertiary survey. In patients presenting with delayed injuries, DPL has sometimes been the only test to have positive results. In some cases, these injuries appeared after a computed tomography (CT) scan with initial negative results. A high index of suspicion must be maintained when multiple shrapnel pieces are identified on radiograph or fluoroscopy. Visceral blast injuries may occur from multiple wounding mechanisms. Primary or tertiary blast injury may cause slow dissection along tissue planes, resulting in delayed peritonitis. In contrast, missile trajectory of secondary blast injury may parallel classic penetrating injury that is described in stab or gunshot wounds.6 Due to the potential for multiple mechanisms of action, a minimum of 5000 red blood cells/ml as a lower-level threshold for DPL in blast visceral injury has been suggested.5 Prioritization of CT scan and ultrasound must be established because these tests must be reserved for immediate, life-threatening, decision-making protocols. Usually, CT scan is available for only the most severe head injuries to support immediate interventional decisions. Total body fluoroscopy should be used liberally to identify all potential projectiles. Routine mapping of such findings is mandatory for documentation and future reference. Bedside ultrasound is of limited use. An obviously positive examination result may expedite diagnosis of hemothorax or hemoperitoneum; however, in many situations ultrasound may not be available due to the volume of injured patients competing for limited resources. Expert clinical judgment is demanded in such scenarios. Because of delayed injury presentation, previous negative examination results require careful reevaluation. Blast injuries may develop exponentially over time, resulting in injuries that are missed initially. For this reason, the tertiary survey has assumed a renewed level of importance in these events. If this examination suggests potential missed injury, further tests such as ultrasound or CT may be available and appropriate as soon as the majority of casualties have been admitted and routed through triage.

UNIQUE CONSIDERATIONS When a complex of injury patterns occur simultaneously in the same patient, as described, this has been termed the multidimensional injury pattern.5–7 This subgroup of patients is not predicted adequately by the classic injury severity score system. Parameters such as length of hospital stay, length of stay in the intensive care unit, and mortality appear significantly different than other groups of patients, emphasizing the unique nature of this subgroup. The management of multidimensional injury can be contrasted with that of other, conventional traumatic injury. Due to the multiple wounding mechanisms, the SUICIDE BOMBER 755

CASE PRESENTATION A 45-year-old man was a bystander in a bus explosion. The patient was triaged to the closest facility along with 45 other multiple-injured patients. The initial emergency department evaluation noted a Glasgow Coma Scale score of 3 with bilateral hemopneumothoraxes. The patient was promptly endotracheally intubated with concomitant placement of bilateral chest tubes and moderate blood return. An examination of the patient then revealed a perforation of the right eye, a periorbital laceration, peppering of the facial region and scalp, and an extensive laceration of the scalp. The initial abdominal examination revealed a soft and scaphoid abdomen. On closer inspection, a small round wound was noted in the left lower quadrant. A skeletal survey disclosed that the left arm had a comminuted humoral fracture with active bleeding; this was controlled with a pressure dressing. In addition, a 30% body surface area burn encompassing the chest, abdominal wall, and lower extremities was noted, as were multiple lacerations to both legs. Due to lack of neurosurgical coverage, the patient was prepared for transfer to a level I trauma center (to occur in approximately 40 minutes). Before the transfer, bedside abdominal ultrasound was normal. In addition, CT scan of the head, chest, and abdomen revealed moderate cerebral swelling and multiple shrapnel injuries with metallic spheric balls throughout the body but no penetration of the chest or abdominal cavity. The patient arrived in the trauma center with stable vital signs. A small spherical ball was noted in the right lower chest area. There was concern that this ball could have traversed the abdominal cavity from the left lower quadrant abdominal wound previously noted. Despite the otherwise normal abdominal examination results, the Focused Assessment with Sonography for Trauma (FAST) examination was repeated. Although this ultrasound had negative results, a DPL was then found to have a positive result of 5000 red blood cells/ml. Further evaluation noted the absence of a pulse in the right hand distal to the injury. Multiple surgical teams were mobilized. Personnel from the plastic surgery and ophthalmology departments worked on the facial region. The right eye required enucleation. Vascular surgery and orthopedics personnel treated the extremity injuries. A transection of the left brachial artery with comminuted humorous fracture was treated with a temporary arterial shunt. External fixation was placed over the fracture. Abdominal exploration (via the burned abdominal wall) disclosed lacerations of the sigmoid colon, small bowel (mid jejunum), a tear of the right diaphragm, and grade 2 injury of the right lobe of the liver. An ulnar nerve injury required reconstruction. One week of mechanical ventilation was required for blast lung injuries, and early tracheostomy was performed. Neurosurgical follow-up confirmed resolution of the brain swelling, and the patient regained full neurologic function with rehabilitation.

likelihood that these patients will require some type of surgical intervention is high. Such multiple injuries result in difficult challenges in diagnosis, decision-making, and treatment. Providing care to a patient with multidimen756 EVENTS RESULTING IN BLAST INJURIES

sional injury will often require the careful coordination of multiple surgical teams. This translates into the need for a large operating space to accommodate the teams who may need to be working simultaneously.

PITFALLS Several potential pitfalls in response to a suicide bomber attack exist. These include the following: • Coordination of manpower and medical resources by protocol are the most important requirements for bombing events. • The combined clinical scenario of head injury, burns, blast lung, and intra-abdominal or thoracic injury may create extreme difficulties in decision-making for surgery as well as critical care management. • Due to the vast number of victims, CT scanning equipment may be available only for the most obviously severe injuries. • Constant clinical vigilance is required to time interventional modalities in the case of combined head and other injuries. • Healthcare providers must be wary of profound acidosis and hypothermia. Aggressive warming mechanisms must be used, and the potential for developing coagulopathy must be recognized.11 REFERENCES 1. Frykberg ER. Medical management of disasters and mass causalities from terrorist bombings: how can we cope? J Trauma. 2002;53:201-12. 2. Fryberg ER. Principles of mass casualty managed following terrorist disasters. Ann Surg. 2004;239:319-21. 3. Mellor SG, Cooper GJ. Analysis of 828 serviceman killed or injured by explosion in Northern Ireland 1970-84. The Hostile Action Casualty System. Br J Surg. 1989;76:1006. 4. Katz JE, Ofek B, Adler J, et al. Primary blast injury after a bomb explosion in a civilian bus. Ann Surg. 1989;209:484-8. 5. Kluger Y, Kashuk J, Mayo A. Terror bombings: mechanisms, consequences, and implications. Scand J Surg. 2004;93:11-4. 6. Kluger Y. Bomb explosions in acts of terrorism: detonation, wound ballistics, triage, and medical concerns. Isr Med Assoc J. 2003;5: 235-40. 7. Kluger Y, Sofer D, Mayo A, et al. Bomb explosions in acts of terrorism—from explosion to medical concerns. Presented at the American Association for the Surgery of Trauma, Annual Meeting. Minneapolis, Minn: September 11, 2003. 8. Almogy G, Belzsberg H, Mintz Y, et al. Suicide bombing attacks: update and modification to the protocol. Ann Surg. 2004;239: 319-21. 9. Einav S, Fridenberg Z, Weissman L, et al. Evacuation priorities in mass casualty terrorism related events: implications for contingency planning. Ann Surg. 2004;239:304-10. 10. Peleg K. Patterns of injury in hospitalized terrorist victims. Am J Emerg Med. 2003;21:258-62. 11. Pelez K,Aharouson, Daniel L, et al. Gunshot and explosion injuries: characteristics, outcomes, and implications for care of terror— related injuries in Israel. Ann Surg. 2004;239: 311-8.

chapter 145

Vehicle-Borne Improvised Explosive Devices Michael I. Greenberg, Michael Horowitz, and Rachel Haroz

DESCRIPTION OF EVENT Vehicle-borne improvised explosive devices (VBIEDs) may be used in two general logistical scenarios. They can be used as assassination devices targeting an individual or group of persons or as a weapon intended to damage or destroy a specific target. VBIEDs have been used to attack “high-profile” targets such as specific buildings or targets with symbolic and/or logistical importance. “Soft” targets, or those having inadequate security protection, may also be targeted with the aim of causing substantial casualties in an area where many people are gathered.1 As an assassination device, VBIEDs may be predeployed with the goal of destroying the occupants of the vehicle in which the device has been installed. As an explosive delivery device, the entire vehicle becomes a bomb that can be used against groups of people, buildings, or other targets. In most instances, a VBIED attack involves a single, high-profile event that cannot be readily predicted. However, detailed preplanning for such an eventuality is essential to maximize the effectiveness of a coordinated medical response. VBIEDs are associated with widely varying casualty and mortality rates. The 1993 World Trade Center bombing resulted in approximately 1000 persons injured, whereas the 1998 bombing of the U.S. Embassy in Nairobi, Kenya, injured more than 4000 persons.2,3 VBIEDs provide a readily available delivery system: the vehicle itself. The explosive devices contained therein may be assembled in a safe and remote location prior to delivery to the intended target. Defense against the deployment of a VBIED is exceedingly difficult because the explosive device is easily concealed and precise target prediction is difficult. Trucks used as VBIEDs may have a dual purpose of being able to carry a very large load of explosive material coupled with the potential mechanical ability and power to penetrate and breach protective barriers. In some cases, separate assault vehicles may be used to break through protective barriers, thus allowing unencumbered access to the vehicle containing the VBEID. VBIEDs may combine a variety of combustible chemicals and explosives as well as radiologic materials and devices. No specific vehicle type has been associated with VBIEDs; however, terrorists usually choose vehicles that

are common to and widely available in a given geographic region as well as vehicles possessing routine access to the intended target. Vehicles of virtually any size can be used as VBIEDs. However, the size of the vehicle used may depend on the nature and size of the explosive device being used. In the 1993 World Trade Center attack, approximately 1200 lb of improvised explosives were positioned in a rental van reported stolen by one of the perpetrators. Various large vehicles including limousines, sports utility vehicles, small trucks, delivery vehicles, ambulances, and minivans may have special attraction to be used as VBIEDs, based on their relatively large storage capacity. An example of selective vehicle use for specific access to a target is the use of limousines, which may convey the appearance of authority, thus facilitating access to specific locations within buildings or to facilities generally denied to the public.

PREINCIDENT ACTIONS Although intelligence reports may help to protect against VBIED use in many cases, those who wish to use VBIEDs may often evade preemptive detection. Law enforcement techniques for detection and preemption against VBIEDs are beyond the scope of this discussion. However, response preplanning is a key preincident action and must include coordination between police, firefighters, emergency medical services (EMS) personnel, public works officials, structural engineers, local elected officials, and others. Relationships must be preestablished and roles precoordinated, including who will have overall authority on the scene and who will be the medical authority. Immediately after a VBIED incident, many competing priorities may emerge. These include rescuing the casualties, securing the area and controlling access, searching for a secondary explosive device, determining whether there is a need for evacuation of the surrounding area, preserving the crime scene, directing traffic to allow easy access/egress to emergency vehicles, and preventing further injury. Something as simple as a passing train could shake already damaged buildings, causing further collapse or fall of debris.4,5 Careful preplanning may allow the adverse effects of such factors to be quickly addressed and corrected. 757

Communication is a key element that requires careful preplanning. The medical authority at the scene must be able to communicate with the scene commander, EMS on-scene (including the EMS dispatcher at the staging area), and local hospitals. The medical commander will need information from all of these sources to properly allocate resources. Information from hospitals regarding patient load and remaining available resources will be vital, allowing the medical commander to direct patients appropriately. Information from the scene commander allows for casualty estimates that will influence the amount and type of personnel that need to be called to the scene. The medical commander must also be provided with constant updates from the triage area at the scene to be aware of needs for resupply. In short, the medical commander will require overall situational awareness to effectively direct medical resources both at the scene and at local hospitals.1,6–9 It is important to remember that, in the event that the major trauma center for an area is a target or is quickly overrun by casualties, a large number of patients may flood some of the smaller surrounding hospitals.6,10 Few factors correlate with patient survival that can be influenced in the case of a car or truck bomb. Factors influencing survival that are not in the medical planner’s control include the size of the explosion, the patterns of injury, the number of casualties, and the time of the day of the attack. Some factors important to survival over which a medical planner may have influence include having a well-rehearsed plan, being educated so as to improve triage efficiency, striving to have a minimum interval from injury to treatment, and ensuring that there is a sufficient number of competent medical staff that can be made available if an event occurs.11,12 As every car bomb incident will be unique, it is vital that the medical plan allows for contingencies. After the Oklahoma City truck bombing, the medical triage/treatment area needed to be moved three times after it was initially established because of threats of another bombing.9

POSTINCIDENT ACTIONS The overall emergency response will, in most locales, be initiated by police officers, who are usually first on the scene. Firefighters, EMS personnel, and other public safety responders will be expected to follow local response protocols. It is of critical importance that the initial responders survey the overall situation before becoming actively involved in the rescue because the danger of unstable buildings and the potential for the detonation of secondary devices will be high. In addition, the area should be surveyed for the presence of radiation by first responders because the use of radiologic dispersion devices must be considered.13 Those on the higher echelons of medical control will need to be made aware of the nature of the event and should receive an initial estimate of the number of casualties. EMS supervisors should alert area hospitals and begin to determine what resources will need to be deployed to the scene of the incident. 758 EVENTS RESULTING IN BLAST INJURIES

Police and/or military bomb units or hazardous materials teams will need to survey the scene to assess the risk for secondary devices while EMS responders initiate rescue efforts and treat casualties. This may engender a variable degree of risk for first responders, as it is likely that the scene will not be completely secured prior to the start of the rescue operation. Triage and treatment operations should follow local preestablished protocols. A covered and protected area, out of view of the survivors, should be designated as a morgue. Also, a possible air evacuation site can be determined, although there may be substantial amounts of loose debris that could become dangerous during helicopter operations.1,4,8 The flow of casualties from the scene should be as regulated as possible by one medical commander who has a good overall situational awareness both at the scene and at the area hospitals. The goal will be to send lessinjured patients to hospitals that are farther from the scene to conserve resources at the closer hospitals for the more seriously injured patients. Real world incidents have demonstrated that the majority of patients bring themselves to the closest hospital by car, by foot, or via public transit.1,7,9 Area hospitals will need to activate individual masscasualty plans. These plans should include the ability to triage patients away from the emergency unit. It is vital that the typical earlier arrival of less-injured patients not interfere with the later treatment of more critically ill patients. Over-triage (i.e., referring patients for potentially serious injuries when only relatively minor injuries exist) at the scene may also result in a hospital being overwhelmed with less-injured patients.

MEDICAL TREATMENT OF CASUALTIES The epidemiology of VBIED incidents may be useful in predicting the patterns and numbers of injuries expected in future events. The literature regarding VBIED attacks reveals predictable patterns, including the fact that many injuries in survivors are relatively minor.13,14 For example, after the Oklahoma City bombing there were 759 casualties; of these, 167 died, 83 were hospitalized, and 509 were treated and released.15 The greatest risk for death after the detonation of a VBIED is building collapse. It is estimated that 95% of the deaths associated with the Oklahoma City bombing were secondary to blunt trauma consequent to the collapse of the building.9 Other factors influencing the mortality rate include an open versus closed blast environment.16–18 A closed environment leads to greater overall mortality, increased risk of blast injury, more severe injuries among survivors, and a higher risk of significant burns.19 Most studies of VBIEDs do not report large numbers of survivors with blast-related injuries. This is likely due to the fact that those close enough to the blast to experience these injuries do not survive the initial explosion. Most survivors therefore sustain injuries from secondary blast effects, including injuries from loose material or frag-

ments propelled by the blast.16 This epidemiology may be helpful not only during medical preplanning, but also in providing the receiving facility with important predictors of what to expect in the immediate aftermath of an event involving VBIEDs. The literature is also helpful in planning what supplies are critical in the initial treatment of casualties. The most heavily used supplies in past events were reported to include antibiotics, narcotics, bandages, and tetanus toxoid.7,20 The most common injuries observed after a VBIED detonation are soft tissue injuries as well as hearing loss, fractures, and musculoskeletal injuries. The most profound challenge to medical resources of the hospital involves the emergency department, where adequate staffing is essential to ensure a proper flow of casualties.7,20 In addition, an increased demand on the radiology services may occur. Thus, in the early hours after an event, the indications for radiology studies may need to be limited to the most critical injuries.21 In some cases, the mode of arrival may give a clue as to injury severity, and it is important to remember that the initial group of presenting patients will generally have only minor injuries. This phenomenon was evident after the World Trade Center bombing in 1993, the Oklahoma City bombing, and the Nairobi Embassy bombing. After the 1993 World Trade Center bombing, just 450 of 1040 patients were transported by EMS, and after the Oklahoma City bombing EMS transported only 33% of patients seen in area hospitals.1,7 Those patients transported by EMS were much more likely to require hospital admission.7 Studies of VBIED events have highlighted the importance of triage both at the scene and at receiving hospitals. It is critical for those performing triage to quickly identify critically injured yet salvageable patients and to initiate treatment. Over-triage is common after VBIED incidents. Even physicians with extensive experience in trauma triage may find it difficult to identify patients with certain blast injuries on initial triage assessment.21 Specific clinical findings may be helpful. Tympanic membrane rupture may be a subtle sign of blast injury in some cases. However, the presence of an intact tympanic membrane does not ensure that a patient has not sustained a significant blast injury.16 Although over-triage places an increased strain on hospital resources, an overtriage rate of 50% is necessary to avoid the less desirable scenario of under-triage (i.e., categorizing a critically injured patient into a delayed treatment category). Frykberg and Tepas14 evaluated 14 terrorist bombing incidents and found an average over-triage rate of 59%. In general, accurate and efficient triage is an important factor in patient survival.

UNIQUE CONSIDERATIONS VBIED explosions stand apart from other explosions because they are, unfortunately, relatively common, unpredictable, and frequently perpetrated by terrorist groups. As numerous domestic and international VBIED incidents have demonstrated, morbidity and mortality are

CASE PRESENTATION At 10:30 AM, a truck carrying approximately 2 tons of explosives detonates in the center of a city’s financial district. The explosion results in the collapse of a portion of a 12-story office building and damages buildings in a 24-block radius. Within minutes several EMS units arrive at the scene, and over the next 30 minutes coordination begins between police, fire, and EMS personnel at the scene. Incident command is established per preplanned protocols, and specific areas are designated as casualty treatment and triage sites. The incident area is cordoned off, and rescue efforts begin. Large numbers of people are exiting buildings and police are directing them to safe locations. Hospitals in the immediate vicinity activate their individual disaster plans, and all local emergency departments are quickly inundated with patients. Most victims arrive at area emergency departments on foot or via private vehicle. Communications from the scene of the explosion to the local hospitals offer limited details of initial casualty estimates. During the course of the day, nearly 700 patients are evaluated at area hospitals as a result of the explosion; of these, 580 patients are treated and released, 12 patients die en route to the hospital or within the first 24 hours, and 115 are admitted to the hospital for further care and/or observation.

high. Another risk to consider with VBIEDs is the potential to use these devices as a dispersal mechanism for various hazardous materials. For example, the bombing of the World Trade Center in 1993 may have involved a cyanide compound, which the perpetrators hoped would be dispersed into the building ventilation system after the explosion. It is not clear whether cyanide was used during this attack; however, it is clear that the terrorists involved possessed cyanide and had plans to use chemicals in conjunction with future explosive devices.22

PITFALLS One potential pitfall in responding to a VBIED attack is the failure to consider the risk of a secondary explosion after the initial explosion. Secondary explosive devices may be designed to kill and injure emergency responders both at the scene as well as at the hospital. It is important to note that secondary devices may be located near the epicenter of the original blast as well as at other locations. An example of the use of a secondary device deployed at a location remote from the original blast was the Thiepval barracks bombing incident.12 In this incident, a second car bomb was deployed and timed to target the local medical treatment facility at a time when arriving patients and medical personnel would be present. Medical treatment facilities must be mindful of this tactic and should have protocols in place to protect against such an eventuality. A second potential pitfall in responding to such an attack is the failure to consider that a VBIED explosion may be used to disperse hazardous materials. VEHICLE-BORNE IMPROVISED EXPLOSIVE DEVICES 759

REFERENCES 1. Maniscalco PM. Terrorism hits home. Emerg Med Serv. 1993; 22:31–2, 34–7, 40–1. 2. Hollander D. Mairobi bomb blast-trauma and recovery. Trop Doct. 2000;30:47–8. 3. U.K. Security Service (MI5). Vehicle Bombs. Available at: http://www.mi5.gov.uk/print/Page42.html. 4. Cabinet Office Civil Contingencies Secretariat. Dealing with Disaster. Revised 3rd ed. June 2003. Available at: http://www. ukresilience. info/contingencies/dwd/index.htm. 5. Hillier T. Bomb attacks in city centers. September 1994. Available at: http://www.emergency.com/carbomb.htm. 6. Doyle C. Mass casualty incident integration with pre-hospital care. Emerg Med Clin North Am. 1990;8:163–75. 7. Hogan DE, Waeckerle JF, Dire DJ, et al. Emergency department impact of the Oklahoma City terrorist bombing. Ann Emerg Med. 1999;34:160–7. 8. Jacobs Jr LM. An emergency medical system approach to disaster planning. J Trauma. 1979;19:157–62. 9. Maningas PA, Robison M, Mallonee S. The EMS response to the Oklahoma City bombing. Prehospital Disaster Med. 1997;12:80–5. 10. Frykberg ER. Principles of mass casualty management following terrorist disasters. Ann Surg. 2004;239:319–21. 11. Hodgetts TJ. Lessons from the Musgrave Park hospital bombing. Injury 1993;24:219–21. 12. Vassallo DJ, Taylor JC, Aldington DJ, et al. Shattered illusions: the Thiepval Barracks bombing, 7 October 1996. J R Army Med Corps. 1997;143:5–11.

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13. Frykberg ER,Tepas III JJ,Alexander RH. The 1983 Beirut airport terrorist bombing injury patterns and implications for disaster management. Am Surgeon. 1989;55:134–41. 14. Frykberg ER,Tepas III JJ. Terrorist bombings lessons learned from a Belfast to Beirut. Ann Surg. 1988;208:569–76. 15. Greenberg M. Routine screening for environmental radiation by first responders at explosions and fires. Ann Emerg Med. 2003; 41:421. 16. Mellor SG, Cooper GJ. Analysis of 828 servicemen killed or injured by explosion in Northern Ireland 1970–84: the hostile action casualty system. Br J Surg. 1989;76:1006–10. 17. Mallonee S, Shariat S, Stennies G, et al. Physical injuries and fatalities resulting from the Oklahoma City bombing. JAMA 1996; 276:382–7. 18. Arnold JL, Halpern P, Tsai MC, et al. Mass casualty terrorist bombings: a comparison of outcomes by bombing type. Ann Emerg Med. 2004;43:263–73. 19. Cooper GJ, Maynard RL, Cross NL, et al. Casualties from terrorist bombings J Trauma. 1983;23:955–67. 20. Adler J, Golan E, Golan J, et al. Terrorist bombing experience during 1975–9 casualties admitted to the Shaare Zedek medical center. Isr J Med Sci. 1983;19:189–93. 21. Hirshberg A, Stein M, Walden R. Surgical resource utilization in urban terrorist bombing: a computer simulation J Trauma. 1999; 47:545–50. 22. Parachini JV. The world trade center bombers, 1993. In:Tucker JB, ed. Toxic Terror: Assessing Terrorist Use of Chemical and Biological Weapons. Cambridge, Mass: MIT Press; 2000:185–206.

chapter 146

Rocket-Propelled Grenade Attack* Marshall Eidenberg

INTRODUCTION Rocket-propelled grenades (RPGs) have been used in combat since World War II, with the American bazooka and German Panzerfaust. All RPGs share one common element: a shaped charge in the warhead designed to penetrate armor.1 In one attack in Vietnam, RPGs caused 12% of casualties.2 More recently, in Operation Iraqi Freedom, RPGs caused 14.5% of battlefield injuries.3 RPGs have been used to bring down helicopters and have been mass fired, reminiscent of American Civil War battles, to attack armored vehicles. Current examples are the American light antitank weapon (LAW) rocket and AT4 and the Russian-made RPG-7. The RPG-7 has a maximum range of 920 meters, at which time it selfexplodes (4.5 seconds from firing). As a result, this weapon is sometimes used as a form of anti-aircraft artillery against slow, low-flying, or hovering helicopters. There is a second class of weapons that physically resembles RPGs, called enhanced blast weapons (EBWs). They also made their debut in World War II. The Sovietmade Katyusha and German Nebelwerfer were the first. EBWs rely primarily on blast overpressure and secondarily on heat for their effects. Confined spaces intensify the blast effect by reflection of the pressure waves from interior surfaces. Current examples are the Russian TBG-7V (which is fired from the RPG-7 launcher) and the Chinese RPO-A.4,5

DESCRIPTION OF EVENTS Shaped-charge warheads cause a mix of wound patterns including thermal, blast, and ballistic trauma. The shaped charge forces a jet of super hot material through armor. These wounds have been described as similar to those caused by a blowtorch. The explosion will cause blast injury, discussed in greater detail below, and fragments of the RPG and spall (i.e., fragments of the vehicle or building hit by the RPG) from the target can cause ballistic damage with perforations and lacerations.6

*Disclaimer: The opinions or assertions contained herein are solely those of the author and do not represent the views of the Army Medical Department or the Department of Defense.

The EBWs cause injuries from the compressive effects of the shock waves transmitted to the victim (i.e., primary blast injury). The lungs and all air-filled organs are most vulnerable to blast overpressure, and injury to these organs increases the risk of mortality. Internal organs such as the intestines, heart, liver, and kidneys are also susceptible to damage from primary blast injury. The most likely result will be the crushing or rupture of the organ, which can lead to rapid loss of blood, accumulation of body fluids, or eventual peritonitis. Air embolism can also occur in coronary and cerebral vasculature. Pneumothoraces may also result from primary blast injury. Secondary blast injuries result from limited fragmentation of the warhead as well as the debris displaced by the blast. In open areas this is limited. In enclosed areas like buildings, debris is usually present, which increases the likelihood of these injuries. Typical secondary blast injuries are perforations of the body, fractures, injuries to the eyes (from dirt or dust), and lacerations. Unless a vital organ is damaged, rapid blood loss is the primary danger from this type of injury. Tertiary blast injury results from the blast throwing the casualty. Typical injuries are blunt trauma, fractures, and amputated limbs. Again, rapid blood loss is the major danger.

PREINCIDENT ACTIONS Aside from having a well-developed and rehearsed disaster response plan, there are no specific preplanning actions to be taken. Body armor helps cut down on secondary injuries from fragmentation but may enhance primary blast injuries in enclosed spaces.4,5

POSTINCIDENT ACTIONS Prehospital trauma life support becomes the primary care at the point of wounding. Simple life-saving skills are necessary to treat airway, breathing, and circulatory problems of persons with these types of wounds. Prehospital personnel should document injuries that occurred within an enclosed space to highlight the possibility of blast overpressure injuries when the casualty 761

reaches the emergency department. Postincident actions include notification of the trauma team and activation of the hospital’s mass-casualty plan. Plans should be in place for casualties who may have unexploded ordinance embedded in their bodies, are still alive, and require care. These weapons can be handled relatively safely during removal from patients, but they will need ultimate disposal by the “bomb squad.” Police bomb disposal personnel should be involved if there are any unexploded RPGs or EBWs retained in the patient’s body. Other considerations consist of mobilization of type O-positive and O-negative blood. The police department and hospital security personnel should be used for crowd control and media control.

MEDICAL TREATMENT OF CASUALTIES Treatment for both RPGs and EBWs are essentially the same as that of any other injury. The primary survey, airway, breathing, and circulation issues must be addressed first. Traumatic injuries are treated in the same way as any other casualty. Frequently, these patients have a multiple modality injury—burn, blast, and fragmentation (foreign body). Recent information from Operation Iraqi Freedom indicates that RPGs are the leading cause of multiple site injury.3 Blast injuries are relatively difficult to diagnose in the prehospital setting and can take time to reveal themselves, especially in the case of chest and abdominal blast injuries. Injuries to the torso and abdomen may have no external symptoms and may initially be indistinguishable from benign causes of respiratory distress, such as hyperventilation, breathlessness, and agitation due to stress reaction. More subtle signs of primary blast injury include deafness, bleeding from the ears, chest or abdominal pain, confusion, and difficulty breathing. Suspected blast casualties should be transported by stretcher because exercise has been shown to worsen pulmonary problems.7 Inappropriate use of intravenous fluids in patients with primary blast injury can cause rapid development of pulmonary problems due to pulmonary contusion (i.e., blast lung). Fluids should not be withheld for

resuscitation but should be used based on clinical parameters such as level of consciousness, urine output, and peripheral pulses. This is slightly different than the current advanced trauma life support guidelines, which recommend the rapid infusion of 2 liters of isotonic crystalloid.8

UNIQUE CONSIDERATIONS Remember that these patients who have been caught in an RPG attack have incurred multiple mechanisms of injury. In addition, these are high–kinetic-energy military weapons, especially compared with civilian modes of wounding, and the amount of energy transfer and tissue damage is likely to be greater. The RPO-A EBW uses isopropyl nitrate as an energetic material in the warhead. Isopropyl nitrate can be absorbed into the skin, ultimately causing formation of methemoglobin.9 Isopropyl nitrate is also a carcinogen. Ordinarily, isopropyl nitrate is a clear fluid, but it may have been dyed pink for ease of identification during maintenance. If a pink fluid is present when the RPO-A malfunctions, avoid contact with this fluid.

PITFALLS Several potential pitfalls in response to an RPG attack exist. These include the following: • As with every trauma patient, finding the first injury necessitates the search for the second, third, etc. Responder should not stop looking until the patient has had the tincture of time to unmask the more subtle injuries. • The anxious patient with no apparent injuries may still have sustained injuries to his or her lungs or abdomen. Rule out the medical causes (e.g., primary blast injury) for this anxiety before obtaining a psychiatry referral. • Large-volume intravenous fluid resuscitation should be avoided. Healthcare providers should treat for shock, but titrate volumes based on mental status, urine output, and peripheral pulses. REFERENCES

CASE PRESENTATION While working in an urban emergency department, you see live video on a news channel reporting there is a terrorist situation occurring nearby. Multiple rockets have been launched at buses and buildings, causing multiple casualties and obvious fatalities. You are at the closest facility, and you know from previous experiences with Oklahoma City and the World Trade Center attacks that patients will go to the nearest facility. You have 5 minutes until the patients start arriving. What are you going to do to prepare yourself and your team for these casualties? What information does your team need? 762 EVENTS RESULTING IN BLAST INJURIES

1. Bellamy RF, Zajtchuk R. The weapons of conventional land warfare and Assessing the effectiveness of conventional weapons. In: Bellamy RK, Zajtchuk R, eds. Textbook of Military Medicine: part I. Volume 5, Conventional Warfare: Ballistic, Blast and Burn Injuries. Washington DC: U.S. Office of the Surgeon General, Department of the Army; 1991:27, 66, 68. 2. Wound Data and Munitions Effectiveness Team. Evaluation of wound data and munitions effectiveness in Vietnam. Alexandria, Va: U.S. Defense Documentation Center of the Defense Logistics Agency; 1970:Vol. 3,Table 4, p. C-7,Table D. 10-3, p. D-19. 3. Dunemn KN, Oakley CJ, Gamboa SR, et al. Profile of Casualties Treated in US Army Medical Treatment Facilities During Operation Iraqi Freedom: 10 March-30 November 2003. Washington DC: Center for AMEDD Strategic Studies; 2004:1-98. 4. Grau LW, Smith T. A ‘crushing’ victory: fuel-air explosives and grozny 2000. The Marine Corps Gazette. Aug 2000;84(8):30.

5. The threat from blast weapons. The Bulletin, for Soldiers by Soldiers, The Canadian Army Lessons Learned Centre. 2001; 7-3:1-10. 6. Dougherty PJ. Armored vehicle crew casualties. Mil Med. 1990;155:417-20. 7. Hamit HF, Bulluck MH, Frumson G, Moncrief JA. Air blast injuries: report of a case. J Trauma. 1965; 5:117-24.

8. Bellamy RF. The nature of combat injuries and the role of ATLS in their management. In: Zatjuk R, ed. Combat Casualty Care Guidelines. Washington DC: U.S. Office of the Surgeon General, Department of the Army; 1991:9-19. 9. Safety (MSDS) data for isopropyl nitrate. October 27, 2003. Available at: http://ptcl.chem.ox.ac.uk/MSDS/IS/isopropyl_ nitrate.html.

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chapter 147

Conventional Explosions at a Mass Gathering Franklin D. Friedman

DESCRIPTION OF THE EVENT The magnitude and severity of primary injuries from a blast explosion are determined by proximity, the quantity and type of explosive, and whether the explosion occurs in an open or enclosed space.1,2 Naturally, when an explosion occurs in the midst of a large gathering of people, other factors that strongly affect overall morbidity and mortality include access of rescuers to the injured and the personnel and resources available to care for an overwhelming number of victims in the immediate aftermath. The increasing prevalence of terrorism and insurgency over the last three decades has increased our understanding of the types of injuries caused by blast in the civilian environment—injuries once seen only on the battlefield—as well as the predictors of survival and management techniques for such incidents.3–5 By the time victims of these injuries reach the hospital, primary blast injuries are uncommon because, so often, they result in immediate death.6 Because they are so rare, and because a bombing often results in so many casualties converging on a single institution, many physicians and other healthcare workers with no prior expertise in trauma or disaster management may be pressed into service to care for trauma patients.7 Although many articles in the medical literature describe the effects of blast injuries,8–11 and others describe medical planning and care for mass gatherings12–15 (i.e., mass “gatherings of potential patients”16), few combine both topics.17–20 As late as 2002, a 25-year review of the literature pertaining to mass gatherings did not reference a single article describing a terrorist incident at a mass gathering, or even discuss the topic.11 Most articles concerning healthcare planning for mass gatherings, in fact, ignore the risk of a major traumatic event such as a bombing, instead focusing on environmental or medical emergencies. An incident in which 60,000 spectators are exposed to an exploding bomb demands a different response. Fortunately, very few incidents of intentional or accidental explosions have occurred, affecting large gatherings such as sporting or entertainment events (e.g., the 764

Atlanta Olympics in 1996 and Bali in 2002). Many of the terrorist bombings from which we have learned about injury patterns occurred in other settings (e.g., U.S. barracks in Beirut in 1983, the Alfred P. Murrah Federal Building in 1995, the World Trade Center in New York in 1993, the Madrid train in 2004, numerous attacks in Israel). By extrapolating from what is known about the nature of explosion injuries, the outcome of explosions that have affected many victims, and the strategies developed to provide medical care at major events, one can build a workable strategy to care for persons with these injuries. The medical usage rate (generally reported as numbers of patients per 10,000 in attendance) at a mass gathering is rarely greater than 50 at a spectator event, and it is most often related to weather. By stark contrast, one author documents a mortality of 7.8% for open-air and 49% of closed-space bombings, although these do not refer to mass gatherings with several thousand persons in attendance.2

PREINCIDENT ACTIONS Preparation for conventional explosions at a large gathering is best when it is preventive, rather than reactive. The best preparations depend on making conditions unfavorable for the bomber and designing structures that are fire resistant, are less likely to collapse, and offer easy egress in the event of an explosion. Measures can be taken, as in the London Underground, to remove waste receptacles in which an explosive device may be hidden. Similarly, although inconvenient, inspecting backpacks and the trunks of vehicles for those entering events have become a necessary precaution. The importance of repeated drilling of all the facets of a hospital and a region’s disaster plan must not be underestimated. After the bombing at the 1996 Atlanta Olympics, Atlanta emergency medical services leaders attributed pre-event training and drills practiced during 5 years leading up to the event as the principal reason why their response went well.19 All 111 injured patients were evacuated to the area hospitals within just 32 minutes of the explosion.19 To best prepare for a

conventional bombing at a mass gathering, perform a drill involving a scenario with a large surge of trauma victims, mixing both critically ill and lightly injured victims.

POSTINCIDENT ACTIONS The potential volume of patients with both critical and noncritical injuries is the greatest risk to successful management of an explosion at a mass gathering. Establishing effective triage, both at the scene and again at the receiving hospitals, will prevent overwhelming limited resources and ensure that the most seriously injured patients are identified rapidly and sent to appropriate medical facilities. Virtually all civilian bombings constitute a criminal act. Therefore, any material from the explosives found on or inside of victims is evidence that may be useful to investigational authorities in solving the crime. Salvaged clothing may contain identifiable explosive residue. Even corpses may yield important clues; consider performing postmortem radiographs to identify shrapnel. Expect to continue to work with law enforcement personnel after an incident, especially in matters such as evidence collection and serving as witnesses as the examining healthcare providers. After treatment of casualties is completed, how should outcomes be assessed? Data points of interest include injury severity scores, specific injuries, morbidity, mortality, and location of persons with respect to the explosive device. By publishing data such as these, and lessons learned, it may be possible to improve the response to the next bombing incident.

MEDICAL TREATMENT OF CASUALTIES When caring for victims of a conventional bombing at a mass gathering, keep in mind the convergence of two types of disaster: injuries unique to conventional explosives and caring for the surge of many simultaneously injured patients. Those close to the actual explosion often will die or suffer serious injuries, but the majority of casualties will receive relatively minor injuries, frequently from flying debris.21 The other traumatic injuries likely seen will be those related to stampede from those trying to escape or burns from a resulting fire. Despite the variety of serious injuries unique to blast injuries, the most common injuries among blast survivors involve standard penetrating and blunt trauma.22 The major medical challenge in caring for the victims of bombs, in addition to the multiple simultaneous casualties, is to identify those who are seriously injured but salvageable and to realize that they will be mixed in with a large number who are lightly injured or psychologically traumatized.1 Children are particularly at risk for the damages inflicted by bomb explosions, yet the physical clues of injury may be less apparent, particularly to rescuers mainly accustomed to treating adults.23 Large numbers of children may also be present at certain mass gatherings. Details concerning the nature, type, and care

CASE PRESENTATION: THE BALI BOMBINGS OF OCTOBER 12, 2002 Shortly before midnight in the town of Kuta, Bali, an electronically triggered bomb exploded in Paddy’s Bar, driving the patrons outside, where moments later, a powerful car bomb (containing ammonium nitrate) exploded in front of the crowded Sari Club.“The place was packed, and it went up within a millisecond” was the description of a visiting Australian football coach24 (the team was in the club, and half were killed). “A huge, massive flame erupted from the floor like a volcano…Everybody rushed to the back steps, but it was too crowded to get out…everything was on fire.”25 Most of the victims were in their 20s and 30s, and most were foreign visitors (primarily from Australia, although at least 22 countries were represented among the deceased).26 The death toll was 202, and several hundred more suffered various injuries including severe burns.

of injuries common to conventional explosions are described in other chapters in this section. In addition to the actual explosions, the other two principal injury-causing features of this attack were the collapse of the Sari Club (a largely open-sided building), which trapped patrons, and the ignition of a huge fire that was apparently caused by exploding gas cylinders. Care of the injured was compromised by a limited medical infrastructure in Kuta; although it has one of the best hospitals in Bali, the care offered there is still rudimentary.27 Many of the foreign nationals were evacuated to Australia and Singapore. Sixty-one patients were transferred to Royal Darwin Hospital in Australia, 28 of whom had major trauma including “severe burns, missile injuries from shrapnel, limb disruption, and pressurewave injury to ears, lung, and bowel.”28 In Bali, beyond the limitations of caring for so many burned and otherwise injured patients, untrained volunteers performed much of the initial mortuary care. Tourists took on the daily responsibility of bringing ice to a makeshift morgue. Unfortunately, they also combined victims’ remains in single bags, commingling DNA and making some identification impossible. Three unidentified bodies were cremated subsequently.26

UNIQUE CONSIDERATIONS Responding to a conventional explosion at a mass gathering is unlike treating either a small number of victims from an explosion or the typical patients presenting from a large event (usually medical complaints, minor injuries, or environmental-related problems). A carefully placed explosive device at a major indoor event can result in hundreds or potentially thousands of casualties suffering assorted trauma, including burns. Triage, both at the scene and again at the receiving hospitals, is one of the most crucial aspects of the response to prevent CONVENTIONAL EXPLOSIONS AT A MASS GATHERING 765

overwhelming limited resources. Keep in mind that, unlike a medical emergency, at a sports event, the EMTs prepositioned in the stadium may be among the victims when a bomb explodes. Delay of care for those truly in need (i.e., those requiring chest decompression, mechanical ventilation, operative exploration) while methodically evaluating and bandaging every patient with an abrasion will mean lives lost. The effective disaster response, as for any surge of trauma patients, will rely on a variety of caregivers pressed into service to treat minor injuries,7 while senior, experienced emergency providers perform rapid triage, directing casualties to appropriate sites for care.

PITFALLS Several potential pitfalls in responding to an explosion at a mass gathering exist. These include the following: • Over-triage could rapidly overwhelm hospitals, resulting in the needless death of casualties who otherwise might have been saved. • Failure to consider the possibility of additional explosive devices after the initial detonation can needlessly result in additional casualties. • Failure to rapidly institute an orderly means to perform triage, both in the field and at hospitals, will result in unnecessary chaos. A military processing station model should be the ideal. REFERENCES 1. Stein M, Hirshberg A. Medical consequences of terrorism. Surg Clin North Am. 1999;79: 1537-52. 2. Leibovici D, Gofrit ON, Stein M, et al. Blast injuries: bus versus open-air bombings—a comparative study of injuries in survivors of open-air versus confined-space explosions. J Trauma. 1996;41: 1030-5. 3. Frykberg ER,Tepas JJ 3rd. Terrorist bombings, lessons learned from Belfast to Beirut. Ann Surg. 1988;208:569-76. 4. Biancolini CA, Del Bosco CG, Jorge MA. Argentine Jewish community institution bomb explosion. J Trauma. 1999;47:728-32. 5. Pahor AL. The ENT problems following the Birmingham bombings. J Laryngol Otol. 1981;95:399-406. 6. Boffard KD, MacFarlane C. Urban bomb blast injuries: patterns of injury and treatment. Surg Annu. 1993;25:29-47. 7. Fisher D, Burrow J. The Bali bombings of 12 October 2002: lessons in disaster management for physicians. Int Med J. 2003;33:125-6.

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8. Phillips YY. Primary blast injuries. Ann Emerg Med. 1986; 15: 105-9. 9. Mallonee S, Shariat S, Stennies G. Physical injuries and fatalities resulting from the Oklahoma City bombings. J AMA 1996; 276: 382-7. 10. Wightman JM, Gladish SL. Explosions and blast injuries. Ann Emerg Med. 2001;37:664-78. 11. Gibbons AJ, Farrier JN, Key SJ. The pipe bomb: a modern terrorist weapon. J R Army Med Corps. 2003;149:23-6. 12. Milsten AM, Maguire BJ, Bissell RA. Mass-gathering medical care: a review of the literature. Prehospital Disaster Med. 2002; 17: 151-62. 13. Michael JA, Barbera JA. Mass gathering medical care: a twenty-five year review. Prehospital Disaster Med. 1997;12:305-12. 14. Arbon P, Bridgewater FHG, Smith C. Mass gathering medicine: a predictive model for patient presentation and transport rates. Prehospital Disaster Med. 2001;16:150-8. 15. Nordberg M. EMS and mass gatherings. Emerg Med Services. 1990;19:46-56, 91. 16. Butler II WC, Gesner DE. Crowded venues: avoid an EMS quagmire by preparing for mass gatherings. J Emerg Med Serv. 1999; 24:62-5. 17. Severance HW. Mass-casualty victim “surge” management: preparing for bombings and blast-related injuries with possibility of hazardous materials exposure. N C Med J. 2002;63:242-6. 18. Frykberg ER. Medical management of disasters and mass casualties from terrorist bombings: how can we cope? J Trauma. 2002;53:201-12. 19. Feliciano DV,Anderson GV, Rozycki GS, et al. Management of casualties from the bombing at the Centennial Olympics. Am J Surg. 1998;176:538-43. 20. Brismar BO, Bergenwald L. The terrorist bomb explosion in Bologna, Italy, 1980: an analysis of the effects and injuries sustained. J Trauma. 1982;22:216-20. 21. Kennedy TL, Johnston GW. Civilian bomb injuries. BMJ. 1975;1:382-3. 22. Explosions and blast injuries: a primer for clinicians. Mass Preparedness and Response. Available at: http://www.bt.cdc.gov/ masstrauma/explosions.asp. 23. Waisman Y,Aharonson-Daniel L, Mor M, et al. The impact of terrorism on children: a two-year experience. Prehospital Dis Med. 2004;18:242-8. 24. Bonner R. Bombing at resort in Indonesia kills 150 and hurts scores more. New York Times on the Web. October 13, 2002. Available at: http://travel2.nytimes.com/mem/travel/article-page. html?res=9F06E7DA103AF930A25753C1A9649C8B63. 25. Mydans S. Terror in Bali: The aftermath—survivors of Indonesia blast are left stunned and searching. The New York Times on the Web. October 14, 2002. Available at: http://travel2.nytimes.com/ mem/travel/article-page.html?res= 9C02E4D9113AF937A25753C1A9649C8B63. 26. 2002 Bali terrorist bombing. Wikipedia. Available at: http://en. wikipedia.org/wiki/2002_Bali_terrorist_bombing. 27. Watts J. Bali bombing offers lessons for disaster relief. Lancet 2002;360:1401. 28. Palmer DJ, Stephens D, Fisher DA, et al. The Bali bombing: the Royal Darwin Hospital response. Med J Aust. 2003;179:353-6.

chapter 148

Conventional Explosion at a Hospital Donald MacMillan

DESCRIPTION OF EVENT Although a highly unlikely event, a hospital explosion and its impact on the infrastructure, patients, staff, and the community must be considered. The hospital setting is rich in flammable and toxic materials, making it a potentially hazardous environment. The ever-increasing use of hazardous materials, nuclear agents, and toxic substances makes most medical centers vulnerable to explosions.1 Although there is a paucity of reports of hospital explosions in the literature, the increasing frequency of terrorist events makes such an event more likely.2 The experience gained from damage to healthcare facilities by earthquakes and terrorist incidents provides some insight into how to respond to this type of emergency. This chapter will discuss the types of explosions that may affect a hospital, and the associated injuries will be described. Potential pitfalls and successes from similar events will also be discussed. All will be considered in the context of the Incident Command System (ICS). Conventional explosions in hospitals are exceedingly rare. When a hazard vulnerability analysis is performed, the probability of such an event would be given a low score; however, the impact of the event on the institution warrants a high score, making the overall score low to intermediate. Explosions can result from either a terrorist event or an internal mishap, such as a ruptured gas line. No matter the source, the result is essentially the same. A terrorist incident will most likely involve the detonation of an improvised explosive device. These devices come in a variety of shapes and sizes, ranging from small pipe bombs composed of metal pipe and rapidly burning gunpowder to large truck bombs like the one used to destroy the Alfred P. Murrah Federal Building in Oklahoma City in 1995. Secondary devices, which are devices timed to detonate after the primary explosion, must be considered. Although they failed to function as intended, the suspects in the Columbine High School shooting in 1999 had many secondary devices, which were designed to maim and kill emergency responders.3 Secondary devices were also used in the Centennial Park bombing at the 1996 Atlanta Olympics as well as the Atlanta abortion clinic bombing in 1997. Until the source of the explosion can be identified, the presence

of secondary devices must be considered. Unlike terrorist bombings, explosions caused by flammable gases or liquids may continue to burn, resulting in secondary explosions that can cause further damage to the structure. The storage of compressed gases, including oxygen and air, can be the source of an explosion at a healthcare facility. No matter what the source of the explosion, damage to the building can include the structural components or infrastructural components (e.g., ventilation, water supply, and sprinkler systems). Fires ignited from the initial explosion can generate injured patients, even among those who avoided injury in the initial event. Damage to anything other than a small confined area requires the consideration of a partial or facility-wide evacuation.

PREINCIDENT ACTIONS An ICS is the foundation of the hospital’s emergency operations plan. Repeated drills using the ICS are a must. An ICS is an organized system of command and control that allows the user to employ procedures for organizing personnel, facilities, equipment, and communications during an emergency response. A full discussion of the ICS can be found in Chapter 30. Table 148-1 briefly outlines the immediate tasks of the sector chiefs.

POSTINCIDENT ACTIONS The Incident Commander will determine when the incident is over or determined to be under control and when to discontinue or contract the ICS. The incident may be turned over to the top-ranking police or fire agency during the investigative phase. The primary function is to restore the hospital to its preincident state. Partial restoration of services may begin as soon as the building is deemed structurally sound and certain patients may be returned to their beds or the hospital can start accepting new patients. The determination of whether severely damaged structures can be repaired or will have to be razed must be addressed. After the 1994 Northridge, Calif, earthquake, four of the eight hospitals that evacuated patients because of that disaster required demolition.4 767

TABLE 148-1 IMMEDIATE TASKS OF SECTOR CHIEFS IN EMERGENCY RESPONSE TITLE

TASKS TO CONSIDER

Incident Commander

1. Activate Emergency Operations Center. 2. Set agenda for status report by sector chiefs (i.e., operations, logistics, planning and finance). 3. Assign liaisons to coordinate with responding agencies. 4. Assign a public information officer 5. Prepare staff for extended operations. 6. Determine whether patient evacuation will be required. 1. Determine the structural integrity of the affected building and advise the Incident Commander. 2. Secure the utilities, including medical gases. 3. Ensure adequate supplies to treatment area. 4. Activate emergency communications plan. 1. Consider alternative care sites. 2. Secure transportation for patients to alternative care sites. 3. Ensure accurate patient tracking. 4. Develop a plan for convergent volunteerism. 1. Organize triage and treatment of all casualties. 2. Ensure continued care of all unaffected patients. 1. Immediately track all costs associated with response, recovery, and mitigation of event.

Logistics Sector Chief

Planning Sector Chief

Operations Sector Chief

Finance Sector Chief

Immediate real-time cost tracking may become important for reimbursement. The finance officer should work closely with outside agencies, including the institution’s insurance carrier, to provide accurate costs. This must include personnel costs as well as replacement costs for material. Determining what types of disaster relief or grant money will be available and how best to access these funds will assist the institution in returning to its preincident condition. In the event the source of the explosion is unknown and possibly the result of a terrorist attack, the facility also becomes a crime scene. Evidence preservation and limited access to the scene are critical. Jurisdictional issues, particularly with law enforcement agencies, may become complicated. All agencies should understand that safety issues take priority, but responders should try to minimize their impact on the scene. Working with these agencies during drills and appreciating one another’s roles and capabilities will greatly enhance the working relationship and allow both missions to be accomplished in overlapping time frames. Finally, since hospitals have large amounts of hazardous and radioactive material, patient decontamination may be required. Contaminated patients cannot enter the general population without first being decontaminated. Depending on the location of the explosion and the damage sustained, the hospital’s own decontamination facility may be unavailable. Even if the facility is undamaged, the 768 EVENTS RESULTING IN BLAST INJURIES

personnel who usually provide decontamination may be unavailable. Contamination with radioactive material has some special considerations. Working closely with the hospital physicist or the radiation safety officer will greatly enhance decontamination efforts. In addition, educating staff about radioactive decontamination will reduce the anxiety of treating these patients. Although explosions at hospitals are rare, they must be considered during the hazard vulnerability analysis. The best way to prepare for these and all types of events is to implement an Incident Command–based hospital emergency management plan. This plan should be exercised frequently and should involve as many community agencies as possible. This experience will be invaluable no matter what type of emergency disrupts the function of a hospital.

Medical Treatment of Casualties Victims of a conventional explosion at a hospital will have the myriad of injuries seen in blasts and structure collapse. The care of these victims will follow those guidelines described thoroughly in Chapters 141, 142, and 162. In a hospital setting, however, some casualties may have underlying medical conditions for which they are being hospitalized.The management of such patients should also take into account these underlying conditions.

CASE PRESENTATION An explosion and fire occurs at 11 PM in the main power plant of a large inner-city hospital, severely damaging that part of the hospital structure. An adjacent building with inpatient wards on seven floors, including the emergency department, operating rooms, and medical and surgical intensive care units, is damaged from the explosion. The backup power supply initiates, then fails after 1 minute and another explosion. Electrical power is lost throughout the hospital. All of the lights as well as some ventilators and monitors turn off, elevators stop, and communications cease. As first responders arrive, one section of the hospital is enveloped in flames, and the remainder of the hospital is in complete darkness. Inside, hospital staff in every unit frantically attempt to locate patients in the dark, rescue patient and staff victims of the explosion and fire, assist those whose ventilators have failed, and begin the evacuation procedure.

UNIQUE CONSIDERATIONS There are unique considerations with hospital explosions. The first is operating in an oxygen-rich environment. The potential for increase in fire is directly related to the amount of oxygen available from ruptured medical gas lines. It should be an absolute top priority of the operations sector chief to have the oxygen lines shut down as soon as possible. This may mean shutting down the entire facility until the affected area of the building can be isolated.

Whether the explosion is due to a terrorist event or is an accident, there is an increased potential for the dispersal of radioactive material. Contamination will add a level of complexity to the management of the incident because decontamination will have to be executed in consultation with the facility’s radiation safety officer. If the explosion is the result of a terrorist event, the involvement of law enforcement personnel adds yet another level of complexity. To ensure that potential radiation contamination is considered, the radiation safety officer should be notified whenever the emergency operations plan is implemented. He or she is a staff officer or liaison to the Incident Commander and needs to be incorporated into the operations plan. The Incident Commander can quickly dismiss him or her if the officer’s services are not required, or the officer can be reassigned to the operations sector as needed. The risk of evacuating patients from a structure that is potentially unstable must be considered. These risks include moving unstable patients through an environment that is immediately dangerous to life and health. If the building is damaged similar to what was seen in Oklahoma City, technical rescue experts will be required and the evacuation will be lengthy. Sheltering in place also has its risks, including turning a potentially stable structure into an unstable one as a result of any secondary explosions. The important point to determine is whether a patient is going to be exposed to greater risk during evacuation than he or she would if sheltered in place.

PITFALLS Several potential pitfalls exist in responding to an explosion at a hospital. These include the following: • Lack of an ICS-based emergency operations plan • Failure to participate with local agencies that will respond in the event of an explosion • Operating outside the ICS, allowing “freelancing” to occur • Not incorporating ICS into all facets of drills, tabletop scenarios, and events • Not getting to know all of the responders’ capabilities and limitations before an event occurs REFERENCES 1. Aghababian R, Lewis CP, Gans L, et al. Disasters within hospitals. Ann Emerg Med. 1994;23:771-7. 2. Hodgetts TJ. Lessons from the Musgrave Park Hospital bombing. Injury 1993;24:219-21. 3. Administration UF. Wanton Violence at Columbine High School. 1999. 4. Schultz CH, Koenig KL, Lewis RJ. Implications of hospital evacuation after the Northridge, California, earthquake. N Engl J Med. 2003;348:1349-55.

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chapter 149

Conventional Explosion in a High-Rise Building Ryan Friedberg

DESCRIPTION OF EVENT High-rise buildings are architectural wonders that shape the skylines of many cities across the United States. Explosions in high-rise buildings were essentially unheard of until 1993, when these structures became targets of terrorism. Until then, healthcare workers in the United States had no experience with mass casualties from explosions in high-rise buildings. There have been three large-scale attacks on highrise buildings in the United States since 1993. The first was the bombing of the World Trade Center in New York in 1993. This event resulted in six deaths and 1042 injuries.1 The second attack was in Oklahoma City in 1995, when a truck bomb exploded adjacent to the Alfred P. Murrah Federal Building. This attack killed 167 persons and injured more than 750 persons.2 The most recent attack, and the worst single act of terrorism in the history of the United States, was the attack on the World Trade Center towers in New York on Sept. 11, 2001. The actual death toll from this attack is unknown. There have been 1527 identified bodies, but it is believed that the actual death toll is between 2726 and 2742 persons.3,4 Thousands of persons suffered injuries from the attack, and 1103 were treated in hospitals for their injuries.5 The attack has changed the way people in the United States live and created an urgent need not only to attempt to prevent another such attack, but also to prepare for the possibility of future attacks on high-rise buildings. There are many different types of explosives that terrorists may attempt to detonate in high-rise buildings. High explosives, including trinitrotoluene (TNT), composite C4, and ammonium nitrate are powerful enough to cause building collapse. However, the explosions and resulting fires from massive amounts of less-explosive aviation fuel in the World Trade Center attack resulted in the greatest structural failure in human history. Trauma after an explosion in a building can be categorized into primary, secondary, and tertiary blast injury. Primary blast injuries are due to the direct effect of the pressure wave on the victim.6 The most sensitive organ affected by the primary blast is the ear.7 Other systems that are 770

affected include the respiratory, circulatory, and digestive systems, as well as the eye and orbit. Secondary blast injuries are incurred due to objects propelled by the blast. These projectiles can be very significant in a high-rise building explosion and may extend far beyond the distance of the initial blast effect. These fragments that become projectiles can be both large and small and can cause both penetrating and blunt injuries. Tertiary blast injuries occur when a person is propelled by the blast against another structure. These are typically blunt injuries including soft tissue injuries, lacerations, head injuries, and fractures. Less commonly seen are flash burns and thermal injuries. Crush injuries are common if a building explosion results in structural collapse, and these frequently cause immediate death. In the Oklahoma City bombing, 97% of fatalities were immediate, and most were killed in the building collapse.2 This was also true in the World Trade Center attack.3 The risk of building collapse and resultant high fatality rates distinguish explosions in high-rise buildings from other types of explosions. Medical personnel are unlikely to care for victims crushed in a highrise collapse because survival is rare.

PREINCIDENT ACTIONS Prevention is the most effective method of reducing morbidity and mortality in the aftermath of an explosion in a high-rise building. In addition to the obvious goal of preventing such an explosion in the first place, constructing high-rise buildings that can withstand an explosion without structural failure should significantly reduce mortality. Other safeguards will help to prevent secondary and tertiary injuries. Currently, significant focus is being placed on design guidance, including site location, layout, building envelope and interior, and on the mechanical and electrical systems used in high-rise construction.When designing a new building, design guidance is provided for limiting or mitigating the effects of terrorist attacks. It is beyond the scope of this chapter to discuss each of these methods. The U.S. Federal Emergency Management Agency’s Web site (http://www.fema.gov) extensively describes

each of these strategies in their risk management series as of December 2003. Another critical element to have in place in the aftermath of a building explosion is a disaster plan that involves all medical and rescue personnel of a given area. Any city or large community must have a well-rehearsed disaster plan in place in case of a mass-casualty event.

POSTINCIDENT ACTIONS Immediately after a conventional explosion in a highrise building, there are three phases that need to be addressed. The first is the prehospital management, followed by the emergency department management, and finally, in-patient hospital management of the victims. Each of these will be addressed in this section. The prehospital management starts with the activation of the mass-casualty alert that makes local, state, and federal agencies as well as all medical personnel aware of a disaster event. The first aspect of the disaster that needs to be addressed is the scene itself. Secondary explosive devices designed to explode on a delay, and directed at the personnel trying to rescue the victims, are unfortunately very common in terrorist attacks.8 The safety of the remaining structure must also be assessed. Building collapse is always a significant risk during a bombing, and it is never acceptable to lose rescue workers when attempting to save victims. Once the building is as secure as possible, it is of utmost importance to quickly triage the victims according to standard protocols and determine which of them has life-threatening injuries. Prehospital and emergency department staff must be prepared to triage patients appropriately, as the more severely injured patients are not usually the first wave of patients seen. Scene triage and separate emergency department triage may be necessary to direct patients to the most appropriate venue for care and maximize use of resources. Prehospital personnel should expect to see familiar injuries including blunt, penetrating, and thermal injuries. After an explosion, all medical personnel need to maintain a high index of suspicion for primary blast injury. It is very important to evaluate the scene while performing rescue operations. Presence of a crater, injuries to closer victims, and building collapse are important observations regarding blast strength. Likewise, assessment of damaged objects near a casualty situation might yield a gross estimate of the pressures that existed in the vicinity. For example, shock waves able to rupture a tympanic membrane are about the same needed to shatter automobile glass.9 It is also important to get a quick history. Phillips and Zajtchuk10 recommend the following questions when evaluating a bombing casualty: • What type of ordinance was used? How large was the explosion? • Where was the casualty located with respect to the blast? • Did the blast occur inside an enclosed space, such as a room or vehicle?

• What was the casualty’s activity after exposure? • Were fires or fumes that might lead to an inhalation injury present? • What was the orientation of the casualty’s head and body in relation to the blast? Prehospital medical personnel should be ready to perform life-saving interventions, including intubations, resuscitations, field amputations, and chest decompressions, although the most common procedures performed are spinal immobilizations, field dressings, and intravenous fluid administration.11 Prehospital personnel should also be well equipped for the extrication of victims after complete or partial building collapse. Extricating these victims as quickly as possible greatly improves their chance of survival. The second phase of treatment occurs in the emergency department. It is very important for medical control to direct the prehospital personnel to the most appropriate emergency department. Designated trauma centers should receive the most severely injured patients, even if they are not the closest hospital. Once the patient reaches the emergency department, the emergency staff needs to be prepared for the many types of injuries occurring in a blast. Emergency staff must be prepared for victims to arrive by all modes of transportation, most of whom will have only minor injuries. In the Oklahoma City bombing, Hogan and colleagues11 report that 55% of victims came by private vehicle whereas only 33% came by emergency medical services transport; 80% were discharged that day. As soon as hospitals are made aware of an explosion, emergency staff must mobilize the equipment necessary to treat numerous victims. This includes wound care trays, tetanus immunizations, antibiotics, fracture care, endotracheal tubes, thoracostomy tubes, cricothyroidotomy trays, and medications for conscious sedation, rapid sequence induction, and advanced cardiac life support. It is also the role of the emergency physician to ensure that the hospital disaster plan goes into effect. This includes making sure trauma teams are aware of any incoming patients and that the hospital is ready to accommodate the many injured patients that will need rapid admission to the hospital. This will improve throughput in the emergency department and create space in the emergency department for incoming wounded. Preparing for this type of disaster includes drilling the plan by hospital staff, and the plan should be well known by all staff members. The importance of adequate communication from the scene and prehospital providers to hospitals and emergency departments about the number of victims and types of injuries cannot be overstated.

MEDICAL TREATMENT OF CASUALTIES The treatment of casualties after an explosion in a highrise building can be very challenging due to the different types of injuries seen and the pattern in which injured persons arrive at healthcare facilities. Healthcare professionals should be prepared for all three types of blast CONVENTIONAL EXPLOSION IN A HIGH-RISE BUILDING 771

injuries as well as flash injuries, thermal burns, and crush injuries. It is very important to properly triage patients who arrive from a blast event. The most common injuries are superficial, including abrasions and lacerations, and these patients are often the first group to present for care. The emergency physician must always be aware of the potential for primary blast injury and internal injuries that may present with delayed symptoms.When patients are examined, standard trauma protocols should be followed. For those patients with seemingly minor injuries,it is still necessary to do a thorough examination of the entire body. This will decrease the risk of missing an injury or any sign of an internal injury. Blast injuries differ from many other types of injuries because serious injuries may not manifest themselves immediately, particularly with primary blast injury, and careful observation of the patient is often necessary. Primary blast injury may result after any explosion but is amplified when it occurs in a building due to the enclosed surroundings. The management of primary blast injuries is discussed in more depth in earlier chapters in this section. Secondary blast injuries are caused from projectiles due to the blast. These types of injuries make high-rise building explosions different from other conventional blasts. With many of the high-rise buildings today made with significant amounts of glass and steel, projectiles traveling at a high speed are very dangerous. It is these types of injuries that are most often seen in the emergency department. This is because the shrapnel that comes from a high-rise building can reach victims well outside the reach of the primary blast zone. During the Oklahoma City bombing, glass laceration injuries occurred as far as 10 blocks from the explosion. The most important thing to remember when treating patients with lacerations is to rule out other more serious injuries. Once more serious injuries have been ruled out, lacerations should be treated as time and resources allow. Delayed closure should be used if resources aren’t available to treat both the critically ill and those with minor injuries. Injury to the eye often results from secondary blast injuries and should not be overlooked. Of the surviving victims of the Oklahoma City bombing, 8% sustained eye injuries, including lid lacerations, open globe injuries, orbital fractures, corneal abrasions, retinal detachment, and intraocular foreign bodies.12 The most worrisome type of secondary blast injury is the penetrating injury. Every part of the building and its contents has the ability to become shrapnel moving at high velocity. Victims with penetrating injuries should be treated promptly and with the involvement of the surgical trauma team. As with all penetrating injuries, the practitioner should be ready to treat hemorrhagic shock. In a stable patient, deep penetrating shrapnel should only be removed in a safe, controlled environment, usually the operating room. Penetrating injuries are obvious; however, blunt trauma must not be overlooked. Blunt trauma can occur from secondary or tertiary blast injury after a high-rise explosion. Severe entrapment or crush injuries are rare

772 EVENTS RESULTING IN BLAST INJURIES

in survivors but may be seen in the emergency department. Patients with crush injuries are at risk for amputation, compartment syndrome, and rhabdomyolysis. These patients should be treated according to standard trauma protocols. Flash burns and thermal injuries are usually superficial injuries and should be treated with standard burn care.

CASE PRESENTATION It is 9:30 AM, and you are the only attending physician working at the only level one trauma center in a small rural city. You receive a call from emergency medical services alerting you that there was just a large explosion from the ground floor of a commercial bank building. The building is made mostly of steel and glass. It is 22 stories high, and there are approximately 650 persons in the building. You are providing medical control for the paramedics. What do you tell them? What do you need to do immediately with regard to your emergency department and hospital staff? Who else should be notified? What type of injuries do you expect to see, and what special equipment will you need to treat these injuries?

UNIQUE CONSIDERATIONS Preparing for a conventional bombing in a high-rise building is a difficult task because of the large variety of injuries seen and the great numbers of victims. Unique to these types of attacks is the pattern in which patients arrive. The first wave of patients is usually the furthest from the blast. These are usually secondary blast injuries, most of which are minor. The second wave of patients is usually the most critical. Another consideration in the explosion of a high-rise explosion is the presence of toxic substances, which may necessitate decontamination of victims and rescuers. A final consideration is emergency department patient flow. A triage system needs to be in place that will properly direct the large flow of injured victims.

PITFALLS Several potential pitfalls in response to an explosion in a high-rise building exist. These include the following: • Failure to make sure the building is secure and safe for rescue personnel • Failure to have a rehearsed disaster plan in place for a mass-casualty incident involving an explosion in a high-rise building • Underestimation of the severity of injuries sustained by victims as a result of a conventional explosion in a high-rise building

REFERENCES 1. Federal Bureau of Investigation Bomb Data Center. General Information Bulletin 96-1: 1996 Bombing Incidents. Washington, DC: US Department of Justice; 1996. 2. Mallonee S, Shariat S, Stennies G, et al. Physical injuries and fatalities resulting from the Oklahoma City bombing. JAMA 1996; 276:382-7. 3. Schwartz SP, Li W, Berenson L, Williams RD. Deaths in World Trade Centers Terrorist Attacks: September 11th, 2001. MMWR 2002;51:16-8. 4. Hirschkorn P. New York reduces 9/11 death toll by 40. October 29, 2003. Available at:. www.cnn.com/2003/US/ Northeast/ 10/29/wtc.deaths 5. Centers for Disease Control and Prevention. Rapid assessment of injuries among survivors of the terrorist attack on the World Trade Center—New York City, September 2001. MMWR 2002;51:1-5.

6. Phillips YY. Primary blast injuries. Ann Emerg Med. 1986;15: 1446-50. 7. Adler OB, Rosenberger A. Blast injuries. Acta Radiol. 1988;29:1-5. 8. Boffard KD, Macfarlane C. Urban bomb blast injuries: patterns of injury and treatment. Surg Ann. 1993;25:29-47. 9. Wightman JM, Gladish SL. Explosions and blast injuries. Ann Emerg Med. 2001;37:6. 10. Phillips YY, Zajtchuk JT. The management of primary blast injury. In: Bellamy RF, Zajtchuk R, eds. Conventional Warfare: Ballistic, Blast, and Burn Injuries. Washington, DC: Office of the Surgeon General of the US Army; 1991:295-335. 11. Hogan DE, Waeckerle JF, Dire DJ, et al. Emergency department impact of the Oklahoma City terrorist bombing. Ann Emerg Med. 1999;34:160-7. 12. Mines M, Thach A, Mallonee S, et al. Ocular injuries sustained by survivors of the Oklahoma City Bombing. Ophthalmology 2000;107:837-43.

CONVENTIONAL EXPLOSION IN A HIGH-RISE BUILDING 773

chapter 150

Conventional Explosion at a Nuclear Power Plant Michelle McMahon-Downer

DESCRIPTION OF EVENT Since the attack on the World Trade Center in New York City on Sept. 11, 2001, there has been increased worldwide concern over the safety of nuclear power plants. In the United States, there are over 100 such plants.1 Security has been heightened around nuclear power plants. Barricades are in place and armed guards are present.2 All commercial nuclear power plants in the United States house the reactor core in a thick stainless steel vessel within a concrete building.3 Nonetheless, studies have shown that if a jet aircraft crashed into a nuclear reactor and only 1% of its fuel ignited after impact, the resulting explosion could compromise the integrity of the reactor core containment building. Thus, these reactor core containment buildings, although designed to withstand impacts, are certainly destructible and vulnerable to largescale explosions. Nuclear power plants harbor additional radioactive materials in the form of spent fuel pools. The spent fuel pools are housed in corrugated steel buildings, which are much more vulnerable to attack than the reactor core containment structure.4 An example of a conventional explosion at a nuclear power plant took place at Chernobyl Nuclear Power Plant in 1986. An accidental steam explosion during a safety test destroyed the reactor core. An atmospheric plume of radioactive substances was released into the environment during the explosion and fire.5 Approximately 600 persons were hospitalized within a week due to injuries and ailments linked to the Chernobyl explosion.6 Two died the first day as a result of trauma, combined with thermal burns and irradiation.7 One hundred thirty-four persons were confirmed to have acute radiation sickness. Twentyeight of those with acute radiation sickness died within the first 3 months, and 14 died in subsequent years.8 Nineteen of the 28 who died in those first 3 months had severe radiation skin injuries that complicated their course of treatment in the hospital.7 At the time of the explosion, approximately 100,000 persons lived within a 30-km radius around Chernobyl Nuclear Power Plant. When the explosion occurred, radioactive substances were released into the atmosphere and continued to do so for 10 days, until the fire was 774

finally contained. Winds and rainfall distributed the radioactive substances throughout the northern hemisphere, with the highest concentration around the power plant in the former U.S.S.R. Contamination of the area around the power plant was patchy in that distribution of the fallout depended largely on where it happened to rain. The volatile radioisotopes of iodine and cesium were the most important in terms of health risk.6 Radioactive iodine has a half-life of just 8.05 days, but radioactive cesium has a half-life of approximately 30 years.5,7 A total of 350,400 persons were resettled due to concerns over contamination caused by the Chernobyl explosion.5 Long-term effects of exposure to radiation, mainly carcinogenesis, are being seen in the population affected by the Chernobyl explosion. A clear association has been made between exposure to radiation and thyroid cancer, especially in children.5 An increase in the incidence of leukemia in Russian clean-up workers has been seen, and Ukrainian scientists have indicated that there is an increase in other solid cancers (e.g., breast, lung, urologic) among the inhabitants of contaminated areas and clean-up workers.8

PREINCIDENT ACTIONS Each nuclear power plant is required to have an emergency response plan,as are the local and state government agencies in which the power plant is housed. Some federal agencies have emergency response plans in the event of a power plant explosion.1 Control and command procedures must be clarified before an incident occurs, as must organizational responsibilities. Assessment of type and quantity of materials and equipment needed, along with decontamination plans and healthcare worker protection, should be addressed. Location of Geiger meters and other radiation survey instruments should be posted along with reference material on what the various readings mean in terms of patient care. An adequate supply of potassium iodide to combat exposure to radioactive iodine should be available for the entire affected population.3 Each community surrounding a nuclear power plant should have a designated person who makes decisions

about evacuation and other issues concerning the potentially exposed population. Communication during the incident is of vital concern, and emergency communication systems must be tested in advance.3 There are two emergency planning zones—the first is within a 10-mile radius of the event, where the threat of direct radiation is highest, and the second is within a 50-mile radius, where the radioactive plume is the biggest threat to residents. A warning system, such as sirens or flashing lights, is required to be provided by the nuclear power plant to alert all inhabitants within a 10-mile radius of an event. Each year, the nuclear power plant is required to distribute emergency information materials to all people who live within a 10-mile radius so that, in the event of an explosion, the public in the vicinity of the plant are prepared.1 Every hospital, regardless of the proximity to a nuclear power plant, should have a radiation control officer. This officer is responsible for monitoring all patients and medical personnel with radiation counters, supervising clean-up of the potentially radioactive waste, and devising a plan to minimize contamination. Training for physicians to prepare for a disaster involving radiation exposure is offered by the Radiation Emergency Assistance Center/Training Site, which can be contacted by phone at 1-865-576-1005.3 The World Health Organization suggests that the general population, particularly those in the vicinity of nuclear power plants, be prepared for a nuclear incident. One recommendation is that they become aware of possible solid shelter areas in the local area. A second is to have disaster supplies on hand; these include food and water for 3 to 5 days, a first-aid kit, respiration protection, flashlights and batteries, a battery-operated radio with extra batteries, and stable iodine.9

POSTINCIDENT ACTIONS Immediately after a conventional explosion at a nuclear power plant, the local emergency personnel will be activated. The disaster area must be designated as safe for these personnel to enter. Geiger counters and other devices used to detect radiation should be used. If the level is 0.1 Gy/hour or above, emergency personnel should not enter the area and should return to the control point until further notice. Specialized protective equipment is needed to enter the area safely. As with any mass-casualty event, on-scene triage should be performed. Those with life-threatening injuries are to be taken directly to the hospital.3 For these patients, emergency personnel are to use gloves and gowns, remove the patients’ clothes, cover their hair with surgical caps if available, and wrap the patients in sheets for transport. Simply removing the clothes reduces the patient’s contamination by approximately 80%.10 Those who are uninjured or suffering from minor injuries should be relocated upwind, and decontamination should be performed. Decontamination in these situations consists of removing the victim’s clothes and placing them in hazardous material bags and washing

the person’s skin and hair with soap and warm water.11 All those with nausea, vomiting, diarrhea, or rash should be referred to the emergency department for evaluation of possible acute radiation syndrome.3 In mass-casualty situations, approximately 80% of victims are decontaminated at hospitals; thus, the hospital facility must be prepared to decontaminate patients both inside and outside the emergency department.10 For those whose conditions are stable, decontamination should be done immediately, and if possible, it should be done outside of the hospital. Those who must be brought into the emergency department immediately should be treated in an area roped off from the rest of the department. Hospital personnel should wear disposable clothing, gowns, gloves, and shoe covers when treating these patients.12 The radiation control officer is responsible for monitoring the exposure of hospital staff. Personnel involved with care of contaminated patients should wear dosimeters to monitor radiation exposure.10 The dose limit for persons providing emergency services other than lifesaving actions is 5 rem per event, whereas for lifesaving activities the recommended maximum dose is 25 rem per event. In the event of a disaster, the recommended limit increases to 150 rem per event.3 The U.S. Federal Bureau of Investigation is the lead federal agency during crisis management, that is, during the period when the focus is on ensuring that there is no further threat and establishing the site of attack as a crime scene. The Federal Emergency Management Agency takes the lead during consequence management, where the focus is on limitation of damage, protection of the public, decontamination, and disposal of the radioactive material. These two agencies will be lead coordinating organizations and should be contacted with questions. Also, the Radiation Emergency Assistance/ Training Site should be contacted with any concerns via telephone (1-865-576-1005) or via their interactive Web site (http://www.orau.gov/reacts).3

MEDICAL TREATMENT OF CASUALTIES A conventional explosion at a nuclear power plant will lead to a variety of injuries. Blast, thermal burns, and smoke inhalation will be responsible for most immediate deaths. Radiation injuries will include whole-body or localized exposure (i.e., irradiation) and internal deposition of radioactive substances (i.e., contamination).12 Whole-body irradiation by gamma rays can lead to acute radiation syndrome. The most susceptible cells to radiation damage are rapidly dividing cells such as those in the intestinal mucosa and bone marrow.3 However, with massive irradiation, even the central nervous system, with its relatively low cellular turnover rate, will show the effects.12 The degree of whole-body radiation exposure is estimated using clinical signs and symptoms, the minimal lymphocyte count within the first 48 hours, the severity of thrombocytopenia and reticulocytopenia, and cytogenic studies looking for chromosomal CONVENTIONAL EXPLOSION AT A NUCLEAR POWER PLANT 775

abnormalities in bone marrow and red blood cells.3,12 Lymphocytes are the most radiosensitive cells in the blood, and a substantial dip is apparent within the first 8 to 12 hours.13 The faster the fall and the lower the nadir of lymphocytes, the greater the whole-body radiation dose.3 Furthermore, the sooner the onset of signs and symptoms for each phase of radiation illness, the greater the whole-body irradiation.1 Nausea, vomiting, diarrhea, and rash are the first presentation after gamma irradiation. Later, the clinical manifestations of acute radiation syndrome are related to the level of leukocytes and platelets (Table 150-1). Fever, infections, and hemorrhaging occur. Also, with sloughing of the intestinal mucosal surface, mucositis and enteritis occur.3 In addition to the whole-body, uniform irradiation discussed above, the skin is susceptible to local radiation injury. The distribution tends to be nonuniform, and the skin radiation dosage absorbed is estimated to be 10 to 20 times greater than the bone marrow doses. The signs of a radiation burn are very similar to those of a thermal burn, with the difference being that the signs of radiation burns appear after a period of days in contrast to thermal burns, where the results appear immediately.3 In the Chernobyl explosion, a period of primary erythema was seen in the first few days, followed by a 3- to 4-day period of latency. In severe cases, secondary erythema and the full extent of the burn manifested as early as 5 to 6 days and as late as 3 weeks in milder cases. The most frequent locations early on were the wrists, face, neck, and feet. As time went on, burns were also seen on the chest and back, and later on the knees, hips, and buttocks.12 Vascular insufficiency can develop at any time after the radiation exposure, even years later, with necrosis occurring. Treatment includes control of pain, vasodilator therapy, and prophylaxis against infection.3 Surgery and plastic surgery consultants should be involved because extensive debridement, skin grafting, and amputation are often required.14 Burns to the eyelids and eyes are often seen, requiring ophthalmology consultation. Internal contamination occurs through inhalation, ingestion, and absorption through open wounds. Inhalation can lead to radiation pneumonitis. Early bronchopulmonary lavage may be helpful in removing some of

TABLE 150-1

SYMPTOMS

>30

Hypotension, high fever, mental status change, syncope, seizures Immediate nausea, vomiting, diarrhea Delayed (by hours) nausea, vomiting, diarrhea

4–10 2–4 10

the radioactive contaminants. Chronic low-level inhalation of radioactive substances is more common and was seen among those involved in the clean-up efforts from the Chernobyl explosion. Radiation fibrosis was seen,and treatment with interferon was of some benefit.12 Ingestion of radioactive substances is either treated with specific antidotes and/or general measures to decrease absorption, both of which should be instituted as soon as possible after exposure. Specific antidotes include blocking agents that saturate a tissue with a nonradioactive element, thus reducing the uptake of the radioisotope, and chelating agents that bind metals into complexes, preventing tissue uptake and allowing urinary excretion.12 As in all poisonings, the local or regional poison control center should be contacted.3 Contaminated wounds should be rinsed with saline until the Geiger meter reads no evidence of radioactive material. If the patient has received a dose of whole-body radiation that leads to decreased lymphocyte count (above 1 to 2 Gy to the bone marrow), the wound should be closed as soon as possible to decrease the chance of the wound serving as a portal of entry for infection.3 Surgical debridement is necessary for the usual indications of dirt and nonviable tissue as well as for continued high readings of radioactive contamination despite saline rinses.12

Delayed (by days) nausea, vomiting, or no symptoms Less than 10% with delayed (by days) nausea and vomiting

TPN,Total parenteral nutrition.

776 EVENTS RESULTING IN BLAST INJURIES

LYMPHOCYTE NADIR

TREATMENT

2

Oil Gasoline Petroleum Petroleum

29 3

Gasoline Oil

7 12 2 26

2 167

122

2

161 45 >60 82

76 >43 26

15,000

60 1 35 42

2 16 >100

>1,000

30,000 430 153 26

48 2 26 350 500 17 35

33

37

60 220 100

130 23

89 51

12,000

40,000 25,000

2,500

PCBs, polychlorinated biphenyls. Data from United Nations Environment Programme. Awareness and Preparedness for Emergencies on a Local Level Disasters Database. Available at: http://www.uneptie. org/pc/apell/disasters/lists/disasterloc.ht (accessed October 2005).

chemical that requires specific treatments and antidotes. Patients should be immediately removed from the area and be evaluated for signs of respiratory decompensation as a result of pulmonary edema, pneumonitis, pul788 EVENTS RESULTING IN BLAST INJURIES

monary hemorrhage, or systemic toxicity. Administering 2.5% or 3% calcium gluconate inhalational solution by nebulizer as a therapy has been suggested for respiratory exposures. Treatment of hydrofluoric acid dermal

injury consists of immediate irrigation with copious amounts of water for at least 15 to 30 minutes, removal of all blisters because they may harbor fluoride ions, and calcium gluconate (2.5%) gel applied to the debrided skin surface. Systemic toxicity from hydrofluoric acid exposure can cause dysrhythmias and hypocalcemia, thus warranting cardiac and electrolyte monitoring. A 10% calcium gluconate solution should be administered intravenously or intra-arterially in patients exhibiting significant hydrofluoric acid systemic toxicity. Ammonia is another compound that is found throughout the refining process. Ammonia is widely used as a cleaning agent and as a coolant. The release of ammonia causes injury to the patient in two ways: (1) because of its low freezing point (−33°C), frostbite injury occurs to any skin in direct contact; and (2) ammonia vapors readily dissolve in the moisture of the skin, eyes, and mucosa, causing chemical burns through liquefaction necrosis. Exposures require prompt irrigation of the eyes and skin with water and management of inhalation injury.

CASE PRESENTATION A mist develops after a pipe rupture at an oil refinery. Multiple workers at the plant begin complaining of cough, sore throat, and difficulty breathing. Disaster plan management is implemented, and emergency medical services are called into action. Plant supervisors notify personnel that the pipe delivers hydrofluoric acid. Prehospital healthcare workers are notified to use personal protective equipment. Patients are treated with nebulized calcium gluconate solutions, and the evacuation of potential personnel and the surrounding community is initiated. The pipe is later repaired, and the hydrofluoric acid spill is contained and dissipates.

UNIQUE CONSIDERATIONS A common scenario in a petroleum industry disaster is the explosion of oil and gasoline drums. Bak and colleagues21 reported a series of incidents where these containers were inappropriately handled. The typical scenario was that in which a worker attempted to divide or cut through a presumably empty 55-gallon drum with a grinder or a blowtorch. These drums often contain residual quantities of flammable material in liquid or vapor form. Once the container is penetrated, the metal drum explodes. Nearby workers suffer from significant trauma from projectiles, the blast force, and burns.

PITFALLS Many different and potentially toxic chemicals are used throughout a petrochemical refinery. When a refining column is damaged as in an explosion, lighter components are released. These hydrocarbons composed of

fewer carbon and hydrogen atoms vaporize, leaving behind a heavier, less volatile fraction. Gasoline contains relatively high proportions of toxic and volatile hydrocarbons, such as benzene (which is known to cause cancer in humans) and hexane (which can affect the nervous system). Gasoline and kerosene releases are exceptionally hazardous due to their high flammability. Crude oils and semirefined products such as diesel and bunkering oils may contain cancer-causing polycyclic aromatic hydrocarbons and other toxic substances. These differing chemicals have various thresholds for combustion, and multiple explosions can occur at differing times. This poses a serious threat to healthcare workers who arrive on the scene after the initial incidents.

REFERENCES 1. Snodgrass WR. Petroleum industry. In: Greenberg MI, Phillips SD, eds. Occupational, Industrial, and Environmental Toxicology. 2nd ed. St Louis, Mo: Mosby; 2003. 2. U.S Environmental Protection Agency. Types of petroleum oil. 2004. Available at: http://www.epa.gov/oilspill/oiltypes.htm. 3. Yapa PD, Zheng L, Chen F. A model for deepwater oil/gas blowouts. Mar Pollut Bull. 2001;43:234-41. 4. Leese WL. Some medical aspects of North Sea oil industry. Scott Med J. 1977;22:258-66. 5. Gabbay DS, De Roos F, Perrone J. Twenty-foot fall averts fatality from massive hydrogen sulfide exposure. J Emerg Med. 2001;20:141-4. 6. Trevino MA, Herrmann GH, Sprout WL. Treatment of severe hydrofluoric acid exposures. J Occup Med. 1983;25:861-3. 7. Dayal HH, Brodwick M, Morris R, et al. A community-based epidemiologic study of health sequelae of exposure to hydrofluoric acid. Ann Epidemiol. 1992;2:213-30. 8. Harrison BF. Blast resistant modular buildings for the petroleum and chemical processing industries. J Haz Mater. 2003;104:31-8. 9. Skrbic B, Miljevic N. An evaluation of residues at an oil refinery site following fires. J Environ Sci Health Part A Tox Hazard Subst Environ Eng. 2002;37:1029-39. 10. Skrbic B, Novakovic J, Miljevic N. Mobility of heavy metals originating from bombing of industrial sites. J Environ Sci Health Part A Tox Hazard Subst Environ Eng. 2002;37:7-16. 11. Attias L, Bucchi AR, Maranghi F, et al. Crude oil spill in sea water: an assessment of the risk for bathers correlated to benzo(a)pyrene exposure. Cent Eur J Public Health. 1995;3:142-5. 12. Hull AM, Alexander DA, Klein S. Survivors of the Piper Alpha oil platform disaster: long-term follow-up study. Br J Psychiatry. 2002;181:433-8. 13. Alexander DA. Burn victims after a major disaster: reactions of patients and their care-givers. Burns 1993;19:105-9. 14. Campbell D, Cox D, Crum J, et al. Initial effects of the grounding of the tanker Braer on health in Shetland. The Shetland Health Study Group. BMJ. 1993;307:1251-5. 15. Crum JE. Peak expiratory flow rate in schoolchildren living close to Braer oil spill. BMJ. 1993;307:23-4. 16. Dayal HH, Baranowski T, Li YH, et al. Hazardous chemicals: psychological dimensions of the health sequelae of a community exposure in Texas. J Epidemiol Community Health. 1994;48:560-8. 17. Palinkas LA, Petterson JS, Russell J, et al. Community patterns of psychiatric disorders after the Exxon Valdez oil spill. Am J Psychiatry. 1993;150:1517-23. 18. Qiao B. Oil spill model development and application for emergency response system. J Environ Sci (China). 2001;13:252-6. 19. Qiao B, Chu JC, Zhao P, et al. Marine oil spill contingency planning. J Environ Sci (China). 2002;14:102-7. 20. Li J. A GIS planning model for urban oil spill management. Water Sci Technol. 2001;43:239-44. 21. Bak B, Juhl M, Lauridsen F, et al. Oil and petrol drum explosions: injuries and casualties by exploding oil and petrol drums containing various inflammable liquids. Injury 1988;19:8-5.

PETROLEUM DISTILLATION/PROCESSING FACILITY EXPLOSION 789

S E C T I O N

T W E L V E

Events Resulting in Burn Injuries

chapter 155

Introduction to Fires and Burns Marianne E. Cinat and Victoria M. Vanderkam

Burn injuries are commonly seen in disasters. In addition to being associated with structure fires, they may also occur in conjunction with explosions; wild land fires; plane, train, or automobile crashes; or other serious events. Injuries may be the result of flame, flash, chemicals, or electricity. More recently, there has been increased concern about nuclear, biologic, and chemical warfare disaster management, all of which can result in significant burn injury to a large number of victims. Burn injury can involve only the skin or may have an inhalational component resulting from heat exposure to the face and upper airway or from smoke inhalation causing damage to the distal airways and bronchial tree. Burn injury with inhalation may result in rapid loss of airway and shock. Immediate triage and resuscitation are essential to survival and optimal outcomes.Many authors have described burn injuries associated with major disaster. Recent events and lessons learned will be reviewed.

CURRENT PRACTICE Preincident Action: Disaster Planning Firefighters, rescue workers, and emergency medical personnel should have a good working knowledge of the treatment of burns. Disaster preparedness in a specific geographic area should include a plan to triage burn victims to burn centers in the area that are equipped for and experienced in handling critically injured patients. Burn care should be prioritized as a curriculum item for instruction to emergency medical services (EMS) workers including emergency medical technicians, paramedics, and firefighters. All EMS responders should be aware of the nearest burn center as well as nearest receiving centers. Collaboration among burn centers should be proactive.Working relationships among centers with specific plans and transfer agreements will be effective in ensuring the triage and early care of burn victims. Burn centers must be prepared to receive multiple burn patients that may have other associated injuries.

Prehospital Management of the Incident The American Burn Association (ABA) endorses the Advanced Burn Life Support course curriculum.A section 790

of this course is devoted to the management of multicasualty burn incidents as well as scene safety with fire hazards.1 Excerpts of this course are provided in Boxes 155-1, 155-2, and 155-3. Organizational components for incident management by all responding units are listed in Box 155-1. The triage area should have adequate lighting and be located in an area where the triage officer can visualize the entire scene. It should be located away from hazards, at a site between the scene of the incident and transport vehicles. Four treatment categories are recommended and are summarized in Box 155-2. Stabilization in the field is managed by EMS using protocols and communication with base hospitals. Airway control is the top priority. The airway should be established and maintained with endotracheal intubation based on local protocols. In general, burn patients without other injuries typically do not go into shock within 60 minutes from the time of injury, even if no treatment is provided.1 Therefore, a burn victim who develops shock soon after an incident should be evaluated immediately for underlying injury, occult hemorrhage, respiratory failure, or other causes of shock (e.g., cardiac, neurologic). Masellis and others2 provide guidelines for the general public regarding immediate first aid in the care of burn victims.They are as follows: 1. 2. 3. 4. 5. 6. 7.

Maintain self-control—don’t panic. Protect yourself. Reduce the activity of the fire. Extract and transfer victims to open air if possible. Extinguish burning clothing. Remove burning clothing. Provide emergency treatment of burns. a. Thermal burns: Leave blisters intact. Cool the burn for up to 10 minutes. Avoid hypothermia. Cover body with dry, clean sheet. Avoid ointments or other medications. b. Chemical burns: Flush the exposed area with water thoroughly. Collect detailed information about the chemical agent, and be prepared to provide this information to the emergency medical personnel. c. Electrical burns: Remove the source of electricity and protect the airway.

BOX 155-1 BURN DISASTER MANAGEMENT A. The medical command post should: 1. Be established in a safe area. 2. Serve as the communication center for dispatch and medical control. B. Security and hazard control: 1. Should minimize risks of injury to rescuers and onlookers. 2. Is coordinated at the medical command post. 3. Are the responsibility of all members of the rescue team. 4. Should ensure crowd and hazard control. C. A communication center at the medical command post should: 1. Communicate patient information to incident managers, including the number of victims and their condition. 2. Ensure casualty distribution to appropriate facilities. 3. Communicate to the receiving facility the number of casualties and treatment provided. Reproduced from Advanced Burn Life Support–Pre-Hospital Course Manual. Chicago:American Burn Association; 2001:19–20, with permission.

BOX 155-2 TRIAGE TREATMENT CATEGORIES 1. Immediate care (red) a. Burns >20% TBSA in patients aged 10 to 50 years b. Burns >10% TBSA in patients aged 50 years c. Inhalation injury d. Chemical injury e. Electrical injury f. Associated, life-threatening injuries 2. Delayed care (yellow) a. Burns 120/minute) Macroscopic abnormal urine findings White blood cell count Hyperkalemia

Hemodialysis machines and filters, together with nephrologists, nurses, and technicians, should arrive within 24 to 36 hours as national and international resources are mobilized. Emergency dialysis units should be set up in easily accessible areas to avoid problems of transportation for those patients who may have other serious injuries requiring major surgery. On-scene doctors treating disaster victims can consult with remote renal experts using telemedicine or Internet linkages for advice on treating particularly complex cases. Decisions about which type of dialysis modalities to use should take into account the hypercatabolic state of the victims, the degree of electrolyte disturbances, the presence of polytrauma and bleeding tendency, as well as specific geographic and local conditions, transport problems, and other logistic difficulties. Conventional hemodialysis allows for efficient solute removal, treatment of multiple patients, and application without anticoagulants. Peritoneal dialysis is difficult to administer in patients with abdominal trauma and often is inefficient for

removal of potassium and other catabolic metabolites. It might offer temporary help, however, especially during disaster scenarios where conventional hemodialysis equipment is not ready available.9

MEDICAL TREATMENT OF CASUALTIES The treatment of crushed casualties should begin as soon as they are discovered. Attention should be given to the possibility of concomitant injury such as fractures, solid organ damage, or spinal injury. Intravenous access should be obtained with large-bore intravenous catheters, and the patient should receive fluid as soon as possible.10–12 Multiple intravenous lines are necessary because these patients require large fluid volumes and individual intravenous lines may be dislodged during extrication. Normal saline is an appropriate initial choice for intravenous fluid resuscitation. A saline infusion of 1000 to 1500 mL/hour should be initiated during extrication. When a urine flow has been established, a forced mannitol-alkaline diuresis up to 8 L/day should be maintained (urine pH > 6.5). Once the patient reaches the hospital, 5% dextrose should be alternated with normal saline to reduce the potential sodium load. Since large volume of intravenous fluids may not be available in the first 2 days after a major incident,it is reported that hypertonic saline is also safe and effective in a variety of trauma patients.13 Placement of a Foley catheter is also recommended to have accurate measurements of urine output. Alkalinization increases the urine solubility of acid hematin and aids in its excretion. This may protect against renal failure and should be continued until myoglobin is no longer detectable in the urine. In addition to its protective effect as an osmotic diuretic, mannitol also is an effective scavenger of oxygen free radicals and may help reduce the reperfusion-related components of this injury by this mechanism.4,6 At hospital admission, electrolytes, arterial blood gases, and muscle enzymes should be measured. Performing a simple dipstick test on the urine for hemopositivity in the mildly injured patients can diagnose subclinical rhabdomyolysis and can be useful in identifying this critical condition. If these patients are discharged because of a limitation of facilities, they should be advised to check the color and the volume of their urine daily and to watch for other symptoms of ARF such as weight gain and edema.1 The outcome of the renal victims of catastrophic earthquakes is influenced by the type of trauma, concomitant events, and complications observed during the clinical course as well as epidemiologic features such as age, distance to reference hospitals, and time elapsed between disaster and admission to reference hospitals.14 The earlier one starts intravenous therapy, the better the chance of preventing ARF. When fluid therapy is delayed for 6 hours after extrication, ARF is almost ensured. If the desired urinary output cannot be achieved, the use of diuretics, preferably furosemide, should be considered. The majority of crush injury victims who do not receive intravenous therapy early enough and who do not

818 EVENTS ASSOCIATED WITH STRUCTURAL COLLAPSE/CRASHING/CRUSHING

respond to forced alkaline diuresis go on to develop renal failure and the requirement for hemodialysis.15 There are case reports of hyperbaric oxygen improving the outcome of victims of crush injury.16,17 The use of this modality is obviously limited in disaster situations because of lack of access to hyperbaric chambers.

• • • •

Delayed treatment after the victim extrication Delay in starting intravenous fluids Low index of suspicion for crush injuries Failure to continue the monitoring of patients with a high risk for ARF

REFERENCES

CASE PRESENTATION You are the physician of an emergency medical services ambulance. You are attending a victim of building collapse. You have already assessed the patient’s airway, breathing, and circulation, and you are coordinating with rescue personnel.Which is your next priority?

• • • •

Notify 9-1-1 dispatch center and obtain directions. Consider amputation as soon as possible. Use tourniquets as a treatment of wounds. Obtain multiple intravenous lines and start fluid infusion. • Perform field fasciotomy. Note:To obtain multiple intravenous lines, reduce the possibility of the lack of intravenous access during extrication procedures and allow intravenous effusion of larger amounts of normal saline to prevent ARF and hemodialysis.

UNIQUE CONSIDERATIONS There is no doubt that the majority of deaths occur immediately after structural collapse or a catastrophic event, such as an earthquake.18 And among those still alive, short-term mortality dramatically increases as the time the persons are buried under the rubble lengthens. During the first few hours, a not inconsiderable number are still alive. After 24 hours the survival curve starts to fall more steeply, and after 5 days all those not recovered are dead. Disaster medical plans should comprise a medical care chain in which casualties receive life-supporting measures at the accident scene, with subsequent transport to hospital for more definitive care within a few hours of their rescue. The development of crush syndrome after crush injury is preventable and treatable. Crush injury patients may present with few signs or symptoms; hence, medical personnel must maintain a high index of suspicion in treating crush victims.

1. Sever MS, Erek E, Vanholder R, et al. Clinical findings in the renal victims of a catastrophic disaster: in the Marmara earthquake. Nephrol Dial Transplant. 2002;17:1942–9. 2. Visweswaran P, Guntupalli J. Rhabdomyolysis. Crit Care Clin. 1999;15:415–28. 3. Bywaters EGL, Beall D. Crush injuries with impairment of renal function. BMJ 1941;1:427–32. 4. Better OS. Rescue and salvage of casualties suffering from the crush syndrome after mass disasters. Military Med. 1999; 164:366–9. 5. Erek E, Sever MS, Serdengeçti K, et al. An overview of morbidity and mortality in patients with acute renal failure due to crush syndrome: the Marmara earthquake experience. Nephrol Dial Transplant. 2002;17:33–40. 6. Smith J, Greaves I. Crush injury and crush syndrome: a review. J Trauma. 2003;54:S226–30. 7. Schulz CH, Di Lorenzo RA, Koenig KL, et al. Disaster medical direction: a medical earthquake response curriculum. Ann Emerg Med. 1991;20:470–1. 8. Benson M, Koenig KL, Schultz CH. Disaster triage: START, then SAVE—a new method of dynamic triage for victims of a catastrophic earthquake. Prehospital Disaster Med. 1996;11:117–24. 9. Vanholder R, Sever MS, Erek E, et al. Rhabdomyolysis. J Am Soc Nephrol. 2000;11:1553–61. 10. Better OS, Stein JH. Early management of shock and prophylaxis of acute renal failure in traumatic rhabdomyolysis. N Engl J Med. 1990;322:825–9. 11. Better OS and Rubinstein L. Management of shock and acute renal failure in casualties suffering from crush syndrome. Ren Fail. 1997;19:647–53. 12. Noji EK. Prophylaxis of acute renal failure in traumatic rhabdomyolisis. N Engl J Med. 1990;323:550–1. 13. Vassar MJ, Fisher RP, O’Brien PE, et al. A multicenter trial for resuscitation of injured patients with 7.5% sodium chloride: the effect of added dextran 70: the Multicenter Group for the Study of Hypertonic Saline in Trauma Patients. Arch Surg. 1993; 128:1003–11. 14. Sever MS, Erek E,Vanholder R, et al. Lessons learned from the catastrophic Marmara earthquake: factors influencing the final outcome of renal victims. Clin Nephrol. 2004;61:413–21. 15. Castañer Moreno J. Insuficiencia renal aguda postraumática. Rev Cubana Med Milit. 1999;28:41–8. 16. Siriwanij T,Vattanagomgs V, Sitprija V. Hyperbaric oxygen therapy in crush injury. Nephron 1997;75:484–5. 17. James PB. Hyperbaric oxygen treatment for crush injury. BMJ 1994;309:1513. 18. Pointer JE, Michaelis J, Saunders C, et al. The 1989 Loma Prieta earthquake: impact on hospital patient care. Ann Emerg Med. 1992;21:1228–33.

PITFALLS Several potential pitfalls in response to a structural collapse exist. These include the following: • Failure to plan evacuation routes prior to an event • Failure to know who is in command of disaster operations within your local area

INTRODUCTION TO STRUCTURAL COLLAPSE (CRUSH INJURY AND CRUSH SYNDROME) 819

chapter 163

Train Derailment J. Scott Goudie

DESCRIPTION OF EVENT Railroads provide a vital means of transportation for both passengers and industrial products. The high-volume and varied nature of cargo carried means that railway disasters are an ever-present risk that make possible a wide variety of situations, as demonstrated by past events: • a high-speed passenger train derailment in the rural Southwest1 • a train derailment and hazardous material spill in rural North Dakota2 • a collision of two commuter trains in Chicago3 • a freight train derailment with subsequent hazardous material spill and fire in downtown Baltimore4 Each situation presents its own unique problems, whether it is a remote accident scene, a high-volume of patients, or a hazardous material spill potentially affecting those on the train, those living nearby, and emergency personnel responding to the scene. Although most railway disasters are unintentional, arising either from human error or equipment failure, railways remain prominent targets for terrorism, as demonstrated by the Madrid subway bombings in March 2004. The many miles of railroads crossing the United States make it extremely difficult to provide security for every stretch of track, thus providing a potentially soft target for terrorists.

PREINCIDENT ACTIONS To respond effectively to a train derailment, hospitals, emergency departments, emergency medical services, and fire departments should all develop disaster response plans for mass-casualty and hazardous material disasters. These plans must also be supported by the proper equipment and training with regular tabletop and live disaster drills. A well-established system of communication and coordination between all local emergency services is vital, as well as maintaining points of contact with regional, state, and federal disaster response agencies. A hazard assessment should be performed to identify the potential for railway disasters in a community based on the number of railways, the population density adja820

cent to the rails, the volume of rail traffic, the characteristics of rail services (e.g., subway, high-speed commuter, industrial freight, hazardous waste), and vulnerable facilities adjacent to the railways (e.g., schools, nursing homes, hospitals, apartment complexes, military bases) that may create unique problems for an emergency response.

POSTINCIDENT ACTIONS Initial priority should be given to the extraction, triage, transport, and treatment of the victims. Remote railway locations can present difficulties in reaching the scene, necessitating use of aeromedical assets in addition to land-based responders. Once at the scene, it is vital to do the following: (1) perform a rapid assessment to identify any potential hazardous material spills and (2) establish an incident commander and command center in a secure location. If the potential for a hazardous material contamination has not been determined, the information regarding the contents on board the train should be available, along with their material safety data sheets from the managing railroad company. On-scene triage of victims according to an established system, such as the Simple Triage and Rapid Treatment system, allows for prioritizing medical evacuation of victims back to the medical center according to severity of injury.5 The transportation of victims may include all traditional assets such as ground ambulances and aeromedical transports, as well as “lifts of opportunity” that may present themselves such as buses, police or fire vehicles, and military transport. Identification and tracking of the victims after their extrication and evacuation is vital and may be accomplished by triage tag number if no further identification is available on the scene. Definitive identification must be pursued at the time of presentation at the medical centers, for both the living and the deceased, to ensure all victims are recovered and accurately identified. Early contact and coordination with state, regional, and national organizations such as the National Transportation Safety Board and the Federal Emergency Management Agency are essential in providing an appropriate response to a large-scale railway disaster. Local resources can rapidly be exhausted, thus necessitating

outside aid such as from a National Guard unit or a disaster medical assistance team. All railway disasters are potentially crime scenes and must be approached as such throughout the response. Extrication of victims is of paramount importance; however, attention must be paid to not destroy any potential evidence. In the case of a terrorist attack, there is also the potential for secondary devices targeted at the emergency responders. Coordination of early statements and releases to the press should be handled through a single entity, whether it is the public affairs office of the hospital,the local police or fire department, or an outside agency; for instance, Amtrak manages all public affairs information and press releases for any accidents involving their trains.1

MEDICAL TREATMENT OF CASUALTIES Passengers will present with a broad spectrum of traumatic injuries, ranging from simple lacerations and fractures to severe head injuries and deceleration injuries (e.g., aortic or mesenteric avulsions). Patterns of injury may vary greatly depending on the passenger’s location (e.g., seated versus standing, forward- versus rear-facing seats) at the time of the injury: • Standing patients have a higher incidence of neck and craniofacial injuries.6 • Seated patients have a higher incidence of thoracoabdominal injuries, with those in forward-facing seats having a greater potential for facial injuries and deceleration injuries.7 In prolonged extrications, victims may also be suffering from crush syndrome and effects from exposure such as hypothermia or hyperthermia. There may also be a substantial number of burn or blast injuries, depending on the presence of combustible materials onboard the train or due to terrorist explosives. Traumatic injuries to passengers and railway workers will often be the primary medical challenge; however, in cases of hazardous material exposures, the potential for exposure and illness extends to include rescue workers and residents living near the disaster. After trauma, the most frequent injuries sustained by railroad employees are respiratory irritation, nausea, vomiting, and headache—all suggestive of hazardous material exposure.8 Residents near the derailment and first responders are most likely to present with respiratory, dermatologic, or ophthalmic complaints due to exposure.4 Proper use of personal protective equipment for rescue workers,decontamination of both victims and rescuers upon leaving the scene, and evacuation of any residents nearby can all minimize the effects of a hazardous material spill. Be prepared for a significant number of psychological casualties presenting both immediately and delayed.9 These victims may present with either psychological complaints, somatic symptoms, or both. Posttraumatic stress disorders have been identified in both train passengers as well as nearby residents after a major train derailment.10 Establishment of a critical incident support center to pro-

vide stress management, chaplain services, and psychological support for victims and families, as well as first responders, is helpful in minimizing the short- and longterm psychological sequelae after a railway disaster.

CASE PRESENTATION On a weekday afternoon, the call comes into the emergency department of the county’s only community hospital that there has been a reported train derailment in a small outlying town approximately 40 miles away. Initial reports state that a freight train with six workers on board has derailed adjacent to an elementary school and that there is a large fire burning on scene. Local fire and emergency medical systems crews are rolling onto the scene and requesting medical direction. What are your next moves? How would your response be different if it had been a high-speed commuter train with 100 passengers on board?

UNIQUE CONSIDERATIONS Train derailments are unique in the diversity of potential problems for responders. A derailment may occur in an urban environment with the subsequent risk of injury to the many people living and working nearby, or it can present in an isolated, rural location thus causing delays in response to the accident. The number of casualties can vary from only a handful of railway workers to hundreds of passengers on board a commuter rail. The possibility of hazardous material exposure exists in every train derailment, which may delay extrication of victims as well as present serious problems for rescue workers and those nearby. For a disaster response plan to be effective in the event of a train disaster, it must take into account all of these diverse possibilities.

PITFALLS Several potential pitfalls in response to a train derailment exist. These include the following: • Failure to develop and practice a disaster response plan • Failure to coordinate response with other agencies • Failure to recognize hazardous material release • Failure to maintain integrity of a crime scene for investigators • Failure to address positive identification of both victims and deceased • Failure to communicate with the public regarding risk and need for evacuation REFERENCES 1. Jenkins BM. Protecting surface transportation systems and patrons from terrorist activities. MTI Report. 1997;97:20–7. TRAIN DERAILMENT 821

2. National Transportation Safety Board. Railroad Accident Report, NTSB # RAR-04-01. Washington, DC: 2004. Available at: http://www.ntsb.gov/publictn/2004/RAR0401.htm. 3. National Transportation Safety Board. Railroad Accident Brief, NTSB # RAB-04-07.Washington, DC: 2004.Available at: http:// www.ntsb.gov/publictn/2004/RAB0407.htm. 4. Hsu EB, Grabowski JG, Chotani RA, et al. Effects on local emergency departments of large-scale urban chemical fire with hazardous materials spill. Prehospital Disaster Med. 2002;17:196–201. 5. Super G,Groth S,Hook R.START: Simple Triage and Rapid Treatment Plan. Newport, CA: Hoag Memorial Hospital Presbyterian; 1994. 6. Cugnoni HL, Finchman C, Skinner DV. Cannon Street rail disaster: lessons to be learned. Injury 1994;25:11–3.

7. Ilkjaer LB, Lind T. Passengers’ injuries reflected carriage interior at the railway accident in Mundlestrup, Denmark. Accid Anal Prev. 2001;33:285–8. 8. Orr MF, Kaye WE, Zeitz P, et al. Public health risks of railroad hazardous substance emergency events. J Occup Environ Med. 2001;43:94–100. 9. Hagstrom R. The acute psychological impact on survivors following a train accident. J Trauma Stress. 1995;8:391–402. 10. Chung MC, Easthope Y, Farmer S, et al. Psychological sequelae: posttraumatic stress reactions and personality factors among community residents as secondary victims. Scand J Caring Sci. 2003;17:265–70.

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chapter 164

Subway Derailment Jason Dylik and David Marcozzi

DESCRIPTION OF EVENT Subways are a common means of mass transit found in many urban settings. Subways are essentially electrified trains that can transport hundreds or even thousands of people per train. Since the subway runs on a track, instead of freely on the road, derailment can present a host of problems, ranging from a thump barely noticed by passengers to catastrophic failure resulting in massive injury and death. One of the worst accidents in subway history occurred in New York City on November 1, 1918, when an inexperienced dispatcher (filling in for striking motormen) entered a tunnel too fast and caused the wooden train to derail. The train struck a wall, killing 97 people and injuring 200. This incident led to the Brooklyn Rapid Transit Company going out of business a month later.1,2 Subways have become considerably safer in the years that have followed, but accidents including derailments may still occur. Operator error remains the most common cause of derailment.3 Intentional sabotage of tracks or cars can also lead to derailment. On March 11, 2004, 191 people were killed and more than 2000 injured when 10 bomb explosions occurred simultaneously on 4 commuter trains in Madrid, Spain.4 The location of these events can present unique challenges for emergency responders. Subways may travel underground, on elevated platforms, or on bridges over bodies of water, gorges, and ravines. An underground subway derailment necessitates evacuation of the train in a dark tunnel with possibly a long walking distance to access points. During an above-ground derailment, train cars may tip over. Train derailment from an elevated railway may result in the train falling off the bridge entirely. Passengers and emergency responders risk falling off the elevated railway as well. Elevated railways passing over water present the additional hazard of drowning and exposure to cold for victims falling into the water. A common hazard to all electrified train accidents is the ever-present risk of electrocution that can result on contact with the third rail, which runs along the track in many subway systems and conducts several

hundred volts of direct current, providing power to the train. Contact with the third rail can be fatal.

PREINCIDENT ACTIONS Hazard vulnerability analysis by hospital disaster planners should include a survey of subway or train stations located in the vicinity of the hospital. Any past rail accidents that have occurred within the hospital catchment area should be carefully reviewed to determine whether there are “danger zones”where future accidents may be more likely to occur. The kinetic energy of a traveling train is proportional to the number of cars (mass) and the velocity. The higher the kinetic energy,the greater the risk of injury to passengers in the event of a derailment event.5 An estimate of the potential number of injuries that could result from a theoretical rail accident can be made by multiplying the number of cars per train traveling through local stations and rail routes by the passenger capacity of each car. If the potential number of patients that could result from such a rail accident exceeds the capacity of local prehospital and hospital resources, multiagency disaster plans should be developed for this scenario.

POSTINCIDENT ACTIONS Because of the variety of potential disaster scenes after a subway accident, the responder must pay particular attention to scene safety issues. Adequate resources should be mobilized to address the specific scenarios faced and preconceived evacuation plans for the victims should be implemented. After victim rescue operations, assessment of the rail bed must be made to determine structural integrity before reestablishment of service along that route. Train cars must likewise be inspected to determine future usability. Debriefing with emergency responders should be undertaken by senior members of involved agencies and other trained personnel from specialized organizations after any rescue operation to understand any difficulties that may have been encountered during the rescue and recovery operations.

823

MEDICAL TREATMENT OF CASUALTIES Multiple types of casualties may be encountered in victims of rail accidents. In low-speed derailments, musculoskeletal injuries such as ankle and wrist injuries, and injuries due to falls are predominantly seen. In highspeed derailments, deceleration forces may be significant, with a resulting spectrum of traumatic injuries similar to that seen in other patients with high-speed blunt trauma. High-speed derailments occurring in tunnels may result in collision with tunnel support posts or stanchions, which may remain intact but cause passenger cars to collapse.6,7 Fire, with smoke and release of toxic gases, may complicate injuries resulting from blunt trauma.4 Rail accident scenes are prone to multiple hazards of which emergency responders must be aware and must take precautions to avoid. Live electrical wires or the train’s electrified third rail present the risk of electrocution leading to burns and respiratory and cardiac arrest. Fire in a subway tunnel can result in low oxygen levels and the presence of toxic fumes. If fire is present, effective suppression must take place before rescue attempts can be made. There may be a risk of falling debris or collapse of on-scene structures and train cars, as well as the potential that rescuers and victims could fall from elevated railways. When scene safety is insured, victims should be evacuated from the accident zone as quickly as possible to minimize further risk from on-scene hazards and to allow for appropriate triage, on-scene treatment, and transportation to hospital. High-angle rope rescue techniques may be needed in some cases of elevated railway accidents. The scenario of needing to apply spinal immobilization and extricate hundreds of patients on long boards presents an enormous technical and logistical challenge to emergency responders. In this scenario, deployment of physicians to the field to evaluate and clinically clear patients without evidence of cervical spine injuries can significantly expedite the safe extrication of patients at risk for cervical spine and other injuries. The triage area should be established upwind and outside of the accident zone, away from potential hazards, in an area that is accessible to transporting ambulances. Patients should be triaged using standard algorithms for a mass-casualty incident. A mass-casualty incident exists when: 1. The number of patients and the nature of their injuries make the normal level of stabilization and care unachievable, and/or 2. The number of Emergency Medical Service personnel that can be brought to the site within the time allowed is not enough, and/or 3. The stabilization capabilities of the hospitals that can be reached within the time allowed are insufficient to handle all the patients. Basic trauma stabilization of injured patients can be initiated on the scene in preparation for transport to hospital. Patients with smoke inhalation or exposure to other toxic fumes should receive supplemental oxygen.

Patients with electrical burns or respiratory or cardiac arrest resulting from electrical shock should also be anticipated.

CASE PRESENTATION On a summer Saturday afternoon, an above-ground subway train consisting of 11 cars with approximately 245 passengers and crew is heading toward a popular amusement park and the city aquarium. Unbeknownst to the crew, the track ahead has been vandalized. Spikes joining the track had been pulled, leaving the rails loose although still intact. The first car passes over the section of the break without incident, but as the second car passes, the track comes apart and the rear truck of the third car derails, twisting the train into an “S” shape and slamming into a wall.The train conductor activates an alarm, and a bystander calls 9-1-1.The train crew, who is uninjured, begins identifying injured passengers. Police, fire, and emergency medical services (EMS) units arrive on the scene, and a mass-casualty incident is declared. In total, 116 patients are transported.There is one fatality: a massive epidural hematoma with herniation. Three other red-tagged patients are appropriately admitted, treated, and discharged in good health.The train is recovered from the track, taken out of service, rehabilitated, and returned to service. The train bed, wall, and track are repaired. The National Transportation Safety Board determines the cause of the derailment to be sabotage of the track; operator error was not ruled to be involved. The vandals/saboteurs are never identified or apprehended.

UNIQUE CONSIDERATIONS Subway derailments, when they occur underground or on elevated platforms, may be associated with difficult access issues for rescuers. Underground accidents may be associated with fire, smoke, and toxic gases that present risks to victims and rescuers alike. Rescuers may have to walk long distances through tunnels to reach the accident scene, carrying extrication and other rescue equipment, and then transport patients out on foot. The extrication of passengers from severely damaged or crushed train cars may require the use of heavy equipment outside the scope of standard EMS or fire department capabilities. Planning for such scenarios should occur in advance and involve representation from all relevant response agencies, including the Transit Authority.

PITFALLS Several potential pitfalls in response to a subway derailment exist. These include the following: • Inadequate implementation of an emergency plan with sufficient elements, including fire, police, EMS, and government agencies (e.g., the NTSB) • Slow or incomplete discontinuation of track electricity and service on the line

824 EVENTS ASSOCIATED WITH STRUCTURAL COLLAPSE/CRASHING/CRUSHING

• Accumulation of toxic gases underground • Technically difficult rescues and extrications, either due to entrapment in machinery, conditions other than on level ground (e.g., bridge, tunnel underground or underwater), or remote locations • Patient accountability—some may be entrapped, selfextricated, or transported by private citizens, and there is no way of determining the number of passengers who might be on board at the time of the accident REFERENCES 1. Scores Killed, Many Hurt on B.R.T., New York Times. November 2, 1918:1–2.

2. Death beneath the streets. WGBH, Boston MA, Feb. 17, 1997. Available at: http://www.pbs.org/wgbh/amex/technology/ nyunderground/death.html. 3. National Transportation Safety Board, Railroad Accident Report, Washington DC, June 17, 1997, PB97-916302, NTSB/RAR-97/02, p 153. 4. Gutierrez de Ceballos JP, Fuentes FT, Diaz DP, et al. Casualties treated at the closest hospital in the Madrid, March 11, terrorist bombings. Crit Care Med. 2005;33:S108. 5. Jussila J, Kjellstrom BT, Leppaniemi A. Ballistic variables and tissue devitalisation in penetrating injury-establishing relationship through meta-analysis of a number of pig tests. Injury 2005;36:282–92. 6. Pirmann D. NYC subway accidents. June 15, 2004. Available at: http://www.nycsubway.org/faq/accidents.html 7. National Transportation Safety Board, Railroad Accident Report, Washington DC, October 27, 1992, PB92-916304, NTSB/RAR-92/03, p 12. 8. Available at: http://www.directives.doe.gov/pdfs/doe/doetext/ neword/151/g1511-1v4-3.html.

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chapter 165

Bus Accident Kavita Babu

DESCRIPTION OF EVENT In 2002, Americans traveled 21.8 billion miles by bus.1 Despite these extraordinary numbers, serious bus accidents are still an uncommon event. National Security Council data state that the risk of fatal injury for a bus passenger is 170 times lower than that of an automobile occupant.2 However, a single bus filled only to its stated capacity may hold more than 50 passengers.3 Therefore, the possibility exists for a bus accident to cause an instant mass-casualty event in virtually any setting. Data from transit buses for the year 2000 report more than 20,000 injuries and 82 deaths.4 Although transit and charter bus data are available, the most complete data on bus accidents are derived from analysis of school bus crashes. More than 22 million American children take the bus to school daily.5 In 1999, more than 18,000 people were injured in school bus accidents, resulting in 164 deaths.6 Characteristics of those accidents that produced fatalities included front-end and side-impact crashes, overturned buses, and collisions with trains.7 According to the National Transportation Safety Bureau, death and significant injury were often attributed to sitting at the point of impact.8 Analyses of individual accidents have guided the bus industry safety standards. The primary passenger safety feature of school buses is called compartmentalization. Given the size of buses and the lower crash forces imparted to passengers, legislation was passed in 1977 to make compartmentalization standard in the production of new school buses.9 Padded seats create a compartment for the passenger between high seat backs and the seat in front. The seats themselves are constructed of steel, and designed to absorb energy by bending. However, this method of protection is particularly limited in rollovers, when passengers may be thrown from their seats.10 Continued controversy exists over the use of seat belts in school and transit buses. National transportation authorities argue that seat belts in buses increase the risk of serious neck injuries, and that the cost of seat belt implementation may be better allocated for other safety measures. Additionally, the role of seat belts in buses is questioned because their primary purpose in cars is to prevent ejection, an uncommon event in bus accidents.11 826

Proponents state that seat belts are an essential intervention for preventing injury to passengers during rollover and lateral-impact collisions.11 As this debate continues, research on improving bus safety remains a priority for many government, professional, and parent organizations.

PREINCIDENT ACTIONS Every public safety system, emergency department, and hospital must have a comprehensive plan in place for approaching a mass-casualty event involving a bus. A serious bus accident can rapidly overwhelm the resources of a single hospital. Activation of local, state, and even federal resources may be required. Prehospital triage is critical to avoiding saturation of the nearest hospital. On-scene personnel should transport patients with unstable conditions to the nearest hospital, whereas patients with minor injuries can be diverted to outlying facilities. One unique difficulty faced by prehospital personnel at the scene of a bus accident is the difficulty of extricating victims. The standard extrication tools and techniques used in response to car accidents may not be effective in evacuating victims from a bus. Particular difficulties with extrication were noted in an Omaha,Nebraska,accident in 2003. As a result of this accident, the National Transportation Safety Board recently issued a recommendation that all fire and rescue personnel undergo specialized training in bus extrication techniques.12 Rapid extrication of bus accident victims is particularly vital in cases in which the bus becomes submerged. Recent accidents in China and India resulted in large death tolls after buses left the road and entered nearby rivers.13,14 High numbers of bus accident fatalities in developing countries may also be attributed to older equipment, bus overcrowding, lack of standardized driver training, and hazardous road conditions.

POSTINCIDENT ACTIONS In recent years, national transportation authorities have identified the collection and assimilation of transit and charter bus accident data as a priority in creating applicable safety interventions. The efforts of clinicians and

local rescue and law enforcement personnel to report all bus accidents are critical for surveillance. If the bus accident involves a large number of fatalities, part of the disaster response must involve rapid activation of local, state, and national mortuary teams to identify remains in a rapid and accurate manner.15

MEDICAL TREATMENT OF CASUALTIES An Australian study reviewing school bus–related fatalities in children identified head injury and blood loss as the most common causes of death.16 As in other causes of blunt trauma, immediate attention must be directed to airway, breathing, and circulation. Rapid airway management may be required in patients with a depressed Glasgow Coma Scale score or significant burns. Spinal immobilization must be maintained where appropriate. The secondary survey for injuries should be performed rapidly, with a particular focus on triage in the mass-casualty setting. Patients with life- or limb-threatening injuries must be addressed emergently, whereas other patients may be appropriate for immediate transfer or triage to a less urgent level of care. In most bus accidents, there are far more “walking wounded” than patients with incapacitating injuries.17 However, in the case of multiple serious casualties, the physician or his or her staff must be able to mobilize both hospital and community resources rapidly in avoiding the saturation of any single healthcare site without failing to provide care to all patients.

The nature of patient injuries may be specialized with school bus accidents representing a potential event involving pediatric mass casualties, whereas a charter bus may represent a geriatric mass-casualty event. Additionally, multiple bus accidents have occurred where large numbers of burn victims have been documented, creating need for aggressive airway management and resuscitation.

PITFALLS Several potential pitfalls in response to a bus accident exist. These include the following: • Failure to develop adequate mass-casualty protocols at the emergency services, hospital, community, and state level • Failure to train community EMS personnel in specialized techniques for bus extrication • Failure to educate schoolchildren and public transportation passengers regarding emergency exit operation and use • Failure to anticipate a large number of trauma victims • Failure to anticipate a large number of pediatric victims • Failure to anticipate a large number of burn victims requiring definitive airway management • Failure to inform National Transportation Safety Board or National Highway Traffic Safety Administration of bus accidents (of all severity) to provide better data and improve overall safety

CASE PRESENTATION REFERENCES You are working in a 15-bed emergency department of a small community hospital that is 40 minutes by ambulance to the nearest level 1 trauma center. On a Monday morning, you receive pre-notification of a collision between a dump truck and a school bus. The bus overturned, landing on its left side. Flames were initially noted to the rear of the bus but were extinguished upon arrival of fire department personnel. The on-scene paramedic cannot pinpoint the number of passengers on the bus but estimates 20 children. Extrication is proceeding slowly. There is one reported fatality. Local emergency medical services (EMS) dispatch is contacting neighboring towns for assistance, and EMS personnel will transport the first victims to your hospital within 15 minutes.

UNIQUE CONSIDERATIONS In many ways, the traumatic injuries sustained by any person during a bus accident are not markedly different than those found in a simple motor vehicle collision. However, a bus accident carries the potential to generate far more patients than a car accident, depending on the capacity of the bus and the severity of the accident. Local resources may quickly become overwhelmed.

1. American Public Transportation Association. Table 70: Bus and Trolleybus National Totals. APTA Public Transportation Fact Book. Washington, DC:APTA; 2002. 2. National Safety Council. What are the Odds of Dying? Odds of Death due to Injury, United States 2000. Itasca, IL: National Safety Council; 2000. 3. U.S. Department of Transportation, Office of Public Affairs. NHTSA sends school bus report to Congress. May 7, 2002. Available at: http://www.nhtsa.dot.gov/nhtsa/announce/ press/PressDisplay. cfm?year=2002&filename=pr37-02.html. 4. U.S. Department of Transportation, Federal Transit Administration. 2000 Transit Safety and Security Statistics and Analysis Report. Washington, DC: USDOT; 2002. 5. National Center for Education Statistics. Table 51: Public School Pupils Transported at Public Expense and Current Expenditures for Transportation: 1929–30 to 1999–2000. Digest of Education Statistics.Washington, DC: National Center for Education Statistics; 2002. 6. National Safety Council. School Bus Safety Rules. Fact Sheet Library, National Safety Council. December 23, 2002. Available at: http://www.nsc.org/library/facts/schlbus.htm. 7. National Highway Traffic Safety Administration. Table 5: School Bus Passenger Fatalities by Most Harmful Event. Report to Congress.School Bus Safety: Crashworthiness Research.Washington, DC: NHTSA. 2002. 8. National Transportation Safety Board.Safety Study—Crashworthiness of Large Post-Standard School Buses. NTSB/SS-87/01. Washington, DC: NTSB; 1987. 9. National Highway Traffic Safety Administration. Section 1.3: School Bus Occupant Protection Requirements. Report to Congress. School Bus Safety: Crashworthiness Research. Washington, DC: NHTSA. 2002. BUS ACCIDENT 827

10. Sibbald B. MDs call for new safety features after death in school bus crash. CMAJ 2003;169:951. 11. Lapner PC, Nguyen D. Analysis of a school bus collision: mechanism of injury in the unrestrained child. Can J Surg. 2003; 46:269. 12. National Transportation Safety Board. School Bus Run-off-Bridge Accident. Highway Accident Report. NTSB/HAR-04/01. Omaha, Neb: NTSB. 13. Pratap A. India bus accident kills 28 children. CNN; November 18, 1997. Available at: http://www.cnn.com/WORLD/9711/18/india.bus/ index.html.

14. Reuters. Bus accident in western China kills 34. CNN; 2001. Available at: http://www.cnn.com/2001/WORLD/asiapcf/east/ 08/11/bus.crash/index.html. 15. Valenzuela A, Martin-de las Heras, Marques T, et al. The application of dental methods of identification to human burn victims in a mass disaster. Int J Legal Med. 2000;133:236–9. 16. Cass DT, Ross F, Lam L. School bus related deaths and injuries in New South Wales. J Rehabil Res Dev. 2003;40:309–19. 17. National Highway Traffic Safety Administration. Occupant fatalities in school buses (model year 1997–2001) by person type. Fatality Analysis Reporting System:1999–2000.Washington,DC:NHTSA;2000.

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chapter 166

Aircraft Crash Preparedness and Response Dan Hanfling and Christopher R. Lang

DESCRIPTION OF EVENT There are more than 27,000 commercial flights in the United States each day, making air travel one of the safest means of mass transportation per mile traveled.1 Nevertheless, the crash of an airplane is often considered a major disaster and often generates significant interest for an extensive period of time. As current technologies improve, and the aviation industry tends to fly larger aircraft on longer flights, the need to prepare for the response to an air crash emergency remains a fundamental element of local disaster planning.2 With over 850 airports in the United States handling regional, national, and international air traffic, the potential for response in any given community is more than just theoretical.

PREINCIDENT CONSIDERATIONS Analysis of National Transportation Safety Board (NTSB) data with regard to aircraft size and the severity of injuries in “hull loss”events demonstrate a declining trend in aviation accident rates over time and an improvement in passenger and crew survival. This can be attributed to the increased use of wide-bodied, larger commercial aircraft. This allows for improved structural integrity, enhanced occupant protection mechanisms, improved fuel cutoff and fire extinguishing capabilities,and the suppression of toxic fumes from burning cabin materials.3 A review of 473 civilian airplane crashes with survivors between 1977 and 1986 demonstrated only eight crashes with more than 50 injured casualties of any degree of severity. Additionally, there were only three crashes in which more than 50 seriously injured casualties occurred.4 Another review of eight commercial aviation aircraft crashes in the United States between 1987 and 1991 revealed initial fatality rates ranging from zero to 46%. The number of injured passengers surviving the crash incident averaged over 60 passengers per event.5 However, the potential for significantly larger numbers of casualties rises as passenger payload capacity increases. An example of this occurred in Tenerife, Canary Islands, on March 27, 1977, when two fully loaded Boeing 747 jets

collided on the runway and burst into flames, killing over 500 people on the tarmac and critically injuring 60 passengers, many of whom later died. A significant factor in the survivability of an airplane crash has to do with the aircraft conditions during and immediately after the crash event. An airframe that sustains an impact alone will likely yield many more survivors than an airframe that sustains impact followed by fire and explosion. Highlighting this point is the crash of Avianca Flight 52 in January 1990 on the north shore of Long Island, New York, after running out of fuel. There were 158 passengers on board, of whom 85 survived.6,7 The majority of passengers perished because of trauma, not because of fire or smoke inhalation. The risk to passenger safety increases exponentially with the presence of fire or explosion on impact. Even in what may be an otherwise survivable event, fire contributes to significant morbidity and mortality of passengers, primarily from the rapid incapacitation of passengers by heat, smoke, and toxic fumes. Review of the British Airtours Boeing 737 accident at Manchester International Airport on August 22, 1985, demonstrates that passengers died within 4.5 minutes of the emergency being declared, and probably within 2 minutes of smoke and flames entering the fuselage.8 This exemplifies the aggressive nature of fire and smoke within the confined space of the cabin and their devastating effects. The final significant factor related to planning for air crash response is related to the location of crash events. The vast majority of aircraft accidents (85%) occur during takeoff and landings at an airport or occur within a 5-mile radius of the airport. Such statistics predicate the importance of both airport emergency operations planning, as well as off-airport planning, including waterbased response plans for those airports adjacent to large bodies of water. Under U.S. Federal Aviation Regulations (FAR Part 139.325), each airport operator must conduct a full-scale airport emergency plan exercise at least once every 3 years.9 This exercise ensures that responding agencies are familiar with their responsibilities under the plan and is intended to improve their proficiency in its execution. Response to aviation emergencies on the airport grounds 829

begins initially with the airport rescue firefighting (ARFF) resources, but will often quickly escalate to a mutual aid response event. In the event of an off-airport crash, the affected jurisdiction will have the initial responsibility for providing fire and rescue response. In today’s environment of increased terrorist events, the deployment of a rocket-propelled grenade (RPG) fired at an aircraft becomes an intense concern. This was exemplified by the near miss of a rocket-propelled grenade on a departing Arkia Airlines Boeing 757 departing from Mombassa, Kenya, on November 29, 2002. In the setting of current security risks, any aviation emergency is likely to be considered the result of terrorist action until proven otherwise. Therefore, responses to off-airport incidents are likely to include local, state, and federal emergency responders, including a large contingent of law enforcement assets.10 If an airport is located near or adjacent to water, the off-airport disaster planning must incorporate an offshore response strategy for a downed aircraft in the water. This response is likely to include airport-based water rescue resources and municipal, Coast Guard, and other Defense Department rotor wing and water-based rescue assets.11

POSTINCIDENT CONSIDERATIONS Regardless of the location of an air crash event, disaster operations are likely to follow four distinct operational phases (Box 166-1). The initial phase, emergency response, is primarily focused on life-saving, firefighting, and safety-related operations. It is during this phase that fire suppression, search and rescue, emergency medical care, traffic direction, and control and perimeter security are established. The first arriving emergency personnel will establish a Unified Command post and establish staging area(s) to provide on-scene management of the incident. Note that if there are multiple crash sites or if there is significant wreckage scattered over a large geographic area, it may be necessary to establish multiple Unified Command posts to provide effective command and control of the disaster scene. This element of aircraft disaster operations will be considered complete when the last surviving passenger(s) are transported from the scene and all life safety hazards at the crash site have been stabilized or eradicated. The second phase of operations, the transition and stabilization phase, will often occur simultaneously with the emergency response phase and is intended to serve as a bridge between the initial response to the air crash event and the investigative and recovery aspects of the incident. It is during this phase that the disaster site

BOX 166-1 POSTINCIDENT OPERATIONAL PHASES Phase 1: Emergency Response Phase 2:Transition and Stabilization Phase 3: Investigation Phase 4: Recovery

is assessed and long-term strategic and recovery plans are developed. This includes the anticipation of necessary staffing and resource requirements over time. In coordination with the local or state health departments, morgue operations are established, and provisions are made for requests made by the Chief Medical Examiner’s office. It is also likely that personnel from the NTSB will begin arriving on the scene during this phase of operations. Finally, operational control of the scene is passed from fire department to police department authorities in anticipation of the next phase of operations. The investigation phase, which begins at the conclusion of the stabilization of the crash site, may last for several days, weeks, or months and includes all aspects of the investigation to determine the cause and origin of the crash. The NTSB retains primary responsibility for coordinating all aspects of the investigation, with significant assistance provided by the Federal Aviation Administration; local, state, and federal law enforcement agencies; and representatives of the involved airline. The NTSB may assume direction and control of the “wreckage site” to conduct an investigation into the cause of the crash. This is accomplished in close coordination with law enforcement organizations to manage the incident scene. The NTSB also works with the airline carrier(s) of the plane(s) involved in the crash, other appropriate airline organizations, and local and state governments to coordinate federal resources that may be required to meet the needs of aviation disaster victims and their families. Family counseling, victim identification and forensic services, communicating with foreign governments, and translation services are among the provisions that can be made available to help local authorities and the airlines deal with a major aviation disaster.12 The NTSB will lead the aviation crash investigation until it is determined to have been caused by a criminal act, at which point the Federal Bureau of Investigation is given the lead role in coordinating the crisis management response to acts of terrorism.13 In addition, the U.S. Department of Homeland Security may elect to send a representative to help coordinate the overall federal response to the incident.14 The final phase of the incident, the recovery phase, begins at the conclusion of the investigative phase and likewise may last for several days, weeks, or months. It begins with the transition towards normal flight operations. This assumes the completion of the clean-up operations at the crash site, the demobilization of staff, equipment, and other resources, and the finalization of all reports, incident records, and other documentation. It is completed by the preparation of an after-action report detailing all four phases of the operational response to the air crash event.

MEDICAL TREATMENT OF CASUALTIES The mechanisms of injury in aircraft accidents are primarily related to a combination of blunt, penetrating, and thermal injuries. More than one mechanism of injury is likely to coexist, resulting in multisystem traumatic

830 EVENTS ASSOCIATED WITH STRUCTURAL COLLAPSE/CRASHING/CRUSHING

injuries. These injuries most often result from one of five major causes, which include explosive decompression, crush and entrapment, passenger restraint systems, burn and thermal exposure, and events associated with evacuation. Rapid and explosive decompression may be one of the initial events occurring in a loss of aircraft integrity, leading to a crash. This can affect many organ systems including the lungs, sinuses, and gastrointestinal tract. These air-filled structures are predisposed to injury resulting from barotrauma. Lung injuries are the most serious and are due to rapidly increasing positive pressure leading to tearing of lung tissue and subsequent pneumothorax. In addition, traumatic sinus rupture and tympanic membrane rupture can result from increased pressure in the sinuses. Finally, gastrointestinal effects can lead to possible bowel perforation and ventilatory compromise due to elevation of the diaphragm. Crush and entrapment within the airframe wreckage are also highly likely to result in post-incident casualties. When a plane impacts a surface, there is compression of cabin space that can lead to entrapment and probable crushing. Many injuries seen are fractures, head and neck trauma, and rhabdomyolysis. In addition, the presence of fire, smoke, and water introduce the additional risk of morbidity and mortality related to thermal injuries or drowning. Passenger restraint systems may cause patterns of injury similar to those seen in motor vehicle crashes; however, the velocity of the impact is greatly increased. This leads to a high incidence of blunt force injuries to the head, thorax, pelvis, and abdomen, in descending order of frequency.Examples include epidural and subdural hematoma, aortic dissection, solid organ lacerations, and pelvic fractures. The lack of shoulder restraints with lap belts allows for greater bodily movement and risk for injury. In addition, untethered objects within the cabin may become projectiles, resulting in blunt or penetrating injuries. Thermal and burn injuries present a major cause of death from survivable impact. This is due to the confined space of the aircraft and the inability to egress in rapid fashion. Toxic fumes, especially carbon monoxide, pose a major risk (Table 166-1). In a study of military aircraft fatalities occurring between 1986 and 1990, 535 cases were analyzed for carboxyhemoglobin. There were 23 cases (4%) having elevated levels of carboxyhemoglobin (above 10% saturation.) In each case, the victim survived the crash and died in the post-crash fire.15 Finally, there are many injuries resulting from the evacuation of the aircraft. The crash environment will be chaotic, often with significantly hampered visual perception and significant risk posed by collisions with other passengers or exposed wreckage. Fractures, sprains, and soft tissue injuries predominate. In addition, flash and chemical burns from either jet fuel or hydraulic fluid may pose significant exposure risks. Specific patterns of injuries in survivors can be divided into three major categories. Fractures are the most common injury, representing close to one quarter of all injuries16 (Table 166-2). They range from isolated closed fractures requiring minimal medical attention to

TABLE 166-1 MANIFESTATIONS OF CARBOXYHEMOGLOBIN PERCENT COHB

MANIFESTATIONS

80

Data adapted from Klette K, Levine B, Springate C, et al. Toxicological findings in military aircraft fatalities from 1986–1990. Forensic Sci Int. 1992;53:143–8.

complex vertebral, pelvic, and open long bone fractures that are often associated with hemodynamic instability and the potential risk from fat embolism. Thermal and burn injuries are another major cause of morbidity in surviving passengers, including the risk of inhalation injury to the airway. Finally, blunt and penetrating trauma to intrathoracic and intra-abdominal organs can result in major bleeding and shock. These are usually related to direct impact or the movement of large objects within the cabin postdisaster. Some key issues identified by after-action review of Sioux City, Iowa, crash response include the following17,18: • No identified entry and exit way was available for emergency vehicles. This caused some traffic jams and indecision regarding how to exit the area. • There was inadequate emergency equipment and resource management. Ambulances had extra equipment including include portable oxygen, intravenous

TABLE 166-2 DISTRIBUTION OF NAVY AND MARINE CORPS AVIATION ACCIDENT INJURIES BY DIAGNOSTIC CATEGORIES DIAGNOSIS Fracture/dislocation Contusion Laceration Abrasion Thermal burn Sprain/strain Multiple extreme injuries Amputation/avulsion Hemorrhage Perforation/rupture Concussion Crushing Decapitation Miscellaneous

PERCENT OF TOTAL INJURIES REPORTED 22.8 16.1 12.3 8.3 7.9 7.6 6.3 3.6 2.4 2.1 1.1 1.1 1.1 7.3

Data taken from Table 25-1 in Aircraft Accident Autopsies from United States Naval Flight Surgeon’s Manual: The Virtual Navy Hospital Project. 3rd ed. Chapter 25. 1991. Available at: http: // www.vnh.org /FSManual /25/04 Autopsy.html.

AIRCRAFT CRASH PREPAREDNESS AND RESPONSE 831

CASE PRESENTATION: UNITED FLIGHT 232, JULY 19, 1989 United Airlines Flight 232 departed from Denver Stapleton International Airport for Chicago O’Hare International with 296 passengers onboard. It was a clear day without any weather restrictions. One hour and 17 minutes into the flight, there was a catastrophic failure of the tailmounted engine (#2) that led to loss of hydraulic systems, virtually paralyzing the aircraft. The plane declared an emergency at 3:20 p.m. near the Sioux City, Iowa airport. Five minutes before crash impact, there were five airport rescue firefighting companies and four local fire engine companies positioned just outside the airport perimeter, awaiting the arrival of the crippled aircraft. At 4:00 p.m.,the plane touched down with the right wing making first impact with the ground. The plane’s fuel reserve then ignited, and the aircraft flipped end over end as it ran off the runway into an adjacent cornfield. The tail section was completely severed from the rest of the aircraft. The main cabin and cockpit tumbled forward, finally resting in the inverted position 3700 feet from impact area. Fires and smoke erupted everywhere,and survivors alighted from the crashed plane, screaming for help. There were over 26 different agencies involved in the response to the crash at the Sioux City airport. Out of 296 passengers and crew, 112 died in the crash. Thirtyfive of those deaths were from asphyxia secondary to smoke inhalation (Table 166-3).17 The number of casualties was greatly minimized by the rapid-fire suppression response. After the fires were controlled, the triage of patients was initiated. The emergency medical service response to the event included the transport of 196 patients to hospitals within 90 minutes of the crash impact using ambulances, helicopters, buses, and vans.

supplies, and pressure dressings that would have been tremendously valuable to the on-scene response. However, these were not left on scene and remained on the individual transport units. • Uncoordinated release of public information led to inconsistent reporting by media and news organizations. • Fire engine water pump failure resulted in 10 minutes without adequate supply. • There was an unknown number of passengers. Children who sat on a guardian’s lap were not counted on the passenger manifest.

TABLE 166-3 INJURIES TO UNITED FLIGHT 232 PASSENGERS INJURIES Fatal Serious Minor None Total

CREW 1 6 4 0 11

PASSENGERS

TOTAL

110 41 121 13 285

111 47 125 13 296

Data adapted from National Transportation Safety Board Aircraft Accident Report PBSO-910406NTSB/AAR-SO/06 United Airlines Flight 232, Sioux Gateway Airport. Sioux City, Ia: July 19, 1989. Available at: http://amelia.db.erau.edu/reports/ ntsb/aar/AAR90-06.pdf.

• Many different languages were spoken without available interpreters, leading to miscommunication during the rescue efforts.

UNIQUE CONSIDERATIONS Given the significant risk of repeated terrorist attack in the United States, the response to all air crash events will necessarily invoke a significant law enforcement component, particularly in the initial investigative phase of the event. Such a response was exemplified by the response to the TWA Flight 800 crash off the southern coast of Long Island, New York, in the summer of 1996, and more recently, the crash of American Airlines Flight 587 immediately upon takeoff from New York Kennedy International Airport in October 2001. The implication of such a response is that surviving patients brought to the hospitals may eventually need to undergo law enforcement questioning and evaluation. All clothing and other personal items transported with the patient from the disaster scene must necessarily be considered as evidence and therefore must be collected and stored according to agreed-upon procedures, in conjunction with local law enforcement officials. There is an important caveat regarding the presence of firearms or other weapons that may be found on the person of surviving passengers. These would have traditionally been associated with possible hijackers. However, with the reintroduction of armed federal air marshals on board an increasing number of flights, particularly those departing or arriving from key high-threat urban areas, such weapons may in fact be attributable to law enforcement personnel.

PITFALLS Most disaster scene triage decisions are predicated upon the application of the Simple Triage and Rapid Treatment (START) triage decision-making algorithm. This system is primarily based on the recognition of bodily injuries and the categorization of patients into categories of priority based on specific physiologic criteria, including airway, breathing, and circulation considerations. This is a system that is focused on the treatment and transport of the most emergent patients first, followed by those patients with injuries requiring less urgent attention. It involves a color-coded system that is used to rapidly triage patients into their respective injury status. And although this triage approach works for the majority of mass-casualty situations, it needs to be adapted for use in air crash disasters, particularly those in which there has been a fire or explosion. Patients who may present with only mild throat irritations, without any other injuries, would likely be placed in the lowest transport priority group. However, such symptoms may be the harbinger of a more serious developing inhalation injury, either due to an explosion and fire through the passenger cabin, exposure to toxic fumes, or aspiration of water or toxic fluids in the event of a water ditching. Such patients must be automatically upgraded in

832 EVENTS ASSOCIATED WITH STRUCTURAL COLLAPSE/CRASHING/CRUSHING

response category and transported away from the scene in a more rapid manner. These patients may possibly benefit from early aggressive airway management if the index of suspicion of an inhalation injury remains high based on the assessment of the initial out-of-hospital care providers. This exemplifies the need for constant reevaluation and possible changes in triage and treatment status. REFERENCES 1. Accidents, Fatalities, and Rates, 2004 Preliminary Statistics U.S. Aviation, National Transportation Safety Board. Accessed at: http:// www.ntsb.gov/aviation/Table1.htm. 2. Mollard R, Akestedt T, Cabon P, et al. Summary and recommendations for future ultra-long range operations. Aviat Space Environ Med. 2004;75:B124. 3. Abelson LC, Star LD, Stefanki JX. Passenger survival in wide-bodied jet aircraft accidents vs. other aircraft: a comparison. Aviat Space Environ Med. 1980;51:1266-9. 4. Rutherford WH. An analysis of civil aircrash statistics 1977-86 for the purposes of planning disaster exercises. Injury 1988;19: 384-8. 5. Anderson PB. A comparative analysis of the EMS and rescue responses to eight airliner crashes in the United States. Prehospital Disaster Med. 1995;10:142-53. 6. Dulchavsky SA, Geller ER, Iorio DA. Analysis of injuries following the crash of Avianca Flight 52. J Trauma. 1993;34:282-4. 7. Van Amerengen RH, Fine JS, Tunik MG, et al. The Avianca plane crash: an emergency medical system’s response to pediatric survivors of the disaster. Pediatrics 1993;92:105-10. 8. Hill IR. An analysis of factors impeding passenger escape from aircraft fires. Aviat Space Environ Med. 1990;61:261-5.

9. Code of Federal Regulations Title 14. Volume 2, revised. U.S. Government Printing Office via GPO Access CITE: 14CFR139.325; January 1, 2001:812-3. Available at: http://ecfr.gpoaccess.gov/cgi/ t/text. 10. Fairfax County Emergency Operations Plan, Aircraft Crash Appendix for Off Airport Incidents. Fairfax County, Virginia: Fairfax County Division of Emergency Management; March 2, 2004. 11. Multi-Agency Ocean Rescue Disaster Plan and Drill. Broward County, Florida: United States Fire Administration, Federal Emergency Management Agency. Available at: http://www.usfa. fema.gov/downloads/txt/publications/tr-079.txt. 12. National Transportation Safety Board. Federal Family Assistance Plan for Aviation Disasters. April 2000. Available at: October 28, 2005 at http://www.ntsb.gov/publictn/2000/spc0001_body.htm. 13. Presidential Decision Directive 39: U.S. Policy on Counterterrorism. The White House, June 21, 1995. Available at: October 28, 2005 at http://www.fas.org/irp/offdocs/pdd39htm. 14. National Response Plan: Homeland Security Presidential Directive (HSPD-5). The White House, February 28, 2003. Available at: October 28, 2005 at http://www.fas.org/irp/offdocs/ nspd/hspd-5.html. 15. Klette K, Levine B, Springate C, et al. Toxicological findings in military aircraft fatalities from 1986-1990. Forensic Sci Int. 1992; 53:143-8. 16. United States Naval Flight Surgeon’s Manual: The Virtual Navy Hospital Project. 1991: 3rd ed. Chapter 25. Bureau of Medicine and Surgery, Naval Aviation Medical Institute. Pensacola, Florida Available at: http://www.vnh.org/FSManual/25/04Autopsy.html. 17. National Transportation Safety Board Aircraft Accident Report PBSO-910406NTSB/AAR-SO/06 United Airlines Flight 232, Sioux Gateway Airport. Sioux City, Iowa: July 19, 1989. Available at: http: //amelia.db.erau.edu/reports /ntsb/aar/AAR90-06/pdf 18. Brown G. The Crash of Flight 232.. Lecture series provided at University of Nebraska, Omaha. January 23, 2002. Accessed on October 28, 2005 at http://ai.unomaha.edu/video/

AIRCRAFT CRASH PREPAREDNESS AND RESPONSE 833

chapter 167

Air Show Disaster Peter D. Panagos

DESCRIPTION OF EVENT Typically,an air show is a summertime event during which aviators display their flying skills and aircrafts. Although some air shows are held for commercial purposes, many are arranged to raise funds for charities. Usually air shows occur at military or large civilian airfields, located near the coastline or large cities in which a variety of static aircraft and helicopters are on view. When space allows, other entertainment and market stalls are available, adding further to the attraction of the show. Flight performances by military aerobatic teams and civilian aerobatic aircraft as well as large-scale pyrotechnics are presented to attract larger crowds. Due to the public interest in aviation, crowds at a typical air show can range from a few hundred to tens of thousands of attendees. A disaster at an air show is a multiple-casualty incident in which the primary effects are morbidity and mortality to persons, while the community infrastructure remains intact. Over the last 30 years, there have been air show accidents involving performing aircraft that have caused a significant number of casualties (Table 167-1). Because of the possibility of mass casualties due to ground accidents, aviation mishaps, or terrorism, pre-event planning, incident response, and the post-event reaction must be thoroughly planned to effectively manage any potential situation.

PREINCIDENT ACTIONS Preparations should include the continuum from basic event planning such as addressing the sanitation needs of a large crowd to planning for area evacuation in case of a large-scale aviation mishap involving significant casualties and a hazardous materials risk.1–8 An effective disaster plan will identify potential problems by performing a risk analysis of chemical and environmental hazards,7 personnel and physical resources, and transportation elements available to the planners (Box 167-1). Once a plan has been outlined, it must be evaluated for effectiveness and completeness through the implementation of a disaster drill. A thorough mishap plan includes contingency arrangements with appropriate activities for rescue, firefighting, explosive ordnance disposal, logistical support, 834

medical support, coordination with public affairs/media, coordination with law enforcement officials, wreckage location, security, recovery and preservation, and notification of key personnel.9 Disaster preparedness officials have long recognized the value of good training and exercises. Most of the principles of disaster planning are based on the painful lessons learned under actual catastrophic conditions.10 Exercises provide the opportunity to learn how to perform in realistic and controlled settings that are relatively free of risk.

POSTINCIDENT ACTIONS In any unannounced event, the alert mechanism must be expeditious because the survival of severely injured individuals is often time sensitive. In an air show disaster involving ground casualties on the airfield, knowledge of the disaster will often be immediate. Notification of a crash may come over primary or secondary communication networks, and a crash message is disseminated to include aircraft type, nature of emergency, location of crash or landing runway, number of persons on board, hazardous cargo, potential ground casualties, and other pertinent information. If there are survivors at the scene, the urge to charge in to render care should be avoided. Trained rescue teams will bring casualties to a safe area or allow the medical team into the area when it is safe. When multiple casualties are involved, a system of triage may be needed.3 Specific areas for casualty management should be predesignated with standard nomenclature. It is the medical leader’s responsibility to keep the Incident Commander abreast of numbers and types of casualties, the need for additional support, and any other facts the command post needs to make decisions.11,12 If an aircraft crashes in a remote setting, all responding personnel from the airfield will proceed to a prearranged assembly point for convoy to the area. In any disaster, medical personnel should enter the area only when it is declared safe. Once the survivors have been taken care of and the remains of the deceased secured or removed, an assessment of the adequacy of response should be made as soon as possible to include supplies and equipment eval-

TABLE 167-1 FATAL CRASHES AT AIR SHOWS OVER THE LAST 30 YEARS DATE

LOCATION

DESCRIPTION

July 2002

Western Ukraine

June 1999

Bratislava, Slovakia

July 1997

Ostend, Belgium

September 1997

September 1982

Chesapeake Air Show, Glenn L Martin State Airport, Baltimore, MD Ramstein Air Force Base,West Germany Mulhouse-Habsheim, FrenchSwiss border Mannheim,West Germany

Russian Sukhoi Su-27 performing maneuvers crashed into crowd British Royal Air Force Hawk 200 crashed during air show Light aircraft mounting an aerobatics display crashed into crowd around a Red Cross tent F-117A crashed during flyby

June 1973

Paris, France

August 1988 June 1988

Three Italian Air Force jets collided midair and crashed into crowd New Airbus A320 crashed during low-level demonstration flight U.S. Army Chinook helicopter carrying multi-nation sky divers crashed Prototype Russian Tupolev Tu-144, a supersonic airliner, dubbed “Concordski” exploded midair during Paris air show

uations (e.g., too little? inappropriate? not available?) and personnel (e.g., adequately training? management performance?). These evaluations should be used to make changes in the disaster response plan and improve future response. The psychological impact of the mishap on the response team members and the community should not be overlooked. A critical incident debriefing or other intervention by mental health workers should be considered for the responding or on-site workers.13,14 Other interventions must be considered for family and friends.

MEDICAL TREATMENT OF CASUALTIES In any large-scale disaster, once the site has been deemed safe, the next priority is the triage, treatment, movement, and evacuation of casualties. During an air show without a mass-casualty event, the types of injuries and illnesses treated vary based on meteorologic conditions and geographic location. The conditions encountered are typical complaints seen in emergency departments such as dehydration, intoxication, sunburn, animal/insect bites, trips/falls,exacerbation of chronic illness,and altercations.1 In the event of an aircraft crash involving ground personnel, the potential for multisystem life-threatening injuries increases. In many aircraft accident fatalities, the injuries appear extensive from multiple trauma, burns, or both. Explosive and blast injuries involving penetrating and blunt trauma will result from the sudden deceleration of the airframe into the ground with ignition and disbursement of aircraft flammable materials and ordnance. Explosive-related injuries will affect most organ systems and produce unique patterns of injury seldom seen outside the combat arena. The management of these injuries in the field will often be limited to triage, stabilization, and transportation to an appropriate level of care.15–21 If the aircrew successfully exits the aircraft, rescue personnel should be aware of human impact injury patterns.

NO. OF PERSONS INJURED/KILLED 84/115 1/1 9/57 5/0 70/100s 3/133 46 killed 15 (6 crew, 9 ground)

Although aircraft structures are designed to improve crash survivability, the human tolerance to deceleration and postcrash explosions is a complex function of many factors.22–24 Based on Armed Forces Institute of Pathology injury analysis, there are four major injury types to be considered: thermal, intrusive, impact, and deceleration.22,23,25 Though protected by flame retardant clothing, aircrew often sustain thermal injuries secondary to ignition of aircraft fuel and materials, inhalation of soot and combustion products including carbon monoxide, skin and soft tissue burns, soft tissue contraction and charring, thermal fractures and amputations, and severe burns. Intrusive injuries from the loss of occupiable space due to the intrusion of main rotor blades, propellers, trees, or wires are also common causes of severe injury. Finally, impact and deceleration forces cause injuries based on the position during deceleration and the distribution of force over the body parts (Table 167-2). For example, the pilot who ejects before impact may survive but may sustain extremity fractures resulting from the violent extremity movements involved in a high-speed ejection. Aircraft wreckage sites can have multiple hazards. Personnel involved in the recovery, examination, and documentation of wreckage may be exposed to physical hazards posed by such things as hazardous cargo, flammable and toxic fluids, sharp or heavy objects, and disease. Hazardous materials, such as cartridge-actuated devices, tires, and oxygen bottles are major concerns. Explosive ordnance disposal personnel should target items such as pressurized bottles, hydraulic reservoirs, and canopy detonation cord to secure the scene and prevent further injury.9,24,26–33 Finally, once all injured or trapped victims have been cleared from the crash site, the area should be considered a crime scene. Wreckage and cargo should not be disturbed or moved except to the extent necessary for personnel safety. Arrangements should be made for security at the accident scene to protect the wreckage from additional damage and to protect rescue personnel and the public from injury. AIR SHOW DISASTER 835

BOX 167-1 PRE–AIR SHOW RISK ANALYSIS Security Requirements • Isolation of air show and base operations • Terrorism/vandalism/theft concerns Parking Plan and Traffic Control • General public • Handicapped • VIP • Crowd arrival and departure plan FAA Coordination • Schedule practice for dynamic shows • Airspace coordination Emergency Planning and Drills • Published and practiced • Community resources informed Communications and PA System • Many methods and backup communication systems available • Phonebook of key personnel and services Crowd Control Barriers • No-smoking signs in hazardous areas • Parking away from sensitive areas Pedestrian Concerns • Trip hazards • Sound and sun mitigation options • Comfort stations • Lost-parent stations • Published safety guidelines • Medical response plan Medical Response Plan • First-aid stations clearly identified • Medical personnel placed in crowd • Airfield and local EMS transportation • LZ identified for rotary ring evacuation Restroom Facilities • Sufficient numbers for crowd • Contract for routine cleaning • Handwash stations Vendor Setup • Area and infrastructure available to support FAA, Federal Aviation Administration; PA, public address; EMS, emergency medical services; LZ, landing zone.

UNIQUE CONSIDERATIONS Most advanced military aircraft contain composite structures consisting of light, strong, stiff fibers embedded in a matrix material. Although these materials offer a significant structural advantage, they present a danger to rescue and medical personnel. Studies have shown that composite fibers can cause mild short-term skin, eye, and respiratory problems, but the long-term carcinogenic potential is unknown. Therefore, prudence is required in using personal protective equipment. The reinforcing fibers most commonly used in aircrafts are graphite, bismalemide, and boron fibers (such as Kevlar). For example, in the F-18A/B, there are 1000 lbs (or 9.8% total aircraft structural weight) of composite material.22 These fibers, when released from an epoxy matrix, become fine splinters that can easily be driven into the skin and will cause irritation. Graphite fibers

TABLE 167-2 DECELERATIVE INJURIES AND APPROXIMATE G FORCES INVOLVED BODY PART/INJURY

DECELERATIVE FORCE (G)

Pulmonary contusion Nose fracture Vertebral body compression

25 30 20–30 (less in thoracic region or if poor body position) 20–40

Fracture dislocation of C-1 or C-2 Mandible fracture Maxilla fracture Aorta intimal tear Aorta transection Pelvic fracture Vertebral body transection Total body fragmentation Concussion

40 50 50 80–100 (at ligamentum arteriosum) 100–200 200–300 (through body, not intervertebral disc) 350 60 G over 0.02 sec 100 G over 0.005 sec 180 G over 0.002 sec

Adapted from The U.S. Naval Flight Surgeon’s Pocket Reference to Aircraft Mishap Investigation. 4th ed. Pensacola: The Naval Safety Center,Aeromedical Division in conjunction with The Society of United States Naval Flight Surgeons; 1995.

CASE PRESENTATION It was supposed to be the grand finale to a beautiful, family day event; then everything went wrong for the low-flying Russian-built Sukhoi Su-27, a 5.5-ton supersonic fighter aircraft (a long-range air fighter comparable to the U.S. F-15). More than 1500 people watched the free air show, part of celebrations to mark the 60th anniversary of a local Air Force unit. Witnesses said the jet was performing complex aerobatic maneuvers before it reportedly lost power, clipped some trees and another plane, cartwheeled across the ground, and crashed into a huge fireball. The two-pilot crew safely ejected from the aircraft before the plane hit the crowded spectator stands. As one witness stated, it was “a huge ball of fire, as big a house, and black smoke…I barely had enough time to clutch my young daughter before the explosive wave threw us to the ground, and severed arms and legs were flying all over.” In all, 84 persons were killed (26 were 18 years of age or younger), and more than 116 were hospitalized with various injuries. The crash of the fighter jet was caused by pilot error, an official report into the incident has concluded. The head of the commission set up to investigate the crash said the pilots had failed to follow the flight plan and performed difficult maneuvers they had not done before. Additionally, operational issues, organizational problems, and a lack of safety measures had contributed to make it the world’s worst air show disaster. These events occurred at Sknyliv Airport, near Lviv, Ukraine, on July 27, 2002.

are very small and light and pose a respiratory threat similar to asbestos. While the aircraft is still burning or smoking, only firefighters should be in the immediate vicinity. Once the fire is completely extinguished and cooled, the composite material is normally sprayed with a fixant, such as polyacrylic acid or aircraft firefighting

836 EVENTS ASSOCIATED WITH STRUCTURAL COLLAPSE/CRASHING/CRUSHING

foam to contain release of composite fiber material. Finally, it is recommended that all personnel around the released fibers wear a National Institute for Occupational Safety and Health–approved disposable air-filtering mask, Tyvek disposable overalls, puncture-resistant gloves and goggles while on scene and take a shower before leaving the scene.22,25,29,30 Additionally, the risk of being exposed to blood and body fluids is possible in any mishap involving human injury. Human immunodeficiency virus, hepatitis B, Lyme disease, and tetanus pose a threat to rescue personnel. Hepatitis B virus can survive in a dried state for several weeks. Therefore, it is recommended that all crash scene rescue and medical personnel become familiar with potential on-scene hazards, adhere to Occupational Safety and Health Administration work practice controls,31 and make use of personal protective equipment.32

PITFALLS Several potential pitfalls in response to an air show disaster attack exist.These include the following: • Failure to identify, prepare for, and properly train for a mass-casualty event by not developing contingency plans and periodically reviewing and correcting errors in the plans • Failure to plan for the medical needs of a mass gathering composed of both geriatric and pediatric persons, many with significant preexisting diseases, exposed to a wide range of environmental elements and stresses unique to an airfield • Failure to recognize the unique injuries sustained by ground personnel from explosive-related forces in close proximity to an aircraft crash • Failure to appreciate that emergency responders may become casualties themselves if they do not recognize the hazardous dangers of a modern aircraft crash scene containing composite materials, biologic hazards, and unexploded ordnance. (Use of personal protective gear is paramount to avoid responder injury.) • Failure to recognize the unique injury patterns of aircraft crash survivors who have experienced sudden deceleration forces (high G) and exposure to hazardous materials REFERENCES 1. Mears GD, Batson DN. Mass gatherings. In: Bosker G, ed. Textbook of Adult and Pediatric Medicine. Atlanta: American Health Consultants; 2000. 2. Schultz CH, Koenig KL, Noji EK. A medical disaster response to reduce immediate mortality after an earthquake. N Engl J Med. 1996;334:438–44. 3. Schultz CH, Koenig KK, Noji EK. Disaster preparedness and response. In: Rosen P, Barkin RM, eds. Emergency Medicine: Concepts and Clinical Practice. 4th ed. St Louis: Mosby; 1998:324–33.

4. Hogan DE, Burstein JL, eds. Disaster Medicine. Philadelphia: Lippincott Williams and Wilkins; 2002. 5. De Lorenzo RA. Mass gathering medicine: a review. Prehospital Disaster Med. 1997;12:68. 6. Waeckerle JF. Disaster planning and response. N Engl J Med. 1991;324:815. 7. Levitin HW, Siegelson HF. Hazardous materials: disaster medical planning and response. Emerg Med Clin North Am. 1996;14:327. 8. Auf der Heide E. Disaster Response: Principles of Preparation and Coordination. St Louis: Mosby; 1989. 9. Edwards M. Airshow disaster plans. Aviat Space Environ Med. 1991;62:1192–5. 10. de Boer J.Tools for evaluating disasters: preliminary results of some hundred of disasters. Eur J Emerg Med. 1997;4:107–10. 11. Christen H, Maniscalco P. The EMS Incident Management System. Upper Saddle River, NJ: Prentice-Hall Inc; 1998;1–15. 12. Irwin RL. The incident command system (ICS). In Auf der Heide E, ed. Disaster Response: Principles of Preparation and Coordination. St Louis: Mosby; 1989. 13. Burkle FM Jr. Acute-phase mental health consequences of disasters: implications for triage and emergency services. Ann Emerg Med. 1996;28:119–28. 14. Linton JC, Kommor MJ, Webb CH. Helping the helpers: the development of a critical incident stress management team through university/community cooperation. Ann Emerg Med. 1993;22:663. 15. Pepe PE, Kvetan V. Field management and critical care in mass disasters. Crit Care Clin. 1991;7:321–7. 16. Dunne MJ Jr, McMeekin RR. Medical investigation of fatalities from aircraft accident burns. Aviat Space Environ Med. 1977;48:964–8. 17. Mason JK. Aviation Accident Pathology. London: Butterworths; 1962. 18. McMeekin RR. Patterns of injury in fatal aircraft accidents. In: Mason JK, Reals WJ, eds. Aerospace Pathology. Chicago: College of American Pathologists Foundation; 1973. 19. Mariani F. Spinal and spinal cord injuries in aviation medicine [Italian/English]. Minerva Med. 1978;69:3621–30. 20. Shanahan DF, Mastroianni GR. Spinal injury in a U.S. Army light observation helicopter. Aviat Space Environ Med. 1984;55:32–40. 21. Boyarsky I, Shneiderman A. Natural and hybrid disasters—causes, effects, and management. Top Emerg Med. 2002;24:1–25. 22. Aircraft Mishap Investigation Handbook. Brooks Air Force Base, TX:The Society of USAF Flight Surgeons; 2002, 23. The US Naval Flight Surgeon’s Pocket Reference to Aircraft Mishap Investigation. 4th ed. Pensacola: Society of United States Naval Flight Surgeons; 1995. 24. US Naval Flight Surgeon Manual. 3rd ed. Washington, DC: The Bureau of Medicine and Surgery, Department of the Navy; 1991. 25. McMeekin RR. Aircraft accident investigation. In: DeHart RL, ed. Fundamentals of Aerospace Medicine. Philadelphia: Lea & Febiger; 1985. 26. Rayman RB. Aircraft accident investigation for flight surgeons. Aeromedical Rev. 1979;3:79. 27. Thompson RL. Cause of death in aircraft accidents: drowning vs. traumatic injuries. Aviat Space Environ Med. 1977;48:924–8. 28. Ernsting J, Nicholson AN, Rainford DJ, eds. Aviation Medicine. 3rd ed. London:Arnold; 2003. 29. Department of the Air Force Human Systems Center. Response to Aircraft Mishaps Involving Composite Materials (Interim Guidance). Consultative Letter, AL-OE-BR-CL-1988-0108. Brooks Air Force Base,Tex:AFMC; 1998. 30. Mishap Risk Control Guidelines for Advanced Aerospace Materials: Environmental, Safety, and Health Concerns for Advanced Composites. LT John M. Olson (Project Engineer), McClellan Air Force Base, CA; October 1993. 31. Bloodborne Pathogens 29 CFR Part1910.1030. Washington, DC: Occupational Safety & Health Administration; 2001. 32. National Institute of Justice, Guide for the Selection of Personal Protection Equipment for Emergency First Responders, NIJ Guide 102–00 (Volumes I, IIa, IIb, and IIc), November 2002. Available at: http://www.osha.gov.

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chapter 168

Asteroid, Meteoroid, and Spacecraft Reentry Accidents Jay Lemery and Faith Vilas

DESCRIPTION OF EVENT From its origins 4.6 billion years ago, the natural history of our planet is replete with evidence of extraterrestrial impacts. Comets, asteroids, and meteoroids are the cosmic “impactors” that are theoretically both the originators (first organic molecules) and destructors (demise of the dinosaurs) of terrestrial life.1,2 Evidence of these impacts on our world remains, for example, in the milewide meteor crater in Arizona and in the impact site off the coast of the Yucatan Peninsula, believed to have caused the extinction of the dinosaurs 65 million years ago. Impacts of such magnitude are exceedingly rare, yet even less than 100 years ago, a small meteoroid 60 m in diameter is thought to have exploded 8 km over a sparsely populated region of Siberia, leveling all vegetation for hundreds of square kilometers. Most meteoroids incinerate while entering Earth’s atmosphere, as can be witnessed by any falling star on a clear night. In fact, about 100 tons of cosmic material fall to Earth daily, mostly in the form of tiny dust particles.3 As our understanding and interaction with the cosmos has broadened over the last few decades, we have realized that there are quantifiable risks from impactors to humanity, ranging from locally traumatic to globally cataclysmic. We will address these events as three distinct entities: 1. Local-effect near-Earth object (NEO) impacts 2. Global-effect NEO impacts 3. Artificial orbital debris reentry The risk posed by an impactor is directly proportional to its size2 (Table 168-1). Those less than 50 m in diameter will most likely incinerate. Impactors 1 to 2 km in diameter will devastate the area surrounding the impact site. Impactors larger than 2 km in diameter have the potential to cause obliterative local damage, as well as displace large amounts of dust into the stratosphere. The consequent effects would resemble a “nuclear winter,” affecting the entire globe, changing entire ecosystems with a resultant drop in global temperature, loss of agricultural productivity, and possible societal breakdown.2 Since over 70% of the Earth is covered with water, an 838

ocean impact could cause tsunamis with inland flooding extending tens of kilometers into the coastal plains. Orbital debris, the artificial residual of the last 40 years of human endeavors into space, is another source of a potential terrestrial impactor. According to the U.S. Air Force Space Command, there are currently over 8900 objects orbiting Earth.4 Although the vast majority of orbital debris pieces incinerate upon reentry, some components could survive, whether due to heat-resistant material (e.g., shuttle tiles) or a design that sheds heat fast enough to keep object temperatures below the component’s melting point. As the Columbia space shuttle tragedy demonstrated, controlled reentry can fail, in which case suborbital debris would be expected to survive reentry in greater quantity with a commensurate impact potential on life and property.

PREINCIDENT ACTIONS Asteroids and comets are classified as NEOs when they orbit close to the sun (and therefore Earth). NEOs of interest to astronomers addressing the impact hazard are those greater than 150 m in diameter that pass Earth within 1.3 times the average distance from the sun to Earth (93 million miles). The National Aeronautics and Space Administration (NASA)’s goal is to discover 90% of all NEOs with a diameter more than1 km by 2008. As of spring 2004, 2883 NEOs have been discovered: 719 of these are asteroids with diameters larger than 1 km, and 607 have been classified as potentially hazardous asteroids. The risk of impact by any specific potentially hazardous asteroid is extremely small, on the order of 10 to 100 times less than the annual risk of a single person being struck by lightning.5

NEOs 50 to 1000 m in Diameter An impactor with a diameter larger than 50 m will reach Earth’s surface on average once every 100 years. The composition of the impactor could determine the extent and type of local damage. If the object has less physical coherence, such as a loosely bound, low-density comet

TABLE 168-1 TERRESTRIAL EFFECTS OF IMPACTORS

From: Chapman CR, Durda DD, Gold T. The comet/asteroid impact hazard: a systems approach. Southwest Research Institute Web site. Available at: http://www.boulder.swri.edu/clark/neowp.html; and Toon OB, Zahnle K, Morrison D, et al. Environmental perturbations caused by the impacts of asteroids and comets. Rev Geophysics. 1997;35:41–78.

body containing ice, it might not remain whole prior to impact and could explode in the atmosphere over Earth’s surface. Scientists believe this happened in the Tunguska explosion over Siberia on June 30, 1908. Generally, the diametrical sizes at which incoming objects will break apart when they enter Earth’s atmosphere are 540 m for icy objects, 330 m for rocks, and 200 m for solid iron. These objects will change shape, flattening out to 5 to 10 times their original diameters because of the immense heat and pressure generated as they pass through the atmosphere. A surface impact will excavate material dependent on incoming velocity and angle of impact, resulting in a crater 10 to 25 times the size of the impactor. One model estimates that the 40-km-diameter Puchezh-Katunky crater in Russia was created by a 2-km diameter rocky asteroid moving at a velocity of 20 km/sec with a 45-degree angle of impact.6,7,8 This impact destroyed near-surface layers of land to a depth of 100 m up to 40 km from the center of the impact. Impactors less than 1 km in size are expected to have locally devastating effects, including total destruction within the resulting crater, thermal radiation surface fires, air blast compression, tidal wave flooding of lowlying areas, and compression wave injuries well beyond the crater zone. An event such as the Tunguska explosion might have occurred with minimal impact on humanity; however, if delayed by only a few hours, the more populous regions of Europe (and millions of lives) would have been in jeopardy.

NEOs 1 to 2 km in Diameter Impacts from NEOs larger than 1 km in diameter are thought to occur, on average, every few hundred thou-

sand years. NEOs of this size can have globally devastating effects; the resulting crater could reach 50 km in diameter. Debris would be launched into the stratosphere, blocking sunlight and threatening agricultural production globally. Super-heated impact debris would rain back down on Earth’s surface. An ocean impact would produce flooding tens of kilometers inland. Although rare, we have witnessed such an impact in the last decade within our solar system. The comet Shoemaker-Levy 9 impacts on Jupiter in 1994 were a series of 20 discernible impact fragments ranging up to 2 km in diameter. Had this comet hit Earth, it would have killed billions of people and risked most species on our planet.9

NEOs 10 to 15 km in Diameter NEOs 10 to 15 km in diameter will strike Earth even less frequently, on the order of once every 500,000 years. Global “earthquakes”from the impact, tsunamis, and total destruction over hundreds of kilometers would culminate in nuclear winter that would ensue for decades. The effect of such an impact would result in major global climate change, such as that which triggered the demise of the dinosaurs.

Orbital Debris Orbital debris is the artificial byproduct of the last 50 years of human endeavors into space. According to U.S. Strategic Command, orbital debris can be categorized as 7% operational satellites, 15% rocket bodies, and about 78% fragmentation and inactive satellites.4 The further degradation of these objects is facilitated by solar heating ASTEROID, METEOROID, AND SPACECRAFT REENTRY ACCIDENTS 839

and solar radiation, component explosions, and debris collisions. Motor casings, aluminum oxide exhaust particles, motor-liner residuals, release bolts, solid-fuel fragments, paint chips, and insulation are only some of the 70,000 objects approximately 2 cm in size that have been observed at altitudes 850 to 1000 km above Earth (Space Shuttles and the International Space Station orbit at 340–400 km).10 Although the intense pressure and heat of reentry will incinerate much of the mass of orbital debris, some satellite components can withstand this process. Components that have a sufficiently high melting temperature or a shape that allows rapid heat dispersal will have a higher probability of persisting. When debris pieces enter the lower regions of the atmosphere, they will lose velocity, begin to cool, and fall virtually straight down from the sky at relatively low speeds (terminal velocity); these are clearly a potential hazard to life and property. Although NASA attempts to track orbital debris and predict where debris from a randomly reentering satellite will hit Earth, it is an uncertain science: the atmospheric density varies greatly at high altitudes, thus confounding the calculation of reentrant drag. Other confounding factors include variations in the gravitational field, solar radiation pressure, and atmospheric drag. The predicted time to reentry is generally accurate to within 10% of the actual time, although this translates to a margin of error of several miles on the ground. Over the last 40 years, more than 1400 metric tons of materials are believed to have survived reentry without report of injury.4 In the event that Earth becomes at risk of being hit by a moderate to large impactor, we would likely know well in advance, perhaps by several years to decades. There would be an immediate, intense psychological reaction in the public, with likely intense media coverage and speculation. An incredible challenge would be posed to scientists, public health officials, and political leaders to relay the known risks and possible solutions to the public accurately. A discordance between calculated risks and publicly perceived risks can be expected, contributing to widespread fear and even mass hysteria.11 Familiar doomsday scenario patterns of behavior are likely to emerge on the fringes of society. Mental health providers could expect an increase in anxiety, depression, or both among a large portion of the population.

POSTINCIDENT ACTIONS As previously discussed, the risk of damage of an impactor is related to its size, and casualties and property damage should be treated as patients would be in other mass-casualty incidents. Meteorites are classified as “irons” (nickel-iron metal) or “stones.” Stones can be divided into two subgroups: chondrites and achondrites. Chondrites (about 86% of stones) are aggregates of early solar system materials that have not been significantly altered since formation of the solar system. Achondrites (about 8% of stones) are the products of melting and recrystallization of mostly magnesian silicates. One percent of meteorites are a conglomerate of those two types (called stony irons).

When a meteorite strikes, it does so at terminal velocity and has therefore cooled from the intense temperatures of atmospheric entry. The outer layer, or fusion crust, is usually 1 to 2 mm thick, the rest having burned off during entry and generally posing no risk of burn from contact (silicate materials are traditionally poor conductors of heat). There are reports of eyewitnesses picking up an object that has fallen, cracking it in two, and discovering ice particles. Meteorites are composed of materials that are abundantly found on Earth and pose no toxic or radiation risk. Historically, the controlled reentry of large components of artificial orbital material (Skylab, Mir) has been directed to remote, uninhabited parts of the planet (oceans). As seen with Columbia, however, spacecraft components can return to Earth relatively intact. Beyond the risk of impact, they can pose a toxicologic risk. Rocket propellants such as hydrazine and nitrogen tetroxide pose a chemical burn and inhalation risk. Structural materials such as beryllium have been known to cause pulmonary damage. Other potential hazards include ammonia, radiation sources (e.g., radioactive altimeters, live ordnance (e.g., pyrotechnics for emergency hatch opening), and other exotic compounds (e.g., scientific payloads, solar arrays, environmental control items such as lithium perchlorate and permanganate). Currently, there are no known nuclear-powered devices (e.g., powered by uranium) in orbit. Once an orbital debris piece is committed to a reentrant trajectory, it will fracture and scatter over a predictable pattern based on mass. The “footprint”of debris will consist of heavier objects at the “heel” of the footprint and lighter objects at the “toe.” In the certain cases of reentry events, forensic and possibly national security concerns will necessitate the mobilization of law enforcement personnel across several jurisdictions. As seen with Columbia in 2002, a concerted effort between law enforcement agencies in several states and NASA, coupled with direct appeals to the public, were initiated to preserve the integrity of the debris sites and to preclude souvenir hunters from disturbing debris fields. In such cases, mobilization of the military (national security concerns or naval salvage) may be deemed necessary, as well as international coordination if debris fields cross national borders.

MEDICAL TREATMENT OF CASUALTIES There is nothing unique to the medical treatment of casualties from the events discussed in this chapter. Blunt trauma is the likely mechanism of smaller impactors, expanding to burn and blast injuries for larger impactors. For large-scale impactors approaching the 1km-diameter mark, humanitarian/refugee crises will be a major concern. Psychological treatment will be another important consideration in any impactor scenario. Often even the smallest meteorite impacts are covered widely in the news media and may trigger anxiety and concern in otherwise unaffected portions of society. Mental health will

840 EVENTS ASSOCIATED WITH STRUCTURAL COLLAPSE/CRASHING/CRUSHING

be a major concern in the event of an orbital debris impact involving the loss of life. The scope of such a tragedy on the national psyche can affect all segments of the population, and there is a risk of the infliction of depression and posttraumatic stress disorder. Special concern should be made for those suffering personal loss. Despite efforts to shield them from further anguish, astronauts and other NASA staff (not unlike the New York City firefighters after the World Trade Center bombings on September 11, 2001) played a major role in the search for the remains of Columbia, prompting concerns of exacerbating already severe mental trauma.

UNIQUE CONSIDERATIONS Perhaps unique to this chapter is the potential scope of the disaster. If an NEO larger than1 to 2 km in diameter was identified as a probable Earth impactor, the need for international coordination would be unprecedented. The logistical scope of such an endeavor would be daunting. Whereas protocols are in place among astronomic groups to verify impactors and their risks before a public announcement,the ramifications of living in the age of the Internet could easily unglue efforts to sequester such proceedings. Initial efforts would likely focus on understanding the shape, configuration, mineral composition, and spin state of an impactor. These characteristics would further clarify risk and, potentially, a strategy for deflection using existing technology of conventional rockets and explosives.12 Future strategies could include attaching solar sails or engines to the NEO to deflect its path. A final consideration should be mentioned. As spacerelated technology proliferates and becomes more accessible over the next decades, satellites and space vehicles may become susceptible targets for terrorists, particularly as an impactor over urban areas, power/chemical complexes, or military targets.

PITFALLS One pitfall that should be anticipated with any impactor event is relying on uninterrupted global communication. The effects of an impactor entering the ionosphere may disrupt satellite communication and possible security net-

works. It is reported that those who have observed meteor “fireballs”before impact experience a metallic taste sensation, possibly due to an electromagnetic disturbance.

HELPFUL WEB SITES • http://impact.arc.nasa.gov; NASA asteroid and comet impact hazards • http://neo.jpl.nasa.gov; NASA Near Earth Orbit Program Web site REFERENCES 1. Chyba CF, Owen TC, Ip W-H. “Impact Delivery of Volatiles and Organic Molecules to Earth.” In: Gehrels T, ed. Hazards Due to Comets & Asteroids. University of Arizona Press. Tucson, AZ. 1994:9–58. 2. Morrison D, Chapman CR, Slovic P. “The Impact Hazard”. In: Gehrels T, ed. Hazards Due to Comets & Asteroids. University of Arizona Press. Tucson,AZ. 1994:59–92. 3. Kyte FT,Wasson JT. Accretion rate of extraterrestrial matter: iridium deposited 33 to 67 million years ago. Science 232:1225–9, 1986. 4. U.S. Air Force Space Command Web site. Available at: http://fas.org/spp/military/ program/track/mccall.pdf.McCall, G.H. “Space Surveillance.” Last accessed October 27, 2005. 5. Chapman CR, Durda DD, Gold RE. The comet/asteroid impact hazard: a systems approach. Southwest Research Institute Web site.Available at: http://www.boulder.swri.edu/clark/neowp.html. 6. Ivanov BA. Geomechanical models of impact cratering [abstract]. Presented at the International Conference On Large Meteorite Impacts and Planetary Evolution. Sudbury, Canada, 1992:40. 7. Pevzner LA, Kirijakov A,Vorontsov A, et al. Vorotilovskay drillhole: first deep drilling in the central uplift of large terrestrial impact crater [abstract]. Lunar Planet Sci. 1992;XXIII:1063–4. 8. Shoemaker EM. “Interpretation of lunar craters.” In: Kapal Z, ed. Physics and Astronomy of the Moon. 1962:283–359. New York: Academic Press (Elsevier). 9. A’Hearn M. “The impacts of D/Shoemaker-Levy 9 and bioastronomy.” In: Astronomical and Biochemical Origins and the Search for Life in the Universe. Proceedings of the 5th international conference on bioastronomy (held in Capri, Italy July 1–5, 1996), IAU Colloquium 161. Published in Bologna, Italy: Editrice Compositori, 1997: 165. 10. NASA Office of Space Operations Website (Dawn Brooks, editor). Available at: http://www.hq.nasa. gov/osf/station/viewing/history.html. 11. Benjamin GC. Managing terror: public health officials learn lessons from bioterrorism attacks. Physician Exec. 2002;28:80–3. 12. Ahrens TJ, Harris AW. “Deflection and Fragmentation of Near-Earth Asteroids.” In: Gehrels T, ed. Hazards Due to Comets & Asteroids. University of Arizona Press. Tucson,AZ. 1994:897–928.

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chapter 169

Building Collapse Catherine Y. Lee and Timothy Davis

DESCRIPTION OF EVENT The attacks on Sept. 11, 2001, shocked the American public with the destruction of the World Trade Center towers. It also brought to the forefront of disaster medicine the danger of building collapse,or progressive collapse,a principal if not the leading cause of injury and death in building failures.1 In the engineering world, progressive collapse has been studied for 40 years since the 1968 Ronan Point disaster.2 Progressive collapse is a “chain reaction of structural failures that follow from damage to a relatively small portion of a structure” or “the spread of an initial local failure from element to element that eventually results in the collapse of an entire structure or a disproportionately large part of it.”3,4 Simply stated, progressive collapse is a “domino effect,” causing the sequential collapse of one floor on top of lower floors.3 In this chapter, the terms building collapse, structural collapse, and progressive collapse are used interchangeably. There are six causes of building collapse: bad design, faulty construction, foundation failure, extraordinary loads, unexpected failure, and a combination of these causes. Some causes of bad design are errors in engineering computation, failure to consider all stresses and weights, reliance on inaccurate data, and poor choice of materials.5 Faulty construction may be the most common reason for building collapse around the world. It results from the use of inferior steel, bad riveting, infirm fastening and securing, and bad welds.5 In the case of foundation failure, the earth beneath a building may be unsuitable to support the weight of the building. Such is the case during an earthquake, when buildings are shaken off their mountings if built on top of unstable soil or not properly tied to their foundations.6 Extraordinary loads, which exceed the normal calculated stress that a building can withstand, include earthquakes, tornadoes, tsunamis, or man-generated events such as a motor vehicle striking a key support pillar, a gas explosion, or a bombing.4 For example, explosions damage buildings due to extremely high, instantaneous pressures from the blast wave.3 Depending on the size of the explosion, distance from the building, and sturdiness of building construction, an explosion can induce progressive collapse in a matter of milliseconds.3 The blast will first target the weakest point of the building closest to the detonation 842

and push onto the exterior walls of the lower floors, leading to wall failure and window breakage.3 While the shock wave expands, it enters the structure and pushes upwards and downwards, onto all floors of the building, inducing collapse.3 The reflection of the oncoming, or incident, blast wave against hindering structures like hard surfaces of a building’s exterior, can lead to additional pressures up to 13 times greater than the peak incident pressure.3,7 Laboratory tests have shown that surfaces exposed perpendicularly to the incident blast wave may experience pressures up to 5000 psi,3 yet typical window glass breaks at an incident overpressure of 0.15 to 0.22 psi.3

PREINCIDENT ACTIONS Although engineers note that progressive collapse cannot be totally prevented from occurring, they agree that tools can be designed to improve building performance to resist or improve building performance against collapse.1,8 National institutes encourage designing multihazard resistance and mitigation suitable to withstand progressive collapse from all threats including natural and technologic disasters.1 Specific mitigation against terrorist bombings focuses more on window and glass hazards, stand-off distancing, and “hardening” of the exterior. Site design and modification for perimeter defense using soil, bollards, planters, and retaining walls in addition to increasing stand-off distance between the facility and possible threats (such as a truck bomb) can deter and delay terrorist attack capable of insinuating building collapse.3 Strategies to limit parking,vehicular entry,and access inside or near the structure are additional methods for mitigation.3 But once these measures have failed,structural “hardening”to fortify the building’s exterior is used to mitigate the effects of an explosion once it has occurred. The objective of designing the exterior wall is to ensure that structures like walls, doors, and windows fail in a flexible mode, as opposed to a brittle mode that would induce shear and result in multiple fragments of cement, glass, and other materials capable of serious injury.3 In the 1998 bombings of the U.S. Embassies in Kenya and Tanzania, the U.S. Department of State found:“Although there was little structural damage to the five-story reinforced concrete building, the explosion

reduced much of the interior to rubble—destroying windows, window frames, internal office partitions and other fixtures on the rear side of the building. The secondary fragmentation from flying glass, internal concrete block walls, furniture, and fixtures caused most of the embassy casualties.”1,8,9 Nonstructural components such as ceiling fixtures, lights, windows, office equipment, computers, files, air conditioners, electrical equipment, and objects stored on shelves and hung on walls can also become an injury hazard.3,6 In an earthquake, these nonstructural elements are likely to be unhooked, dislodged, and flung, causing injury and damage.3 Additionally, the U.S. Federal Emergency Management Agency recommends that building design be optimized to facilitate emergency rescue and response, allowing feasible evacuation, rescue, and recovery efforts through effective placement, structural design, and redundancy of emergency exits and electrical/mechanical systems.3

POSTINCIDENT ACTIONS After a building collapse, trapped survivors requiring quick rescue “where minutes count” are rare. An expeditious headlong, poorly planned ingress into the “hot zone” can risk valuable human assets with limited potential benefit. The rules for traumatic arrest still apply— attempts to resuscitate persons with blunt traumatic arrest are typically futile. The bulk of surviving casualties will arrive over a 60minute period at the closest hospitals(s), either selftransported or transported by emergency medical services (EMS). Disaster managers should expect high resource utilization from hospitalized survivors, far exceeding the benchmark comparisons for similar injury severity score (ISS) casualties. Critically injured progressive collapse survivors can be compared with casualties of explosive injury, and they require an extraordinary amount of hospital resources. Hospitalized explosion survivors have longer than usual hospital and intensive care unit length of stay, more surgeries, and more ventilator time, and they are more often discharged to a rehabilitation facility compared with ISS-equivalent casualties of motor vehicle or gunshot wounds.10,11 Some general emergency management options apply: 1. Follow your hospital and regional disaster system plan. 2. Expect increased severity and delayed arrival of casualties. 3. Expect an “upside-down” triage—the most severely injured arrive after the less injured, who bypass EMS triage and go directly to the closest hospitals.12 4. Double the first hour’s casualties for a rough prediction of total first wave of casualties.12 5. Obtain and record details about the nature of the event, potential toxic exposures and environmental hazards, and casualty location using all reliable informants including local police and fire departments, EMS, Incident Command System, regional emergency management agency, local health department, and eyewitness casualties. The need for epidemiologic injury data is an imperative national agenda.13

MEDICAL TREATMENT Progressive structural collapse produces casualty and injury patterns similar to earthquakes and can be more severe than blast injuries alone.14 The final casualty toll and injury pattern depend most on preexisting circumstances: time of day, occupancy, warning, evacuation proficiency, individual health status, and building design and materials. The majority of casualty survivors will have minor injuries and require only outpatient or self-care. Standard penetrating and blunt trauma to any body surface is the most common injury seen among survivors, with the most severely injured consisting of burns, traumatic amputations, and head, chest, and abdominal injuries.14–16 Characteristic injuries seen in building collapse are shown in Table 169-1. Frykberg notes a substantial amount of immediate death and constant critical mortality rate among victims of a terrorist bombing building collapse, despite differences in TNT-equivalents of blast force.16 Most persons caught in the direct path of the collapse will not survive and will either be dead on-scene or dead on arrival, regardless of postcollapse rescue efforts. Trapped survivors are most often found in air spaces adjacent to partially intact support structures. Few survivors are rescued after the first 24 hours, although young children can be an exception. More than half of all children may have head or face trauma. Because children’s airways can be easily occluded, the primary cause of cardiopulmonary arrest in children may be respiratory. Therefore, children in cardiopulmonary arrest should first have their airways cleared. If there is no spontaneous pulse or respirations, they too are unsalvageable and CPR should not be initiated. Most casualties will meet either anatomic, physiologic, or mechanism of injury criteria to be transported immediately to a level I or II trauma center, and limited scene time remains the standard. Assume crush syndrome and rhabdomyolysis for any casualty trapped for longer than 1 hour. Compartment syndrome, rhabdomyolysis, and acute renal failure are associated with structural collapse, prolonged extrication, severe burns, and some poisonings. All casualties with substantial blunt injuries should be screened for acidosis, electrolyte imbalance, and renal failure. Resuscitation efforts should focus on correcting the underlying cause—for example, fasciotomy or benzodiazepine for agitation or seizures; crystalloid for treating volume depletion, correcting acidosis with sodium bicarbonate; and hemodialysis for renal failure or intractable hyperkalemia.

UNIQUE CONSIDERATIONS Traumatic amputation of any limb may be a marker for multisystem injuries, since such injuries usually result from close proximity to a blast.17,18 Wounds can be grossly contaminated. Consider delaying primary closure until after an assessment of tetanus status has been performed. Ensure close follow-up of wounds, head BUILDING COLLAPSE 843

TABLE 169-1 MECHANISMS OF INJURY ASSOCIATED WITH PROGRESSIVE COLLAPSE CATEGORY

CHARACTERISTICS

BODY PART AFFECTED

TYPES OF INJURIES

Penetrating Injury

Results from flying debris and fragments. Results from falling objects, blown debris, or persons being thrown by the blast wind. Unique to high explosives, results from the impact of the overpressurization wave with body surfaces.

Any body part may be . affected Any body part may be affected.

Penetrating ballistic (fragmentation) Eye penetration (can be occult) Fracture and traumatic amputation Closed and open brain injury

Gas-filled structures are most susceptible (i.e., lungs, GI tract, and middle ear).

Blast lung (pulmonary barotrauma) TM rupture and middle ear damage Abdominal hemorrhage and perforation Globe (eye) rupture Concussion (TBI without physical signs of head injury) Burns (flash, partial, and full thickness) Crush injuries Closed and open brain injury Asthma,COPD, or other breathing problems from dust, smoke, or toxic fumes Angina Hyperglycemia, hypertension

Blunt Injury Primary Blast Injury

Other

All injuries, illnesses, or diseases not due to penetrating, blunt, or primary blast injury. Includes exacerbation or complications of existing conditions

Any body part may be affected.

GI, Gastrointestinal;TM, tympanic membrane;TBI, traumatic brain injury; COPD, chronic obstructive pulmonary disease.

CASE PRESENTATION Newham, London, was a newly developed borough in 1968, spotted with brand new apartment towers and promising an upgraded lifestyle from the previous dirty and rundown homes that had characterized West and East Ham towns. Using an engineering method that was perceived as safe and quick in construction, the Ronan Point Apartment Tower was built in 2 years, opening in 1968 as a 210-foot-high building consisting of over 100 flats. Tenants moved in immediately. The apartment building had been occupied for only 2 months when a natural gas explosion on an 18th floor apartment triggered the structural failure of an entire corner of flats. Subsequent floors below were blown out, allowing a domino-effect collapse of wall and floor sections from the top to the ground. The majority of the 260 residents fled down stairwells in advance of the collapse that toppled floors like a deck of cards. However, four people died immediately as a result of the blast although more could have died if the flats were completely occupied. An elderly patient died later in hospital, leading to a total of 17 injured survivors. Residents saw the design failures such as use of costcutting when choosing building materials, poor workmanship, and lack of adequate building inspection as the reasons for the building collapse. Ronan Point was demolished in 1986, and fewer towers have been built since the disaster.

silent until signs of acute abdomen or sepsis are advanced.21 Primary blast lung and blast abdomen after explosions are associated with high mortality rates.22,23 The symptoms of mild traumatic brain injury (e.g., concussion) and posttraumatic stress disorder might be identical.24 Auditory system injuries and concussions are easily overlooked. Communications and instructions may need to be written because of tinnitus and sudden temporary or permanent deafness.25 Consider the possibility of exposure to inhaled toxins and poisonings (e.g., carbon monoxide, cyanide, methemoglobin) in both industrial and criminal explosions.26 In August 2003, a military hospital in Mozdok, Russia, was bombed, resulting in the partial building collapse of the 3-story structure killing 41 people and entrapping nurses, doctors, and personnel.27 A hospital building collapse can result in the loss of a critical community resource that cannot be easily replaced. Lastly, crowd surge or stampede can be more deadly than the original event. On January 27, 2002, a large military ammunition dump in Lagos, Nigeria, exploded, immediately killing 300. But another 800 persons, including small children, were trampled to death during the mass exodus that left several blocks of buildings completely and partially collapsed.28

PITFALLS injuries, and complaints related to the patient’s eyes, ears, and stress level. Air embolism can occur and can present as stroke, myocardial infarction, acute abdomen, blindness, deafness, spinal cord injury, or claudication. Hyperbaric oxygen therapy may be effective in some cases.19,20 If collapse was preceded by an explosion, clinical signs of blast-related abdominal injuries can be initially

Several potential pitfalls in response to a building collapse exist. • Do not discourage buddy rescue and self-transport of casualties. The majority of rescue is conducted by survivors and bystanders. Self-evacuation clears the scene and moves the bulk of the exposed population out of harm’s way.

844 EVENTS ASSOCIATED WITH STRUCTURAL COLLAPSE/CRASHING/CRUSHING

• Do not hold critical casualties in temporary triage sites instead of immediately transporting. Trauma never improves in the field, and trauma’s golden hour does not stop for a disaster. • The U.S. Federal Emergency Medical Treatment and Active Labor Act prevents the expeditious movement of excess outpatient casualties to hospitals with excess outpatient capacity.29 • Another pitfall is activating an entire hospital’s disaster plan for a distant regional event and not releasing recalled staff in a timely manner. Only the closest one to three hospitals receive the majority of the casualties, and half of all casualties arrive over a 60-minute period. • Lack of ventilators and cardiac monitors is a common limit or delay in inter-hospital transfer of critical casualties. • It should not be assumed that all ambulatory casualties are “worried well.”All have been exposed to a variable amount of physical trauma and environmental hazards. Israeli pediatric traumatologists have proposed eliminating “Green” or “Minimal” from the triage protocol.30 • Adult casualties in cardiopulmonary arrest are either dead or unsalvageable. No attempt should be made to resuscitate beyond confirming the absence of vital signs.

10.

11. 12. 13. 14. 15. 16. 17. 18. 19. 20. 21.

REFERENCES 1. National Research Council. Blast Mitigation for Structures: 1999 Status Report on the DTRA/TSWG Program. Washington, DC: National Academy Press; 1999. 2. BBC News Online. 1968: Three die as tower block collapses. Available at: http://news.bbc.co.uk/onthisday/hi/dates /stories/ may/16/ newsid_2514000/2514277.stmA. 3. U.S. Federal Emergency Management Agency. Risk Management Series: Reference Manual to Mitigate Potential Terrorist Attacks Against Buildings. Washington, DC: FEMA; 2003. 4. Gould NC. Quantifying the risk for progressive collapse in new and existing buildings. International Risk Management Institute, March 2003. Available at: http://www.irmi.com/expert/Articles/ 2003/Gould03.aspx. 5. Calvert JB. The collapse of buildings: why the World Trade Center towers collapsed. Available at: http://www.du.edu/~jcalvert/tech/ failure.htm. 6. U.S. Federal Emergency Management Agency. What is an earthquake? National Earthquake Hazards Reduction Program. Available at: http://www.fema.gov/hazards/earthquakes/quake. shtm. 7. Boffard KD, MacFarlane C. Urban bomb blast injuries: patterns of injury and treatment. Surg Ann. 1993;25:29-47. 8. Multihazard Mitigation Council. Prevention of Progressive Collapse: Report on the July 2002 National Workshop and Recommendations for Future Efforts. Washington, DC: Multihazard Mitigation Council of the National Institute of Building Sciences; 2003. 9. U.S. Department of State. Report of the Accountability Review Boards on the Embassy Bombings in Nairobi and Dar es Salaam on

22.

23.

24. 25. 26. 27. 28.

29. 30.

August 7, 1998. U.S. Department of State; January 1999. Available at: http://www.state.gov/www/regions/africa/kenya_tanzania. html. Peleg K,Aharonson-Daniel L, Stein M, and the Israeli Trauma Group (ITG). Gunshot and explosion injuries: characteristics, outcomes, and implications for care of terror-related injuries in Israel. Ann Surg. 2004;239:311-8. Peleg K,Aharonson-Daniel L, Michael M, Shapira SC, and the Israel Trauma Group. Patterns of injury in hospitalized terrorist victims. Am J Emerg Med. 2003;21:258-62. U.S. Centers for Disease Control and Prevention. Explosions and Blast Injuries: A Primer for Clinicians. Available at: http:// www.cdc. gov/masstrauma/preparedness/primer.htm. National Research Council. Protecting People and Buildings from Terrorism, Technology Transfer for Blast-Effects Mitigation. Washington, DC: National Academy Press; 2001. Butcher TP. Explosive emergencies treating blast injuries in the field. JEMS 1991:50-54. Frykberg ER, Tepas JJ 3rd. Terrorist bombings: lessons learned from Belfast to Beirut. Ann Surg. 1988;208:569-76. Frykberg ER. Medical management of disasters and mass casualties from terrorist bombings: how can we cope? J Trauma. 2002;53:201-12. Hull JB. Traumatic amputation by explosive blast: pattern of injury in survivors. Br J Surg. 1992;79:1303-6. Hull JB, Bowyer GW, Cooper GJ, Crane J. Patterns of injuries in those dying from traumatic amputation caused by bomb blast. Br J Surg. 1994;81:1132-5. Guy RJ, Glover MA, Cripps NP. The pathophysiology of primary blast injury and its implications for treatment. Part I: The thorax. J Royal Nav Med Serv. 1998;84:79-86. Vavrina J, Muller W. Therapeutic effect of hyperbaric oxygenation in acute acoustic trauma. Rev Laryngol Otol Rhinol (Bord). 1995;116:377-80. Wightman JM, Gladish SL. Explosions and blast injuries. Ann Emerg Med. 2001; 37:664-78. Leibovici D, Gofrit ON, Stein M, et al. Blast injuries: bus versus open-air bombings—a comparative study of injuries in survivors of open-air versus confined-space explosions. J Trauma. 1996; 41:1030-5. Stuhmiller LH, Phillips YY, Richmond DR. The physics and mechanisms of primary blast injury, a brief history. In: Bellamy RF, Zajtcjuk JT, eds. Conventional Warfare: Ballistics, Blast, and Burn Injuries. Textbook of Military Medicine series. Washington, DC: Office of the Surgeon General at TMM Publications; 1991:241-70. Barrow DW, Rhoades HT. Blast concussion injury. JAMA 1944; 125:900-2. Hirsch FG. Effects of overpressure on the ear: a review. Ann NY Acad Sci. 1968;152:147-162. Quenemoen LE, Davis YM, Malilay J, et al. The World Trade Center bombing: injury prevention strategies for high-rise building fires. Disasters 1996;20:125-32. Tavernise S, Myers SL. Toll in Russia climbs to 41 in bombing at a hospital. New York Times. August 3, 2003. Available at: http:// www.sullivan-county.com/bush/41_russia.htm. United Nations Disaster Assessment and Coordination Team, UNDAC Mission to Lagos, Nigeria. United Nations Disaster Assessment 31 January – 7 February 2002 Munitions Depot Explosion Environmental and Humanitarian Assessment Report. Geneva, Switzerland, UNDAC (UN Disaster Assessment and Coordination Team), Feb. 7, 2002. American College of Emergency Physicians. EMTALA. Available at: http://www.acep.org/webportal/PracticeResources/ IssuesBy Category/EMTALA/default.htm. Waisman Y, Aharonson-Daniel L, Mor M, et al. The impact of terrorism on children: a two-year experience. Prehospital Disaster Med. 2003;18:242-8.

BUILDING COLLAPSE 845

chapter 170

Bridge Collapse Laura Diane Melville and Najma Rahman-Khan

DESCRIPTION OF EVENTS On the morning of May 9, 1980, the Summit Venture had just entered a difficult portion of the shipping channel leading into Tampa Bay that passed under the Sunshine Skyway Bridge. The boat was a tanker the size of two football fields. A sudden squall blew up and created almost zero visibility, and the ship’s radar ceased to function. Based on a number of factors, the captain made the decision to go forward and try to pass under the bridge. The ship rammed the south pier 700 feet from the center of the channel, causing the center span of the Skyway to collapse into the channel below. Several cars and a Greyhound bus disappeared into the Bay. Thirty-five people died in the disaster.1 There is such a dearth of medical or disaster planning literature specifically addressing the collapse of bridges that information must be gathered from newspaper and other stories to understand what has happened and what could happen. Most of the time a bridge collapses due to structural failures; however, there can be other causes such as weather (including floods, tornados, earthquakes), explosions (both accidental or nonaccidental), acts of war or terrorism, objects crashing into the bridge (such as a barge), and potential nuclear or dirty bombs. Since the events of Sept. 11, 2001 in New York City, we can easily imagine scenarios in which a bridge with major traffic burdens (including pedestrian, motor, and rail) and significant symbolism (such as the Golden Gate Bridge or the Brooklyn Bridge) becomes a target of a terrorist attack. During war, bridges become targets for those same reasons. The T-shaped Aioi Bridge was the target for “Little Boy”—the atomic bomb dropped on Hiroshima. It is important to remember that not all bridges cross water. Highway overpasses are essentially bridges, and the collapse of such structures also occurs. This kind of collapse would require interventions more like those required for structural collapses,such as urban search and rescue teams and confined-space medical interventions. A brief description of the different types of bridges may be useful in understanding the types of risks they are subject to. There are several different types of bridges, such as arch, cable-stayed, suspension, draw span, truss, and beam bridges, with the first three being the most common. Arch bridges are relatively small, usually 130 to 500 846

feet in length. This type of bridge allows no movement in horizontal bearing, so these bridges are usually located on stable ground and cross over valleys and rivers. Cable-stayed bridges are usually 300 to 1600 feet long with a continuous bridge that has one or two towers erected in the middle with support cables attaching the bridge to the towers. The towers bear the brunt of the load. This design provides strong support against earthquakes and strong winds but remains vulnerable to shifting or uneven sinking in the ground. The new Sunshine Skyway Bridge is an example of a single-tower cable-stayed bridge. Suspension bridges,such as the Golden Gate Bridge,usually span about 2000 to 7000 feet. These bridges have cables that are attached to either end to transmit the load to either anchorage. These anchorages at either side provide strong support,but the construction makes the bridge vulnerable to strong winds. The collapse of the Tacoma Narrows Bridge, also known as “Galloping Gertie,” is a famous example of the failure of a suspension bridge.2–4 The Tacoma Narrows Bridge is a case of a suspension bridge gone wrong. It collapsed in 1940 because of strong winds, but the bridge’s undulations were an attraction to locals and tourists for years before the actual collapse. Due to its suspension wire construction, there were both vertical and horizontal undulations in the bridge that contributed to its failure. During some winds, there was as much as a 28-foot disparity between the left and right sides of the bridge. Before that event, there was pressure to construct bridges to maximize “lightness, grace, and flexibility”; however, this collapse forced a reevaluation of this in favor of safety and stability.2 The impressive amateur video taken just before the collapse can be viewed on the Internet.3 Another famous bridge disaster was the May 26, 2002 collapse of the Oklahoma I-40 bridge across the Arkansas River after it was rammed by a empty oil barge. More than a dozen cars and tractor-trailers went into the river, and 14 people died. This disaster was reminiscent of the Sunshine Skyway disaster. Like the former event, there had been a number of prior incidents that could have served as a warning that this was a real possibility. The rescue effort had to be delayed several days because of the murky water conditions. Thirteen people died by drowning, and one died by blunt trauma to the head. According to the National Transportation Safety Board,

the bridge may have collapsed because of its old design; had it been retrofitted to modern standards, it may have withstood the impact.5,6 Not all bridges transport cars. During the 1997 Israeli Maccabiah Games, a pedestrian bridge (footbridge) passing over the polluted Yarkon River collapsed, killing four athletes and injuring many more. Three of the deaths were attributed to infectious complications caused by ingesting the polluted water. Medical data on the types of injuries sustained in any bridge collapse are exceedingly difficult to access, but the one available abstract reported on the minor injuries sustained by these athletes. Of the 65 people who sustained nonfatal injuries as a direct result of the bridge collapse, the most common anatomic regions of musculoskeletal injuries were the thigh (20.9%), lumbar spine (15.3%), and the foot and ankle (13.3%). The types of injury most commonly reported were sprains (49.0%) and strains (27.6%).7 However, the abstract had no information about any victims being seriously injured. It seems that all of the athletes who actually fell into the river suffered severe consequences. Information gleaned from newspaper coverage suggests that when motor vehicles or trains are involved, the degree of injury can be much more wide ranging. Material from the Sunshine Skyway collapse and the Oklahoma bridge disaster demonstrate that most of those who died had suffered major trauma, drowning, or in some cases both. Under most circumstances, it is rare for drowning victims to suffer any trauma other than cervical spine injuries.8,9 This is important for those planning to treat potential victims of injuries resulting from a collapsed bridge.

PREINCIDENT ACTIONS Each government agency (state, county, city, township) that manages a public bridge is required by the Federal Highway Administration to have a crisis management plan.2 These involve such agencies as the police, sheriff, fire, rescue, emergency medical services, coast guard, Army Corp of Engineers, Federal Aviation Administration, and railroads. Hospitals should be aware of the plans for bridges in their area and should have an understanding of how loss of the transportation route and the influx of patients will affect their facilities. This should be one of the many scenarios envisioned in the hospital disaster plan. A critical factor in this planning should be the expectation that many staff members may not be able to get to or from work—this could mean anyone from cleaning staff to a hospital’s only two trauma surgeons. Hospital representatives should be involved in the creation of the federal state and local plans because emergency departments (EDs) can expect to be the center point of any medical consequences. Important issues will be traffic re-routing, designation of receiving hospitals, etc. There are software programs available such as the Geographical Resource Intranet Portal, created by the Oklahoma Department of Transportation (ODOT), that can overlay all the area roads with information about ability to handle trucks and high traffic volume, locations

of hospitals, and other information that can allow a quick return of traffic flow. This program allowed the ODOT to detour traffic within 2 hours after the 2002 collapse of an I-40 bridge.10 Those hospitals with hyperbaric chambers should be identified in case they are required for victims or rescuers. Communication issues, both within the hospital and with outside agencies, are paramount and must be addressed prior to the event itself. This is often one of the most challenging parts of developing and implementing a disaster plan, and it should be emphasized in planning and drilling. Search and rescue teams, with divers, will likely be needed for recovery of victims trapped under structures and underwater. There must be planned routes for emergency vehicles and rescue personnel to get to and from the event site. Knowledge of the body of water (e.g., currents and pollutants) could also be critical to effective rescue efforts. If the collapse occurs due to weather, earthquake, or terrorism, there will be damage to other structures and resources including the hospital itself; chemical or nuclear weapons may be involved.11 Those who will be performing triage must be clear about the rules of mass-casualty triage, based on the principle of “the greatest good for the greatest number.”This is based on the likelihood of successful resuscitation and the resources available. Most mass-casualty triage systems tag patients with black, red, yellow, and green tags corresponding to dead, emergent, urgent, and the walking wounded, respectively. Two examples of this kind of system are the Simple Triage and Rapid Treatment (START) system and the Jump START for pediatric triage.12 A person removed from cold waters with no vital signs would be extensively resuscitated in non–mass-casualty settings and would be black-tagged in the event of a mass-casualty incident. If the bridge collapse is part of a large event, the Federal Emergency Management Agency and disaster medical assistance teams may become part of the response after the first few days. Disaster medical assistance teams are designed to be a rapid-response element to supplement local medical care until other federal or contract resources can be mobilized, or until the situation is resolved.13

POSTINCIDENT ACTIONS It is often impossible to attempt rescue without risk to the rescuer, but it is vital to secure the area as much as possible and ensure the maximum possible safety for everyone on-scene. A collapsed bridge can be particularly dangerous because the elevated structure may continue to break down. Large amounts of debris underwater can endanger divers, as can weather and current conditions. Under certain circumstances, this may include evaluation for any coincidental biologic, chemical, or radiation terrorism. Plans that are in place must be implemented in an orderly fashion. It is paramount that communication between agencies occurs as smoothly as possible. As in all of the situations addressed in this book, coordination of federal, state, and local resources will lead to the most BRIDGE COLLAPSE 847

effective and efficient handling of the situation. The conventional wisdom is that a response team must be able to stand alone for 12 to 24 hours.11,13 This isolation may be prolonged if the bridge has collapsed due to severe weather conditions or a geologic event such as an earthquake. If the hospital itself has been compromised by the surrounding events (e.g., the power is out because of an earthquake), internal as well as external disaster plans may need to be implemented. Urban search and rescue teams will likely require activation, and preliminary medical care may have to be delivered at the scene for victims who are trapped alive. If there are large numbers of victims, it will be important to bring stable patients to hospitals farthest from the scene. The walking wounded and the worried well often take themselves to the closest hospital, and the severely injured are transported there.11 Other disaster management issues that warrant inclusion in hospital disaster plans for bridge collapse include what to do with medical and nonmedical volunteers; hospital capabilities regarding trauma and pediatrics; how and where to transfer patients who require care that cannot be provided; and how to get staff to the facility if the usual traffic routes are not available.

MEDICAL TREATMENT OF CASUALTIES It is beyond the scope of this chapter to cover the detailed medical treatment of the many types of injuries that could be seen in the event of a bridge collapse. These topics are covered in other sections of the book. For any bridge over water, near-drowning will be an important mechanism of injury to expect. Although near-drowning injuries are not typically associated with other trauma, this scenario has been shown to produce both blunt injury and drowning. It is likely that the trauma victims in this situation were incapacitated by their injuries and drowned secondarily. Blast injuries will occur if there are any explosions. Primary blast injury occurs as a direct effect of changes in atmospheric pressure caused by a blast wave. Secondary blast injuries occur when objects accelerated by the energy of the explosion strike a victim, causing either blunt or penetrating ballistic trauma. Tertiary blast injuries result from a victim’s body being displaced by expanding gases and high winds; trauma then occurs from tumbling and colliding with objects. Primary blast injury mostly occurs in gas-containing organ systems, notably the middle ear, lungs, and bowel. Few victims of primary blast injury survive to require treatment.14 Hypothermia may be a factor complicating the care of both submersed and entrapped patients; however, it may in fact improve survival and neurologic outcome in some patients, particularly the drowning victims. The principle that the patient is “not dead till warm and dead”is the norm for emergency medicine,11 but if disaster triage protocols have been implemented, patients who do not have respirations or a pulse will not be resuscitated regardless of their temperature. These are the patients who will likely present the most difficult ethical and

emotional challenge for personnel on-scene and at receiving hospitals. Any victims trapped under rubble or in crushed vehicles can sustain crush injuries and may require treatment based on principles of confined-space medicine at the scene and on arrival in the ED. Head injuries are also common. As described above, pollution may complicate the treatment requirements of submersion victims. As in any disaster, stress-related exacerbations of medical illness and psychological issues will require intervention for victims, responders, and family members.11,15

CASE PRESENTATION It is mid-February, and you and one other ED attending physician are working the night shift at a level II trauma center. About 2 miles away is an interstate highway that crosses the large river in your area. The university level 1 trauma center is across the river. In fact, quite a few of your staff work at both hospitals and live on the other side of the river.The bridge is old and scheduled for repairs in the next fiscal year. Your hospital has participated in the local Office of Emergency Management and Federal Highway Management Office’s disaster planning. It is 6:00 AM,and you are getting ready for change of shift. A couple of residents come in from a smoke break and tell you they think they heard thunder, but it is a bright, beautiful day. You tell them they should quit smoking and get ready to hand over the ED.About 15 minutes later,your EMS phone rings and you are notified that there has been a terrible accident—a large fuel truck has exploded and caused the bridge to collapse. You are on standby to receive up to 50 patients. There are several vehicles on fire, and several have plunged into the icy waters below. No one is quite sure what happened, and rumors of terrorism are already spreading among your staff. Because the traffic was twoway,there are injured persons on both sides of the bridge— those on your side will be coming to your hospital regardless of their degree of injury. You notify your hospital administrator and initiate your disaster plan, including additional triage areas, notifying the operating room and all your surgeons.The clinic down the hall from your ED is opened to handle non-urgent patients. Your department chairman calls to say she is on her way in by police department helicopter, which will land nearby because your facility does not have a helipad. Patients are beginning to come in now, and your beds are filling up. Several are critically injured, with burns and blunt trauma. No victims have been recovered from the waters yet, but the coast guard is almost on scene and the search and rescue team is also en route. There are questions about chemical exposure. Several cardiologists who live next to the hospital have just arrived in the ED to help, along with a number of neighbors who want to give blood. You are the Incident Commander for your hospital and are constantly on the phone with EMS, police and fire personnel, and your counterpart at University General. More staff is on the way in. You hear the rescue divers are having trouble getting to victims because of river conditions, but your first hypothermic near-drowning victim is on his way in,by Basic Life Support (BLS) with a faint pulse and an unobtainable blood pressure reading….

848 EVENTS ASSOCIATED WITH STRUCTURAL COLLAPSE/CRASHING/CRUSHING

UNIQUE CONSIDERATIONS Bridges are most likely to collapse due to a combination of severe environmental circumstance, structural flaws, and wear and tear. However, sudden collapse caused by structural failure, impact, or attack can occur. Staff may not be able to come to work or get home if the bridge is critical for access to that area or if traffic becomes intensely snarled. Although drowning victims rarely have concurrent traumatic injuries other than cervical spine injuries, people in vehicles that slam into water and then submerge will suffer both insults. Most are unlikely to survive severe traumatic injury followed by submersion, but a patient with these types of injuries should be anticipated in this scenario. Collapse of bridges that do not cross water may lead to trapped and crushed victims requiring intervention more like those for other structural collapses, as described in studies of confined-space medicine. In addition, exposure to polluted water could lead to chemical toxicity and overwhelming sepsis.

PITFALLS Several potential pitfalls in response to a bridge collapse exist. These include the following: • Failure to plan for collapse of any local or important bridge • Failure to be aware of and incorporate plans already in place by state and local authorities • Failure to have hospital disaster plans in place prior to an incident • Failure to include the possibility of bridge collapse in plans for larger events such as earthquakes, flooding, or a terrorist attack • Failure to consider larger events (e.g., earthquake or flood) when planning for a possible bridge collapse • Failure to consider that such larger events (e.g., earthquake or flood) may compromise the functioning of the hospital itself

• Lack of knowledge regarding water conditions, including level of pollution and chemical content of polluted water • Failure to plan alternate ways for staff to get to the hospital REFERENCES 1. “A blinding squall, then death” St. Petersburg Times. Available at www2.sptimes.com/weather/SW.2.html. 2. Northwestern University’s Infrastructure Technology Institute’s Bridge Disaster Links Page. Available at: http://www.iti.nwu. edu/links/bridges/disasters.html. 3. Mark Ketchum’s Bridge Collapse Page. Available at: http://www.ketchum.org/bridgecollapse.html. 4. NOVA Online. Super Bridge: Resources. Available at: http://www. pbs.org/wgbh/nova/bridge/resources.html. 5. CNN.com Divers find three victims from bridge collapse May 27, 2002 Available at: http://archives.cnn.com/2002/US/05/26/ barge.bridge. 6. CBS news Web site. Still searching for the bodies. Available at: http://www.cbsnews.com/stories/2002/ 05/28/national/main 510320.shtml. 7. Kolt GS, Wajswelner H, Adonis M, et al. Injury Toll Following the Maccabiah Games Bridge Collapse: Implications for Sports Medicine Coverage. Adelaide, Australia: Australian Conference of Science and Medicine in Sport; 1998. 8. Olshaker JS. Submersion. Emerg Med Clin North Am. 2004;22:357. 9. Orlowski JP, Szpilman D. Drowning rescue, resuscitation and reanimation. Pediatr Clin North Am. 2001;48:627–46. 10. Adams J. ODOT gets a GRIP on transportation. May 1, 2003. Available at: http://www.geospatial-online.com/geospatialsolutions/article /articleDetail.jsp?id=56069. 11. Hogan DE, Burnstein JL, eds. Disaster Medicine. Philadelphia: Lippincott,Williams and Wilkins; 2002. 12. Lovejoy JC. Initial approach to patient management after largescale disasters. Clin Pediatr Emerg Med. 2002;3:217–23. 13. U.S. Department of National Security. National Disaster Medical System Web site. Available at: http://www.oep-ndms.dhhs.gov. 14. Wightman JM, Gladish SL. Explosions and blast injuries. Ann Emerg Med. 2001;37:664–78. 15. Barbera JA, Lozano M. Urban search and rescue medical teams: FEMA task force systems. Prehospital Disaster Med. 1993; 8;349–55.

BRIDGE COLLAPSE 849

chapter 171

Human Stampede Angela M. Mills and C. Crawford Mechem

DESCRIPTION OF EVENT Human stampede is one of the most disastrous examples of human crowd behavior. Triggers include building fires and evacuations and a rush for ingress or egress at large sporting events or concerts. In large crowd stampedes, there are often serious injuries and fatalities resulting from crushing and trampling. On Nov. 28, 1942, a fire began at the Coconut Grove, a popular Boston nightclub, causing widespread panic and a stampeding crowd. Inward-opening doors and doors sealed shut prevented escape. As a result, 491 persons died and over 400 were injured.1 On Apr. 15, 1989, during a semifinal cup soccer game in Sheffield, England, there was a large crushing incident of late-arriving fans who entered a confined area at the Hillsborough stadium. Persons were unable to escape this area due to a surrounding fence; 95 died and more than 400 required hospital treatment.2,3 These are only two examples of countless episodes of human stampede. A model for crowd disasters aids in understanding the causes, prevention, and alleviation of an ongoing incident. The four elements of this model form the acronym FIST and include the force (F) of the crowd or crowd pressure; information (I), whether real or perceived, on which the crowd acts; physical space (S) involved in the disaster; and time (T) or duration of the event.4 Forces are generated by persons pushing and leaning against each other. There is often a lack of communication from front to back in a crowd, with persons in the rear pushing forward, injuring those in front. As individuals are injured or fall, they become obstacles to the movement of others. Access to the fallen becomes impossible.4,5 Large numbers of humans involved in a disaster event tend to exhibit mass behavior and do what others do. As people crowd and jamming occurs,alternative exits are frequently overlooked or not used adequately, resulting in additional injuries.6 Escape panics have been studied extensively and have the following characteristics. Panicking persons attempt to move faster than usual and begin pushing and having physical contact with others. This movement, especially around bottlenecks, becomes uncoordinated. Exits become clogged. The pressures generated by a crowd may exceed 4500 N (1000 lb), allowing steel railings to bend and brick walls to fall.4,6,7 850

The widening of a corridor has been demonstrated to slow down movement of panicking persons rather than allowing for faster movement. In a study performed with mice, the most efficient escape was a door large enough for only one mouse to fit through at a time. As door widths were increased, the mice ceased lining up and began competing with one another, prolonging the escape rate.8 This behavior also pertains to rushing pedestrians who will block an exit that they could safely pass through at walking speed. Jamming and clogging may be minimized in the construction of venues by avoiding bottlenecks and placing columns asymmetrically in front of exits to improve outflow.6 A human stampede leads to various injuries and fatalities, with traumatic asphyxia being the most common cause of death and serious injury.The majority of deaths are due to compressive asphyxia as persons are stacked vertically on top of one another or horizontally with associated pushing and leaning forces. Traumatic asphyxia is caused by a severe crush injury to the chest or upper abdomen. The mechanism is believed to be acute, severe venous hypertension.9,10 The various presentations include asystolic cardiac arrest, status epilepticus, prolonged confusion, and cortical blindness.2 The majority of signs are confined to the upper torso, with the lower torso being spared. Clinical manifestations include facial edema and petechiae, cranial cyanosis, subconjunctival hemorrhage, exophthalmos, and ecchymotic hemorrhages of the face and upper chest. Life-threatening pulmonary, cardiac, and gastrointestinal injuries may occur with traumatic asphyxia. These include pulmonary contusion, pneumothorax, myocardial contusion, flail chest, liver and splenic lacerations, and gastrointestinal hemorrhage. Superior vena cava syndrome may mimic the features of traumatic asphyxia and should be ruled out. Basilar skull fractures may also present similarly. Skull fractures are rare in traumatic asphyxia because the compressive force is usually to the chest or upper abdomen. Morbidity and mortality are associated with the severity and duration of compression and the high incidence of associated injuries. These injuries should be ruled out by computed tomography scan, duplex ultrasound, or echocardiogram as dictated by the physical examination. Long-term neurologic sequelae are rare, and full recovery may be achieved with

early reestablishment of ventilation and correction of hypoxia.9,10 In addition to traumatic asphyxia and its associated injuries,many other injuries may occur secondary to stampede including musculoskeletal trauma, soft tissue crush injuries, acute right heart strain,3 and brachial plexus injuries.2 Crush injuries, including crush syndrome, compartment syndrome, and acute traumatic ischemia, lead to hemorrhage, edema, and hypoperfusion with resulting tissue hypoxia and ischemia. Although any tissue may be affected, nerve and muscle located in myofascial compartments are at increased risk. Cellular death leads to release of potassium, phosphate, and myoglobin as part of crush syndrome with rhabdomyolysis. Most crush syndromes occur as a result of compression for 4 or more hours. Complications include hypovolemia, hypotension, and disseminated intravascular coagulation, with renal failure being the most serious complication. Peak creatine kinase level has been shown to correlate with the occurrence of renal failure and mortality.11–13

PREINCIDENT ACTIONS Human stampedes can occur at venues with or without organized mass-gathering medical care. Mass-gathering events require extensive coordination of various agencies including emergency medical services, fire and police departments, local emergency departments and hospitals, local government agencies, and others. Factors in planning for large events may include the type and duration of event, physical plant and location characteristics, routes of ingress and egress, and age of attendees. As a result of previous stampedes, much has been learned for the prevention of future incidents. Factors used in prevention may include providing reserved seating rather than general admission to large events, avoiding use of fixed barricades, ensuring availability of multiple exits, minimizing bottlenecks, limiting access to alcohol, and having the crowd form into queues.4,14,15

POSTINCIDENT ACTIONS The Incident Command System, a standard emergency management system used throughout the United States, should be activated to coordinate the response to a human stampede. Establishment of effective communication is vital. Prehospital providers must commence triage and rapid treatment and determine the most sensible distribution of patients to area hospitals. Hospitals, and in particular emergency departments, should have disaster protocols available to effectively handle masscasualty events.16

MEDICAL TREATMENT OF CASUALTIES Standard trauma protocols should be followed when caring for victims of human stampede. Treatment of traumatic asphyxia is largely supportive and aimed at the

associated injuries, which include pulmonary and myocardial contusion, pneumothoraces, intra-abdominal injuries, and neurologic injuries. Prompt delivery of oxygen and effective ventilation compose the mainstay of treatment, as well as elevation of the head of bed. Prognosis is excellent for those persons who survive the initial crush injury, with a recovery rate of approximately 90% for patients surviving the initial hour.10 As massive compression occurs, one needs to evaluate a patient who has incurred injury in a stampede for crush injuries including the sequelae of crush and compartment syndromes. The goal of therapy is to prevent renal failure by avoiding hypotension and maintaining urine output. The administration of appropriate intravenous fluid therapy with crystalloid solution should be initiated as early as possible, even before extrication, to maximize intravascular volume and renal perfusion. Urine output should be maintained at approximately 200 mL/hour. Alkalinization of the urine has been shown to increase the solubility and excretion of myoglobin and prevent renal failure. The urine pH level should be maintained between 6 and 7. The use of mannitol is controversial but may aid in diuresis. If compartment syndrome is suspected, compartment pressures should be measured directly, and, if elevated, fasciotomy may be required.11–13 Hyperbaric oxygen therapy has also been shown to be effective in severe extremity crush injuries.17

CASE PRESENTATION It is Saturday night, and more than 1200 persons have gathered at a large downtown nightclub to hear a famous rock band perform. A fire starts as a result of patrons smoking in the lavatory and spreads quickly through the building. Persons panic and rush to the closest exits, only to find many of them locked. Those in the rear of the crowd push forward, causing many of those in front to fall and become obstacles for those rushing forward. A call is placed to 9–1–1 and emergency responders arrive but have difficulty reaching patients. There are well over 100 persons injured. Patients begin arriving at your emergency department. A 22-year-old woman is transported receiving oxygen and having facial edema and petechiae. A 23-year-old man is brought in unconscious with multiple ecchymoses about the face and torso. Other patients continue to arrive.

UNIQUE CONSIDERATIONS In the event of a human stampede, access to patients early on, as well as extrication of patients, may be difficult if not impossible. The safety of emergency responders must be considered. Traumatic asphyxia and the crush syndrome are rare clinical entities that may be associated with high morbidity and mortality. Early and aggressive therapy, often initiated in the prehospital setting and even before extrication, may be required to ensure the best possible outcome. Adequate planning, public education, and interagency cooperation play key HUMAN STAMPEDE 851

roles in minimizing the risk of human stampede and its associated injuries and deaths.

PITFALLS Several potential pitfalls in response to a human stampede exist. These include the following: • Failure to adequately plan and coordinate the necessary agencies needed to respond to mass-gathering events • Failure to alert appropriate persons, hospitals, and emergency departments to a human stampede event • Failure to rapidly restore oxygenation and ventilation to victims of a human stampede • Failure to identify and aggressively treat associated injuries of traumatic asphyxia and massive compression REFERENCES 1. Saffle J. The 1942 fire at Boston’s Cocoanut Grove nightclub. Am J Surg. 1993;166:581-91. 2. Wardrope J, Hockey M, Crosby A. The hospital response to the Hillsborough tragedy. Injury 1990;21:53-54. 3. Grech E, Bellamy C, Epstein E, et al. Traumatic mitral valve rupture during the Hillsborough football disaster: case report. J Trauma. 1993;35:475-6.

4. Fruin J. The causes and prevention of crowd disasters. In: Smith R, Dickie J, eds. Engineering for Crowd Safety. Amsterdam: Elsevier Science Publishers; 1993:99-108. 5. Johnson N. Panic at “The Who Concert Stampede”: an empirical assessment. Soc Probl. 1987;34:362-73. 6. Helbing D, Farkas I, Vicsek T. Simulating dynamical features of escape panic. Nature 2000;407:487-90. 7. Low D. Statistical physics: following the crowd. Nature 2000;407:465-66. 8. Saloma C, Perez G, Tapang G, et al. Self-organized queuing and scale-free behavior in real escape panic. Proc Natl Acad Sci USA. 2003;100:11947-52. 9. DeAngeles D, Schurr M, Birnbaum M, et al. Traumatic asphyxia following stadium crowd surge: stadium factors affecting outcome. Wisc Med J. 1998;97:42-5. 10. Dunne J, Shaked G, Golocovsky M. Traumatic asphyxia: an indicator of potentially severe injury in trauma. Injury 1996;27:746–9. 11. Smith J, Greaves I. Crush injury and crush syndrome: a review. J Trauma. 2003;54:S226-30. 12. Malinoski D, Slater M, Mullins R. Crush injury and rhabdomyolysis. Crit Care Clin. 2004;20:171-92. 13. Delaney J, Drummond R. Mass casualties and triage at a sporting event. Br J Sports Med. 2002;36:85-8. 14. Grange J. Planning for large events. Curr Sports Med Rep. 2002;1:156-61. 15. Milstein A, Maguire B, Bissell R, et al. Mass-gathering medical care: a review of the literature. Prehospital Disaster Med. 2002;17: 151-62. 16. Schultz C, Koenig K, Noji E. Disaster preparedness. In: Marx J, Hockberger R, Walls R, et al, eds. Rosen’s Emergency Medicine. 5th ed. Vol III. St Louis: Mosby; 2002:2631-40. 17. Bouachour G, Cronier P, Gouello J, et al. Hyperbaric oxygen therapy in the management of crush injuries: a randomized doubleblind placebo-controlled clinical trial. J Trauma. 1996;41:333-9.

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chapter 172

Mining Accident Dale M. Molé

DESCRIPTION OF EVENT The Industrial Revolution significantly increased the demand for fossil fuels. In America, outcrop deposits of coal along the James River in Virginia supplied fuel for blacksmith forges as early as 1702, and when surface supplies diminished, miners followed the coal seams underground. Deeper mines combined with poor ventilation increased the formation of explosive mixtures of methane. The inevitable occurred in 1810 with the first coal mine explosion.1 Mine disasters in the first half of the twentieth century involved hundreds of deaths in each accident. Advances in mine technology and safety have greatly reduced the hazard of underground occupations since the early days, but they have not completely eliminated danger. In the United States alone, 169 miners have lost their lives in coal mine mishaps since 1980.2 In the immediate aftermath of a mine accident, surviving until rescue is the first priority of trapped miners. Obstacles to survival include poor communication, extreme darkness, confined space, hypothermia, toxic atmosphere, and injuries. One of the most challenging aspects of any rescue operation is establishing the existence, location, and condition of any survivors. Mine communication systems are often damaged or unreachable in a disaster. Lowfrequency radio waves can penetrate rock and offer promise for minewide alarm and communication devices. Seismic locators can detect the vibrations produced by trapped miners in some circumstances. If a survival borehole is drilled, tapping on the drill using prearranged tap codes provides useful information. Shutting off electricity to reduce ignition sources for fires or explosions is often the first action after a mine accident. Plunged into absolute darkness, the miners must rely on limited-duration battery-powered helmet lights, making survival efforts more arduous. Cool ambient mine temperatures combined with water from mine operations, aquifers, rain, or flooding creates a major problem for miners who get wet. Immersion in water increases conductive heat loss by as much as fivefold, hastening the onset of hypothermia. Adaptive survival mechanisms (e.g., shivering thermogenesis) increase metabolic heat production by two to five times,

but they also significantly increase oxygen consumption and carbon dioxide production—a major problem in small, airtight spaces.3 Hypothermia depresses the central nervous system, impairs judgment, and prevents the accomplishment of appropriate survival actions. The atmosphere within a mine is composed of many gases. Early miners used canaries as biologic atmosphere monitors because the birds are overcome by relatively small amounts of noxious gases or damps. The word damp, originally derived from the German word dampf meaning “fog” or “vapor,” is the mining vernacular to describe any mixture of gases in a underground mine, usually noxious or oxygen deficient. Firedamp primarily refers to methane resulting from the decomposition of coal or other carbonaceous material decaying in an anoxic environment and is explosive when present in air in concentrations of 5% to 15%. The Davy safety lamp, one of the earliest detection devices, detects concentrations as low as 1%. Flame color and height indicates the amount of methane present. Low oxygen levels extinguish the flame entirely. Special colorimetric detectors are now used. Blackdamp, referring to an anoxic mixture of nitrogen and carbon dioxide, extinguishes flame and causes death by suffocation. Carbon dioxide is produced by the complete combustion of carbonaceous material, metabolism of miners and animals, decay of organic matter, oxidation of coal, or the chemical action of acid water on carbonates. Chokedamp is any anoxic mixture of mine gases. Whitedamp contains large amounts of carbon monoxide; is found in the exhaust of diesel engines, detonated explosives, wood or coal fires; and is the result of the incomplete combustion of carbonaceous materials. This colorless, tasteless, odorless gas competes with oxygen for hemoglobin binding sites and binds with an affinity 218 times greater. The oxyhemoglobin dissociation curve is transformed from the normal sigmoid to an asymptotic shape, impairing or preventing oxygen transport to the tissues. Tissues with high oxygen demands (e.g., brain and heart) are among the first affected. Symptoms include fatigue, dizziness, headache, seizures, unconsciousness, and hypotension. Afterdamp is the gas produced by an explosion. It almost always contains dangerous amounts of carbon 853

monoxide and oxides of nitrogen, reported in terms of nitrogen dioxide that can form nitric acid in the lungs. Stink damp, or hydrogen sulfide gas, has a characteristic pungent smell of rotten eggs. The byproduct of organic decomposition, the action of mine acid on sulfur minerals, or the burning of explosives containing sulfur such as black powder or dynamite, it is soluble in water and may be liberated whenever a mine pool is agitated. It is extremely poisonous and has a mechanism of action similar to cyanide. High concentrations produce loss of consciousness, seizures, and death with just a few breaths. Other gases include highly explosive hydrogen gas from battery-charging stations; sulfur dioxide, which creates sulfuric acid in the lungs; and acetylene resulting from methane heated in a low-oxygen atmosphere or the interaction of calcium carbide with water. Oxygen is essential for survival. It is the partial pressure of oxygen, not the absolute percentage, that determines whether the ambient atmosphere can sustain life. Fire or metabolic activity can rapidly consume the available oxygen in a confined, airtight space. Flooding can compress air pockets, raising the total pressure and therefore the partial pressure of oxygen to dangerous levels. Since air is 21% oxygen and normal atmospheric pressure (1 atmosphere absolute [ata]) is equivalent to 760 torr, the partial pressure of oxygen is 760 times 0.21, or 160 torr. Expressed in atmospheres absolute, this would be 1 ata times 0.21, or 0.21 ata. If the atmospheric pressure were doubled to a total pressure of 1520 torr, or 2 ata, the partial pressure of oxygen could be expressed as (1520 torr × 0.21) = 320 torr, or (2 ata × 0.21) = 0.42 ata. Pulmonary oxygen toxicity results from prolonged exposure to high-oxygen partial pressures in excess of 0.5 ata. Breathing 0.6 ata oxygen produces respiratory symptoms in the majority of humans in less than 24 hours.4 Conversely, as survivors in a closed space consume the available oxygen, the partial pressure of oxygen falls, producing signs and symptoms of hypoxia such as dyspnea (i.e., air hunger), cyanosis, impaired cognition, poor muscle coordination, and unconsciousness. Nitrogen composes 79% of our atmosphere and is generally considered an inert (metabolically inactive) gas. When breathed at increased pressure, however, it produces a narcotic effect in a dose-dependent fashion; that is, the higher the partial pressure of nitrogen, the greater the narcosis. Nitrogen narcosis causes both cognitive and psychomotor disturbances. Breathing room air at 4 to 7 ata results in exposure to elevated partial pressures of nitrogen high enough to cause delayed response to auditory and visual stimuli, impaired neuromuscular coordination, a loss of clear thinking, and a tendency toward idea fixation. The effect is similar to ethanol intoxication, and it can significantly impair the ability of miners to take the necessary steps to ensure survival. Carbon dioxide comprises only 0.001 ata, or one-tenth of 1% of the atmosphere. It is a by-product of cellular metabolism, and for each standard cubic foot of oxygen consumed an almost equal amount of carbon dioxide is produced. If the carbon dioxide level climbs past 0.10 ata, unconsciousness is soon followed by death. In an airtight space, it is the carbon dioxide level that limits survival, not the amount of oxygen.5

In prolonged survival situations, food and water also become important considerations. Inadequate caloric intake can produce starvation diarrhea, making survival less likely.6

PREINCIDENT ACTIONS One of the most significant advances in mine rescue operations occurred in 1856 with the introduction of self-contained breathing apparatus, allowing rescuers to conduct operations with increased safety. Part 49 of Title 30 of the Code of Federal Regulations requires every mine in the country to have mine rescue teams. It stipulates how many members each team should have and outlines physical and training standards and required equipment, maintenance, and storage. Modern mine rescue, with enhanced team training and improved equipment, has transformed chaotic, uncoordinated rescue attempts into efficient, well-coordinated group efforts. The full integration of medical elements into the team is essential for a successful outcome to rescue operations. Today’s teams use modern gas detection and communication equipment, seismic locators, geophones, and other devices to locate miners. Rescue vans are outfitted with breathing apparatus, recharging facilities, hand tools, medical supplies, and gas analysis equipment. A qualitative and quantitative knowledge of constituent gases within the mine provides important clues to past events, as well as current atmosphere conditions such as elevated carbon monoxide levels suggestive of a fire. Mine emergency operations teams can drill boreholes down from the surface to reach miners. Once a smalldiameter “survival hole” is drilled, rescuers can lower microphones, lights, and cameras into the mine to help locate the miners, to determine their situation, and to lend support and assistance while a rescue hole is drilled. Trapped miners can be safely hauled to the surface in specially designed “rescue capsules.”

POSTINCIDENT ACTIONS The first few hours after the emergency are the most critical. Coordination of mine rescue teams, mine personnel, and local, state, and federal officials is essential. A command center forms the hub of mine rescue operations and contains communications equipment, underground diagrams, and local area maps. As mine rescue teams arrive, a rotation schedule is prepared, designating which teams are to be the exploration team, backup team, and standby team. A bench area with running water allows breathing apparatus to be cleaned, tested, and prepared. Establishing perimeter security is essential to keep roads open for emergency personnel and to ensure that curious bystanders do not hinder rescue efforts or become injured while on mine property. Company personnel or police officers should guard all routes to the mine. A press center should be established away from the disaster site and should be the only area where news media

854 EVENTS ASSOCIATED WITH STRUCTURAL COLLAPSE/CRASHING/CRUSHING

receive information. A public affairs officer will authorize, issue, and ensure the accuracy of the information being released to the public. The family waiting area should be away from any rescue activity and the media center. Provision should be made to feed and house rescue personnel during an emergency. Food can be catered or brought in from a nearby restaurant. The American Red Cross is skilled at providing disaster relief services. Nearby motels can often provide sleeping quarters, or if none are available, tents and cots can be set up at the rescue site. Ensuring adequate field hygiene is critical to preventing infectious disease outbreaks among rescue personnel. Mine exploration is the process of assessing conditions underground and locating miners during a rescue or recovery operation. The safest route into the mine is determined before anyone goes underground. In a shaft mine, the cage (i.e., elevator) is thoroughly tested for proper operation, and the shaft is tested for the presence of gases, smoke, or water. In some disaster situations, conditions may make it possible to begin the initial exploration without selfcontained breathing apparatus. This “barefaced” exploration is conducted only when the ventilation system is operating properly and gas tests demonstrate a safe atmosphere. Backup crews with apparatus are stationed nearby, ready to perform a rescue if necessary. Barefaced exploration stops where disruptions in ventilation are discovered, when gas analysis indicates the presence of noxious or explosive gases or an oxygen deficiency, or when smoke or damage is encountered. A “fresh air base” is usually established at the point where conditions no longer permit barefaced exploration. Teams equipped with breathing apparatus continue exploration from the fresh air base. Typical mine rescue equipment includes gas detectors, oxygen indicators, communication equipment, thermal imaging cameras or heat-sensing devices, link-line, map board and marker, scaling bar, walking stick, stretcher, first aid kit, fire extinguisher, tools, blankets, and extra breathing apparatus. Before going underground, each team is briefed about what has happened in the mine and what conditions currently exist. Since every underground coal mine contains harmful gases, dust fumes, and smoke, a ventilation system draws air from the surface via the main intake shaft. Ventilation controls force air to move in certain directions and at certain velocities to safely ventilate all sections of the mine. The main fan creates a pressure differential and must be monitored or guarded to ensure the rescue team’s safety while underground after the fresh air base is established and exploration is under way. Changes in ventilation are only made by the command center. As the team advances through the mine, all ventilation controls are examined. Team members must be able to recognize damaged ventilation controls, determine the direction and velocity of ventilation air by using an anemometer or smoke tube, measure the cross-sectional

area of a mine entry, and calculate the volume of air by using the area and velocity. The quantity of air (measured in cubic feet) is equal to the area (in square feet) multiplied by the velocity (in feet per minute.) Fires in underground mines are especially hazardous because they pose explosion hazards, consume oxygen, and produce smoke, toxic gases, and heat. Ventilation is always maintained during a fire to carry off explosive gases and distillates away from the fire area and to direct the smoke, heat, and flames away from the team. The most frequent cause of explosions in coal mines is the ignition of methane gas, coal dust, or a combination of the two. Explosions can blow out roof supports, damage ventilation controls, twist or scatter machinery, and ignite numerous fires. Roof and ribs can be weakened, and fires can be spread. Further explosions may occur because of damage to the ventilation system during the initial explosion.

MEDICAL TREATMENT OF CASUALTIES In a disaster in which several miners are trapped underground, or in which injuries are sustained after an explosion, roof fall, or fire, a temporary medical treatment facility should be established. After initial stabilization, a carefully considered means of patient transport may include ambulances or evacuation aircraft, with medical crew on standby. If large numbers of corpses are being recovered from the mine, a temporary morgue is necessary.

UNIQUE CONSIDERATIONS Delayed care for contaminated wounds and crush injuries, as well as the synergistic effects of toxic gases, hypothermia, and inadequate nutrition make medical management of the victims of a mining accident especially challenging. Provision for decontamination is essential after prolonged underground dwelling. Carbon monoxide poisoning may require treatment with hyperbaric oxygen.

PITFALLS Several potential pitfalls in response to a mining accident exist. Failure to consider the effects of elevated pressure in mine flooding situations may result in death or permanent disability upon rescue due to decompression sickness. In addition, inadequate medical integration into mine rescue team training may result in suboptimal performance in real emergencies, leading to preventable morbidity and mortality.

MINING ACCIDENT 855

CASE PRESENTATION: QUECREEK MINE DISASTER On the evening of July 24, 2002, miners working 240 feet underground in the Quecreek coal mine breached a wall separating them from the water-filled Saxon mine. One hundred fifty million gallons of water flooding into the mine compressed the air to more than twice the normal atmospheric pressure. At the request of local officials, U.S. Navy recompression chambers, normally used for submarine rescue operations, were set up in a barn on the William Arnold family farm within 18 hours of the first call for assistance. Nine multiplace recompression chambers, five small monoplace chambers, and 60 Navy personnel were on site and ready to receive patients. After the correct position was determined via global positioning system coordinates,a 6-inch survival hole was drilled. When the drill was shut down, tapping was heard on the other end. Nine taps were sent from topside and nine taps were returned from below, indicating that nine miners were alive. High-pressure air pumped down through the drill rig provided a source of fresh air and helped to prevent water from rising within the mine. Turbine pumps at the mine entrance pumped water out of the mine, but at a rate that would take weeks to pump the mine dry. A 32-inch rescue hole was drilled. A cylindrical yellow steel cage, the rescue capsule, would lift miners one at a time up 245 feet through the hole. A remote video camera attached to the capsule would assist in determining conditions within the mine and look for signs of life. Since most of the rescue hole was unsheathed and could collapse at any time, food, water, and blankets were loaded into the basket for the first trip below.

REFERENCES 1. Kravitz J. An Examination of Major Mine Disasters in the United States and a Historical Summary of MSHA’s Mine Emergency Operations Program. Available at: http://www.msha.gov/ S&HINFOTECHRPT/MED/MAJORMIN.pdf. 2. United States Mine Rescue Association. Available at: http://www. usmra.com. 3. Danzl D, Prozos R, Hamlet M. Accidental hypothermia. In Auerbach PS,ed:Management of Wilderness and Environmental Emergencies. St Louis: Mosby; 1989.

To prevent rapid depressurization when the drill pierced the mine, a special cap for the rescue hole was designed and rapidly constructed on site, allowing the removal of miners while maintaining pressure in the mine. Once at normal pressure, the miners had about 15 minutes before the onset of decompression sickness symptoms. During this latent period, they had to be moved from the rescue hole, had to undergo a quick medical examination and decontamination, and had to be returned to depth in the recompression chambers and then decompressed using tables developed at the Navy Experimental Diving Unit in Panama City, Florida, for submarine rescue. Working at full capacity, pumps were able to lower the water level and reduce the pressure in the mine at a rate of about 10 cm of water per hour in what turned out to be an almost perfect air saturation decompression schedule. Shortly after midnight, the first miner reached the surface. Covered in coal dust from head to toe, he was carried up the hillside to the decontamination tent, where his clothes are cut away and a cursory medical history and examination were conducted. After soap and warm water decontamination, he was quickly moved to the medical treatment area. While the civilian emergency medical technicians started an intravenous line for the patient, Navy personnel obtained vital signs and performed a physical examination. The process was repeated eight more times, with the last miner being brought to the surface at 2:45 AM. One patient required treatment in the recompression chamber after suffering symptoms of decompression sickness.7

4. Dougherty J, Styer D, Eckenhoff R. The Effects of Hyperbaric and Hyperoxic Conditions on Pulmonary Function During Prolonged Hyperbaric Chamber Air Saturation Dives. Bethesda, Md: Undersea Biomedical Research; 1981. 5. Molé D. Submarine Escape and Rescue: An Overview. San Diego, Calif: Submarine Development Group One; 1990. 6. House C, House J, Oakley H. Findings from a simulated disabled submarine survival trial. Undersea Hyperb. Med. 2000, Winter; 27(4):175–83. 7. Molé D. Steaming to assist at the Quecreek Mine disaster. Navy Med. 2002;93:18–29.

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chapter 173

Submarine or Surface Vessel Accident Steven T. Cobery and Dale M. Molé

DESCRIPTION OF EVENT Vessels that travel on the surface of the water fulfill many vital needs in support of the nations of the world today. Oversea shipping remains the preeminent means for transporting large amounts of material internationally.Naval vessels actively deploy, conducting missions throughout the world with conventional and special weapons aboard. Within coastal and near-land waters, millions of fishing vessels of varying sizes scour the seas, providing both a vital food source and a substantial addition to many local economies. Huge cruise liners offer every conceivable type of enjoyment and relaxation for the millions of vacationers they entertain each year. Submarines, almost exclusively military in usage, silently and stealthily patrol every ocean on earth, often under adverse conditions and far removed from readily available medical attention. Each of these segments of the shipping world poses very unique problems when it comes to the medical care of the personnel and passengers aboard. The medical facilities aboard most ships are sparse because space is a scarce commodity on most vessels. The capability of first responders is impaired both by their level of knowledge and training and the amount and quality of available medical equipment. Dedicated, medically trained personnel exist only on larger ships; the role of the “ship’s doc” is often a collateral duty of nonmedical personnel on smaller commercial vessels. Diagnostic imaging and laboratory testing are nonexistent in almost all cases. Communication equipment capabilities vary from very advanced satellite voice communications to visual line-ofsight signaling. The challenges posed by a seaborne masscasualty incident or disaster to shore-based facilities are enormous. All sea traffic faces the common foe of an unpredictable and often hazardous work environment. The inner workings of any vessel afloat are choreographed in an effort to conserve energy, personnel, money, and space. Imagine the occupational hazards present in a land-based facility that combines a power plant powerful enough to light several neighborhoods, a processing facility capable of independently handling tons of material daily, and a mechanical plant with a vast array of rotating machinery and high-pressure systems. The occupational hazards of these facilities alone produce

huge risks for their workers. Now take this facility, place it on a moving platform that has approximately onequarter the footprint, and operate it with efficiency in an external environment that can range from dead calm to “the perfect storm”—that is, 30-foot waves with wind gusting to 100 miles/hour. The risks for mass casualties and accidents exponentially increase due to the constraints placed by operating at sea in a dangerous environment, both internal and external to the ship. Three types of casualties commonly plague all shipping vessels: fire, high-pressure/high-temperature occupational exposures, and flooding/drowning. Fires are often called a ship’s worst enemy. Because of the myriad of flammable and combustible materials onboard the ship, all classes of fires represent an omnipresent and often fatal danger at sea. In addition to the fire itself, smoke inhalation, electric shock, exposure to toxic gases, and chemical burns secondarily compound the casualties generated by an onboard fire. Consequently, firefighting skills and equipment occupy important places in the priorities of the crew. Fires can occur virtually anywhere on the ship and from any source. The power plant and hydraulic plants represent the majority of fire locations.1 The priority of the crew in the event of a fire is first to extinguish the fire, and second to attend to the casualties. This prioritization can sometimes delay bringing injured persons to the attention of medical facilities, particularly when the fire occurs at sea rather than pier side. In addition to fires in the propulsion plant, occupational exposures to high-pressure and high-temperature gases and fluids uniquely challenge the onboard medical capabilities. Most ships are powered by one of four means: steam, diesel-electric, gas turbine, and nuclear.2 Each employ high-temperature, high-pressure gases to turn the prime mover, a turbine, often rotating at speeds in excess of 2000 revolutions per minute. Catastrophic rupture of the piping system in the propulsion plant can rapidly lead to death within minutes in the closed compartments of the engine room. Focal exposure to these fluids causes burns, high-pressure stream-penetrating injuries, toxic inhalation or ingestion, or blunt trauma. With nuclear propulsion, radiologic exposure complicates both the injury and its treatment. A unique feature of maritime engineering applications is that the mechanical and auxiliary systems of the ship are not restricted to 857

a defined industrial space; high-pressure air, hydraulics, and inert gas systems run the length of the ship, including living, recreation, food service, and open deck spaces. In any maritime setting, water supports, passes through, and sometimes surrounds the hull of the vessel. The sheer power of the ocean adds a dimension of hazard not seen on land. Flooding on board is often not the result of a breach in the hull itself; most often, it is the result of a cooling water system failure or hull penetration interlock failure. The force of a sudden inrush of water can easily cause primary blunt trauma or secondary trauma associated with falls or impact. Drowning casualties, whether due to persons being swept overboard or occurring as a result of catastrophic flooding, frequently present themselves in a more delayed fashion by nature. Anoxic brain injury, hypothermia, and cardiorespiratory failure are common complications.3 The constant presence of the power of the sea makes these types of casualties a continuous threat. Submarine disasters provide their own unique challenges. Submarines sink because of uncontrolled flooding. Only marginally buoyant by design, relatively small amounts of flooding can prevent a submarine from surfacing, especially if propulsion is lost. If this happens in the deep ocean, there are no medical issues since the submarine implodes once crush depth is exceeded. However, since collisions are most likely to occur over the continental shelf, having survivors trapped in a sunken submarine is a real possibility. The decision to await rescue or to begin escape depends on the external as well as the internal environment of the submarine. In water deeper than 180 m, escape is not currently an option, despite a hostile internal submarine environment (i.e., high pressure, low oxygen, toxic gases). Weather over the disaster site may prevent the timely rescue of survivors. The ability for a submarine crew to survive for between 5 and 7 days is the ideal goal, but the nature of the disaster may result in significantly shorter times. Barriers to survival are many. The ingress of water reduces the internal submarine volume, compressing the air and subjecting the crew to an elevated atmospheric pressure. As the total pressure increases, the partial pressure of constituent gases increases as well. Oxygen and nitrogen, the primary constituents of air, are lethal at high partial pressures. Central nervous system oxygen toxicity can cause death in a matter of minutes. High partial pressures of nitrogen produce narcosis in a dosedependent fashion, as well as loading tissue with excess nitrogen. Survivors with nitrogen-saturated tissues must be decompressed or slowly returned to normal atmospheric pressure to avoid potentially fatal decompression sickness. Carbon dioxide produced by human metabolism is the limiting factor for submariners trapped in an airtight compartment, since carbon dioxide climbs to deadly levels before oxygen becomes insufficient to sustain life. Since the average ocean temperature is 4˚C, clothing wet from flooding can quickly lead to hypothermia. Shivering helps to maintain core temperature but markedly increases the consumption of oxygen and the production of carbon dioxide. Toxic gases from fire or chlorine produced by flooded batteries may force the

crew to use emergency breathing apparatus or escape under unfavorable conditions.4 Submarine escape is potentially hazardous under the best conditions. Pulmonary barotrauma resulting in arterial gas embolism, as well as fulminate decompression sickness, are conditions that may occur and require immediate hyperbaric oxygen treatment.

PREINCIDENT ACTIONS Hospital staff, emergency department personnel, outpatient facilities, and port control authorities should have an established, well-rehearsed plan to initiate reliable communications in a timely manner to ensure the prepared receipt of casualties. Assigning geographic areas of responsibility to primary receiving facilities will simplify routing of the injured and improve response times. Mass-casualty plans, which integrate local, state, and federal agencies, including both the coast guard and naval bases in the region, will establish the most efficient means of conveyance, triage, and treatment. Knowledge of receiving facility flight pad capabilities, including global positioning system coordinates of the helipad, the capacities in terms of type and number of helicopters capable of being accommodated, and special local area flight considerations, should be evident in these plans. Special decontamination procedures to be used in the event of radiologic contamination or exposure to hazardous materials should be in place to handle these unique potentialities. Secondary facilities should be identified to receive overflow casualties for which the primary facility cannot provide care.

POSTINCIDENT ACTIONS Once notified of incoming casualties from a seaborne platform, feedback to the port control authorities and U.S. Coast Guard/U.S. Navy will assist in refining masscasualty planning for future events.

MEDICAL TREATMENT OF CASUALTIES Because of the relatively wide variety of casualties that can be encountered from a shipborne accident, the treatment of the injuries should follow the standard of care for that specific injury. Two common complicating factors, however, should be addressed. Prolonged exposure to the elements at sea can rapidly lead to hypothermia. In most oceans, hypothermia (Tc< 35˚C) occurs in less than 30 minutes. The onset varies with multiple factors, including water temperature, sea state, amount and type of clothing worn by the patient, body habitus, and other factors.5 Although exposure suits are required aboard many sea-going vessels, due to the exigency of the casualty or their physical location, many casualties may not be able to access these suits. Hypothermia becomes a primary injury that can sometimes be overlooked in the face of other, more obvious injuries.

858 EVENTS ASSOCIATED WITH STRUCTURAL COLLAPSE/CRASHING/CRUSHING

Contamination with toxic or hazardous material, including radioactive fluids or waste, is a silent, invisible complicating factor in the treatment of these casualties. Before any intake, treatment, or care, proper containment or decontamination, in accordance with the masscasualty plans, must occur to ensure the safety of the treating personnel and the other patients at the receiving facility. However, disaster management planning must include the provision for providing life- or limb-saving medical treatment for contaminated injured personnel while maintaining a safe environment for the medical staff. Every emergency department must have a wellrehearsed treatment/decontamination plan for contaminated patients. Most radioactive surface contamination can be removed using soapy, lukewarm water to gently wash the affected area. Scrubbing runs the risk of embedding these contaminants and should be avoided.4 Chemical exposures should be assessed for their acidity/basicity to ensure proper usage of neutralizing agents. Once patients have been verified clean/decontaminated, physical entrance into the treating facility can safely occur. Life-saving interventions for the contaminated patient must be weighed against the risk of exposure to the treating personnel.

Radiologic controls, in the event of a radioactive release or spill, can greatly slow response, recovery, and treatment times. Very specific regulations govern the management of radiologic sites. These regulations are written in an effort to minimize the exposure of radioactive materials to the public. In the event of a casualty involving contaminated, injured personnel, public exposure will be limited by the reliance on the receiving facility to safely decontaminate the injured in an effort to minimize any delay in medical attention. However, the benefit of life- and limbsaving measures must outweigh the risk of low-level radioactive exposure of the medical responders. Explosive hazards are real potentials on many vessels, particularly warships. Most disasters occurring on U.S. naval vessels will be managed by the regional commander and the organic medical facilities and personnel in that command. However, disasters remote from dedicated U.S. naval medical centers capable of handling mass casualties may require civilian assistance, particularly when deployed out of territorial waters. Knowledge of and planning for the treatment of injuries associated with explosive trauma (e.g., blunt/penetrating trauma, amputations, blast injury) complete any plan dealing with seaborne disasters.

PITFALLS CASE PRESENTATION Several potential pitfalls in response to a naval vessel accident exist. These include the following: On the evening of August 26, 1988, the Peruvian submarine Pacocha with 49 persons aboard was struck by a Japanese fishing vessel while returning to the port of Callao, Peru. The submarine sank in 140 feet of water about 6 nautical miles from land. Twenty-three crewmembers managed to scramble overboard, but three of those later drowned or succumbed to exposure in the 14˚C water prior to rescue. The captain and three of his crew drowned immediately while attempting to save the submarine. Twenty-two submariners were trapped in the forward compartment, where flooding had increased the internal pressure to about three times normal atmospheric pressure. After about 20 hours, rising carbon dioxide levels forced the survivors to begin escaping from the submarine. Upon reaching the surface, all required recompression treatment in a hyperbaric chamber for decompression sickness. Of these 22 submariners, 1 died and another suffered severe brain damage/quadriplegia.6

• Failure to fully exercise the sea disaster mass-casualty plan • Failure to consider radiologic or toxic contamination in the process of providing treatment for affected persons • Allowing low-level radioactive contamination to delay life- or limb-saving medical treatment • Poor communications hampering efforts to properly coordinate patient transport • Failure to anticipate and properly treat hypothermia in casualties exposed to the environment • Failure to adequately communicate instructions for basic medical care to on-scene personnel lacking medical expertise • Lack of knowledge regarding the location of hyperbaric facilities REFERENCES

UNIQUE CONSIDERATIONS Shipboard spaces are often difficult to navigate, particularly with bulky medical gear and stretchers. Consequently, initial assessment, extraction, and transport to the weather decks can present challenges that hamper the provision of care. Accurate relaying of patient location on the ship can speed recovery times, particularly on smaller ships that will rely on outside medical assistance on board the ship.

1. Tyrell D. Accidental fire causes. In: Guide for Conducting Marine Fire Investigations. 2000:25–37. 2. Jane’s Marine Propulsion. 2002. 3. Ibsen LM. Submersion and asphyxial injury. Crit Care Med. 2002;30(11 Suppl):S402–8. 4. Molé DM. Submarine medicine. In: Edmonds C, Lowry C, Pennefather J, eds. Diving and Subaquatic Medicine. 3rd ed. 1992:499–512. 5. Willis D. The dirty bomb: management of victims of radiological weapons. Medsurg Nurs. 2003;12:397–401. 6. Harvey C, Carson J. The B.A.P. Pacocha (SS-48) Collision: The Escape and Medical Treatment of Survivors. Submarine Development Group One; 1988. San Diego.

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S E C T I O N

F I F T E E N

Other Events, Combination Events

chapter 174

Aircraft Hijacking Kurt R. Horst

DESCRIPTION OF EVENT Aircraft hijacking is defined as the armed takeover of an aircraft.1 Prior to the events involving the World Trade Center in New York City on Sept. 11, 2001, most hijackings involved the use of the aircraft as transportation and the passengers as hostages. The hijackers would then typically present specific demands, which would be negotiated.1 The first recorded aircraft hijacking occurred in 1931 in Peru when a group of armed revolutionaries approached a Ford Tri-motor aircraft and attempted to force the pilot to fly them to their destination.1,2 The pilot refused, and after a 10-day standoff during which the revolution had been successful, the pilot was released.1,2 Unfortunately, many aircraft hijackings do not end so peacefully. A few noteworthy incidents are presented in Table 174-1. Before the events of Sept. 11, 2001, anti-hijacking training followed what was termed the Common Strategy. This philosophy was based on prior experiences with hijackers. It instructed aircrews to avoid attempts to overpower these persons, and encouraged actions to resolve hijackings peacefully,even by accommodating the hijackers when necessary. But the goal of the Sept. 11 hijackings was to use the aircraft to perform a suicide attack, rendering the Common Strategy obsolete.5 Since this attack, training has been altered and is now referred to as the Crew Training Common Strategy. It now instructs pilots to not open the cockpit door and new Federal Aviation Administration regulations require the reinforcement of those doors. However, if the door is breached, the flight crew will attempt to protect the aircraft from being taken over.6 New legislation,including the Arming Pilots Against Terrorism Act of 2002, has opened the way for the training and deputization of pilots.6,7 This will allow pilots to carry a firearm and provide an added safeguard to the security of the flight deck.6,7 In November 2001, the Aviation and Transportation Security Act was passed and the Transportation Security Administration (TSA) was created to oversee travel security.8,9 Initially placed under the U.S. Department of Transportation, the TSA now falls under the Department of Homeland Security.9 The TSA is now responsible for overseeing the screening of passengers, baggage, and cargo to detect possible threats, including explosives.8,9 860

As seen with historical examples of aircraft hijackings, many hostage situations are resolved with force. The emergence of the field of tactical emergency medical support over the last decade may provide a key role in such operations. Emergency medical providers, optimally trained at the paramedic level, serve as members of special weapons and tactics (SWAT) teams. SWAT teams often have a role in resolving hostage situations involving aircraft. The ability to provide immediate,high-level medical attention to hostage victims after entry is made may increase survival of those injured in the incident.10,11

PREINCIDENT ACTIONS Much of the focus on aircraft hijackings has centered on modalities to detect and prevent them from occurring. As outlined in detail previously, the TSA was developed to spearhead many of the changes that have occurred since the Sept. 11, 2001, hijackings in the United States.8,9 Medical personnel should be aware of the various injury patterns that may be present in victims involved in an aircraft hijacking and hostage situation. Knowledge and participation in tactical emergency medical support operations will improve survivability.10,11 Acute exacerbations of pre-event medical conditions among victims may occur during the hostage situation. This may be precipitated by the stress of the event itself or due to the lack of availability of the patient’s own routine medications. For example, a diabetic might develop a hyperglycemic reaction due to lack of access to his insulin that he placed in his checked luggage for an anticipated short flight. As such, emergency responders should be prepared to treat a myriad of primary medical conditions. Continued training of airline personnel using the Crew Training Common Strategy will be imperative in preventing future suicide hijackings.6,7 The arming of pilots is clearly a controversial issue. However, if carried out, proper training in firearms safety and use is required.7 The presence of air marshals, law enforcement officers who fly aboard commercial flights, may also provide added protection because they have specialized training in the prevention of hijackings.12 Finally, aircraft passengers may find themselves in a position where they must

TABLE 174-1 SELECTED AIRCRAFT HIJACKINGS 1968 1969

1970

1970

1976

1982 1984

1985

1986 1988

1996

2001

Three members of the Front for the Liberation of Palestine (PFLP) hijack an El Al plane. After 40 days, the hostages and hijackers are released.1,2 Eight U.S. airliners are hijacked to Cuba in 1 month. This leads to development of a Federal Aviation Administration task force that creates a hijacker “profile” used in conjunction with weapons-screening devices.2 Four airliners, including one operated by a U.S. carrier, are hijacked by the PFLP. Three are successful and force landings in the Jordanian desert, where they are exploded after the passengers deplane. All hostages are subsequently freed after seven PFLP members are released from prison.1-3 A copilot is fatally wounded by a hijacker on an Eastern Airlines flight. The copilot shoots and severely wounds the hijacker. The pilot, who was also injured, safely lands the aircraft.2 Palestinians hijack an Air France aircraft. After landing in Uganda, Israeli commandos free 105 passengers after they storm a building where the hijackers had relocated the hostages. Three passengers, all the hijackers, and one commando are killed.1 Fifty-nine people die when Egyptian commandos infiltrate an EgyptAir plane after it is hijacked by Palestinians and flown to Malta.2 Four Arab hijackers aboard a Kuwait Airways jetliner force the aircraft to land in Iran. Once there, they kill two American citizens and commit other brutalities against the passengers. Iranian forces storm the aircraft, freeing the remaining hostages.3 Lebanese Shiite Moslems hijack a TWA airliner in Athens and kill a U.S. serviceman onboard the flight. The rest of the passengers are released in stages over the course of 2 weeks. The International Security and Development Cooperation Act of 1985 is signed 2 months later and provides monies for development of new airport security devices and hiring of additional security inspectors to serve as air marshals.3,4 After a 16-hour standoff, 22 people are killed when Pakistani forces storm a hijacked Pan Am flight in Karachi.1,2 The explosion of a Pan American jetliner over Lockerbie, Scotland, by an explosive device in a cassette player prompts the institution of a number of security measures, including installation of devices to detect explosives and stricter penalties for trying to take a gun through airport screening sites.3,4 One hundred twenty-five passengers are killed when an Ethiopian Airlines flight crashes into the Indian Ocean when hijackers refuse to allow the pilot to land and refuel. Fifty passengers survive.2 On September 11, three American aircraft are hijacked and deliberately used to cause destruction at the World Trade Center towers in New York City and the Pentagon in Washington, DC. A fourth hijacked aircraft crashes in Pennsylvania after passengers attempt to retake the plane.1,2,4

act. This will certainly be a hard decision, and giving advice in this particular manner is difficult. However, as seen on Sept. 11, 2001, the action of private citizens prevented the fourth airliner from reaching its target.5

POSTINCIDENT ACTIONS The information just described can be used to develop a specific action plan in the event that a hijacking attempt has begun. Once on the ground, negotiations

may occur between the hijackers and law enforcement personnel. Alternatively, the aircraft may be entered by specialty teams that will use an array of techniques to gain entry and incapacitate the hijackers. Medical personnel must be readily available to treat injuries to hijackers and hostages alike.

MEDICAL TREATMENT OF CASUALTIES A variety of injury patterns are likely to be expected among victims of aircraft hijackings. With more stringent screening of passengers and luggage, there may be a lesser chance of seeing gunshot wounds, especially compared with prior hijackings. However, with some pilots now carrying weapons and the possibility of armed rescue attempts by military special forces and SWAT teams once the aircraft is on the ground, the possibility of seeing such patterns of injury remains. As such, emergency personnel attached to these teams and in the emergency department must be prepared to provide appropriate immediate care. Additionally, penetrating trauma from an array of instruments such as knives, screwdrivers, and other sharp objects should be treated in a manner similar to gunshot wounds. Evaluation, as always, should begin with an assessment of airway, breathing, and circulation and then progress to a secondary survey. Intubation should be performed as needed, and intravenous resuscitation should begin with crystalloid solutions. Penetrating trauma to the chest may result in cardiac injury leading to pericardial tamponade, which must be immediately recognized and treated with fluid boluses, needle aspiration, and subsequent surgical intervention.13,14 Beck’s triad,while not always present,is indicative of pericardial tamponade and consists of hypotension, distended neck veins, and muffled heart sounds. Ultrasonography is used to confirm the diagnosis. Thoracotomy may also play a role in the treatment of this condition.14 If a tension pneumothorax is suspected (evidenced by hypotension, distended neck veins, unilateral decreased breath sounds, and tracheal deviation), immediate needle decompression must be performed before obtaining a chest radiograph.13,15 A tube thoracostomy may then be performed.15 Simple pneumothorax, hemothorax, and a variety of injuries to the great vessels and lung parenchyma may also occur and must be identified early as surgical therapy may be indicated.13,14 Penetrating abdominal trauma can be recognized by the identification of a penetrating wound,evisceration,and the presence of tenderness and peritoneal signs on physical examination. Any aberration in vital signs may also point to the presence of internal hemorrhage.16 Diagnostic peritoneal lavage, focused abdominal sonography for trauma (FAST), and computed tomography (CT) scan all may play a role in the management of a stable patient. However, emergent exploratory laparotomy may be required, especially if the patient becomes unstable.16,17 Penetrating trauma to the neck may result in damage to a number of structures including vasculature, the esophagus, AIRCRAFT HIJACKING 861

and trachea. Specialty surgical services are necessary to further evaluate these injuries as many may require surgical intervention.18 Penetrating head wounds produce brain injury and hemorrhage and require CT scan and neurosurgical evaluation. Complications include infection, seizure disorders, and variable neurologic dysfunction.19 The potential for blunt trauma also exists. Blows to the head may result in an array of injuries, including epidural and subdural hematomas and intraparenchymal hemorrhage, which may be diagnosed by CT and should prompt neurosurgical consultation.19 Blows to the chest may result in rib fractures, pneumothorax, and hemothorax, which can be treated with needle decompression and tube thoracostomy when necessary.15 Blunt trauma to the abdomen can cause solid organ injury and internal hemorrhaging. Physical examination findings include abdominal tenderness, peritoneal signs, and abdominal abrasions or areas of ecchymosis. Evaluation with ultrasound (FAST examination), CT scan, or diagnostic peritoneal lavage is indicated, and positive findings may warrant monitoring or surgical intervention.20 The management of extremity trauma includes control of hemorrhage and stabilization of possible fractures until the patient reaches definitive care. Exposure to chemical incapacitants such as 1chloroacetophenone (Mace) and oleoresin capsicum (i.e., pepper spray) may also occur. These agents are irritants that affect the eyes, respiratory tract, and skin. Rescuers and healthcare providers should wear appropriate protective equipment to avoid exposure to the irritant, which may be more persistent in enclosed spaces, and the victim should be removed immediately from the area of release. Skin should be washed with soap and water. Respiratory symptoms may require the use of inhaled beta2 agonists such as albuterol.21 Eye symptoms

should be treated with contact lens removal (if they are present) and eye irrigation. After improvement of symptoms, the eyes should be examined with the use of a slit lamp to detect corneal abrasions, and topical antibiotic should be prescribed if abrasions are present.22 Additionally, a number of victims will likely have underlying medical conditions that may require treatment. A major area of concern among all victims is that of psychological trauma. This may take the form of acute stress reactions, and some may develop posttraumatic stress disorder. One possible method of intervening to prevent this disorder or decrease its symptoms is a debriefing of the event soon after its occurrence. After the December 1994 hijacking of an Air France plane, passengers underwent a debriefing of the incident by a team of psychiatrists. During the hijacking, two passengers were killed by hijackers in front of passengers in the first 5 hours, and a third was executed the next day. Thirty-five passengers were released before the aircraft departed for Marseilles. The other 188 were released after a total of 54 hours after a military assault of the aircraft. It was found that the group of passengers who were initially released suffered from more psychological reactions, perhaps as a result of concern over being executed by hostages immediately after being freed.23 Unfortunately, this study did not follow up with patients to determine whether this single debriefing prevented worsening or occurrence of psychological symptoms. Although many support the use of an immediate debriefing technique (e.g., critical incident stress debriefing), some reviews have not found this form of single-session therapy to be beneficial.24 A better technique may be to use the debriefing as a bridge to further outpatient therapy if it is determined that the patient would benefit from ongoing care.

CASE PRESENTATION Three men board a plane at Baltimore Washington International (BWI) Airport bound for Los Angeles. Moments after the plane lifts off, the three men brandish pepper spray containers and announce that they are taking over the plane. They are also holding some type of sharpened wooden instruments. Members of the flight crew attempt to disable one of the men, but they become incapacitated when they are exposed to the pepper spray. One of the men begins hammering at the cockpit door, ordering that it be opened immediately or he will begin killing hostages. The pilot and copilot verify that the door is secure and immediately radio the air traffic controller who quickly diverts them back to BWI. The air traffic controller also notifies local authorities, who immediately respond to the airport. An air marshal sitting near one of the hijackers is able to incapacitate him. One of the remaining hijackers grabs a person from a seat near him and holds the sharpened object to his throat, threatening to kill him. The air marshal, realizing they are now on final approach back at BWI airport, stands back and attempts to negotiate with the hijacker. The aircraft lands and is quickly met by members of the local SWAT team who also possess a dedicated medical 862 OTHER EVENTS, COMBINATION EVENTS

component. They know the number of hijackers at this point and determine the best location for entry of the airplane. The team storms the plane and ultimately shoots the hijacker who was holding the man hostage. The other two hijackers are arrested without incident. The paramedics attached to the SWAT team attempt to treat the hijacker, but he has sustained a fatal injury to the head. They recognize that many people in the front of the aircraft, including three members of the flight crew, are experiencing some difficulty breathing and tearing of the eyes. They recognize a possible exposure to a chemical irritant and don masks and gloves. These victims are rapidly extricated from the airplane and their eyes are irrigated. Those experiencing respiratory symptoms are treated with oxygen and albuterol. These patients are evaluated at a local hospital and released a few hours later. A passenger with a history of myocardial infarction reports that he has had chest pain for the last hour but had forgotten to pack his nitroglycerin in his carry-on luggage. He is diaphoretic, tachypneic, and notes that the pain radiates into his left arm. Paramedics administer oxygen,aspirin,and nitroglycerin with some improvement. He is admitted at a local hospital and diagnosed with acute myocardial infarction.

UNIQUE CONSIDERATIONS Elements of an aircraft hijacking that are unique include the following: • Although historical examples of hijackings involved hostage taking and negotiating of demands, the possibility of suicide hijackings is now present. • Airplanes represent a relatively small, closed space, and if they are in flight, hostages are prevented from attempting to escape. • The flight deck must remain locked down at all times, irrespective of events occurring in the passenger compartment. • Pilots on the flight deck may be carrying guns to prevent hijackers from taking over the aircraft. • Air marshals may be present to assist in overcoming a would-be hijacker. • Due to the confined space, an increased number of injuries may be expected if special teams gain entry to eliminate the threat posed by the hijackers. • Exposure to chemical incapacitants in this closed space may result in a large number of occupants becoming symptomatic after exposure. • Many passengers will experience some form of psychological reaction after the event. • Passengers may experience acute exacerbations of underlying medical conditions.

PITFALLS Several potential pitfalls exist in response to an aircraft hijacking. These include the following: • Not having appropriate and rigid screening practices in place to detect potential weapons that may be placed on the aircraft • Assuming that hijackers only wish to divert the flight and land at another locale • Allowing hijackers to overtake the flight deck by opening the flight deck door • Improper training of the flight crew regarding the Crew Training Common Strategy on how to deal with an attempted hijacking • Not incorporating medical assets into special response teams that may gain entry into the aircraft in an attempt to rescue hostages • Medical personnel not wearing appropriate protective equipment, especially when exposure to chemical incapacitants is likely

4. Rumerman J. Aviation security. U.S. Centennial of Flight Commission. Available at: http://www.centennialofflight.gov/ essay/Gove rnment_Role/security/POL18.htm. 5. National Commission of Terrorist Attacks upon the United States. Staff statement no. 4: the four flights. Initially presented January 26-27, 2004, in Washington, DC, at the Seventh Public Hearing of the Commission. Available at: http://news.findlaw.com/hdocs/doc:/ terrorism/911comm–SS4.pdf. 6. Loy J. Statement of Admiral James M. Loy Administrator, Transportation Security Administration before the Committee on Commerce, Science, and Transportation. United States Senate; September 9, 2003. Available at: http://www.tsa.dot.gov/public/ display? theme=47&content=0900051980069a68. 7. Homeland Security Act of 2002. Title XIV – Arming Pilots Against Terrorism. Available at: http://thomas.loc.gov/cgi-bin/ query/z?c107:h.r.5005.enr. 8. Aviation and Transportation Security Act. Public Law 107-71. November 19, 2001. Available at: http://frwebgate.access.gpo.gov/ cgi-bin/getdoc.cgi?dbname=107_cong_public_laws&docid=f: publ071.107.pdf. 9. Transportation Security Administration. Report to Congress on Transportation Security. March 31, 2003. Available at: http://www.tsa.gov/interweb/assetlibrary/Report_to_Congress_on_ Transportation_Security_ Final_March_31_2003.pdf. 10. Heck J, Pierluisi G. Law enforcement special operations medical support. Prehospital Emerg Care. 2002;5:403-6. 11. Heiskell L, Carmona R. Tactical emergency medical services: an emerging subspecialty of emergency medicine. Ann Emerg Med. 1994;23:778-85. 12. Federal Aviation Administration. FAA federal air marshal program (September 2001). Available at: http://www.faa.gov/Newsroom/ factsheets/2001/factsheets_0109.htm. 13. Shahani R, Galla JD. Penetrating chest trauma. Updated June 11, 2004. Available at: http://www.emedicine.com/med/topic2916.htm. 14. Schouchoff B. Penetrating chest trauma. Top Emerg Med. 2001;23:12-19. 15. Schouchoff B, Rodriguez A. Blunt chest trauma. Top Emerg Med. 2001;23:1-11. 16. Kaplan L,Alson R,Talavera F, et al. Abdominal trauma, penetrating. Updated May 16, 2003. Available at: http://www.emedicine.com/ emerg/topic2.htm. 17. Kirkpatrick A, Sirois M, Ball C, et al. The hand-held ultrasound examination for penetrating abdominal trauma. Am J Surg. 2004;187:660-5. 18. Thompson E, Porter J, Fernandez L. Penetrating neck trauma: an overview of management. J Oral Maxillofac Surg. 2002;60:918-23. 19. Shepard S, Dulebohn SC, Talavera F, et al. Head trauma. Updated July 26, 2004. Available at: http://www.emedicine.com/med/ topic2820.htm. 20. Salomone JA, Salomone JP. Abdominal trauma, blunt. Updated May 16, 2003. Available at: http://www.emedicine.com/emerg/ topic1.htm. 21. Smith J, Greaves I. The use of chemical incapacitant sprays: a review. J Trauma. 2002;52:595-600. 22. Rega PP, Mowatt-Larssen E, Sole DP. CBRNE-irritants: Cs, Cn, Cnc, Ca, Cr, Cnb, PS. Updated June 29, 2004. Available at: http://www.emedicine.com/emerg/topic914.htm. 23. Cremniter D, Crocq L, Louville P, et al. Posttraumatic reactions of hostages after an aircraft hijacking. J Nerv Mental Dis. 1997;185:344-6. 24. Rose S, Bisson J,Wessely S. Psychological debriefing for preventing post traumatic stress disorder (PTSD) [systematic review]. Cochrane Depression, Anxiety and Neurosis Group. Cochrane Database of Systematic Reviews. Volume 3. 2004. Available at: http://www.cochrane.org/cochrane/revabstr/AB000560.htm.

REFERENCES 1. Wikipedia. Aircraft hijacking. Available at: http://en.wikipedia.org/ wiki/Aircraft_hijacking. 2. Worldhistory.com. Aircraft hijacking. Available at: http://www. worldhistory.com/wiki/a/aircraft-hijacking.htm. 3. Federal Aviation Administration. FAA historical chronology: civil aviation and the federal government, 1926-1996. 1998 Available at: http://www.faa.gov/docs/b-chron.doc. AIRCRAFT HIJACKING 863

chapter 175

Aircraft Crash into a High-Rise Building Kurt R. Horst

DESCRIPTION OF EVENT The attacks on the World Trade Center in New York City on Sept.11,2001,are a grim example of the immense damage and destruction that can result when an airplane impacts a high-rise structure. A thorough examination of this disaster may yield a greater understanding of the effects of such an event. Within 20 minutes of each other, two Boeing 767 jets collided with the north and south towers of the World Trade Center, instantly killing the 157 passengers and crew and countless others in each building. In less than 2 hours, both towers had collapsed.1 The World Trade Center towers were completed in 1973 and stood over 1300 feet high.2 They were constructed using a lightweight perimeter tube design, essentially creating a structure akin to an egg crate.2,3 As such, the design was redundant and, if a few columns failed, the load would be transmitted to adjacent columns.3 The design allowed for toleration of enormous wind loads and withstanding the impact of an airplane—specifically, a Boeing 707.3,4 Why, then, did the towers ultimately collapse? Investigations and research are ongoing, but one possible theory points to the resulting fires that occurred as likely being the chief cause. Immediately after each impact, the initial explosion ignited tens of thousands of gallons of jet fuel, which spread rapidly through the involved floors. It is believed that the immense heat, coupled with the nearinstantaneous spread of the fire throughout the structure, led to structural damage and distortion of the steel beams. Eventually, multiple beams at that level failed, and the floor below the impact site could not withstand the massive weight of the 10 to 20 floors above that came crashing down. The buildings ultimately fell because of the inertia of their massive weight, the fact that the buildings themselves were 95% air, and that there was an insignificant lateral load applied to the structure.3 As a result of these attacks, more than 2800 people were killed, including over 400 emergency responders.5 In each tower the catastrophic event consisted of a largescale mass-casualty incident (MCI) with many varying components. It began with an explosion (likely to have resulted in blast-type injuries) followed by a high-rise fire, which presented its own unique challenges. The subsequent building collapse created a potential need 864

for confined-space rescue.6 Injuries surrounding the buildings included blast injury, inhalation injury, and thermal injury.7 Additionally, the involvement of not one, but two high-rise structures added to the complexity of the event, whereby two asynchronous crashes essentially led to two MCI events.6 After these attacks, the U.S. Federal Aviation Administration halted all aircraft activity in the United States. The military diverted resources to the East Coast of the United States and military air patrols were begun.8,9 General aviation slowly resumed as new security measures were implemented.10 Initial confusion and incorrect communication may have led to a delay in evacuation of one or both buildings.11 Communication difficulties also occurred during the response to the incident. As would be expected, radio transmissions increased, many of which were incomplete or unintelligible after the first aircraft struck the first tower. Of note, a New York Police Department helicopter communicated information regarding the impending collapse of the towers, but this information does not appear to have been relayed to emergency responders on-scene.12 Finally, a large number of private citizens, physicians, nurses, and other healthcare providers arrived on-scene to provide assistance after the attacks. This process, termed convergent volunteerism, although well intentioned, presents a problem on many levels. These persons, in general, are not trained to work in the prehospital setting. They generally lack appropriate safety and personal protective equipment for field operations and may put their lives and the lives of others in jeopardy. These persons also typically engage in freelancing, creating their own triage and treatment areas that have no ability to communicate with the Incident Commander. Verification of credentials and the process of ensuring personnel accountability may be compromised.13

PREINCIDENT ACTIONS A number of lessons can be learned from this tragic event, many of which are intuitive from the discussion above. One primary goal would be to investigate ways to improve the structural integrity of high-rise buildings to

ensure that they will withstand this threat. Although the World Trade Center towers did withstand the initial impact, they ultimately collapsed as a result of loss of structural integrity due to the heat of the subsequent fires.3,4 Many organizations are continuing to investigate the cause of the collapse, and perhaps this will lead to improved integrity of buildings in the future. In addition, the availability of structural engineers to assess buildings immediately after impact will be of great benefit to determine the likelihood of impending collapse. They will also be useful in evaluating the damage to surrounding structures, as was seen after the Sept. 11, 2001, attacks.5 In light of the relatively short time available for evacuation, coupled with the tremendous size of high-rise buildings, it is imperative that emergency egress routes are well planned, easily understood, and practiced. The addition of clear, concise, and correct information broadcast over multiple loudspeakers may aid in decreasing the time that occupants spend debating whether the threat is serious enough to warrant evacuation.5,14 From the perspective of emergency personnel, it is imperative that strict adherence to all protocols and the Incident Command System is maintained. Personnel accountability must be enforced, and the safety of rescue personnel must be maintained.15 Additional and redundant systems of communications must be instituted to decrease system failures.16 At the same time, contingency plans (e.g., using runners) for total systems failure must be devised. Training specific to this environment must be provided to all emergency personnel and may include high-rise and structural fire suppression and rescue operations, recognition of precursors to building collapse, and confined-space rescue. Medical triage systems must be used and practiced before an MCI occurs.17 Specific information about hospitals in the immediate and distant areas, bed status, and specialty capabilities must be available to aid in patient distribution from patient-collection sites. Mutual aid agreements with surrounding ambulance and fire services must be in place before the event to ensure that adequate resources are available for the incident.18-20 The Federal Emergency Management Agency can also provide a variety of mutual aid resources at the federal level when requested.21 In addition, it is important to recognize that all resources should not be deployed to the single incident because the average daily number of emergency calls received will continue to arrive.13 Finally, hospital disaster plans should augment normal staffing with additional resources.13 This should minimize the problem of convergent volunteerism, which creates a hazard at the hospital and at the scene of the incident. Hospitals must also be prepared for the presentation of patients in waves, with large numbers of walking wounded presenting with minor injuries first, followed by more severely injured patients. The next groups of patients will likely include those rescued from the structure as well as injured emergency personnel.7 Certainly, the prevention of this type of incident from occurring again is a paramount concern. In November 2001, the Aviation and Transportation Security Act was approved in the United States, creating the Transportation Security Administration. It also provided for a number of

new security measures, including enhanced screening at airports and the strengthening of flight deck doors aboard commercial aircraft. Provisions for the deployment of specially trained law enforcement agents (i.e., air marshals) onto commercial flights were also outlined.22 Lastly, a final line of defense should be in place in the event that an aircraft is overtaken and poses a threat to a high-rise structure in a large city. As seen after Sept. 11, 2001, this last-resort option included military flight patrols capable of rapidly responding to a potential threat and exerting deadly force when necessary.8

POSTINCIDENT ACTIONS An action plan can be developed based on the experience of the New York World Trade Center attacks that can be used to guide an effective emergency response, minimizing injury and loss of life. After an aircraft has crashed into a high-rise structure, the following measures should be undertaken: • Airspace restrictions should be instituted around the site and likely around the city and local airports. In many cases, as in the Sept. 11, 2001, attacks, the restrictions will be broader. • A military air presence should be put into place around the area of the incident to provide for possible protection if the incident was the result of a terrorist act. • Fire or police helicopter assets should be placed around the structure and should continually monitor for any signs of impending collapse. • Police should set up a perimeter around the incident site to prevent access from bystanders and nonemergency personnel (this includes volunteers who arrive on scene to assist). • The Incident Command System should be initiated. • Redundant communication systems should be in place and must be able to handle the ensuing increased amount of radio traffic. • Mutual aid agreements with surrounding services and private companies should be called into effect. Designated staging areas should be assigned to prevent congestion at the scene. • Rescue and fire suppression operations should be initiated. • Designated triage sites around the area of the incident should be set up and staffed by emergency medical services and fire personnel. These areas should be far enough from the actual site of the incident to prevent them from becoming involved if the structure were to collapse. • Immediate evacuation of the involved building should begin. There should be no debate among occupants about whether to do so, and emergency egress routes should be used. • During the rescue operation, as safety issues arise or if there is concern for building collapse, a clear warning signal notifying all crews to immediately evacuate should be broadcast. • All resources at local and outlying hospitals should be available, and patients must be properly dispersed AIRCRAFT CRASH INTO A HIGH-RISE BUILDING 865

• • •

•

throughout these facilities rather than over-triaging to the nearest facilities. Hospitals should institute their disaster plans, retaining on-duty employees and calling in additional resources as needed. Emergency medical and fire resources should also be in place to continue to handle the usual daily emergency call volume. Crews should rest frequently and remain hydrated. Rescue and emergency medical “go teams” should be set up to respond to emergency personnel entrapment or injury. In the event of a building collapse or simply a prolonged incident scene that will overwhelm local resources, plans should be in place to request additional local, state, and federal assets. This may include specialty teams, including search and rescue, disaster medical assistance teams, disaster mortuary assistance teams, and veterinary medical assistance teams.

MEDICAL TREATMENT OF CASUALTIES Blast-injury patterns will be seen in victims of this type of incident. Victims may be located either inside the structure at varying distances from the impact site or below the impact as a result of falling debris. The typical array

of blunt and penetrating trauma will be caused by the initial impact, flying debris, and blast winds.23 As a result, victims may suffer open and closed head injury that must be rapidly diagnosed. The possibility of spinal injury is also present if the victim is struck by an object or impacts a wall or other structure after being displaced by the blast wind. Lacerations and fractures, as well as all forms of thoracic and abdominal trauma, can result.24 Primary blast injury, which affects gas-containing organs, such as the lung, bowel, and middle ear, can present special challenges to healthcare providers and must be diagnosed early.23,24 Thermal and inhalation injury can result from the ensuing fires as jet fuel and room contents ignite after the initial impact.5 These may be severe in many cases, especially in those close to the initial impact site. Burns should be characterized by type and severity and referred to burn centers when necessary. Treatment may be as simple as the application of antibiotic ointment; however, full-thickness and circumferential burns of the chest may require escharotomy.25 Occupants must be examined for signs of inhalation injury, including soot in the nasopharynx or oropharynx, difficulty breathing, and stridor, and they must be continually monitored for a change in condition. Early aggressive airway management should occur if there is suspicion of such injury.25,26 Toxic inhalation of carbon monoxide or cyanide must be identified early and may require hyperbaric oxygen therapy or

CASE PRESENTATION At 10:30 AM, an air traffic controller at Chicago’s O’Hare International Airport loses radio contact with a Boeing 757 and recognizes that its flight path has changed. After multiple attempts at radio contact, he recognizes a possible emergency and notifies his superior. Two F-15 military jets are diverted from a nearby training mission to investigate. As the military pilots approach the aircraft, they report that it is losing altitude and is heading for the Sears Tower in Chicago. Before they are able to gather more information, the 757 impacts the 87th floor. A resulting fireball is seen as debris falls from the structure. Recognizing that this may be a possible terrorist attack, Federal Aviation Administration representatives immediately set air restrictions for the city of Chicago, and all airlines leaving Chicago’s airports are grounded. Aircraft en route to O’Hare and Midway airports are diverted. The military launches multiple groups of F-16 and F-15 fighters, which are now patrolling major cities across the United States. Chicago police set up a perimeter around the incident and launch helicopters to survey the damage and provide immediate updates of changes or spread of the incident. Local fire and emergency medical services respond. The Incident Command System is put into place immediately, and triage areas are set up outside the immediate danger areas in case of collapse to serve as collection points for walking wounded and rescued occupants from the structure. Teams for initial treatment and evacuation of those who are injured are placed nearer the incident to provide immediate care and transport. 866 OTHER EVENTS, COMBINATION EVENTS

Immediately after the impact, the evacuation of the Sears Tower commences. Hundreds of persons exit the building and are directed through streets away from the incident. Firefighters entering the building begin assisting occupants and extinguishing the fire,which has spread to the 85th floor. At 11:25 AM, Chicago police helicopters notice an area of the structure near the 86th floor that appears to be bowing outward. This is communicated to the Incident Commander, who orders an immediate evacuation of rescue personnel. A structural engineer is taken via helicopter to inspect the impact site. He feels that,at least at this point,the building remains structurally sound. He does note that with the continued spread of the fire,this will not remain the case. After another 2 hours, the fires are extinguished. A few stairwells above the impact site remained intact,and a number of occupants above the 87th floor were able to be rescued. It was estimated there were 8000 occupants at the time of the impact. Three hundred casualties were treated by emergency medical services at the designated triage areas and were distributed to local hospitals. It is estimated that 7300 occupants were evacuated. Two hundred ten passengers aboard the 757 and 700 occupants of the building were killed. While an investigation is ongoing, it does appear to have been a terrorist act. All local hospitals immediately instituted hospital disaster plans on viewing television news reports and on receiving notification from the Chicago Fire Department. Hospital employees remained on duty, and those at home either came to the hospital or tried to rest in case they were needed as per their specific disaster plans.

the administration of a cyanide antidote kit, respectively.26 In the context of a collapse, the large amount of dust and debris may also contribute to inhalation injury, as was seen on the attacks on the World Trade Center.7 Such injury may trigger asthma attacks and exacerbate underlying pulmonary conditions.24 Emergency personnel should be trained in the proper use of personal protective equipment, including goggles, gloves, and respirators, when there is dust present after a collapse.27 Standard treatment of blunt and penetrating trauma should be performed, including an initial assessment of airway, breathing, and circulation followed by a thorough secondary survey to identify other injuries. Supplemental oxygen should be applied, and intubation should be performed when needed. Wounds should be covered and likely fractures splinted. Early neurosurgical, surgical, and orthopedic evaluation should occur in the emergency department and appropriate interventions performed.

UNIQUE CONSIDERATIONS An aircraft crash into a high-rise structure represents a unique environment. There tend to be a number of potential injury patterns, encompassing blunt trauma, penetrating trauma, thermal injury, and inhalation injury. Due to the large size of the structure, it may be difficult to obtain access to patients because the impact site generally will be among the upper levels of the building. The resulting fires may impede occupants from escaping and prevent rescue personnel from reaching victims and fighting the fires. The ongoing concerns around the resulting structural integrity of the building may be difficult to ascertain, and the possibility of secondary collapse is ever present. The locations of these incidents, typically within cities, will likely result in damage not only to the structure impacted, but also to surrounding buildings. Falling debris may damage nearby structures, making them structurally unsound.5 These secondary impacts may therefore force the evacuation of nearby businesses and homes. The potential for secondary fire spread to these buildings is also not outside the realm of possibility. There will likely be injury and mortality below the impact side from falling debris. Evacuation may not only include the impacted highrise, but also a substantial portion of the area around that locale. The egress of thousands of people, not just from one building but perhaps from an entire area of a city, presents its own unique challenges. Evacuation routes in the city should be well marked, and plans for moving this populace should be developed before the occurrence of such an incident. The concern over a possible terrorist attack must make rescuers wary of a possible secondary explosive device which, as seen on Sept. 11, 2001, may take the form of a second aircraft.23 As such, a strong police and possibly military presence will be required to protect the scene and surrounding air space. The impact on air travel and the airlines will likely be dramatic.

PITFALLS Several potential pitfalls in response to an aircraft crash into a high-rise building exist. These include the following: • Failure to institute and follow the Incident Command System • Failure to develop a series of redundant communications systems as well as contingency plans for total systems failure • Failure to immediately evacuate the involved high-rise as well as buildings near-by • Failure to recognize signs of potential or impending building collapse • Failure to control access to the scene (Note: This is sometimes difficult to accomplish based on available resources and the size of the area involved.) • Failure to prevent unsolicited volunteers from entering the scene • Failure to adhere to triage protocols • Failure to have a hospital disaster plan in place in each facility to provide for an influx of large numbers of patients • Failure to recognize the need to continue to staff the daily emergency medical and fire service needs of the community that occur outside of the incident on a daily basis REFERENCES 1. In-depth special war against terror: interactive attacks explainer. Available at: http://www.cnn.com/SPECIALS/2001/trade. center/ map.html. 2. Public Broadcasting System. Building big: wonders of the world databank—World Trade Center. Available at: http://www.pbs.org/ wgbh/buildingbig/wonder/st ructure/world_trade.html. 3. Eager T, Musso C. Why did the World Trade Center collapse? Science, engineering, and speculation. JOM. 2001;53:8-11. 4. NOVA Online. Why the towers fell. Available at: http://www.pbs. org/wgbh/nova/wtc. 5. McAllister T, ed. World Trade Center Building Performance Study: Data Collection, Preliminary Observations, and Recommendations. FEMA Report 403. Washington, DC: Federal Emergency Management Agency; 2002. 6. Arnold J, Halpern P, Tsai M, et al. Mass casualty terrorist bombings: a comparison of outcomes by bombing type. Ann Emerg Med. 2004;43:263-73. 7. Centers for Disease Control and Prevention. Rapid assessment of injuries among survivors of the terrorist attack on the World Trade Center, New York City, September 11, 2001. MMWR 2002;51:1-5. 8. Center for Cooperative Research. Complete 911 timeline. Available at: http://www.cooperativeresearch.org/timeline. jsp? timeline=complete_911_timeline. 9. September 11: chronology of terror. Available at: http://www.cnn. com/2001/US/09/11/chronology.attack. 10. FAA orders new safety measures. Available at: http://www.cnn. com/2001/TRAVEL/NEWS/09/12/faa. airports/ index.html. 11. Averill JD. Federal building and fire safety investigation of the World Trade Center disaster. World Trade Center investigation status, project 7: occupant behavior, egress, and emergency communications. June 23, 2004. National Institute of Standards and Technology. Available at: http://wtc.nist.gov/pubs/June2004 OccupantBehavior EmergencyCommunications.pdf. 12. Sunder SS. NIST response to the World Trade Center disaster:World Trade Center investigation status. National Institute of Standards and Technology. Available at: http://wtc.nist.gov/pubs/June2004 WTCStatusprint.pdf. AIRCRAFT CRASH INTO A HIGH-RISE BUILDING 867

13. Cone D, Weir S, Bogucki S. Convergent volunteerism. Ann Emerg Med. 2003;1:457-62. 14. Proulx G. Terrorist attack on the World Trade Center findings on evacuation issues. CIB Global Leaders Summit on Tall Buildings. Available at: http://www.bre.co.uk/cibtallbuildingssummit/pdf/ proulx.pdf. 15. Jackson B, Baker J, Ridgley M, et al. Protecting emergency responders. Vol 3. In: Safety Management in Disaster and Terrorism Response. NIOSH Publication 2004-144. Washington, DC: National Institute for Occupational Safety and Health. 16. Garrison H. Keeping rescuers safe. Ann Emerg Med. 2002;40:633-5. 17. Frykberg E. Principles of mass casualty management following terrorist disasters. Ann Surg. 2004;239:319-21. 18. The White House. Mutual aid agreements: support for first responders outside the major metropolitan areas. Available at: http://www.whitehouse.gov/homeland/firstresponder s/mutualaidagreements.html. 19. Harrald JR. Observing and documenting the inter-organizational response to the September 11 attacks. Presented at: Countering terrorism: lessons learned from natural and technological disasters. February 28–March 1, 2002. Available at: http://dels.nas.edu/ dr/docs/harrald.pdf. 20. Tierney K. Lessons learned from research on group and organizational response to disasters. Presented at: Countering terrorism:

868 OTHER EVENTS, COMBINATION EVENTS

lessons learned from natural and technological disasters. February 28-March 1, 2002. Available at: http://dels.nas.edu/dr/docs/ tierney. pdf. 21. Federal Emergency Management Agency. National mutual aid and resource management initiative. Available at: http://www.fema. gov/preparedness/mutual_aid.shtm. 22. Aviation and Transportation Security Act. Public Law 107-71. November 19, 2001. Available at: http://frwebgate.access.gpo.gov/ cgi-bin/getdoc.cgi?dbname=107_cong_public_laws&docid=f: publ071.107.pdf. 23. Wightman J, Gladish S. Explosions and blast injury. Ann Emerg Med. 2001;37:664-78. 24. Centers for Disease Control and Prevention. Explosions and blast injuries: a primer for clinicians. Available at: http://www.bt.cdc. gov/masstrauma/explosions.asp. 25. Alson R. Burns, thermal. Updated October 28, 2003. Available at: http://www.emedicine.com/emerg/topic72.htm. 26. Lafferty KA. Smoke inhalation. Updated August 1, 2001. Available at: http://www.emedicine.com/emerg/topic538.htm. 27. Centers for Disease Control and Prevention. Use of respiratory protection among responders at the World Trade Center site: New York City, September 2001. MMWR 2002;51(Special Issue): 6-8.

chapter 176

Airliner Crash into a Nuclear Power Plant Rick G. Kulkarni

DESCRIPTION OF EVENT Nuclear power plants have been recognized as being potential targets of future terrorist attacks. Following the tragic events of Sept. 11, 2001, at the World Trade Center and the Pentagon in the United States, awareness has increased considerably among the public, federal regulatory agencies, and legislators regarding inadequacies in the ability of nuclear power plants to withstand direct attacks by large, high-speed passenger jets with full or nearly full fuel tanks.1 The U.S. Nuclear Regulatory Commission (NRC), the federal agency responsible for security at the 100-plus nuclear power plants in the United States, has issued several regulatory orders to all licensed nuclear power plants to meet the increased security threat.2,3 After the 1979 accident at Three Mile Island near Harrisburg, Pennsylvania, U.S. Congress enacted legislation mandating that all nuclear power plants be covered by emergency contingency plans. A direct consequence of this act was the imposition of a requirement by the NRC that operators of nuclear power plants maintain a 10-mile emergency planning zone equipped with warning sirens all around the plant.1 Off-site preparedness (i.e., state and local government emergency preparedness activities that take place beyond the nuclear power plant boundaries) is the responsibility of the Federal Emergency Management Agency.4 Nuclear power plants are designed to withstand extreme events such as earthquakes and hurricanes. However, direct impacts by large, fuel-laden airliners into the containment building of the plant are not specifically addressed in the design specifications. The risk of a meltdown and subsequent contamination leading to the exposure of a large number of persons to escaping radioactivity by a direct impact of an airliner into the containment building can occur only if structural integrity of the building is compromised.5 Without a breach caused in the containment building, the radioactive fission products would mostly remain where they are. Such largescale damage to the containment building could occur either as a direct consequence of the impact itself—a possibility especially for older plants where degradation of the building’s construction materials over time may be a factor—or through a delayed loss of strength of the structural members resulting from a sustained and intense conflagration, similar to the one that melted the

structural steel in the World Trade Center buildings in New York. Additionally, for a meltdown to occur, there would also have to be subsequent or concomitant direct damage to the reactor vessel and its control equipment or disruption of normal functioning of the cooling mechanism designed to control the heat generated from the nuclear reaction within the fuel rods.1,5 The NRC is currently conducting a detailed engineering analysis of the possible effects of such a crash scenario. Spokespersons for the NRC have repeatedly testified to Congress and other regulatory federal agencies that “most plane crashes into containment buildings would not result in significant releases of radiation.”2 If a large-scale contamination event were to occur, the immediate effects of radiation exposure on humans would most affect the rapidly dividing radiosensitive cells in the gastrointestinal tract and the integument. The central nervous system is also affected due to edema. Hematopoietic effects are ultimately the cause of delayed death if patients survive the immediate effects of radiation poisoning.6

Gastrointestinal Manifestations Gastrointestinal manifestations can occur within 30 minutes of a severe exposure (for example, >10 Gy) or after 6 hours with a lesser exposure (e.g., 2000/mm3 Moderate GI symptoms ALC at 48 hours > 1200/mm3 Severe GI symptoms ALC at 48 hours < 1200/mm3 Severe GI symptoms within 30 minutes ALC at 48 hours < 300/mm3

ALC, Absolute lymphocyte count; GI, Gastrointestinal. *LD50 = 4.5 Gy with medical treatment (100% without medical treatment).

mination areas. Security personnel should control access to minimize the spread of contamination.6 All rescue and medical personnel should use universal precautions with gowns, gloves, masks, and shoe covers. Radiation survey monitors should be used to prevent contamination beyond known areas. All equipment and clothing suspected to be contaminated should be placed into secured plastic bags for proper storage and disposal. The release of a radioactive form of iodine would be a significant component of a release event from a nuclear power plant. Radioactive iodine is absorbed and remains concentrated into the thyroid glands of humans, thus posing a long-term increased risk of cancer of the gland.7,8 All exposed persons, especially within the emergency planning zone, should be administered potassium iodide pills within 1 hour of exposure to prevent the absorption of the radioactive iodine.6,7

MEDICAL TREATMENT OF CASUALTIES Cleary,the first layer of casualties will present with blast and burn injuries. These patients should be cared for per standard trauma protocol. The concern for decontamination should be only for those patients not requiring immediate, life-saving medical intervention. Such intervention should be done first, and decontamination should then follow. Treatment should be tailored to the degree of exposure to radiation and the manifestation of symptoms. However, there are core measures common to all victims of radiation exposure. All wounds should be irrigated with saline followed by 3% hydrogen peroxide or a soapy solution. Gastrointestinal decontamination with whole-bowel irrigation with activated charcoal is indicated within 2 hours of exposure for those with moderate or greater levels of exposure. Supportive treatment with intravenous antiemetic agents, intravenous fluid to replace gastrointestinal losses, and the dressing of open wounds and burns is indicated. Also indicated is early transport to a medical facility where advanced treatment such as the institution of viral prophylaxis, administration of hematopoietic growth factors, and bone marrow transplantation can be performed.4

CASE PRESENTATION Local police officials report that a group of men have been stopped on a California highway between Los Angeles and San Diego in a car laden with weapons and documents pointing to an attack on the San Onofire nuclear power plant. The incident is reported immediately to the U.S. NRC and to the Department of Defense (DoD). At the same time, the North American Aerospace Defense Command alerts the NRC and the DoD that a 767 Boeing passenger jet seems to be heading for San Onofire and it not responding to direct communication efforts. Military personnel in jet aircrafts are scrambled from Edwards Air Force Base in Lancaster, California. Their mission is to intercept the passenger jet and order it to change course and land immediately at San Diego International Airport. Additionally, emergency measures to shut down the nuclear power plant are implemented at San Onofire. Minutes later, before the Air Force jets can make visual contact with the passenger jet’s cockpit crew, the Boeing 767 crashes into the main containment-building tower of the power plant. Although the crash does not immediately compromise the structural integrity of the reactor’s core

UNIQUE CONSIDERATIONS Gross structural failure of the containment building is essential for a large-scale contamination event occurring from a reactor material release. Although the containment building may not be compromised by the direct impact of an airliner, the effect of a subsequent jet fuel fire or explosion could cause further mechanical and thermal damage to the containment facility, resulting in a structural collapse of the building. Nuclear power plants house many more times the amount of radioactive substances than do stored nuclear weapons. If there is an accidental disaster or a deliberate act of sabotage, the release of only a small portion of this material will have severe consequences. Radiation cannot be detected by sight, smell, or any other sense. This should be a consideration of responders and other personnel. Another element to be kept in mind is that the ingestion of a nonradioactive iodine pill will prevent the absorption and concentration of radioactive iodine released during a nuclear power plant meltdown. Although there have been no incidents of an airliner crash into a nuclear power plant, the possibility of this type of terrorist attack cannot be excluded. Increased vigilance and preparedness of local, regional, state, and federal agencies as well as of the medical staff in areas with operational nuclear power plants is indicated.

PITFALLS

concrete containment building, it wipes out off-site power to the reactor necessary for the shutdown process. Backup generators fail, and a leak of reactor coolant raises the specter of a meltdown. An emergency is declared in the area surrounding the nuclear power plant. Persons living in northern San Diego County, Orange County, and adjoining Los Angeles County are ordered to evacuate. Those who have potassium iodide are advised to “swallow one dose now.” Protesters quickly organize behind barricades outside the San Diego International Airport conference room—the headquarters for operations—where reporters receive intermittent briefings on the situation. It seems that a core reactor meltdown has been averted through the use of secondary backup generators, quick response, and the efficient action of local firefighter crews to extinguish the fire from the airliner’s impact, and the competent implementation of emergency shutdown protocols by the power plant’s staff. Two hundred forty-five persons in the passenger airliner and five persons on the ground were killed in the incident.

• Failure to quickly isolate affected persons • Failure to notify receiving hospitals in a timely manner • Failure to properly categorize victims based on their degree of exposure • Failure to identify and treat emergent traumatic injuries • Failure to create a plan for mass treatment in the event of an attack REFERENCES 1. Behrens CE. Nuclear Power Plants: Vulnerability to Terrorist Attack. Congressional Research Service Report for Congress; 2003. 2. United States Nuclear Regulatory Commission. Nuclear reactors. Available at: http://www.nrc.gov/reactors.html. 3. Nuclear Regulatory Commission. Nuclear security—before and after September 11. Available at: http://www.nrc.gov/what-wedo/safeguards.html. 4. U.S. Federal Emergency Management Agency. Radiological Emergency Preparedness Program. Available at: http://www.fema. gov/preparedness/repp.shtm. 5. Lyman ES. The vulnerability of nuclear power plant containment buildings to penetration by aircraft. Nuclear Control Institute. September 21, 2001. Available at: http://www.nci.org/01nci/09/ aircrashab.htm. 6. Jones MP. Radiation injury. In: Schaider J, Hayden S, Wolfe R, et al. Rosen & Barkin’s 5-Minute Emergency Medicine Consult. 2nd ed. Philadelphia: Lippincott,Williams & Wilkins; 2003:932-3. 7. Kahn LH, von Hippel F. Nuclear power plant emergencies and thyroid cancer risk: what New Jersey physicians need to know. N Engl J Med. 2004;101:22-7. 8. Parfitt T. Chernobyl’s legacy. 20 years after the power station exploded, new cases of thyroid cancer are still rising, say experts. Lancet 2004;363:1534.

Several potential pitfalls in response to an aircraft crash into a nuclear power plant exist. These include the following: • Failure of rescue personnel to use appropriate personal protective equipment AIRLINER CRASH INTO NUCLEAR POWER PLANT 871

chapter 177

Dirty Bomb (Radiologic Dispersal Device)* George A. Alexander

DESCRIPTION OF EVENT A dirty bomb is a device that combines radioactive materials with conventional explosives. Global terrorist organizations are believed to be interested in and capable of constructing dirty bombs and launching attacks with them.1 There are only two documented cases of terrorist use of dirty bombs in the world today.2 Both incidents occurred in Russia. In 1995, Chechen insurgents buried a cesium-137 dirty bomb in a park in Moscow and alerted the media before its detonation. In 1998, a container of radioactive materials was found attached to an explosive mine near a railroad line in Chechnya. Dirty bombs are attractive to terrorists because they are relatively easy to acquire and have the potential of causing casualties, contamination of widespread areas, adverse psychological effects, and economic disruption. A dirty bomb threat potentially poses a medical and public health disaster. A dirty bomb can be made from traditional dynamite, trinitrotoluene (TNT), ammonium nitrate, or a variety of other explosive materials.3 When detonated, it kills or injures by the initial blast, which causes damage from the expansion of hot gases, and by dispersing radioactive materials that are highly toxic over a wide geographic area without a nuclear explosion. The dispersal effects of a dirty bomb depend on the amount of explosives used, the physical form of the radioactive source, and the atmospheric conditions.4 A dirty bomb is also known technically as a radiologic dispersal device. Many different radioactive sources can be used to fabricate a dirty bomb. Radioactive sources can be obtained illicitly from hospitals and medical clinics, industrial radiography and gauging devices, food sterilizers, power sources, communication devices, navigator beacons, oil well logging, and scientific research laboratories. Some common radioactive sources that have a high probability of being used as a dirty bomb based on their availability include cobalt-60, strontium-90, cesium137, iridium-192, radium-226, plutonium-238, americium241, and californium-252. *The views expressed in this chapter are those of the author and do not necessarily represent the official policy or position of the National Cancer Institute, the National Institutes of Health, or the Department of Health and Human Services.

872

Alpha-emitting radiation sources pose serious health hazards if they are inhaled, ingested, or deposited in an open wound. Beta-emitting sources can cause deep beta burns on the skin. Gamma rays may penetrate body tissues and cause deep tissue injury. The most likely dirty bomb scenarios would involve the use of either a few small low-level radioactive sources or a large amount of highly radioactive sources combined with high explosives. The first scenario considers use of a dirty bomb containing a few curies of a gamma-ray source such as cobalt-60 or cesium-137 combined with a few kilograms of high explosive. In this case, the dirty bomb might be used with the primary intent of causing fear or panic among people and disrupting their community. Since the amount of radioactivity is small, the radiation exposure to individuals would be low, and no immediate effects on health would be expected. The probability of long-term health effects would be small. The second scenario considers use of a dirty bomb containing large sources of penetrating radiation coupled with sophisticated high explosives. The detonation would disperse considerable amounts of radioactive material over a large area. Persons injured by the blast are likely to be contaminated with radioactivity and may receive life-threatening doses of radiation. Such a device is intended to kill tens or hundreds of persons, to injure and sicken hundreds or thousands, and to cause widespread panic.5 Recognizing that a conventional explosive device has been detonated may be simple because of the associated blast. However, it may take considerable time before the radioactive component of the dirty bomb attack is recognized. Therefore, it is important that first responders use radiation-detection equipment to identify a radioactive component after any explosion.6 Recognition of acute radiation injury is based on the patient’s medical history and clinical findings.7 The extent of radiation injury depends on three factors: depth of penetration of the radiation,dose of radiation absorbed, and volume of tissue irradiated. For localized radiation exposure, the initial signs of injury might be a radiation burn including erythema, blistering, or desquamation. With a low whole-body dose of 0 to 100 cGy from a dirty bomb, a patient would generally have no symptoms. With a moderate whole-body dose of 100 to 200 cGy, the

patient may exhibit the prodromal phase (nausea and vomiting) of acute radiation syndrome. At doses exceeding 300 cGy, patients would experience nausea, vomiting, diarrhea, erythema, and fever. A useful method of predicting the clinical severity of radiation injury is the time to onset of vomiting. If the time to vomiting is less than 4 hours, the patient has received a high dose of radiation. Laboratory data show that early changes in lymphocyte counts are associated with the severity of radiation injury. Absolute lymphocyte counts less than 1000 mm3 and greater than 500 mm3 indicate moderate and severe levels of radiation exposure, respectively. Complete blood counts can be repeated every 4 to 6 hours to evaluate lymphocyte depletion kinetics. The appearance of chromosome dicentrics in peripheral blood lymphocytes is also useful in calculating exposure dose. In patients who have developed acute radiation syndrome, within 2 to 3 weeks bone marrow suppression may occur with associated neutropenia, lymphopenia, and thrombocytopenia.

PREINCIDENT ACTIONS One of the most important preemptive actions that emergency medical service agencies, hospital-based emergency departments, and outpatient facilities should do is to determine whether their community is a possible target for a terrorist dirty bomb attack. Coordinating with local and state law enforcement and response agencies should provide a framework in which to assess the dirty bomb threat and develop a medical radiation incident or injury protocol. The protocol should be incorporated into the overall disaster plan. The radiation disaster plan should address decontamination, security, radiation monitoring, and decorporation of radioactive materials. The hospital radiation safety officer should be included in the medical radiation response team. Hospital staff should understand the hazards of radioactive contamination and be trained in radiation-monitoring techniques. Staff would need access to dosimeters, Geiger-Mueller counters, and personal protective equipment. Radiation-detection capabilities are critical to an effective medical response. Hospitals should have a realistic decontamination plan for patients, a lockdown plan to control access, and evacuation plans. A radiation risk communication program is required for the public.

POSTINCIDENT ACTIONS Emergency medical first responders arriving on the scene of a dirty bomb incident should initiate actions to treat or evacuate casualties. All response personnel should be advised of the explosive and radiologic hazards that may be present. Healthcare providers should advise others regarding safety measures to be taken to protect the public and to mitigate the radiation health effects. Patients evacuated from the scene and arriving at hospitals or medical clinics should be routinely monitored for radiation and decontaminated as needed.

Healthcare providers should control any exposure of hospital personnel to contamination. Clinicians should seek the assistance and cooperation of state and local authorities and inform them of casualties and possible hazards. Hospital radiation safety staff should periodically monitor the emergency department for radioactive contamination.

MEDICAL TREATMENT OF CASUALTIES Injuries associated with dirty bombs pose new and significant challenges for clinicians. Since radiation affects many organ systems, it can complicate blast and thermal injuries associated with a dirty bomb. Conventional injuries should be treated first, since radiation contamination is not a life-threatening medical emergency. Patients with traumatic blast and radiation injury should be resuscitated and stabilized. The assessment of patient airway, breathing, and circulation always takes priority. Victims of radiation exposure require more specialized treatment, and specialists in hematology, oncology, radiation, and infectious disease should be consulted. Effective treatment of internally contaminated patients requires knowledge of both the relevant radioactive isotope and its physical form. Treatment should be instituted quickly to ensure its effectiveness. However, with a terrorist incident, initially the radioactive source or sources are not known.8 Several general approaches may be used to treat internal radiation contamination, including reduction of absorption (administer Prussian blue), dilution (force fluids), removal of blockage (use potassium iodide), rectification of displacement by nonradioactive materials (administer oral phosphate), mobilization as a means of elimination from tissue (use ammonium chloride), and chelation (achieve with Ca-DTPA and Zn-DTPA).9 Patients who have received a low whole-body radiation dose may develop gastrointestinal tract distress within the first 2 days. Antiemetic agents may be effective in reducing the gastrointestinal symptoms, which will usually subside within the first day. If not, the administration of parenteral fluids should be considered. The prognosis for patients who have suffered traumatic blast, burn, and radiation injury is worse than for patients with radiation injury alone.10 A wound that is contaminated with radioactive materials should be rinsed with saline and treated using conventional aseptic techniques.4 Wounds contaminated with alphaemitting radioactive isotopes are usually excised. In patients who receive whole-body doses of radiation greater than 100 cGy, the wound should be closed as soon as possible to prevent it from becoming an entry for lethal infection. In spite of the wide availability of antibiotics, infections from opportunistic pathogens pose a major problem among patients exposed to intermediate and high doses of radiation. In these cases, the primary determinants of survival are treatment of microbial infections and aggressive resuscitation of the bone marrow.10 DIRTY BOMB (RADIOLOGIC DISPERSAL DEVICE) 873

CASE PRESENTATION On a busy Thursday morning, you hear a radio news report of a massive explosion in a crowded downtown district of your large city. Casualties are being evacuated from the scene to local area hospitals. Officials believe the explosion may be due to a natural gas leak. Later, you see a 47-year-old man who was brought to the emergency department of your hospital after being trapped for nearly 3 hours by fallen debris in a collapsed building at the scene of the explosion. He complains of left thigh pain, dizziness, nausea, weakness, and a burning sensation in his chest. Your high index of suspicion prompts radiation monitoring to be performed, and this

UNIQUE CONSIDERATIONS In contrast to popular belief, a dirty bomb is not considered a weapon of mass destruction.5 Instead, it is used as a weapon of mass disruption.3 Because radiation is colorless, odorless, tasteless, silent, and invisible, the uncertainty of not knowing whether one is being or has been exposed to radiation instills fear and panic in most people. The psychological effects of a dirty bomb incident require special consideration. Recognition of the importance of social and psychological issues will be essential in responding to a terrorist dirty bomb attack.6 Such an incident can cause profound psychosocial effects at every level of society including individual, family, community, and the nation. A dirty bomb attack has the capability of causing widespread fear, an increased sense of vulnerability, and loss of trust and confidence in societal institutions.6 The effects can be emotional, physical, cognitive, or interpersonal in nature. Significant numbers of people may suffer chronic distress years after an attack. Although a dirty bomb attack will create unique challenges, basic tenets of disaster mental health should still be followed in treating those affected.

PITFALLS Obstacles to the provision of optimal medical care include the following: • Failure to adequately prepare of medical response planning for possible terrorist dirty bomb attacks before they occur • Failure to coordinate with local and state emergency response agencies

874 OTHER EVENTS, COMBINATION EVENTS

reveals a significant level of radioactivity from a betagamma emitter. A cursory examination reveals multiple superficial facial and upper extremity lacerations and a deep penetrating wound of the left thigh. The results of an initial complete blood count are unremarkable. Meanwhile, the mayor has announced that the explosion may have been caused by a terrorist radioactive dirty bomb. Two more patients with multiple injuries are brought to the hospital by ambulance. The emergency waiting room is now filled with a dozen walk-in patients complaining of nausea and vomiting.

• Lack of understanding by medical providers of the basic science of radioactive isotopes • Failure to consult with specialists who have clinical experience in the medical management of the effects of radiation exposure • Lack of recognition that anxiety-induced nausea and vomiting may occur after a dirty bomb attack (This phenomenon has been observed after radiation accidents in which people thought they had been exposed to radiation even in the absence of actual exposure.11) REFERENCES 1. Meyer J. Al Qaeda feared to have “dirty bombs.” The Los Angeles Times. February 8, 2003:A1. 2. Edwards R. Only a matter of time? New Sci. 2004;182:8-9. 3. King G. Dirty Bomb: Weapon of Mass Disruption. New York: Penguin Group; 2004. 4. Mettler FA, Voelz GL. Major radiation exposure—what to expect and how to respond. N Engl J Med. 2002;346:1554-61. 5. Zimmerman PD, Loeb C. Dirty bombs: the threat revisited. Center for Technology and National Security Policy, National Defense University. Defense Horizons. No. 38, January, 2004. 6. National Council on Radiation Protection and Measurement. Management of Terrorist Events Involving Radioactive Material. Report No. 138. Bethesda, Md: National Council on Radiation Protection and Measurement; 2001. 7. Gusev I, Guskova AK, Mettler FA Jr, eds. Medical Management of Radiation Accidents. 2nd ed. Boca Raton, Fla: CRC Press; 2001. 8. Leikin JB, McFee RB, Walter FG, et al. A primer for nuclear terrorism. Dis Mon. 2003;49:485-516. 9. Voelz GL. Assessment and treatment of internal contamination: general principles. In: Gusev I, Guskova AK, Mettler FA Jr, eds. Medical Management of Radiation Accidents. 2nd ed. Boca Raton, Fla: CRC Press; 2001:319-36. 10. Conklin JJ,Walker RI. Diagnosis, triage, and treatment of casualties. In: Conklin JJ, Walker RI, eds. Military Radiobiology. San Diego, Calif:Academic Press, Inc; 1987:231-40. 11. International Atomic Energy Agency. The Radiological Accident in Goiânia. Vienna: International Atomic Energy Agency; 1988.

chapter 178

Explosion at a Nuclear Waste Storage Facility Constance G. Nichols

DESCRIPTION OF EVENT Nuclear waste is the radioactive by-product of radionuclides used in medicine, industry, research, weapons development and manufacture, and power generation. Any facility that uses radionuclides is,in theory,a nuclear waste storage facility. Each site must have safe, secure storage for spent radionuclides until they are taken to a more definitive storage facility. Currently 131 facilities exist in the United States, with the Yucca Mountain, Nevada, site is the planned final repository for nuclear waste. A fire, natural disaster, or intentional detonation of explosives in such a facility will potentially result in the release of radioactive materials of varying levels of injury and lethality. In 1982, the U.S. Congress directed the Department of Energy to construct a permanent underground storage facility for spent nuclear reactor fuel and other forms of high-level nuclear waste. In 1987, Congress directed the Department of Energy to develop only Yucca Mountain, Nevada, as a potential site, and President Bush recommended Yucca Mountain as a site in 2002. Due to problems with development, it is unlikely that Yucca Mountain will open as scheduled in 2010. Sites holding waste pending long-term disposal are now trying to expand their wet pool storage (a less expensive option) because the existing wet pool storage is reaching capacity. Some are looking at the more expensive dry storage (i.e., steel containers in concrete bunkers) as a temporizing measure.1 The U.S. Nuclear Regulatory Commission has felt that exposure of citizens to spent fuel would be unlikely because it is contained in a ceramic material. Exposure would require that the spent fuel be pulverized, such as in a high-speed impact or explosion, or the spent fuel would need to burn at high temperatures in a sustained fire.1 Unfortunately, very similar conditions occurred with the use of airliners as bombs on Sept. 11, 2001. The development of the Nevada site has been slow and controversial, and the area will not be available for many years. Therefore, it is necessary to regard any place that uses radionuclides as a potential nuclear waste storage facility.

A conventional non-nuclear explosion at a site of nuclear waste storage would be similar in some ways to that of a radiation dispersal device or “dirty” bomb. It would differ in the concentration, amount, and variety of radionuclides dispersed. Another important factor would be whether the explosion was accidental or planned in such a way as to maximize dispersal of radionuclides.

PREINCIDENT ACTIONS Cities and hospitals all have general disaster plans. Sites storing nuclear waste have procedures for dealing with contamination. Before an event, it would be important to communicate to the city and hospital disaster planners the amounts and types of radionuclides present in a local facility. Although national security interests might preclude an exact accounting of amounts of materials, the general nature of the materials should be available to emergency services and healthcare providers who would be dealing with victims of such an event. Drills covering radiation scenarios such as accidental release, conventional explosions, or terrorist attack should be considered and performed to acquaint all providers of emergency care with the special considerations for radiation disasters. Locations of radiation detectors in hospitals and ambulances should be part of the knowledge base of every provider working in those settings, as should basic decontamination principles.

POSTINCIDENT ACTIONS Immediately upon notification of an explosion at a nuclear waste storage facility, hospitals and emergency services should begin responding according to their disaster plans. Fire and police set up hot and cold zones and begin with victim decontamination. In this scenario, the contamination is assumed to be external,with contaminated wounds and inhalation of dust or debris the exception. Special plans for radiation safety should be implemented as soon as the nature of the event is determined. The need for scene decontamination and the timing of transport must 875

be determined in the decontamination zone and should be part of planning for radiation events. At receiving facilities, nonemergent patients should be screened for radiation contamination before entering. Emergent patients have life-saving care provided immediately and are then decontaminated. The ambulatory casualties who have not gone through decontamination at the site must be decontaminated before entering the treatment facility. This may entail police or security personnel equipped with adequate personal protection directing potentially contaminated patients to the appropriate part of the facility to ensure they do not contaminate the treatment area. If possible, all emergency services and hospital personnel should wear dosimeter badges. Hospital radiation safety officers should monitor treatment areas, casualties, and staff to prevent secondary victims.

MEDICAL TREATMENT OF CASUALTIES After decontamination, either at the site of the event or at the treatment facility, patients should be treated for their injuries and medical complaints. However, lifesaving care should be provided even before decontamination. Most casualties will have blast and thermal burn injury. Basic trauma care should be provided to these patients. (For detailed care information for patients with radiation injury, see Section Eight.) Patients should be reevaluated by the hospital radiation safety officer to determine whether they are decontaminated before admission to the hospital or discharge home. Patients need to be informed of the adverse effects of radiation poisoning, and a system should be established to follow up with potential victims for signs of radiation sickness and secondary illnesses from radiation exposure. The Federal Emergency Management Agency toolkit for radiologic incidents defines hospital treatment as follows: “Radiation damage can be repaired if the dose received is not too high and if the dose is received over a long period of time. Injured victims who are suspected of being contaminated by radiological hazards should be treated at

hospital facilities that have the capacity for this specific type of treatment. Local officials must ensure that such facilities are identified in the Emergency Operations Plan. Note: The U.S. medical community is currently illequipped to deal with a large-scale incident involving radiation poisoning. Only one hospital emergency room—in Oak Ridge, TN—is dedicated to treatment of this type of injury.”2

Postexposure prophylaxis with iodine would need to be instituted if the facility contained spent nuclear fuel or other iodine-containing waste. The World Health Organization guidelines for use of iodine after radiation exposure are presented in Table 178-1.3

CASE PRESENTATION “Oh my God!” The sound erupts from the waiting room. The triage nurse comes running back and tells the staff there has been an explosion at the nuclear power plant. As you watch the television, horrified, the local news program reports that there has been radiation released. The Nuclear Regulatory Commission and Federal Emergency Management Agency are going to be involved. Four people come running through the ambulatory door of the emergency department claiming they have been “irradiated,” while the patients waiting to be seen gather their belongings and run to the parking lot. You call the administrator and ask to go to your highestlevel disaster plan. The resource nurse hands you the “triage officer” vest and directs you to the ambulance entrance.

UNIQUE CONSIDERATIONS Internal Contamination Patients with inhalation or ingestion of radiation sources cannot be decontaminated by traditional washing methods. Contaminated wounds can be debrided.

TABLE 178-1 REFERENCE LEVELS FOR DIFFERENT POPULATION GROUPS FOR CONSIDERATION IN PLANNING STABLE IODINE PROPHYLAXIS* POPULATION GROUP

EXPOSURE PATHWAYS TO BE CONSIDERED

REFERENCE LEVELS

Neonates, infants, children, adolescents to 18 years and pregnant and lactating women Adults younger than 40 years Adults older than 40 years

Inhalation (and ingestion†)

10 mGy‡ avertable dose to the thyroid

Inhalation Inhalation

100 mGy‡ avertable dose to the thyroid 5 Gy§ projected dose to the thyroid

(From Guidelines for Iodine Prophylaxis following Nuclear Accidents Update 1999.) *These idealized levels do not take into account the practicalities involved in planning to respond to an accident involving many radionuclides in unknown quantities in real time. For this reason, a generic intervention level of 100 mGy has been specified in the Basic Safety Standards. Nevertheless, this does not preclude the need to consider the practicality of planning to implement iodine prophylaxis for specific age groups. †Ingestion of milk by infants where alternative supplies cannot be made available. ‡Adherence to these values would ensure that doses for all age groups would be well below the threshold for deterministic effects. §Intervention for this group is undertaken to ensure prevention of deterministic effects in the thyroid. Five Gy is the recommended limit for deterministic effects given in the Basic Safety Standards.

876 OTHER EVENTS, COMBINATION EVENTS

Decontamination of the pulmonary tree is difficult, but irrigation of the nasal mucosa may remove a large amount of trapped particles. Use of agents to speed passage through the gastrointestinal tract is the treatment modality of choice. All effluent must be collected for a 24-hour period or until no radiation is detectable.

Pregnant Women Pregnant women would need to be counseled regarding the effect of radiation on their fetus. Consideration would need to be given to amount of exposure and stage of fetal development.

Mental Health Issues A radiologic incident can be expected to cause widespread public panic and fear related both to the current dangers and to the possibility of long-term health effects. Crisis counseling should be available for incident victims, and a greater demand can be expected on longterm mental health services.

Chronic Health Issues Exposure to radiation has the potential for stochastic effects, including cancer and genetic effects. The local medical community should expect an upsurge in patients seeking treatment, and anyone exposed to unsafe levels of radiation will require long-term monitoring.

PITFALLS Several potential pitfalls in response to an explosion at a nuclear waste storage facility exist. These include the following: • Lack of knowledge about a nuclear waste storage facility in the area • Lack of training in radiation-decontamination procedures • Contamination of ambulances and treatment facilities • Possible contamination of treatment facility, if located near the event • Location necessitating evacuation of treatment facility • Loss of staff due to fear for family and safety REFERENCES 1. Report to the Chairman, Subcommittee on Energy and Air Quality, Committee on Energy and Commerce, U.S. House of Representatives. Spent nuclear fuel: options exist to further enhance security. U.S. General Accounting Office; July 2003. Available at: http://www.gao.gov/new.items/d03426.pdf. 2. U.S. Federal Emergency Medical Agency. Toolkit for managing the emergency consequences of terrorist incidents. Appendix C: radiological incidents. July 2002. Available at: http://www.fema.gov/ preparedness/toolkit.shtm. 3. World Health Organization. Guidelines for iodine prophylaxis following nuclear accidents: update 1999. Geneva: 1999. Available at: http://www.who.int/ionizing_radiation/pub_meet/Iodine_ Prophylaxis_guide.pdf.

EXPLOSION AT A NUCLEAR WASTE STORAGE FACILITY 877

chapter 179

Maritime Disasters Lucille Gans

DESCRIPTION OF EVENT Although maritime disasters no longer occur with the frequency of past centuries, when tens of thousands of ships sinking to the bottom of the world’s oceans left thousands of persons dead, they remain a major source of tragedy and loss for the transportation industry.1 Maritime disasters include incidents involving cruise ships, yachts, ferries, barges, container and cargo vessels, fishing boats, submarines, offshore oil platforms, and other watercraft. The loss of seaworthiness of a ship can result from several causes, often occurring in combination. Disasters are most often caused by storms, fires, and explosions, although loss of life generally results from human error. Contributing factors may include excessive reliance on technology, which can result in the loss of basic and advanced sailing techniques, plus underestimation of potential vessel vulnerabilities and risks posed by weather and sea conditions. Technologic advances have meant increases in the size and carrying capacity of ships, with concomitant increased potential for loss of life and property. Human factors also include failure to establish or follow procedures to enhance the safety of ships, their passengers, and crew; inexperience; and “cutting corners” to save time and money. If commercial concerns such as competitiveness, maintaining schedules, and cargo take precedence over passenger and crew safety, disasters can and do result. Survival is enhanced by diligent compliance with appropriate procedures and standards combined with knowledge, experience, and resourcefulness.2 Drowning is the most common cause of death due to maritime disasters, followed by hypothermia,2 although traumatic injuries may also occur because of the event that produced the disaster. These injuries include but are not limited to burns, blast injuries from explosions, and both blunt and penetrating trauma.3 In addition, victims who survive the initial sinking of the ship but who are not rescued in a timely manner may ultimately die from dehydration, starvation, or exposure while occupying life rafts or floating in the sea. Maritime disasters also include events when no human lives are lost but loss of the ship’s cargo results in pollution and damage to the ocean waters, marine life, 878

and shoreline. Such situations have most often involved oil tankers, as in the cases of the Exxon Valdez in Alaska and the Sea Empress in Australia. Other cargo ships carrying hazardous materials that have been damaged while near shore and habitation include the Multitank Ascania, carrying highly explosive vinyl acetate, and the Bilboa, carrying ferrosilicon (which can release toxic and explosive gases when exposed to moisture), to list only a few of the hundreds of incidents that have occurred in recent decades.4 There are huge costs associated with rescue, salvage, and recovery in such situations. For example, the cost for clean-up after the Exxon Valdez spill is estimated at $2.2 billion (U.S.).

PREINCIDENT ACTIONS Before leaving port, both cargo and passenger vessels are subject to various laws and maritime agreements. These requirements include the national laws of the country under which the ship is registered. Many ocean-going vessels are registered under “flags of convenience” to take advantage of national marine laws that may be less stringent than those of the country from which the passenger or cargo company most often sails.3 In addition, there are further security requirements imposed by the individual ports that the ship enters. The International Maritime Organization (IMO) is the specialized agency of the United Nations that has the responsibility for the safety of shipping and the prevention of marine pollution by ships.5 As well, following the Sept. 11, 2001, terrorist attacks on the World Trade Center in New York City, the IMO developed and adopted port security measures as outlined in the International Ship and Port Facility Security Code, which came into effect in 2004.6 All ships should be required to sail with adequate life jackets and lifeboats or rafts aboard for all passengers and crew. National standards for life jackets or personal flotation devices (PFDs) vary among countries. In addition, PFDs designed to allow greater freedom of movement for participation in water sports, such as windsurfing, may provide lesser degrees of buoyancy. PFDs should be adjustable to fit various body shapes and statures and volumes of clothing, including specialized

protective gear. Ideally, the PFD should be self-righting, should maintain the wearer at the water surface, and should keep the airway clear of water, which requires a minimum of 34 lb (150 newtons) of buoyancy. PFDs should be fitted with a crotch strap to prevent the device from riding up over the shoulders. Even with a properly fitted PFD, however, the dependent legs of the wearer act as a sea anchor, turning the face toward the waves. A person with impaired consciousness, a condition that may develop with hypothermia after immersion in cold water, may be unable to coordinate breathing with the irregular pattern of wave splash over face, and death by drowning may occur.2 Lifeboat drills and other safety instruction should be provided once the vessel leaves port. However, there is no guarantee that such information will be provided in multiple languages or that passengers will understand, remember, or comply with directions at the time of an emergency. Lifeboats, life rafts, and their launch equipment must be maintained to ensure that they are functional and seaworthy. At the bare minimum, each lifeboat should be supplied with a container of survival supplies including water, food rations, raft repair equipment, a sea anchor, and signaling equipment such as flares, lights, and mirrors.The IMO stipulates the equipment that survival craft must carry, based on the number of persons to be carried. Anyone aboard a vessel should consider assembling a grab bag containing additional supplies, clothing, and medications should it become necessary to abandon ship, using as a guide the requirements listed by maritime regulators or sailing race authorities.2,7 Because factors external to the ship such as weather and sea conditions can affect the safe passage of the vessel, technologic advances such as Doppler weather radar and Global Positioning Systems, combined with enhanced global communication systems, have contributed greatly to improved ocean safety records in recent years.7

POSTINCIDENT ACTIONS Once the integrity of a ship is breached, or as soon as some other threat to passenger or crew safety is recognized, it is essential that rescue procedures be initiated. Alarms both onboard and via radio transmission to appropriate sea- and land-based rescue facilities should be raised. The extent of the potential danger to the ship and those onboard should be assessed, with consideration for potential worsening of conditions. If the problem can be adequately managed with onboard resources, appropriate personnel should be advised and intervention measures initiated. Procedures for fire suppression must be well understood and initiated immediately once a fire is detected. If the incident is thought to be manageable with the resources available onboard,a “Pan Pan”message should be sent via radio transmission. If the vessel is in immediate danger, a “Mayday”message should be transmitted. In both cases, the radio message should include the vessel name,

nature of the incident, number of persons onboard, and geographic location with latitude and longitude. Maritime history includes many cases in which rescue was delayed by either incomplete information or failure of notification from the stricken vessel, often resulting in loss of life.2 Generally, those onboard will be better off remaining on the ship unless the captain determines that the ship is in danger of sinking. Before leaving the ship, each person should put on a lifejacket or PFD. If available, survival suits should also be worn. Lifeboats and rafts are smaller and less comfortable than a full-size ship, especially in rough ocean waters. In addition, there is no mechanism for steering or sailing most rafts. The crew should instruct passengers in how to get into lifeboat or rafts and the procedures for launching them. Once afloat, occupants should attempt to rescue survivors in the water, which may be hampered greatly by hypothermia of both parties. Therefore, bailing and drying procedures must be adopted early on in the survival craft.2 Additionally, rationing of food and water should be initiated, even if rescue is anticipated in a short time.7 No one should drink seawater, in any quantity, as this markedly reduces the chance of survival.2 Measures should be taken to reduce seasickness, including taking antinausea medications, if available, because seasickness will worsen most medical conditions and has further negative effects on hygiene and morale for all persons in a survival craft.7

MEDICAL TREATMENT OF CASUALTIES Rescuers may include those specially equipped and trained for water rescues—for example, the U.S. Coast Guard Search and Rescue program.8 Often, however, rescue comes from those closest who may not have the knowledge or gear to mount the most effective rescue or resuscitation. The most common conditions suffered by those rescued from the water are near drowning and hypothermia. Rescuers should remove wet clothing and dry the skin and hair of victims before providing warm and dry clothing. If survival suits are available, it may be adequate to dress the victims in these for passive rewarming. However, particularly in the setting of multiple victims rescued from cold ocean waters, the rescuing vessel may not have enough gear for all persons rescued. It may be necessary to put two persons into each suit, and in this case, a warmer victim should be paired with a colder one.2 Although hypothermia causes deterioration more commonly and more rapidly, victims rescued from lifeboats and rafts may suffer heat illnesses, including sunburn, heat exhaustion, and heat stroke, the last of which requires urgent medical intervention.2 Survivors who are rescued after a prolonged time adrift at sea may be suffering from dehydration or starvation plus exposure and may require intensive or prolonged resuscitation and medical care. MARITIME DISASTERS 879

CASE PRESENTATION It is shortly after midnight on an international cruise ship carrying 1200 passengers and 700 crew members. It is the third day of a transatlantic voyage,and the ship is 1000 miles from the mainland. Suddenly there is a large explosion, followed by a fire in the engine room. The crew members on duty reduce ship speed and institute emergency fire suppression measures immediately, with limited success. An initial assessment of damage indicates no significant hull damage, but there has been loss of electric power to areas of the ship. A crew member who had been working in the engine room is missing. Seven other crew members have been injured by the initial explosion or during efforts to fight the fire. Although many passengers had already gone to bed and are unaware of the situation, a large percentage of those still awake are increasingly concerned and some are agitated, which is worsened by prior consumption of alcohol over the course of the evening. Emergency lighting is on throughout much of the ship. Less than 1 hour later, the fire has spread. The two nearest large ships that could provide assistance are 250 and 300 miles away, but both have responded to the distress call and are proceeding toward the stricken cruise ship. Smoke is spreading through the many corridors of the lower decks of the ship, so the captain and crew decide to raise a general fire alarm and alert the passengers. Many are slow to waken and are confused by the noise and lack of normal lighting. Some panic when they see and smell smoke in the passageways. Most do not take their lifejackets with them upon exiting their cabins, despite the instructions accompanying the fire alarm. If rescue does not occur speedily, many passengers who have not donned PFDs and who do not board lifeboats may enter the water unprepared, by jumping in panic or by failing to follow the instructions of the crew. Those without PFDs may drown or suffer hypothermia before a rescue vessel arrives, unless they are assisted into lifeboats by others.

UNIQUE CONSIDERATIONS Maritime rescues are frequently complicated by the very factors that caused the incident. Poor visibility, strong winds, and rough seas may prevent rescuers from reaching or finding damaged ships or floating victims. Once located, high waves and cold temperatures further endanger both rescuers and victims and may damage rescue and medical equipment. Salt water can reduce the effectiveness of equipment immediately or over time. Noise, impaired visibility, and hypothermia can interfere with communications between rescuer and victim, and language barriers may exist. Victims are often hypothermic, dehydrated, and exhausted, which reduce their ability to assist with their own rescue. Victims who are rescued from immersion in cold water may experience temperature afterdrop as a complication of hypothermia, with this postimmersion collapse often resulting in death. This condition occurs when chilled blood from peripheral tissues circulates to the body core 880 OTHER EVENTS, COMBINATION EVENTS

with rewarming, causing a drop in the core temperature and a drastically worsened clinical practice.9,10 The clinical status of survivors rescued after neardrowning may worsen gradually or abruptly due to the development of respiratory distress syndrome with hypoxia and subsequent respiratory failure. Pulmonary edema, cardiovascular complications, and multisystem organ failure may develop, even with intensive medical care.11 Supportive care and prompt transport to a tertiary care center are essential. Victims may be covered with fuel oil or may have swallowed or aspirated oil while immersed. They may develop vomiting, aspiration pneumonia or pneumonitis, or conjunctivitis.2 Oil contamination also complicates the healing of skin wounds such as abrasions or punctures, as does seawater containing bacteria or other contaminants. Prolonged exposure to damp conditions or clothing in a lifeboat may allow saltwater boils, pustules, or even ulcers to develop. Immersion foot can occur in survivors aboard lifeboats and rafts when feet remain cool, damp, dependent, and inactive, with the development of blood stagnation and tissue swelling.2 Survivors rescued from the sea may have swallowed significant quantities of salt water and may develop osmotic diarrhea and hypernatremia, which will require volume replacement and careful monitoring of electrolyte levels.2 After rescue from the sea, there may be delays in reaching definitive medical care. Although the rescue vessel may have adequate personnel and equipment to provide first aid or even major resuscitation for victims, weather and sea conditions may delay transport to a site where surgery or intensive care could be provided, such as a mainland tertiary care center. As well, distances to the nearest appropriate healthcare facility may be significant, particularly in the case of mid-ocean rescues. The same conditions that complicate rescue also make investigation of ship and submarine accidents difficult and hazardous. Evidence may be scattered over the ocean floor, resting several kilometers below the surface in cold, dark water, subject to strong ocean currents.12 There may be no survivors to describe the events leading up to a tragedy or any actions taken in response, whether or not they were effective, heroic, or foolhardy. There may be no conclusive determination of the cause of a tragic event at sea—rather, only conflicting theories and conjecture—but experts must nevertheless attempt to identify what went wrong so that they may recommend methods to prevent future disasters.13

PITFALLS Several potential pitfalls exist in response to a maritime disaster. These include the following: • Failure to appreciate dangerous weather and sea conditions, especially when combined with ship weaknesses or damage • Failure to adapt course or sailing techniques to changing conditions

• Failure to follow rules of sailing, navigation, and sea transport • Excessive reliance on technology and failure to identify deficiencies or weakness in ship structure and function • Failure to request assistance or rescue in a timely manner • Failure to follow safety procedures and lack of familiarity with evacuation and emergency exits and equipment • Failure to abandon ship or deploy emergency escape equipment, such as lifejackets or PFDs, survival suits, and lifeboats • Failure to activate the emergency position indicator rescue beacon before abandoning ship • Failure to ration water and food supplies after abandoning ship REFERENCES 1. Bonsall TE. Great Shipwrecks of the 20th Century. Baltimore, Md: Bookman Publishing; 1988:6-12. 2. Golden F, Tipton M. Essentials of Sea Survival. Champaign, Ill: Human Kinetics; 2002.

3. Roberts SE. Work-related mortality among British seafarers in flags of convenience shipping, 1976-95. Int Marit Health. 2003;54:7-25. 4. Australian Maritime Safety Authority. Available at: http://www. amsa.gov.au. 5. International Maritime Organization Web site. Available at: http://www.imo.org. 6. International Maritime Organization. IMO adopts comprehensive maritime security measures. Conference of Contracting Governments to the International Convention for the Safety of Life at Sea, 1974: December 9-13, 2002. Available at: http://www.imo. org/Newsroom/mainframe.asp? topic_id=583&doc_id=2689. 7. Howorth F, Howorth M. The Grab Bag Book. London:Adlard Coles Nautical; 2002. 8. U.S. Coast Guard Web site. U.S. Department of Homeland Security. Available at: http://www.uscg.mil. 9. Giesbrecht GG, Bristow GK. A second postcooling afterdrop: more evidence for a convective mechanism. J Appl Physiol. 1992;73:1253-8. 10. Giesbrecht GG. Prehospital treatment of hypothermia. Wilderness Environ Med. 2001;12:24-31. 11. Volturo GA. Submersion injuries. In: Harwood-Nuss A,Wolfson AB, Linden CH, et al, eds. The Clinical Practice of Emergency Medicine. 3rd ed. Philadelphia: Lippincott Williams & Wilkins; 2001:194-6. 12. Bird L. The Wreck Diving Manual. Ramsbury, Marlborough: The Crowood Press; 1997:9-43. 13. Krieger M. All the Men in the Sea. New York: The Free Press; 2002:1-221.

MARITIME DISASTERS 881

chapter 180

Cruise Ship Infectious Disease Outbreak Scott G. Weiner

DESCRIPTION OF EVENT Throughout the ages, infectious diseases traveling by boat have affected the course of history. For instance, the Black Death caused by Yersinia pestis was brought by boats coming from the east to Europe. The plague caused the death of at least one-third of the European population during the 1300s. This epidemic led to the practice of refusing the landing of ships with suspected cases of plague for 40 days—the first practice of “quarantine,” from the Italian word quaranta for “forty.” Shipborne smallpox also played a role, actually saving England from a French invasion in 1779 after an outbreak spread among the French sailors.1 The closed environment of the ships and the prolonged duration of voyages led to a high infection rate. In modern times, airplanes have replaced the boat for long-range passenger transportation, but recently a steadily increasing number of people choose to go on cruises as a form of vacation. Over 9.5 million people went on cruise vacations in 2003, an increase of 10.2% from 2002 and 198% from 1994.2,3 The average length of cruise in 2003 was 6.88 days.2 And with the standard capacity of the newer cruise ships reaching well over 2000 passengers, hundreds of people may potentially be at risk from an infectious disease outbreak onboard. The infectious diseases that affect cruise ships can be divided into three categories: gastrointestinal, respiratory, and miscellaneous infections.

Gastrointestinal Illness Gastrointestinal illness is by far the most common result of cruise ship outbreaks. A study of 31 investigated cruise ship gastroenteritis outbreaks between 1986 and 1993 found that 39% were from bacterial sources (including enterotoxigenic Escherichia coli, Shigella species, Salmonella species, and Staphylococcus aureus), 29% were from Norwalk or Norwalk-like virus (collectively called norovirus), and 32% were of unknown etiology.4 Of the determined sources, 48% were from onboard exposures (particularly food), 10% were obtained during onshore excursions, and 42% of sources were unknown.4 A more recent study found a shift in epidemiology, with an increase in the incidence of norovirus.5 Twenty882

one outbreaks of acute gastroenteritis were studied, of which nine episodes were caused by norovirus, three were caused by bacteria, and nine were of unknown etiology. The rate of passenger infection ranged from 5% to 19%.5 However, in one outbreak in 1998, more than 80% of the 841 passengers were affected, indicating the highly infectious nature of this virus.6 Because norovirus is so infectious, the organism passes easily between passengers in the confined space of a cruise ship, and hundreds may be at risk.

Respiratory Illness Whereas the most common illness afflicting passengers and crew aboard cruise ships is gastroenteritis, respiratory infections comprise about one-third of sick bay visits.3 Outbreaks of Legionnaires’ disease and influenza have been reported in the literature.7,8 One outbreak of Legionella pneumophila infection in 1994, linked to the ship’s whirlpool spa, affected 50 passengers on 9 different cruises, including the death of 1 passenger.7 Another study documented an outbreak of influenza A and B in 2000, in which 37% of passengers developed an influenza-like illness, 40 passengers were hospitalized, and 2 died.8 Though never reported as outbreaks in the literature, other diseases with respiratory transmission, such as diphtheria, tuberculosis, and meningitis, remain outbreak possibilities.1

Miscellaneous Infections Other miscellaneous infections, including malaria, yellow fever, and varicella, also involve potential pathogens on a cruise ship.1 A 1997 outbreak of rubella among crew members, mostly from countries that did not have routine immunization programs, serves as a reminder that unanticipated outbreaks can arise in close quarters.9

PREINCIDENT ACTIONS Prevention is the single most important action that can be taken to avoid an infectious disease outbreak. To achieve this goal, the U.S. Centers for Disease Control and Prevention (CDC), in a cooperative arrangement

with the cruise ship industry, created the Vessel Sanitation Program (VSP) in 1975.10 The program is designed to prevent the introduction or transmission of infectious diseases in the United States as well as to assist the cruise ship industry in the development and implementation of sanitation programs to protect passengers and crew.10 The VSP also involves unannounced twiceyearly inspections of all cruises traveling to the United States from international ports and publishes its findings as a sanitation score on a biweekly basis.4,10,11 As part of the VSP arrangement, cruise ships must maintain an incident report of gastrointestinal illness for each cruise. A reportable case of gastroenteritis is defined as three or more episodes of loose stools in 24 hours, or vomiting and any additional symptom suggestive of the illness (excluding nausea,which can be a symptom of seasickness).10 It is also essential that cruise lines use adequate infection control measures, including proper disinfection, filtering, and storage of water and regular maintenance of spas and ventilation systems to prevent the spread of airborne infections.6 Another important step is provision of onboard healthcare facilities that will be capable of treating patients with outbreaks. The American College of Emergency Physicians published guidelines for a ship’s medical facilities, and the 16 members of the International Council of Cruise Lines have agreed to meet or exceed these requirements.12,13 Although the guidelines do not identify specifics regarding outbreaks, they do require ships to have properly trained physicians and nurses, an infusion pump, gastrointestinal system medications, respiratory system medications, and an emergency preparedness plan.12 At a minimum, ships should have the capacity to provide oral and intravenous rehydration therapy and have sufficient doses of or ready access via airlift to antibiotics to treat Legionella infection and bacterial gastroenteritis.

POSTINCIDENT ACTIONS Once an outbreak is identified, it is crucial that a predetermined decontamination plan is commenced immediately.5 Rapid implementation of control measures at the first sign of a suspected outbreak is fundamental for three important reasons:(1) many people share the same water, food, and environment, and are all at risk for infection; (2) the ship’s medical resources can quickly become overwhelmed in an outbreak; and (3) without intervention, the infection can spread to subsequent cruises.10 After an outbreak, international quarantine regulations dictate that the master of the ship traveling to a U.S. Port report to the closest quarantine station. Furthermore, the master of a ship carrying more than 12 passengers is required to report the number of passengers or crew who reported diarrhea during the cruise 24 hours before arrival to the United States. If at least 3.0% of the ship’s passengers or crew is ill, the VSP may conduct an investigation.10 The investigation is composed of three phases: (1) an epidemiologic investigation, in which interviews and questionnaires are performed; (2) a laboratory

investigation, in which the CDC attempts to determine the agent responsible for the outbreak; (3) an environmental health investigation, in which the source of transmission (usually water, food, or air) is analyzed. After the investigation is complete, the information, including recommendations for control and prevention, is sent to the cruise line.10 Complete guidelines for stool and water collection are available on the CDC Web site.10 Furthermore, the World Health Organization publishes a Guide to Ship Sanitation, which offers further assistance in the prevention of the spread of infection.6 Once an outbreak occurs, prompt disinfection of the ship and isolation of ill crew members and, if possible, passengers for 72 hours after clinical recovery are ideal.5 Suitable disinfectants such as chlorine, phenol-based compounds, or accelerated hydrogen peroxide products should be used to disinfect the ship.5 Furthermore, the staff should remind passengers and the crew to perform frequent, rigorous handwashing with soap and water.

MEDICAL TREATMENT OF CASUALTIES The first problem facing the medical staff and crew of the ship is the logistics of treating hundreds of casualties onboard and finding an appropriate docking port. The ship’s medical staff will be forced to ration care as they balance resources with numbers of afflicted patients. The most seriously affected should receive care first. For instance, those who are very young, very old, or significantly dehydrated should receive intravenous fluid before the others. The crew should locate a suitable port where hundreds of casualties can be most easily cared for. If there is a choice, the ship should not dock at a small port if a larger port near a large city is available. Calling ahead and warning the receiving port is also crucial. The treatment of the casualties should be tailored to the individual disease process. For patients with viral gastroenteritis, only supportive care is necessary. Norovirus illness lasts 12 to 60 hours and is usually accompanied by sudden onset of nausea, vomiting, and watery diarrhea. Its incubation period is 12 to 48 hours. No specific treatment or vaccine exists.5 Although generally self-limited, viral gastroenteritis may cause problems in children, elderly persons, and persons with serious underlying medical conditions. Treatment should include oral rehydration for mild cases and intravenous fluid for more significant dehydration. If the cause is determined to be bacterial, appropriate antibiotics (e.g., ciprofloxacin) should be administered to the affected passengers. Other treatments will depend on the infectious agent. Legionnaires’ disease may present with a range of systems from a mild febrile illness to a severe pneumonia with malaise, cough, and gastrointestinal symptoms.14 Standard pneumonia antibiotic therapies such as azithromycin or levofloxacin are curative, and these should be stocked on the ship. Regardless of the etiology, air evacuation is indicated for very ill patients.15 CRUISE SHIP INFECTIOUS DISEASE OUTBREAK 883

Fortunately,cruise ship infectious disease outbreaks are rare and are usually self-limited and nonfatal. Between 1986 and 1993, the CDC investigated 1.4 outbreaks per 1000 cruises, or just 2.3 outbreaks per 10 million passenger-days, and more recent research demonstrates that the VSP is effective in helping to further reduce this number.4,11 However, once it occurs, an infectious disease outbreak on a cruise ship can represent a major medical disaster. An outbreak can quickly overwhelm the limited medical resources available on a ship. Proper preparation and planning can help prevent a catastrophic event.

CASE PRESENTATION* A relatively new cruise ship that is able to carry 2500 passengers and 800 crew members embarked on its usual tour. During a 7-day trip from Miami to various ports in the Caribbean, an increasing number of patients began reporting to the ship’s sick bay complaining of diarrhea. By day 3 of the voyage, 30 passengers (1%) and 10 crew members (1%) presented with gastroenteritis. By day 7, a total of 285 passengers (11%) and 25 of the crew members (3%) had reported the illness. As is required, the CDC was notified and an investigation ensued. A questionnaire was distributed to all passengers, and it was determined that the conditions of 523 passengers (21%) met the definition for acute gastroenteritis. Several stool specimens tested positive for norovirus by polymerase chain reaction. Of the patients with gastroenteritis, 418 patients (80%) had symptoms that spontaneously resolved within 48 hours, 89 patients (17%) had symptoms that resolved within 96 hours, and 4 elderly patients were hospitalized after their return to shore and then were subsequently discharged without complication. Despite aggressive disinfection, the outbreak continued on the next cruise. The cruise line then removed the ship from service for 1 week for further cleaning and sanitizing, and no subsequent cases were reported. *Adapted from Outbreaks of gastroenteritis associated with noroviruses on cruise ships—United States, 2002. MMWR Morb Mortal Wkly Rep. 2002;51:1112-5.

UNIQUE CONSIDERATIONS Cruise ships are closed spaces, and the combination of thousands of people contained for several days in this space represents an opportunity for infection to spread rapidly. Only limited resources are available onboard, so a ship’s medical bay may become quickly overwhelmed during an outbreak. Ships often visit ports in countries where infectious disease is more prevalent than it is in the United States, so the potential for bringing an agent onboard is elevated. In addition, the background of the crew is often diverse, and some may be at increased susceptibility to diseases, depending on immunization status. Although there have been no reported incidents of bioterrorism on cruise ships, this possibility cannot be excluded. A cruise ship might become a means for an infectious disease agent to be purposefully transmitted 884 OTHER EVENTS, COMBINATION EVENTS

into a country. Increased vigilance among the ship’s crew and medical staff is indicated. An infectious disease outbreak may represent a huge financial loss to a cruise line because cruises may need to be cancelled and future passengers may be less likely to travel on an affected line. Again, preventive measures are paramount.

PITFALLS Several potential pitfalls exist in response to an outbreak of infectious disease aboard a cruise ship. These include the following: • Failure to properly staff and supply the ship’s medical clinic • Failure to recognize or report an infectious disease outbreak • Failure to quickly isolate and treat affected passengers and crew • Failure to properly sanitize the ship after an outbreak • Failure to create a plan for mass treatment in the event of an outbreak,including provisions for airlifting patients out or supplies in REFERENCES 1. Minooee A, Rickman LS. Infectious diseases on cruise ships. Clin Infect Dis. 1999;29:737-43. 2. Cruise Lines International Association. CLIA member cruise lines post strong passenger growth with over 9.5 million cruisers in 2003. Cruise News. February 2004. Available at: http://www.cruising.org/CruiseNews/news.cfm?NID=156. 3. Peake DE, Gray CL, Ludwig MR, et al. Descriptive epidemiology of injury and illness among cruise ship passengers. Ann Emerg Med. 1999;33:67-72. 4. Koo D, Maloney K,Tauxe R. Epidemiology of diarrheal disease outbreaks on cruise ships, 1986 through 1993. JAMA 1996;275:545-7. 5. Outbreaks of gastroenteritis associated with noroviruses on cruise ships—United States, 2002. MMWR Morb Mortal Wkly Rep. 2002;51:1112-5. 6. World Health Organization. Ship sanitation and health. February 2002. Available at: http://www.who.int/mediacentre/factsheets/fs269/en. 7. Jernigan DB, Hofmann J, Cetron MS, et al. Outbreak of legionnaires’ disease among cruise ship passengers exposed to a contaminated whirlpool spa. Lancet 1996;347:494-9. 8. Brotherton JM, Delpech VC, Gilbert GL, et al. A large outbreak of influenza A and B on a cruise ship causing widespread morbidity. Epidemiol Infect. 2003;130:263-71. 9. Rubella among crew members of commercial cruise ships— Florida, 1997. MMWR Morb Mortal Wkly Rep. 1998;46:1247-50. 10. Centers for Disease Control and Prevention, National Center for Environmental Health. Vessel Sanitation Program. Available at: http://www.cdc.gov/nceh/vsp. 11. Cramer EH, Gu DX, Durbin RE, et al. Diarrheal disease on cruise ships, 1990-2000: the impact of environmental health programs. Am J Prev Med. 2003;24:227-33. 12. American College of Emergency Physicians. Health care guidelines for cruise ship medical facilities. Ann Emerg Med. 1998;31:535. 13. International Council of Cruise Lines. Medical facilities guidelines. January 1, 2002. Available at: http://www.iccl.org/policies/ medical2.cfm. 14. Thibodeau KP, Viera AJ. Atypical pathogens and challenges in community-acquired pneumonia. Am Fam Physician. 2004;69: 1699-706. 15. Prina LD, Orzai UN,Weber RE. Evaluation of emergency air evacuation of critically ill patients from cruise ships. J Travel Med. 2001;8:285-92.

chapter 181

Hostage Taking Dale M. Molé

DESCRIPTION OF EVENT Incidents of hostage taking and kidnapping are on the rise around the world. Some are politically motivated; others involve simple greed. A few are just the result of being in the wrong place at the wrong time. According to the Hiscox Group, a leading international specialty insurer, the number of reported worldwide kidnappings for ransom increased from 1690 in 1998 to 1789 in 1999. Over 90% of those incidents took place in what have been deemed the top 10 riskiest areas: Colombia, Mexico, the former Soviet Union, Brazil, the Philippines, Nigeria, India, Ecuador,Venezuela, and South Africa.1 The rise can be blamed on a combination of factors such as lawlessness, political unrest, and poverty. Kidnapping is an appealing crime for many since the perpetrators are rarely caught and it is a much easier way to make money than drug dealing or robbery. The epidemic of kidnapping/hostage taking is much greater than demonstrated by statistics, since many kidnappings are handled privately and remain unreported. In about 67% of cases, a ransom is paid and usually averages about $2,000,000 in countries where the “business” is well established. If a ransom is not paid chances of survival for the victim are slim, especially in Latin America. According to insurance industry sources, Americans with kidnapping and ransom insurance are four times more likely to survive a kidnapping than are those who have none. This is not only a problem overseas, however. Each year, the U.S. Federal Bureau of Investigation is involved in approximately 400 domestic kidnappings, with about one third involving a ransom demand. Branch bank managers and their families appear to be favorite targets.2 Some kidnapping/hostage taking occurs incidentally to the commission of another crime, with the victim being a target of opportunity for the perpetrator trying to negotiate his way out of a losing situation. With the growing threat of international terrorism and the increasing political value of American hostages, it is the official policy of the U.S. Government not to make concessions to individuals or groups holding official or private U.S.citizens hostage. However,the United States will make use of every appropriate resource to ensure the release and safe return of American citizens. The goal is to deny

the hostage takers the benefits of ransoms, prisoner releases,policy changes,or other acts of concession,which would increase the risk that other Americans would be taken hostage. The State Department will contact representatives of the captors in an effort to secure release. Although very dangerous, hostage rescue is sometimes the only viable option. Local, state, and federal law enforcement agencies have specialized teams to rescue hostages or deal with standoff situations. These teams rely on training, speed, coordination, stealth, and overwhelming force to rescue hostages and take control of the situation.3 The Federal Bureau of Investigation’s Hostage Rescue Team (HRT) was established in 1982 and has been deployed more than 200 times in support of hostage rescue, counter-terrorism, stopping violent crime, and other federal law enforcement activities. Tactical emergency medical services (TEMS) is emerging as a special interest area within emergency medicine to provide medical services within a civilian law enforcement environment for both law enforcement personnel and suspects. Beyond increasing the chances of successful mission accomplishment,TEMS reduces the morbidity and mortality among innocent persons, suspects, and officers. Medical care in a tactical situation is frequently very different from the care provided by routine civilian EMS. Law enforcement agencies manage crisis situations with zones of containment. The inner perimeter is a geographically defined circle around an incident and is controlled by the tactical law enforcement element (i.e., special weapons and tactics teams,special response teams,and the like). The outer perimeter is a larger boundary that excludes the public, provides additional safety, and is controlled by patrol or regular uniformed officers. Similarly, zones of care (i.e., hot, warm, and cold zones) help define appropriate care in a tactical law enforcement environment. The hot zone includes those areas where the threat to safety is direct and immediate and the threat for additional injury is high, where it would be extremely hazardous to provide medical care; for example, the area surrounding a sniper’s position in a building with a clear field of fire. Extraction to a safer area to render medical assistance is about the only option. The cold zone is where no threat exists and care can be provided in much the same manner as in any routine civilian situation. The warm zone is an area where the threat is intermediate 885

between these two extremes; this is often the most challenging regarding medical decision-making. The benefit of a particular intervention must be considered relative to the risk of additional injury to the patient or the medical tactician. Certain actions considered standard for care in normal situations, such as applying a cervical collar for penetrating neck injuries before moving the patient, make no sense in a tactical environment.

PREINCIDENT ACTIONS Personal Taking simple steps and altering certain behaviors can help travelers avoid putting themselves at risk. Anonymity is the best defense for foreign travelers.4 When traveling abroad, persons should keep a low profile and not advertise their wealth. Jewels and expensive clothes should be left at home. Travelers should de-Westernize their attire as much as possible, since a middle class income in the United States places a person in the top few percents of incomes worldwide. Travelers should not follow a regular routine, nor should they make restaurant reservations in their own names. Colleagues, friends, and family should be kept informed as to travelers’ whereabouts. When traveling in third-world countries, travelers should not wear military-style clothing. Blue or other neutral colors should be worn, since green or brown clothing is often associated with the military. Persons taking trips abroad should avoid luggage tags, behavior, and dress identifying them as American. Reading maps in public or carrying a camera around the neck will let others know a person is a tourist and therefore a target of opportunity. If traveling on a bus, the safest areas are the aisle seats near the middle of the bus. When on an airplane, the safest areas are the window seats near the middle of the aircraft. Personal papers should not be left in the hotel room, and hotel guests should not open the door for strangers. Travelers should make sure they have mentally planned an escape route in case of fire or other disaster. Hotel rooms on the first floor should be avoided, if possible. When driving through crowded areas, windows should be kept closed. Travelers are advised to make sure their vehicle is in good condition, and they should plan the route before traveling. They should make mental notes of safe havens such as police stations, hospitals, and hotels. In addition, they should steer clear of rural or isolated areas, especially when traveling alone or in a small group. It is recommended to schedule direct flights when possible and avoid stops in high-risk areas. Travelers should be aware of what they discuss with strangers and what may be overheard. Routines should be varied, especially if one stays in a country for an extended time. Persons should not take the same travel routes, eat at the same restaurants, or jog on the same pathways on a regular schedule. When walking around foreign cities, it is prudent to ignore the attempts of strangers to engage the traveler in conversation. Letting one’s familiarity with a country lull one into a false sense of security is a mistake. 886 OTHER EVENTS, COMBINATION EVENTS

In conflict or disaster areas, travelers should beware of roadblocks. The people controlling the roadblock may desire to extort money or other items of worth. If a person is working with a relief agency, he or she should ensure that proper identification is available and that he or she is traveling in a clearly marked vehicle. Vehicles painted in military colors should be avoided. If a roadblock is encountered, the personnel manning it may be aggressive, undisciplined, untrained, and intoxicated. Travelers should not make any aggressive movements or statements. They should be firm but polite, stating that the authorities have given them permission to travel in the area. If a person is an aid worker, he or she should establish his or her affiliation quickly because it is one of the greatest assets a traveler has.5

Medical Support Elements Integrated medical support for specialized law enforcement/hostage rescue teams is mandatory. Just-in-time training for supporting medical personnel is not an option and places the mission, the hostages, and the rescuers at risk. TEMS training for physicians, paramedics, and emergency medical technicians is available from several organizations. One of the first and most widely recognized is Counter Narcotics and Terrorism Operational Medical Support. Established within the Casualty Care Research Center at the Uniformed Services University of Health Sciences, lessons learned on the battlefield providing care in austere environments are applied to civilian law enforcement situations. The core curriculum of any TEMS course should include didactic and practical exercises in at least the following areas: • • • • • • •

Threat assessment and medical intelligence Care under fire Hostage survival Clinical forensic science Weapons and their effects Medicine across the barricade Toxic hazards (e.g., clandestine drug labs, weapons of mass destruction) • Medical effects of extended operations • Special equipment and medical kits

POSTINCIDENT ACTIONS The two most dangerous times during a hostage situation are at the beginning and at the end, especially if a rescue is attempted. Initially, persons in a hostage situation should make themselves as inconspicuous as possible. They should listen to the terrorist’s commands and respond without questioning. “Passive cooperation” should be enacted. It is recommended to avoid sudden movements or threatening behavior and avoid eye contact or any other actions that may single a person out. If ordered to be silent, hostages should not talk or whisper. If possible, they should dispose of identification or documents that would make the hostage takers more

hostile toward them. Persons should eat or drink sparingly during the first few hours and should not consume alcohol. If taken hostage, persons should help their kidnappers establish contact with their organization as soon as possible. Hostages should try to remain calm and remember that the vast majority of kidnappings end with the hostages released. Death is usually the result of a medical condition, an unsuccessful escape attempt, or perhaps a botched rescue. It is not advisable to act as a spokesperson for the hostages. Persons should rehearse what they will say to the hostage takers if questioned about their documents. Persons taken hostage should look after their health as much as possible. Because they don’t know where, when, or what their next meal will be, hostages should eat all of the food they are offered after the initial few hours, once the hostage situation has stabilized. They should also try to exercise regularly. Since hostages may be guests of their captors for quite a while, they should try to establish rapport. The better the relationship they establish, the harder it will be for the hostage takers to kill or injure them. Escape should not be attempted unless hostages are absolutely certain of success.6 If a hostage is bound by his or her captors, slumping in the chair while they are tying the person up will allow some slack in the ropes. The same can be accomplished by keeping the chest inflated or wrists slightly apart. Hostages should try to catch a gag in their teeth to prevent it from being forced all the way back in the mouth. If a person’s hands are tied behind him or her, if possible, the hostage should pass his or her hands under the feet. With the hands in front of the body, the hostage can use the teeth to untie knots. Wherever hostages are being held, they should look around for safe areas in case of a rescue attempt. It is a good idea to drop to the floor immediately if there is shooting or an explosion. If possible, persons should seek shelter in a ditch, in a depression, or near a solid wall. They should not jump up and try to run.

MEDICAL TREATMENT OF CASUALTIES The medical care required depends on the length and conditions of captivity, preexisting illnesses, and whether the hostage was released or had to be rescued. Rescue attempts are inherently very dangerous situations and may result in injury to rescuers as well as hostages. The three most common causes of preventable death in a tactical situation are uncontrolled hemorrhage, airway compromise, and untreated tension pneumothorax. Perhaps most important is the emotional and mental health support required by all hostages, even those not sustaining any physical trauma. The lack of control over one’s fate in a highly stressful life and death situation will tax the emotional resources of even the most robust person.

CASE PRESENTATION On the evening of May 23, 2004, three suspects abducted South African Deputy High Commissioner Nicky Scholtz on one of Kuala Lumpur’s busiest streets, near the hotel where he was attending a conference. One man confronted him and forced him into a car where two men were waiting. He was struck with a blunt object and then driven away. The abductors rendezvoused with four men, who became the hostage holders, in another car. This demonstrated operational planning, as well as a level of sophistication not usually seen in a random abduction. Scholtz was taken about 12 miles south of Kuala Lumpur and held hostage for a week. He was bound with wire and beaten while the attackers forced him to write checks and withdraw funds on his credit card, to a total of about $4200, sufficient to purchase weapons or explosives. He suffered two fractured ribs, a dislocated jaw, and severe bruising of his back, face, arms, and legs. The kidnappers released Scholtz after his disappearance was reported locally, but they threatened to kill him if he reported the incident. Based on information he provided, seven suspects were later taken into custody. There is no indication the attack was politically motivated, but rather, it is believed that he was simply a target of opportunity. This incident illustrates the importance of good situational awareness, whether an individual is at home or abroad.

UNIQUE CONSIDERATIONS Being kidnapped or held hostage is perhaps one of the most likely events to cause posttraumatic stress disorder (PTSD). PTSD is characterized by reexperiencing the traumatic event (e.g., vivid nightmares, recurring visual images, reacting physiologically to stimuli associated with the event), avoidance behavior (i.e., avoiding things associated with the trauma such as activities, places, or people), and hyperarousal symptoms (e.g., insomnia, startle behavior, attention deficits). PTSD is a normal reaction to an abnormal situation and can be prevented or mitigated with timely intervention. Critical incident stress debriefing (CISD) is an essential component of post-event care. It involves at least one structured meeting with a trained mental health professional between 24 and 72 hours after release or rescue. The first day after the event is necessary for rest—emotionally and physically. After about 3 days, victims will begin to suppress/repress emotions in an attempt to isolate or compartmentalize the traumatic experience, hence the need to act quickly. The CISD usually takes several hours and includes an explanation of the purpose of the debriefing, a brief personal history of the people involved in the event, a discussion of what each person saw or experienced and their emotional reactions, a query regarding symptoms associated with PTSD, education regarding PTSD as a normal response to horrific events, and referral of those who require further treatment. HOSTAGE TAKING 887

PITFALLS

• Lack of properly trained and integrated medical support for specialized law enforcement teams • Failure to perform a CISD in a timely fashion

Several potential pitfalls exist in response to a hostagetaking event. These include the following:

REFERENCES

• Lack of situational awareness in a high-risk environment • Underestimating the danger or threat posed by female terrorists7 • The Stockholm syndrome: First described by Professor Nils Bejerot to explain the phenomenon of hostage victims bonding with their captors, following a 6-day ordeal in which two bank robbers held four hostages in Stockholm, Sweden, in 1973. Symptoms include emotional bonding with captors, seeking approval or favor from the captors, resenting police or other authorities for attempts at rescue, and refusing to seek freedom when the opportunity is available.

1. Hiscox Group Ltd. Kidnapping Reaches Record Peak [press release]. London: Hiscox Group Ltd;April 19, 2000. 2. Boyle C. In the underworld: kidnapping, hostage-taking, and extortion on the rise. Insurance J. July 10, 2000. Available at: http://www.insurancejournal.com/magazines/southcentral/2000/ 07/10/coverstory/ 22644.htm. 3. Whitcomb C. Cold Zero: Inside the FBI Hostage Rescue Team. Boston: Little, Brown and Company; 2001. 4. Savage P. The Safe Travel Handbook. San Francisco: Lexington Books; 1993. 5. Green J. Dealing with trouble—the wilder issues. In: Ryan J, Mahoney PF, Greaves I, et al, eds. Conflict and Catastrophe Medicine: A Practical Guide. London: Springer; 2002. 6. Auerbach A. Ransom. New York: Henry Holt and Company; 1998. 7. MacDonald E. Shoot the Women First. New York:Random House;1991.

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chapter 182

Civil Unrest and Rioting* Denis J. FitzGerald

DESCRIPTION OF EVENT Civil unrest, also termed civil disturbance, is a spectrum of activities progressively disruptive to public order and tranquility. Civil unrest can occur whenever a group in the community feels, accurately or not, that some aspect of society is antithetic or apathetic to their views, rights, or needs. Examples of civil disturbance include labor strikes, large demonstrations, and riots. As the most extreme situation, a riot is a violent disruption of the public order that threatens public safety. In describing civil unrest, it is valuable to consider first a historical perspective, then to discuss the etiology and evolution of these incidents. Civil unrest has been a part of the fabric of life in the United States since before the country was founded, dating back to the Boston Massacre in 1770.1 Governed by a set of laws to define mechanisms for peaceful conflict resolution, American society has nonetheless experienced many instances throughout its history of violent civil unrest. More recent events include the widespread turbulence of the late 1960s, the civil unrest surrounding the Rodney King incident (1992), and the clashes between the police and protesters at World Bank Demonstrations in Washington, DC (2000). Especially when it turns violent, civil unrest can strain or even shatter the delicate equilibrium between the societal need for public order and the individual’s constitutional right to freedom of expression. Civil unrest arises from the interplay of several factors.2 These factors include confrontational participants, catalyst causes, group dynamics, group leadership, and emotional electricity. To better understand civil unrest, it is important to discuss briefly the role of each causal factor. Across the spectrum of various events, participants in civil unrest span all demographic, political, and socioeconomic categories. At baseline, all participants are connected to the group by a variable degree of investment in a specific cause. Some core persons are highly

*The content of this chapter exclusively reflects the view of the author and does not represent official policy of the U.S. Department of Defense or the United States Government.

committed to the issue, while others merely become caught up in the frenzied periphery of the event. Catalyst causes that trigger civil disturbance include any perceived wrongful policy or event felt worthy of active dissent. These issues include special interest topics, perceived law enforcement injustices, and political grievances. Rioting can occur when the group directs its frustration over a given issue toward persons with opposing views or officers charged with keeping the peace. As a behavioral dynamic, groups foster an environment in which individual inhibition is lowered due to a collective sense of anonymity, a diffusion of personal responsibility, a strong social urge toward conformity, and a loss of individual decision-making. Additionally, persons in groups also become more susceptible to suggestion, manipulation, and imitation during moments of uncertainty or frustration by strong leaders who are often the first and most assertive agitators. The emotional volatility of a group can also be a powerful unifying force, creating an almost electric connectivity between participants when sparked. Given the right circumstances, the net effect of these factors is the evolution of group cohesion. The group becomes, in essence, its own autonomous organism with a collective identity, purpose, focus, and coordinated response. In general, members of a group are more prone to participate in activities that they would not do if alone. If the tone of the group shifts toward anger or frustration, a “mob mentality” may take over, violence can erupt, and a riot can ensue. Of note, in the context of a counter-transference dynamic, police and others involved with the response to civil unrest must be constantly vigilant in guarding against any negative impact of these factors on their behavior as well. Two recognized patterns exist for the emergence of civil unrest. First, civil unrest can be a fluid event that escalates along a progressive continuum of disruption. For example, the incident may begin as a planned demonstration. A demonstration is a group of people (termed protestors or demonstrators) specifically called together for a common purpose,such as to protest a political policy. Under ordinary circumstances, demonstrations are peaceful expressions of First Amendment rights and remain law-abiding entities. However, some demonstrations become increasingly disruptive, with individuals 889

in the group engaging in unlawful activity. If violent tactics are adopted, the situation then degenerates into the anarchy of a riot and the group becomes a mob. During a tense confrontation, violence can beget violence, requiring control measures to diffuse the situation. Second, an additional pattern has been clearly identified in many instances of modern civil unrest.3 A crowd is an unrelated group of people assembled together due to similar circumstances, such as for a sporting event or for a court proceeding. A catalyst event, often a verdict in a law enforcement incident, incites a small ultraviolent group in the crowd to riot in immediate response, often fueled by a deep underlying schism along racial, ethnic, or socioeconomic lines within the community. This core group engages in random acts of violence and looting, subsequently engulfing larger segments of the population. These incidents typically overwhelm the initial public safety resources, requiring an influx of outside support to defuse the situation.

PREINCIDENT ACTIONS Preplanning saves lives when time counts. It is critical to plan for civil unrest events because time is limited for life-saving intervention if violence should erupt. Baseline preparation should focus on the development of infrastructure necessary for mitigation of a worst case scenario, such as widespread rioting. Involving both training and resource coordination, effective medical preplanning for civil unrest involves preparation for the continuum of patient care from the field through initial hospitalization. Important planning aspects include: (1) integration of the field medical response with the tactical response; (2) coordination of regional medical resources at all levels; and (3) development of individual hospital response procedures. Building on this underlying foundation, preparation for specific events (such as announced demonstrations) should involve the completion of a medical threat assessment. To ensure optimal medical care for all participants on the frontline, it is important that medical support be integrated into the initial tactical response. At the flashpoint of a violent incident, the tactical response involves containment and control of the riot through use of a mobile field force (MFF), a special response team for civil disturbance. Successful integration of medical support into the MFF requires the establishment of a working relationship between both parties prior to an actual incident. Planning for organic medical support of such tactical operations should focus on many areas, including the following: • Logistics—deploying, training, and equipping medical personnel for the field • Preventive strategies—ensuring that needs are met for hydration and adequate protective equipment during deployment of the MFF • Acute care delivery—coordinating injury treatment and casualty evacuation from the scene • Decontamination systems—identifying and eliminating contamination thrown by protestors 890 OTHER EVENTS, COMBINATION EVENTS

• Advanced care access issues—connecting MFF field response to the emergency medical system and hospitals On a regional level, prior planning must ensure that medical resources will be coordinated on all levels of the healthcare response to function seamlessly within the Incident Command System. First, the regional disaster plan for large incidents of civil unrest should include a medical annex that focuses on the integration of healthcare delivery with other public safety functions under such conditions. Resource planning for patient care should address issues related to emergency medical services (e.g., protection of ambulance crews and field rehabilitation logistics),4 hospital transport (e.g., ensuring safe travel routes), local hospital capabilities (e.g., determining trauma level and diversion status), and mutual aid. Second, the development in advance of a reliable communication system to facilitate information sharing between the lead law enforcement agency, the emergency medical system dispatch, and regional healthcare facilities is essential. This system may be effectively adapted from preexisting disaster networks to function as well in the limited scope of civil unrest incidents. Individual hospitals also need to look at planning for civil unrest incidents, particularly in the emergency department setting. In many respects, this preparation may be incorporated into the existing disaster plan, with such provisions as increased staffing and the establishment of an Emergency Operations Center. Unique aspects of preparation for civil unrest include hospital security concerns in the face of violent agitators outside, management of injured disorderly protestors requiring treatment, contamination issues, the potential for masscasualty situations, and the control of arrested persons. For demonstrations that are announced in advance, it is advisable for regional medical planners to develop a medical threat assessment (MTA). The MTA is an approach used to prepare for the foreseeable medical issues associated with a particular event by analyzing various health threats, assessing medical vulnerabilities, identifying possible countermeasures, and exploring different resources to optimize healthcare delivery. Relevant information tied to the anticipated circumstances can be gathered in advance through several methods, including hospital site surveys, route surveys, open-source material, and information known about the past behavior of the protest group. Specific MTA components may include an analysis of environmental conditions, hospital capabilities, and substances likely to be thrown by demonstrators.

POSTINCIDENT ACTIONS In the wake of violence associated with widespread civil unrest, the medical community should strive to promote recovery efforts both within its ranks and within the region. In the short term, attention should be paid to the emotional impact of the civil disturbance on healthcare workers, and any persons suffering residual critical

incident stress effects should be supported. Hospital personnel should continue to provide needed care for victims and their families, as well as to release appropriate information to the community as indicated. In the long term, it is valuable for medical professionals to meet with civic representatives to debrief medical aspects of the incident. The main focus should be an effort to enhance the medical response to similar situations in the future. By discussing both what worked and what did not, lessons learned can be applied to improve patient care delivery in the event of a future civil disturbance.

MEDICAL TREATMENT OF CASUALTIES Several important factors should be considered with regard to the medical treatment of casualties from civil unrest. For a large-scale incident, the care should be delivered under conditions defined in the disaster plan of the hospital or agency. Important and unique aspects of medical treatment during civil disturbance are the potential for large numbers of patients, the nature of the injuries seen in riots, and the use of less lethal weapons. The number of casualties from an incident varies widely with the scope of the disturbance. Depending on available resources, it is possible that medical providers may need to implement mass-casualty triage protocols in given situations. The need for this approach may also depend on the timing of the injuries over the course of the incident and the distribution of patients among different hospitals. As exemplified in the civil disturbance surrounding the Rodney King incident,5 three main patterns of injury have been identified in civil unrest. The first type of injury involves assaults suffered by active participants in rioting or other criminal behavior such as looting. With a mixture of blunt and penetrating trauma, these persons may present with gunshot wounds, stab wounds, or injuries incurred in beatings. A second category of injury that has been noted in civil disturbance involves automobile accidents. Suffering primarily blunt trauma, these patients include struck pedestrians and victims of motor vehicle collisions that result from disruption of traffic patterns, erratic driving, or broken traffic signals. The last group of patients present with an acute decompensation of a chronic medical condition because they were unable to obtain needed care. Included in this group are patients receiving dialysis and persons with diabetes. Less lethal weapons are routinely used in the context of modern civil unrest. Less lethal weapons are devices designed to incapacitate persons or to disperse crowds without causing serious harm. As reflected in the term less lethal, the potential does exist, however, for serious harm or even death with these devices. There are two general categories of less lethal agents used in the law enforcement response to civil disturbance. Chemical agents, such as tear gas or pepper spray, cause noxious upper respiratory irritation when deployed. Treatment should focus on removing ongoing contamination, maintaining access to fresh air, and applying cool water.

The injury pattern for projectile munitions, such as “bean bag” rounds, ranges from minor lacerations to significant internal injury.6 It is advisable for healthcare providers to be familiar with these less lethal devices and their effects.

UNIQUE CONSIDERATIONS Medical personnel should remember three unique considerations during a response to civil disturbance. These considerations include awareness of the threat environment, the medical-legal context, and the role of field testing. These three considerations are applicable across the spectrum of medical care settings. The most important consideration for healthcare providers during civil unrest is to recognize that care is being delivered in a threat environment. A threat environment is a situation in which a person is at risk for harm or injury during the performance of a given task. In civil unrest, there are several personal safety concerns for the provider such as violent demonstrators, dangerous crowd tactics, contamination from thrown substances, denial of essential supplies, and the presence of improvised weapons. The provider must provide simultaneous care to different categories of patients placed in confrontation by the event—arrested demonstrators, injured bystanders, and wounded law enforcement officers. In addition to using appropriate protective equipment, medical providers must continually maintain situational awareness and practice scene safety in the threat environment posed by civil unrest. Providers should also appreciate the medical-legal environment created by civil unrest and the consequent implications for healthcare delivery. In the care of patients, providers must be careful (to the extent possible) not to destroy evidence such as collected weapons, bullets, or clothing. In the event that court testimony is later required, the medical practitioner should also have a basic understanding of forensics as it applies to recognition of injury patterns. During violent demonstrations, protestors may throw a variety of substances at responding police officers. One significant concern with both medical and legal implications is the potential exposure to contaminated blood in this setting. A field blood sampling protocol to assess

CASE PRESENTATION On a hot summer day, after a well-publicized trial, a jury acquits several police officers of any wrongdoing in a shooting incident earlier that year. Shortly after the verdict is announced, an angry crowd begins gathering downtown amidst cries for justice. The crowd swells in number as it heads for City Hall to protest the verdict. Incited to violence, some members of the crowd then begin breaking windows of nearby buildings, setting fires to trash cans, and pulling drivers out of their cars.

CIVIL UNREST AND RIOTING 891

thrown red liquids can help clarify this issue. This protocol can be developed using screening field assays in conjunction with professional laboratory confirmation.

PITFALLS Several potential pitfalls exist in the medical response to an episode of civil unrest. These include the following: • Failure to understand the dynamics and impact of civil unrest within modern society • Failure to plan for medical contingencies, communication, and coordination along the continuum of healthcare delivery before an event occurs • Failure to understand the nature of medical casualties in civil unrest, including the injury pattern associated with less lethal weapons • Failure to promote recovery in the wake of an incident through both short-term and long-term measures • Failure to consider personal safety while providing care in the threat environment of civil disturbance • Failure to recognize the unique medico-legal implications of civil unrest

892 OTHER EVENTS, COMBINATION EVENTS

REFERENCES 1. Civil disorder. Los Angeles County Sheriff Emergency Operations Bureau; 1997. 2. Civil disturbances. US Army Field Manual 19-15. Washington, DC: Headquarters, Department of the Army; 2005. 3. Law Enforcement Bulletin. U.S. Federal Bureau of Investigation; March 1994. 4. Civil Disturbances in Emergency Medical Services: Special Operations Student Manual. Federal Emergency Management Agency. U.S. Fire Administration, National Fire Academy, Maryland; 2002. 5. Koehler G, Isbell D, Freeman C, et al. Medical care for the injured: the emergency medical response to the April 1992 Los Angeles civil disturbance. State of California Emergency Medical Services Authority; March 1993. Available at: http://www.usc.edu/isd/ archives/cityinstress/ medical/contents.html. 6. Suyama J, Panagos P, Sztajnkrycer M. Injury patterns related to the use of less-lethal weapons during a period of civil unrest. J Emerg Med. 2003;25:219-27.

chapter 183

Massive Power System Failures M. Kathleen Stewart and Charles Stewart

DESCRIPTION OF EVENT Electric power outages can be caused by lightning, high winds, ice storms, hurricanes, and floods, as well as either accidents or deliberate sabotage or attack of the power system.1-5 In some cases, these power failures have been massive and prolonged, creating their own addition to an ongoing disaster such as a flood. In other cases, they have been the sole contributor to the disaster. This chapter will discuss the potential causes of massive power failure, how it may affect disaster operations, and some selected actions that a physician involved in the disaster might encounter. It should be stressed that this chapter is not exhaustive and is intended only to illustrate how the technology base of the world, and emergency medical services (EMS) in particular, are vulnerable to a variety of attacks. A modern electric power system consists of six main components: 1. The power station 2. A set of transformers to raise the generated power to the high voltages used on the transmission lines 3. The transmission lines 4. The substations at which the power is stepped down to the voltage on the distribution lines 5. The distribution lines 6. The transformers that lower the distribution voltage to the level used by the consumer’s equipment Electricity generation stations throughout the United States are interconnected via power grids. This allows electricity generated in one state to be sent to users in another state. It also allows distant power generation stations to provide electricity for cities and towns whose power generators may have failed or been destroyed by some accident or sabotage. In the United States, the electric system is divided into three grid systems: the northeastern grid, the western grid, and the Texas grid. Two major power subgrids, the Ontario–New York–New England pool and the Pennsylvania–New Jersey–Maryland pool (the PJM interconnection), together make up the northeast power grid. Power from these stations is moved around the country on almost a half million miles of bulk transmission lines that carry high-voltage charges of electricity.

In a typical system, the generators at the power station deliver a voltage of 1000 to 26,000 volts (V). From the high-voltage transmission lines of the power grid, electric power is transmitted to regional substations. Transformers step this voltage up to values ranging from 120,000 to 750,000 V for the long-distance primary transmission line because higher voltages can be transmitted more efficiently over long distances. At the regional substation, the voltage can be transformed down to levels of 69,000 to 138,000 V. Another set of transformers at neighborhood substations step the voltage down again to a distribution level such as 2400 or 4160 V or 15, 27, or 33 kilovolts (kV). Finally, the voltage is transformed once again at the distribution transformer near the point of use to a voltage that can be used in homes, hospitals, and offices (220 to 1200 volts). The towers that carry the high-voltage lines present the easiest pathway for a terrorist to destroy the power system. Only modest amounts of conventional explosives detonated at two to three transmission towers are sufficient to interrupt a high-voltage transmission line. Repair and replacement may take days to weeks. Simple explosives can easily be used to sabotage any above-ground high-voltage power distribution system. A below-ground system is somewhat more difficult to access and has some additional security afforded by this limited access. Although this tactic will destroy the distribution system, it will not destroy the equipment that it powers. In this regard, the consequences will be similar to those of a naturally occurring event. Another device—graphite bombs—works by exploding a cloud of thousands of electrically conducting carbon-fiber wires over electric installations and powerdistribution systems. This short-circuits the electric systems. A graphite bomb (sometimes called a G-bomb) was used in the 1991 Gulf War to successfully disable 85% of Iraq’s power supply. The North Atlantic Treaty Organisation (NATO) used a later version in May 1999, to successfully disable 70% of Serbia’s power supply.6 These bombs will destroy the distribution system, but not the equipment that it powers. Finally,electromagnetic pulse (EMP) devices can be used to cause massive power failures. When “detonated,” an EMP weapon (also known as an E-bomb) generates a powerful pulse of energy capable of short-circuiting 893

a wide range of electronic equipment, including computers (even those contained in ignition circuits in cars and trucks and those that operate traffic lights), radios, and public utility power supplies. These weapons can disable practically any nonshielded modern electronic devices within the effective range of the weapon. (Some militarygrade radios are designed to resist EMPs, but most civilian equipment is not adequately shielded for this type of attack.) The damage from burnout or overload of the electronic circuits would extend far beyond the area directly affected by the blast and radiation of the EMP. It is unknown whether the nation’s air traffic control system has been “hardened” against EMPs.6 The extent of the risk to Federal Aviation Administration systems from EMPs is probably (and appropriately) classified. Civilian airliners may be lost. They will not have communication, navigation aids, or landing lights, and in some cases they may not even be able to control the aircraft after electronic fly-by-wire circuits are destroyed by a massive EMP. Commercial computer equipment is particularly sensitive to EMPs,4 as are UHF and VHF radio receivers, televisions, and cell phones.5 The consequences of disabling such equipment are mind boggling for the now technology-dependent healthcare community. However, although devastating to electronic equipment, EMPs, at least in theory, do not hurt humans.7 Three basic types of EMP weapons exist: nuclear weapons, flux compression generators, and high-power microwave generators. Although an in-depth discussion of each is beyond the scope of this chapter, suffice it to say each weapon would create differing levels of havoc. Those who have only basic engineering and technical skills can harness EMP technology. EMP weapons can be built with materials available to governments and terrorists alike. Fully developed, ready-to-deploy weapons may be available to clandestine markets at any time. Since the United States has actually deployed such a weapon (in Desert Storm, an EMP designed to mimic the flash of electricity from a nuclear bomb was used),8 it is quite possible that the design is available to terrorist nations today. EMP devices are highly portable and can even be operated from a distance. Detonating the EMP in the air or near the top floors of a skyscraper maximizes the effects of the weapon.

PREINCIDENT ACTIONS Even before the terrorist attacks of September 2001, disaster planning in U.S. hospitals was designed primarily for external disasters involving large-scale trauma or mass casualties; for example, airline crashes, radiation accidents, or outbreaks of infectious diseases. Although it is certainly necessary to plan for such events, catastrophic power failures are actually more likely hospital scenarios. By the 1960s, engineers and architects began sealing off buildings from the outdoors, constructing mechanical environments solely controlled by electric power. When this power supply fails, the modern hospital may become totally uninhabitable. 894 OTHER EVENTS, COMBINATION EVENTS

Preparation for an Unscheduled Power Outage The disaster planner must not only consider the usual devices such as lights and power to critical areas, but also must take steps to ensure against unintended actions when power is restored.9 Fiscal restraints often prevent hospitals from spending adequately on emergency power protection. Hospital accountants do not consider absolutely fail-safe 24-hour power for hospitals to be cost-effective. Ironically, when hospitals do provide power protection, it is often used to protect their data systems, not their critical care systems. Devices expected to operate when the power fails need to be inspected, maintained, and tested as part of an equipment preventive maintenance program. Plans and checklists to maintain critical services need to be prepared, implemented, and tested. Many hospitals test their emergency power supply systems at night or early in the morning before the bulk of the hospital’s daily activities begin. This test time is often chosen because it is one of low clinical activity, and will therefore cause less disruption, but normal or peak clinical loads will not be reflected in this emergency power supply system test loading. Many hospitals do not test their emergency power supply systems when their operating rooms are in use. Also, the mechanical, building, radiology, and other clinical processes all vary during a typical hospital day.

Protective Measures Against an EMP Device It is difficult to protect against an EMP weapon without purchasing military-grade communications equipment. Vehicles require computers to satisfy U.S. Environmental Protection Agency requirements, and these computers are vulnerable. Some anti-EMP measures that EMS providers can take include the following: 1. Build a Faraday cage. A Faraday cage can be made from fine metal mesh that is connected to a ground and completely encloses the items to be protected. If any power cables, data cables, or antennae go into the cage, it may be rendered worthless. Keep all equipment in the cage disconnected from batteries and other power supplies. 2. Maintain a supply of spare radio, monitor, and engine ignition spare parts. Keep the spare parts in the Faraday cage. 3. Use one system at a time during a threat period. Disconnect other systems from power and antennae and keep them in the Faraday cage. 4. If your vehicle ignition fails, disconnect the negative battery terminal, wait 2 minutes, and attempt to restart the vehicle. Some computerized ignition systems on late-model cars might be reset in this way.

Continuity of Critical Services Backup power generators and uninterruptible power supplies should be selected and installed by qualified electric service contractors and then coordinated with

the electric utility company. It is particularly important to avoid improper switching from one power supply to another. This can lead to power feedback into the regular power system, resulting in damage to equipment and the generator itself. As plentiful and redundant as backup power sounds, diesel generators alone cannot provide fail-safe backup power to protect hospital patients. The lag between utility shutdown and generator power startup may destroy computerized diagnostic and life-support equipment. Even a 3-second disruption can be perilous to this sensitive electronic equipment. For this same reason, budgets permitting, electric engineers and contractors like to specify uninterruptible power supplies to protect vital equipment from even brief disruptions.

POSTINCIDENT ACTIONS When the power is restored, the following equipment and checklists will be useful: • List manually operated switches that may need to be placed in the off position. • List valves that need to be checked for proper position. • List utilities such as steam, radio, telephone, computers, and pager communications that need to be verified for operability after the power is restored. • List automatic starting equipment that should be shut down for safety and to minimize load demand when the power is restored.

MEDICAL TREATMENT OF CASUALTIES Power outages may cause differing types of injuries. In more rural areas, victims may be trapped for prolonged periods of time without adequate food, water, and medications. In colder climates, this may also result in casualties due to exposure. The risk and type of injury to the general population will be determined by the area in which the power outage strikes.

short-term uninterruptible power supplies and may supply oxygen to patients for a few moments after the power fails. Operating room equipment may fail. Some equipment, such as a heart-lung bypass machine, is mission critical and should be protected by an uninterruptible power supply. Other equipment, such as lights, can be operated by battery power after a short interval of power outage without damage. Laboratory equipment, particularly computerized equipment, may not adequately survive a power loss of only a few seconds. This equipment must be protected by uninterruptible power supply to ensure that data being tested are not lost or degraded.

CASE PRESENTATION: NORTHEASTERN UNITED STATES BLACKOUT, AUGUST 14, 200310

On Aug. 14, 2003, a blackout in the northeastern United States occurred at 4:11 PM. Within 9 seconds, the grid had collapsed with a surge of nearly 300 megawatts moving east on the grid and then reflecting back westward. The power outage affected 24,086 km2 of area, and about 50 million people were without power. One hundred power plants, including 22 nuclear power plants, were shut down. (It takes about 36 hours to restart a nuclear power plant after shutdown.) Because the pumping stations failed, 1,500,000 people in Cleveland were without water. These people were relieved by 7600 gallons of water trucked in by the National Guard. Since the airports and air traffic control systems were without power,an estimated 300 flights were cancelled in North America on August 14. New York City had six serious fires, 800 elevator rescues, more than 80,000 calls to 9-1-1, and over 40,000 police called to duty. Toronto had more than 100 elevator rescues and 1484 fire calls. If the power outage had been deliberately caused by terrorist actions with an EMP bomb, the affected areas might have had no EMS, police, or fire rescue capability (due to transportation failures). Unprotected equipment might have been destroyed.

UNIQUE CONSIDERATIONS Risks to Worker Safety and Health Workers operate machines and power tools and are engaged in chemical processes. These workers could be at risk of injury, exposure to dangerous chemicals, or death from a sudden loss of power without immediate restoration of power for vital systems. People may sustain injuries when trapped in elevators, subways, and mass transit systems. Many of these injuries are sustained during attempts to get out of the local environment to a “safer” area.

Risks to Hospital Patients Ventilator-dependent patients will need supplemental breathing equipment such as a bag-valve-mask operated by qualified personnel. Some ventilators have built-in,

Catastrophic power failure caused by EMP devices may require replacement of all computerized circuitry within the equipment. This means that ambulances may not be operable until the computer ignition control circuitry has been replaced. It may also mean that every computerized piece of equipment from cardiac monitors to laboratory devices within the hospital may need to be replaced.

PITFALLS Several potential pitfalls exist in the response to a massive power system failure. These include the following: • Backup generator failure due to battery failure, insufficient fuel supplies, overheating, or fuel pump failure. MASSIVE POWER SYSTEM FAILURES 895

Many generators are standby rated, meaning that they can reliably perform for only 2 out of 24 hours. • Failure to check that backup generators will run for prolonged periods at anticipated full load. This should be checked at least twice a year for at least 12 hours. REFERENCES 1. Nates JL. Combined external and internal hospital disaster: impact and response in a Houston trauma center intensive care unit. Crit Care Med. 2004;2:686-90. 2. Franklin C. What we learned when Allison turned out the big light. Crit Care Med. 2004;32:884-5.

896 OTHER EVENTS, COMBINATION EVENTS

3. Lewis CP. Disaster planning, Part I. Overview of hospital and emergency department planning for internal and external disasters. Emerg Med Clin North Am. 1996;14:439-52. 4. Dealing with power failure: how Spokane hospitals survived the ice storm. Hosp Secur Saf Manage. 1997;17:3-4. 5. Milsten A. Hospital responses to acute-onset disasters: a review. Prehospital Disaster Med. 2000;15:32-45. 6. Rogers K. Are electromagnetic pulses terrorists’ next weapon of choice? Las Vegas Review-J. September 30, 2001. Available at: http://www.globalsecurity.org/org/news/2001/010930-attack04.htm. 7. Fulghum DA. EMP weapons lead race for non-lethal technology. Aviation Week Space Technol. May 2, 1993; 138:61. 8. Defense News,April 13-19, 1992. 9. CBC News Web site. Blackout by the numbers. Updated November 14, 2003. Available at: http://www.cbc.ca/news/background/ poweroutage/numbers.html.

chapter 184

Hospital Power Outage Marc C. Restuccia

DESCRIPTION OF EVENT The loss of power can be catastrophic for any medical institution, its patients, and its staff. The smooth operation of the facility, the safe treatment and diagnosis of patients, and the comfort of all persons in the facility require the continued availability of heat, cooling, and electric power. Loss of any or all of these can lead to an institutional disaster. In colder climates, loss of heat forces staff to function in uncomfortable and difficult working conditions. For patients, loss of heating can mean they are at risk of hypothermia. Loss of cooling in hotter climates or months will fatigue the medical professionals laboring to diagnose and treat patients. For patients, the loss of cooling could make them susceptible to hyperthermia, dehydration, and worsening of their underlying condition(s). Finally, loss of electric power will severely affect any medical facility. Gone will be the ability to power the many instruments and equipment used to diagnose and treat patients. Computers used to track patients, their past history, and their tests and to order interventions will be offline if an interruption in their supply of electric energy is experienced. Electrically powered ventilators will not function, potentially leading to hypoxia and death for patients in the event of a loss of electric power. Almost all ability to perform laboratory tests and radiographic examinations will not be present in the event of an electric failure. Intravenous pumps, defibrillators, and other life support equipment will suddenly go “dead,” with consequences for the patients who are dependent on them. Likewise, the ability for medical care providers to adequately see their environment, access patient information, perform diagnostic and therapeutic interventions, and function in general will be severely or perhaps totally degraded. Operating rooms will be in the dark, possibly in the middle of procedures. A more mundane, but still important, aspect is the institution’s ability to store and prepare food for patients and staff, which will also be significantly degraded. The stability and potency of many medications and vaccines will be compromised if the facilities necessary to maintain them at their optimal storage temperatures are lost, meaning, at worst, that these medications will not be effective or, at best, they

will be “wasted,” costing the facility money to replace them. Finally, the restoration of power can potentially entail risk for staff and patients. Such power outages can be predicted to be the result of terrorist activities or, much more likely, natural disasters.

PREINCIDENT ACTIONS Hospitals should all have general disaster plans in place. Among the scenarios envisioned must be the loss of electric power, heat, or cooling. Such contingencies must include whether the facility affected is unique, meaning all other local medical facilities are unaffected, or whether the entire local/regional area is affected. In both cases, a plan should be in place for the care, transport, and triage of patients requiring emergent care. Input from and acceptance and knowledge of such a plan and its contingencies must be sought from local and regional emergency medical services (EMS) agencies as well as geographically contiguous medical facilities. In the event of a loss of power, it may be necessary to move patients from the affected facility, move triage patients away from the affected institution, and coordinate local, regional, and perhaps even national resource availability.

Loss of Heating Capacity Although not a common problem to encounter, hospitals in colder climates must have emergency plans in place for the protection of staff and patients in the event of the loss of ability to heat the institution. In the event that such an occurrence was experienced in a remote hospital with no contiguous medical facilities, the difficulties in transferring patients would be magnified. If such a scenario were due to a natural or manmade occurrence, involved multiple contiguous healthcare facilities, and had an attendant increase in the number of affected patients, the complexity would increase. Not only would a far greater number of in-hospital patients be affected, but those in the local population requiring routine, ongoing, and especially emergent medical care would also be affected. Such an event would require regional, state, and most likely federal responses to mitigate the disaster. 897

Preincident actions necessary to prepare for a loss of heating should consist of the following: • Forming a well-planned and drilled disaster strategy • Regularly testing the hospital’s heating system and identifying alternative mechanisms for heating the facility • Identifying means to heat patient care areas in the event of failure of all primary heating capabilities • Adopting and drilling of the hospital Incident Command System (ICS). This must include identifying who should report to the Emergency Operations Center (EOC) and developing a chain of command with clear functions, reporting lines, and expectations for each individual, including both those in the EOC and those throughout the facility • Identifying and equipping an EOC (communications being the weak link in most plans) • Identifying potential alternative sites/facilities for the care of the currently hospitalized patients and for the public seeking healthcare during the emergency • Identifying staff to staff these alternative facilities (if needed) • Developing Memoranda of Understanding with other institutions covering such contingencies. These should include means of transferring patients to unaffected facilities. Such plans should include local, regional, statewide, and other facilities • Involving local EMS personnel in planning for the transfer of large numbers of patients • Determining what group of patients may be continued to be cared for, if any, at the affected facility • Determining how to best notify the general public about the nature of the emergency, how it will affect them, what the capabilities are of the affected facility, and when a return to normal operations can be expected

Loss of Cooling Capability Loss of the ability to effectively air-condition hospitals would lead to similar considerations; however, the problems encountered should be less pronounced than the concerns surrounding a loss of the ability to heat the facility. Planning for such an emergency would be similar. Preincident plans for the loss of hospital cooling should consist of the following actions: • Forming a well-planned and drilled disaster plan • Regularly testing the hospital’s cooling system and identifying alternative mechanisms for cooling the institution • Identifying alternative means to cool patient care areas in the event of failure of all primary cooling ability • Adopting and drilling hospital ICS, as outlined above • Identifying and equipping a hospital EOC • Identifying alternative facilities for the care of currently hospitalized patients and for the public seeking healthcare during the emergency • Identifying persons to staff these facilities if needed • Developing Memoranda of Understanding with other facilities covering such contingencies, including transfer of patients to those institutions 898 OTHER EVENTS, COMBINATION EVENTS

• Involving local EMS in planning for the transfer of large numbers of patients • Determining what group of patients, if any, can be continued to be cared for at the affected facility • Determining how to notify the general public about the nature of the emergency, how it will affect them, what the capabilities are of the affected facility, and when a return to normal operations can be expected

Loss of Electric Power A loss of electric power, having the potential to be extraordinarily disruptive, is an unfortunately common occurance.1 In a modern healthcare facility, the number of critical patient care and ancillary devices, equipment, and services powered by electricity is enormous.2 Interruption of continued, reliable electric power, even of a very brief duration, can be catastrophic. Modern computers, monitoring systems, laboratory instruments, and many more computer driven devices do not function well with even a short duration power loss. This vital dependence on electric power creates an inviting target for terrorist activities. Each healthcare facility must preplan for this event and have a robust disaster plan in place. Multiple redundancies in the delivery of uninterrupted electric power must be ready and able to function immediately in the event of a loss of electric power. Identification of those systems and equipment that cannot function for even a short time without power must be accomplished in advance and these must be continuously tested and ready. Identification of potential events (e.g., an extraordinary heat wave, a tornado, a hurricane, or a manmade event) must be planned for in advance and preparations made for implementing the disaster plan if such an event is anticipated or actually occurs. For loss of electric power to any medical facility, being ready for such an incident in advance of its occurrence, if at all possible, is infinitely preferable to trying to react to such a condition after it has happened.3 Preincident plans for the loss of electric power should include the following actions: • Forming a robust, well-thought-out, and drilled disaster plan • Identifying the primary source of electric power. This should include potential scenarios for the loss of this electric input • Identifying alternative sources of electric power. This would include uninterruptible power system(s) for equipment not able to tolerate the delay for emergency generators (usually 3 or more seconds1) to begin operation. In addition, emergency generators, usually diesel motors, in adequate number and/or capacity are available for use • Continued interfacing with electric utilities and equipment suppliers of electricity-generating equipment to ensure prompt response to a loss of power • Testing the primary electric source and all emergency systems on an ongoing basis

• Making ongoing training of hospital personnel in the use of all of the emergency backup electric systems a top priority • Ensuring that adequate fuel for any emergency electric generating systems be on hand or immediately available • Identifying alternative methods of delivering care to patients and allowing staff to function in the event of the failure of all electric generation capability • Adopting and drilling hospital ICS and identifying the command structure that would ultimately order the evacuation of the hospital patients to another facility • Identifying and equipping a hospital EOC, making allowance for the loss of all electric power • Identifying alternative facilities for care of currently hospitalized patients and for the general public who may be seeking routine and emergency care in the event of a loss of all electric power • Identifying personnel to staff such facilities, if needed • Developing Memoranda of Understanding with other facilities covering such contingencies, including transfer of patients to those institutions • Involving local EMS personnel in planning for the transfer of large numbers of patients • Determining what group of patients, if any, can continue to be cared for at the affected facility • Identifying means of informing the general public about the nature of the emergency, its impact on the hospital, what services will and will not be available, and the expected duration of the emergency • Identifying which medications and vaccines are temperature dependent (most are) and making alternative plans for those thought to be most critical for the immediate care of in-patients in the hospital • Identifying alternative means of feeding patients and staff

MEDICAL TREATMENT OF CASUALTIES Cooling Loss The loss of cooling power for a medical institution would not usually be expected to lead to an influx of new patients. The exception to this rule would be if the loss of cooling were due to an accident, manmade or natural, affecting a local or regional area. Examples of such would include explosions, fires, earthquakes, hurricanes, or tornadoes. In such a case, it would be expected that the local resources would be overwhelmed and outside resources would be needed. It would take time to get these resources into place,and contingency plans should be made to care for the patients in the hospital,care for new patients from the community, as well as prepare for transferring patients to other unaffected facilities in the meantime. The hospital’s disaster plan would guide treatment of patients in a hospital experiencing a loss of cooling. Patients at the highest risk of heat injury—very young children, elderly persons, and those with concomitant medical conditions (such as cardiac disease)—would need to be rapidly identified and arrangements made to either warm their environment or transfer them to unaffected hospitals. The decision whether continue to care for other patients in the hospital would need to be a joint one involving the medical staff leadership, medical staff, and hospital leadership. Consideration of evacuating the hospital must be guided by the best interests of each patient, the availability of beds in alternative facilities, and the ability of EMS personnel to effect such transfers. Just as each medical facility is unique, each such disaster is unique, requiring preplanning, strong leadership, good communication, and commitment from the hospital and its staff.

Heating Loss POSTINCIDENT ACTIONS Once a loss of power of any type is experienced, the medical facility must activate its disaster plan, staff its EOC, and begin to follow the plan’s steps. Notification of local, state, and federal public health and public safety agencies would be necessary, depending on the type of emergency, its scope, its expected duration, and its source of origin. The response made by any of these agencies would be contingent on the factors listed above. The disaster plan, and its implementation, should be flexible enough to adapt to any new information about the disaster, as it is obtained. The medical facility should take great pains to document the resources needed to meet the healthcare needs of its patients and to address the crisis. Initial attempts to bring the facility to a predisaster state of operation should be attempted rapidly, but if unsuccessful, the order to evacuate patients should be made through the ICS. Potential state and federal reimbursement of the costs incurred will be absolutely dependent on such documentation.

A loss of the ability to heat a hospital will engender most of the same difficulties and issues as in loss of cooling. A key difference is that, in most cases, loss of the ability to heat the hospital in a colder climate will lead to the need to evacuate all of the patients in the hospital and to divert all new patients.

Electric Loss In the event of a loss of electric power to a hospital, the first priority is those patients who are dependent on electrically driven life support systems. Such patients are patients breathing via ventilators,patients using intra-aortic balloon pumps, patients using electrically driven intravenous infusion pumps with critically important medications (e.g., vasopressor agents), and patients in the operating room. In many cases, if all electric power is lost, battery backup will be available for most of these devices. For patients on ventilators, life-saving alternative means of ventilating include the Oxylator (Lifesaving Systems, Inc, Roswell, Ga), which is an oxygen-powered, nonelectric ventilation device, or hand-powered bag-valve-mask ventilation. Contingency plans for alternative, often HOSPITAL POWER OUTAGE 899

CASE PRESENTATION St. Joseph’s, a community hospital in Minnesota with 200 beds, is located in a city of 200,000 people. The city is served by two other similarly sized institutions: City Hospital, with 250 beds, and Memorial Hospital, which has 275 beds. On a particularly cold January day, the heating unit at St. Joseph’s, an old plant that is scheduled for upgrade as soon as capital funds can be raised, suffers a pre-dawn fire. All ability to heat the institution is lost. Within the hour, the temperature begins to fall. The hospital is 80% occupied with 162 patients in the emergency department (ED), on the floors, and in the single intensive care unit. A disaster is declared, and an EOC is opened. The chief executive officer; chief financial officer; chief medical officer; heads of the ED, the intensive care unit, and the Chief Nursing Officer; nursing supervisor; director of facilities; director of social services; director of safety; chief of police; and director of public relations all convene in the EOC. It is quickly determined that the heating plant is severely damaged and will take days to weeks—perhaps months—to get back online. Alternative sources of heating the patient care areas are being sought. Immediately the chief executive officer issues the following orders:

• A hospital ICS is established • The ED is closed to incoming ambulance traffic (i.e., diversion) via notification of local and regional EMS and regional EMS authority • The ED makes provision(s) for walk-in patients • The facility is secured from unauthorized entrance • All elective admissions and surgeries are cancelled and the affected patients notified

portable, sources of electric power for other devices should be in place. Preplanning, strong leadership, good communication, contingency plans, and hospital staff commitment are essential.4

UNIQUE CONSIDERATIONS A modern medical facility is uniquely dependent on the continued availability of heating, cooling, and most especially electric power. Loss of any of these is most certainly a cause for the implementation of the institution’s disaster plan. Prior planning, contingency identification, practice, and commitment of the facility and staff are crucial to the positive outcome of such an emergency.

• A public announcement of the state of the hospital is prepared for broadcast on local television and radio stations. News outlets are notified • The other area hospitals are notified of the ongoing problems at St. Joseph’s. Assistance is requested in dealing with the ongoing emergency • Local municipal authorities are notified about the nature of the emergency and request their assistance • The director of facilities, ED director, ICU director, the directory of the community nursing organization, and the nursing supervisor are directed to develop an action plan The action plan will consist of: • Securing alternative means of heating patient care areas; for example, space heaters, radiant heaters, and warming blankets • Identifying those patients who require transfer to fully functional facilities such as nearby hospitals, rehabilitation facilities, and nursing homes • Obtaining acceptance from physicians and facility administrators for those patients • Determining appropriate means of transferring those patients • Determining which patients can be safely discharged home, and making arrangements for this • Determining what additional staff will be needed After 12 harrowing hours, all of the critically ill patients have been transferred to other facilities. All other patients have been discharged or have been sent to appropriate care institutions. At this point, the EOC is demobilized and the process of determining the amount of damage, the cost of repair, and the length of time for restoration of normal services is begun.

• Lack of Memoranda of Understanding with other healthcare facilities to support the stricken institution in such emergencies • Failure to adequately inform and train medical and support staff in their expected roles in the event of the loss of power • Lack of training of staff before the occurrence of a disaster • Failure to include the prehospital (EMS) system in predisaster planning • Failure to continuously test the system’s response to a failure of any of the above; this would include failure to test backup systems • Failure to evacuate the hospital soon after attempts to remedy the problem have failed REFERENCES

PITFALLS Several potential pitfalls exist in the response to a hospital power outage. These include the following: • Failure of the disaster plan to adequately address the loss of heat, cooling, or electricity • Failure to address alternative sources of cooling, heating, and most especially electric power 900 OTHER EVENTS, COMBINATION EVENTS

1. Harrington M. Emergency: the critical condition of hospital power. EC&M. August 1, 2002:1-8. Available at: http://ceenews.com/mag/ electric_clarification_ideals_wirenut/. 2. Nates JL. Combined external and internal hospital disaster: impact and response in a Houston trauma center intensive care unit. Crit Care Med. 2004;32:686-90. 3. O’Hara JF Jr, Higgins TL. Total electrical power failure in a cardiothoracic intensive care unit. Crit Care Med. 1992;20:840-5. 4. Franklin C. What we learned when Allison turned out the big light. Crit Care Med. 2004;32:884-5.

chapter 185

Intentional Contamination of Water Supplies Patricia L. Meinhardt

DESCRIPTION OF EVENT The terrorist events of Sept. 11, 2001, have forced the public health and medical community, federal security and regulatory agencies, and state and local water utilities to consider the possibility of intentional contamination of U.S. water supplies as part of an organized effort to disrupt and damage important elements of the nation’s infrastructure.1–4 Water supplies and water distribution systems represent potential targets for terrorist activity in the United States based on the critical need for water in every sector of its industrialized society.2 Even short-term disruption of water service can significantly affect a community, and intentional contamination of a municipal water system as part of a terrorist attack could lead to serious medical, public health, and economic consequences. The magnitude of water service disruption for a community has been vividly demonstrated by the destruction of water supply systems in the Gulf Region as a result of Hurricane Katrina in 2005. As this massive hurricane illustrated, contamination of water with biologic, chemical, or radiologic agents has generally resulted from natural disasters, industrial pollution, or unintentional man-made accidents in the United States. However, the deliberate contamination of the wells, reservoirs, and other water sources for civilian populations has been used as a method of attack by opposing military forces throughout the history of war. Many armies have resorted to using this method of warfare, including the Romans, who contaminated the drinking water of their enemies with diseased cadavers and animal carcasses.4 With enhanced technology and modern scientific advances, the mechanisms of dispersal of biologic, chemical, and radiologic warfare agents have expanded considerably and currently include water as a delivery mechanism. Whether advanced scientific techniques or ancient warfare methods are used by terrorists, overt and covert contamination of water supplies remains a potential public health threat for the U.S. population. The plausibility of intentional contamination of water supplies as part of a terrorist attack has been reinforced by recent congressional testimony, a consensus statement by a governmental review panel, and a joint Centers for Disease Control and Prevention (CDC) and Environmental

Protection Agency (EPA) water advisory health alert.5,6 As part of its 2002 congressional report, the National Research Council of the National Academy of Sciences concluded that water supply system contamination and disruption should be considered a possible terrorist threat in the United States.5 On Feb. 7, 2003, the national terrorism threat level was increased to “high risk”based on information received and analyzed by the federal intelligence community. Subsequent to this heightened alert, the CDC and EPA issued Water Advisory in Response to the High Threat Level, which describes the need for enhanced vigilance by the public health, medical, and water utility communities regarding the risk of a terrorist attack on the nation’s water infrastructure.6 Apprehension regarding a terrorist assault on drinking water systems has also been reinforced by arrests of suspects in 2002 and 2003 who were charged with threatening to contaminate municipal water supplies in the United States.3,4

Spectrum of Disease Resulting from Intentional Water Contamination The biologic, chemical, and radiologic agents that have been designated as potential terrorist weapons may be dispersed through multiple exposure pathways, including water.2,4,7–9 Recognizing and managing a waterborne disease outbreak and the health effects of exposure to water contaminants are diagnostic challenges under normal circumstances, but the challenge will be even more significant during an act of water terrorism.10 Intentional contamination of water supplies with biologic, chemical, or radiologic agents may produce a broad spectrum of disease and involve virtually every organ system, including, but not limited to, the gastrointestinal, respiratory, dermatologic, hematopoietic, immunologic, and nervous systems. In addition, waterborne agents may enter the body through various portals, including the following: (1) ingestion and aspiration of contaminated water, (2) dermal absorption of contaminated water during bathing activities, (3) inoculation of skin lesions from direct contact with contaminated water, (4) consumption of food directly contaminated by water during food preparation, and (5) consumption of contaminated food indirectly contaminated by water through uptake in the food chain or through agricultural practices.4 901

A key factor in the accurate diagnosis and appropriate management of disease resulting from intentional contamination of water supplies is inclusion of water by the healthcare provider as one possible exposure pathway for the dissemination of biologic, chemical, and radiologic agents at the time of initial case presentation. The categories of compounds that may cause a diverse spectrum of water-related disease during an act of water terrorism include many of the agents traditionally associated with other modes of delivery. Biologic, chemical, and radiologic agents that have been designated as possible terrorist agents of public health concern that include the potential for waterborne route of exposure and weaponized agent delivery are presented in Table 185-1.

PREINCIDENT ACTIONS Although medical practitioners may not be able to prevent the first cases of illness or injury resulting from an act of intentional water contamination, they are positioned to play a critical role in minimizing the impact of such an event by practicing medicine with an increased index of suspicion that such an attack may occur in their community. To prevent a missed diagnosis of a case of terrorismrelated waterborne disease, it is vital that medical practitioners understand how water could act as a potential exposure pathway or mode of dispersal for biologic, chemical, and radiologic agents before an incident occurs.4

TABLE 185-1 SELECTED BIOLOGIC, CHEMICAL, AND RADIOLOGIC AGENTS THAT INCLUDE WATER AS A POTENTIAL MODE OF DISPERSAL FOR TERRORISM* BIOLOGIC AGENTS Bacterial Pathogens Anthrax Bacillus anthracis Brucellosis Brucella melitensis, B. suis, B. abortus, B. canis (undulant or Malta fever) Cholera Vibrio cholerae Clostridium perfringens Glanders Burkholderia mallei (formerly Pseudomonas mallei) Melioidosis Burkholderia pseudomallei (formerly Pseudomonas pseudomallei)

Plague Yersinia pestis Salmonella Salmonella typhimurium and S. typhi (acute gastroenteritis and typhoid fever) Shigellosis Shigella dysenteriae and other Shigella sp. Tularemia Francisella tularensis Viral Pathogens Hepatitis A virus (HAV) Smallpox Variola major Viral encephalitides (e.g.,Venezuelan equine encephalomyelitis [VEE])

Viral hemorrhagic fevers (e.g., Ebola, Marburg, Lassa fever, Rift Valley fever,Yellow fever, Hantavirus, and Dengue fever) Parasitic Pathogens Cryptosporidiosis Cryptosporidium parvum and other Cryptosporidium sp. Rickettsial and Rickettsial-Like Pathogens Psittacosis Chlamydia psittaci Q fever Coxiella burnetti Typhus Rickettsia prowazekii

BIOLOGIC TOXINS Bacterial Biotoxins Clostridium botulinum toxins (collectively BTX) Clostridium perfringens toxins Staphylococcus enterotoxin B (SEB) (e.g., protein toxin from Staphylococcus aureus) Fungal-Derived Biotoxins (Mycotoxins) Aflatoxin metabolite of Aspergillus flavus

T-2 mycotoxin extract from Fusarium spp. Anatoxin A product of cyanobacteria, Anabaena flos-aquae Microcystins products of cyanobacteria, Microcystis spp.

Marine Biotoxins Saxitoxin (Paralytic shellfish poisoning or PSP) product of dinoflagellate, Gonyaulax Tetrodotoxin neurotoxin from pufferfish sp.

Plant- and Algae-Derived Biotoxins Ricin extract from castor bean CHEMICAL AGENTS

Nerve Agents (“Gases”)

Vesicant and Skin Blistering Agents

Industrial and Agricultural Agents

G agents (Volatile) GA (Tabun), GB (Sarin), GD (Soman)

Lewisite L, L-1, L-2, L-3

Pesticides, persistent and non persistent

Nitrogen mustards HN-1, HN-2, HN-3

Dioxins, furans, polychlorinated biphenyls (PCBs)

V agents (Nonvolatile) VX

902 OTHER EVENTS, COMBINATION EVENTS

TABLE 185-1 SELECTED BIOLOGIC, CHEMICAL, AND RADIOLOGIC AGENTS THAT INCLUDE WATER AS A POTENTIAL MODE OF DISPERSAL FOR TERRORISM*—CONT’D Blood Agents (Asphyxiant or Systemic Agents)

Incapacitating Agents (Psychotropic or Behavior-Altering Compounds)

Dioxins, furans, polychlorinated bphenyls (PCBs)

Cyanide Compounds Hydrogen cyanide (AC) Cyanogen chloride (CK)

CNS Depressants (e.g., BZ [3-quinoclinidinyl benzilate] and similar compounds)

Explosive nitro compounds and oxidizers (e.g. ammonium nitrate combined w/fuel oil)

Arsine Compounds (Arsenicals) Ethyldichloroarsine (ED) Phenyldichloroarsine (PD)

CNS Stimulants (e.g., LSD [D-lysergic acid and diethylamide])

Flammable industrial gases and liquids (e.g., gasoline and propane) Poison industrial gases, liquids, and solids (e.g., cyanides and nitriles) Corrosive industrial acids and bases (e.g., nitric acid and sulfuric acid)

RADIOLOGIC AGENTS Radiation Terrorism Threat Scenarios

Potential Exposure Pathways and Agent Source

Nuclear Blast Detonation of suitcase-sized nuclear bomb

External Exposure External radiation exposure from nuclides in the plume after detonation External radiation and contamination from surface-deposited contamination and activation products Personal contamination of skin and clothing

Nuclear Reaction Sabotage of nuclear power plant or “meltdown” Radiation dispersal device RDD or “dirty bomb” release

Internal Contamination Internal contamination from plume inhalation due to nuclides in plume after detonation Internal contamination due to inhalation of re-suspended contamination Internal contamination due to inhalation or ingestion from personal contamination Internal exposure due to ingestion of contaminated food and water Internal contamination through skin or wound absorption or deposition from contact with contaminated material, including water

*Modified and reprinted with permission from Physician Preparedness for Acts of Water Terrorism: An On-line Readiness Guide. Accessible at: http://www. waterhealthconnection.org/bt.

Preincident preparedness by the medical community will be critical to reduce the following: (a) the public health impact of a water terrorism incident,(b) the secondary disruption to potable water availability and distribution, and (c) the psychological impact of the public’s lack of confidence in water safety and quality after an incident of intentional contamination of water.2,4 If preincident actions include terrorism preparedness and disaster readiness,educated medical and public health professionals may make the difference between a controlled response to a water terrorism event versus a public health crisis.4,11 It is important to note that a major effort has been undertaken to improve and enhance the ability to detect and characterize deliberate contamination of water systems in the United States as part of a collaborative effort by local water utilities and several federal public health agencies.3,4,12 As a result, U.S. water systems are more physically secure than ever before, with multiple layers of enhanced protection. However, there are several potential points of contamination that could be targeted for acts of water terrorism. Therefore, it is critically important for the medical community to have a basic understanding of these water system vulnerabilities in order to be able to complete an accurate exposure

history when evaluating a suspected case of waterrelated disease. Various scientific consensus groups, public health agencies, and water utility specialists have outlined a series of potential points of contamination of the U.S. water supply and distribution system.4,5 This information is summarized in Table 185-2 and acts as a valuable resource for healthcare providers and public health professionals when evaluating an unusual symptoms complex or an atypical illness pattern that may represent a case of waterborne terrorism.

POSTINCIDENT ACTIONS Although environmental monitoring of water supplies is improving rapidly, the most likely initial indication that a water terrorism incident has occurred may be an increased number of patients presenting to their healthcare provider or emergency department with unusual or unexplained illness or injury, a change in local disease trends and illness patterns, or a community-wide waterborne disease outbreak. Therefore, healthcare providers and public health practitioners may be the first to discover that a waterborne release of biologic, chemical, or radiologic agents has

INTENTIONAL CONTAMINATION OF WATER SUPPLIES 903

TABLE 185-2

POSSIBLE POINTS OF INTENTIONAL CONTAMINATION OF U.S. WATER

Healthcare providers should keep these sources of potential water contamination and unusual modes of delivery of biologic, chemical, and radiologic agents in mind when evaluating a suspected case of terrorism-related disease*:

• •

•

• • •

Upstream of a community water supply system or collection point: Water supply systems are composed of small streams and bodies of water, rivers, service reservoirs, aquifers, wells, and dams that may act as points of deliberate contamination of water. Community water supply intake access point or water treatment plant: Many water supply systems are designed to receive water from source water reserves at a central intake point, with this source water being subsequently filtered and sanitized at the community water treatment facility for eventual distribution as potable water. Both a water intake point and a community water treatment plant may be targeted for terrorist activity and deliberate water contamination. Selected points in the post-treatment water distribution system: Treated water is distributed to water consumers or end-users through transmission pipelines to homes and businesses. Selected portions of a water distribution system or water main are another potential point of water contamination that may be targeted by terrorists and could affect a subdivision, specific neighborhood, school, medical center, or nursing home. Private home or office building water supply connection, individual building water supply, water tanks, cisterns, or storage tanks: Treated water that is stored very close to the water consumer or end-user as well as individual house or building connections may serve as points of contamination of water by terrorists. Water used in food processing, bottled water production, or commercial water: Water used for food processing or preparation as well as bottled water production also represent points of potential water contamination by terrorists. Deliberate contamination of recreational waters and receiving waters: Both treated and untreated recreational waters may serve as a point of potential contamination of water, including swimming pools, water parks, and natural bodies of water (small lakes and ponds). Receiving waters, such as rivers, estuaries, and lakes, may be secondarily contaminated with wastewater from sanitary and storm sewer systems that may have been environmentally contaminated by a biologic, chemical, or radiologic agent used in a terrorist assault.

*Modified and reprinted with permission from Physician Preparedness for Acts of Water Terrorism: An On-line Readiness Guide. Accessible at: http://www. waterhealthconnection.org/bt.

occurred in a targeted population and must understand their critical role as “front-line responders” in detecting water-related disease resulting from terrorist activity.4 Certain clinical manifestations and disease syndromes may be characteristic of a terrorist attack in which biologic, chemical, or radiologic agents are used via a waterborne route. A heightened level of alertness and awareness by the medical community of these patterns of illness and clusters of disease may enhance the initial discovery of a waterborne terrorist attack and are critical to any postincident action plan. Early and accurate clinical detection of a suspicious case of terrorism-related disease will be especially important for timely follow-up epidemiologic investigations to be initiated and appropriate remediation and prevention efforts to be instituted by the public health and water utility communities.4 During the postincident period, healthcare practitioners will need to “think like an epidemiologist” when evaluating any suspect case or unusual pattern of disease in their clinical practice.13 A medical practitioner’s diagnostic acumen for recognizing waterborne disease resulting from intentional contamination of water can be augmented significantly by embracing this epidemiologic approach. Several epidemiologic patterns and sentinel clues have been published and provide a valuable resource for both the medical and public health community facing the challenges of diagnosing terrorism-related disease that may result from multiple exposure pathways, including water, and have universal application in a clinical and public health setting (Box 185-1). Postincident actions also require that healthcare providers become familiar with the appropriate mechanisms for communicating with law enforcement agencies, public utilities, the media, and the concerned public. If a healthcare provider suspects that an act of water terrorism is responsible for a patient’s symptoms complex or an unusual illness pattern in his or her practice, immediate 904 OTHER EVENTS, COMBINATION EVENTS

action to contact the appropriate public health authority is essential, even before laboratory confirmation or final diagnosis. This contact is the critical first step necessary for the public health authority to (1) initiate a prompt investigation; (2) provide guidance to healthcare providers and the affected community; (3) establish communication and cooperation with other local, state, and federal agencies as warranted; and (4) contact local water utilities for prompt remediation and protective measures. Attention to this postincident procedure by healthcare providers is mandatory to initiate the appropriate response to a potentially high-risk public health event that may indicate intentional contamination of drinking water supplies.

MEDICAL TREATMENT OF CASUALTIES The nature of the medical sequelae resulting from exposure to intentional contamination of water supplies depends on a multitude of factors including the following: (1) agent characteristics, including toxicity and virulence; (2) individual host susceptibility and level of immunity; and (3) movement and dilution of the agent in the environment.14,15 Individual host susceptibility and differences in biologic, chemical, and radiologic agent virulence and toxicity may result in a wide variation in the severity of disease resulting from a waterborne terrorist event.16 Water-related disease resulting from intentional contamination may present as benign symptoms or self-limited illness in a healthy patient population, whereas the same waterborne exposure in a vulnerable patient population may result in serious morbidity and mortality. In addition, as is apparent from the 50 agents that may be dispersed in water (see Table 185-1),the medical management and treatment protocols for water terrorism-related disease vary significantly depending on the agent used.4

BOX 185-1 EPIDEMIOLOGIC INDICATORS AND SENTINEL CLUES INDICATING POSSIBLE TERRORISM-RELATED EXPOSURE AND DISEASE Several epidemiologic patterns have been identified as possible sentinel clues of a terrorist attack. However, none of these indicators alone is pathognomonic for terrorism-related disease. These indicators and sentinal clues are presented here as an educational tool for use by healthcare providers and public health practitioners as possible disease trends that may warrant further investigation*: • Point source illness and injury patterns with record numbers of severely ill or dying patients presenting within a short period of time • Very high attack rates, with 60% to 90% of potentially exposed patients displaying symptoms or disease from possible biologic, chemical, or radiologic agent exposure • Severe and frequent disease manifestations in previously healthy patients • Increased and early presentation of immunocompromised patients and vulnerable population patients with debilitating disease since the dose of inoculum or toxic exposure required to cause disease may be less than for the general healthy population • “Impossible epidemiology” with naturally occurring diseases diagnosed in geographic regions where the disease has not been encountered previously • Higher-than-normal number of patients presenting with gastrointestinal, respiratory, neurologic, and fever diagnoses • Record number of fatal cases with few recognizable signs and symptoms, indicating lethal doses of biologic, chemical, or radiologic agents near a point of dissemination or dispersal source • Localized areas of disease epidemics that may occur in a specific neighborhood or sector, possibly indicating contamination of a selected point in a post-treatment water distribution system • Multiple infections at a single location (school, hospital, nursing home) with an unusual or rare biologic pathogen • Lack of response or clinical improvement of presenting patients to traditional treatment modalities • Near-simultaneous outbreaks of similar or different epidemics at the same or different locations, indicating an organized pattern of intentional biologic or chemical agent release • Endemic disease presenting in a community during an unusual time of year or found in a community where the normal vector of transmission is absent • Unusual temporal or geographic clustering of cases with patients attending a common public event, gathering, or recreational venue • Increased patient presentation with acute neurologic illness or cranial nerve impairment with progressive generalized weakness • Unusual or uncommon route of exposure of a disease such as illness resulting from a waterborne agent not normally found in the water environment *Modified and reprinted with permission from Physician Preparedness for Acts of Water Terrorism: An On-line Readiness Guide. Accessible at: http://www.waterhealthconnection.org/bt.

An online clinical management guide has been developed for healthcare practitioners and public health specialists faced with addressing the evaluation and management of water-related disease resulting from terrorist activity.4,10 This free resource, Physician Preparedness

for Acts of Water Terrorism: An On-line Readiness Guide, which is accessible at www.waterhealth connection.org/bt, is highlighted in Figure 185-1 and provides “24/7” access to medical management guidelines addressing water-related disease resulting from intentional contamination of water supplies from biologic, chemical, and radiologic agents.

UNIQUE CONSIDERATIONS 1. Even though environmental monitoring of water supplies continues to improve, the most likely initial indication that an intentional water contamination event has occurred in a population may be a change in disease trends and illness patterns. Therefore, healthcare providers may be the first to recognize that an act of water terrorism has occurred in their community. 2. Use of water as a mode of dispersion for terrorist agents may confound diagnosis, delay treatment, and impede protective public health measures if clinical evaluations and epidemiologic investigations do not include the possibility of a waterborne route of exposure or mode of dispersal. 3. Prompt identification of waterborne disease resulting from water terrorism may be difficult since the signs and symptoms of waterborne disease and the health effects of water contamination are often nonspecific and mimic more common medical conditions and disorders unrelated to water contamination. 4. Co-infections with waterborne pathogens, coupled with multiple chemical agent exposure during an act of water terrorism, may result in exposed patients presenting with both acute and delayed symptoms from mixed agent exposure, complicating accurate and timely diagnosis. 5. Waterborne exposure to biologic, chemical, or radiologic agents may result from both direct and indirect environmental contamination, including contamination through wastewater from sanitary and storm sewer systems receiving run-off from an aerosolized terrorist attack or through decontamination wastewater generated during patient decontamination procedures.

PITFALLS • Failure to include water as a possible exposure pathway or mode of transmission during initial case presentation of a suspected terrorist incident • Failure to recognize that more than 50 potential terrorist agents of public health concern may be distributed through water as a mode of dispersal • Failure to notify appropriate public health authorities immediately of a suspected case of waterborne disease, preventing timely remediation efforts and protective public health measures • Failure to consider the special needs of susceptible populations most at risk for morbidity and mortality from intentional water contamination INTENTIONAL CONTAMINATION OF WATER SUPPLIES 905

• Failure to identify alternative sources of drinking water as part of disaster preparedness plans in order to ensure that affected communities have adequate drinking water for days to weeks after a water contamination event

• Failure to provide effective risk communication regarding water safety to concerned patients and the public

FIGURE 185–1. Physician Preparedness for Acts of Water Terrorism: An On-line Readiness Guide is a free online medical resource accessible at: http://www.waterhealthconnection.org/bt.

CASE PRESENTATION A sensitive communication advisory from the Department of Homeland Security is issued stating that recent intelligence indicates members of Al Qaeda have discussed plans to attack drinking water supplies. Two potential attack scenarios have been uncovered:(1) disruption of the water delivery system through a physical attack on the water infrastructure and (2) introduction of chemical and/or biologic agents into the water distribution system and post-treatment facilities. Several days later, a large medical center’s emergency department (ED) experiences a very active night in which a series of patients complaining of generalized weakness, fatigue, dry mouth,and dysphagia are evaluated. One elderly patient also complained of blurred vision, partial paralysis, and slurred speech. There is no apparent age or sex distribution in the presenting ED cases, but the number of presenting patients with similar symptoms continues to escalate throughout the day. Laboratory confirmation is not yet available,but by early the next morning,the presumptive diagnosis for the unknown epidemic in the community is botulism. The sudden appearance of multiple patients with acute onset of characteristic symptomatology for botulinum toxicity with no common ingestion of high-risk food suggests a possible terrorist event, and the local public health authorities are contacted. Although the cases of botulinum toxicity appear to be mild at this point, the medical center terrorism preparedness team and the health department are concerned that these initial cases herald a mass exposure event. Through excellent history-taking techniques, a waterborne source for the community botulism outbreak is 906 OTHER EVENTS, COMBINATION EVENTS

uncovered. It is apparent that “finished water,” or drinking water that has already been treated, has been intentionally contaminated with botulinum toxin in one of the community water districts. The intentional contamination of post-treatment drinking water with botulinum toxin has generated real fear and distress in the community. Local healthcare providers are bombarded with questions from their patients, including:“Is my water safe?”To make matters worse, the national news media have arrived and are positioned right outside the medical center entrance. The intentional contamination of the community drinking water has lead to the closure of a targeted water treatment facility until further notice. This closure has lead to denial of potable water for several water-dependent sectors in the community. Local businesses, schools, and nursing homes in the affected water district are very concerned about how long they will be expected to be without municipal water supplies. Several days later, the contaminated water treatment facility is still “off line” and local community governing officials are under pressure to address the disruption of potable water and the resulting financial and public health consequences as well as the ongoing public risk communication crisis. The public health and medical community is faced with developing contingency plans for ongoing disruption of the water delivery system, determining when it will be “safe” to bring the contaminated water treatment facility back “on-line,” and then convincing the local residents that their municipal water is safe again.

REFERENCES 1. Clark RM, Deininger RA. Protecting the nation’s critical infrastructure: the vulnerability of US water supply systems. J Contingencies Crisis Manag. 2000;8:73-80. 2. Krieger G. Water and food contamination. In: Chase KH, Upfal MJ, Krieger GR, et al, eds. Terrorism: Biological, Chemical and Nuclear from Clinics in Occupational and Environmental Medicine. Philadelphia:WB Saunders; 2003:253-62. 3. States S, Scheuring M, Kuchta J, et al. Utility-based analytical methods to ensure public water supply security. Am Water Works Assoc J. 2003;95:103-15. 4. Meinhardt PL. Physician Preparedness for Acts of Water Terrorism: An On-line Readiness Guide. Environmental Protection Agency, Arnot Ogden Medical Center. Available at: http://www. waterhealthconnection.org/bt/index.asp. 5. National Research Council. Making the Nation Safer: The Role of Science and Technology in Countering Terrorism. Committee on Science and Technology for Countering Terrorism, National Academies Press:Washington, DC; 2002. 6. Centers for Disease Control and Prevention. CDC and EPA Water Advisory in Response to High Threat Level. Available at: http://www.phppo.cdc.gov/HAN/ArchiveSys/ViewMsgV.asp?Alert Num=00123. 7. Franz DR, Jahrling PB, McClain DJ, et al. Clinical recognition and management of patients exposed to biological warfare agents. Clin Lab Med. 2001;21:435-73. 8. Inglesby TV, O’Toole T. Medical Aspects of Biological Terrorism. American Collage of Physicians. Available at: http://www. acponline. org/bioterro/medicalaspets.htm.

9. Headquarters, Departments of the Army, Navy and the Air Force, and Commandant, Marine Corps. Field Manual:Treatment of Biological Warfare Agent Casualties. Available at: http://www.nbc-med. org/SiteContent/MedRef/OnlineRef/FieldManuals/FM8_284/ fm8_284.pdf. 10. Meinhardt PL. Recognizing Waterborne Disease and the Health Effects of Water Pollution: Physician On-line Reference Guide. Environmental Protection Agency, American Water Works Association, Arnot Ogden Medical Center. Available at: http://www.waterhealthconnection.org. 11. Henderson DA. Bioterrorism as a public health threat. Emerging Infectious Diseases. 1998:4(3). Available at: http://www.cdc.gov/ ncidod/eid/vol4no3/hendrsn.htm. 12. Environmental Protection Agency. EPA Actions to Safeguard the Nation’s Drinking Water Supplies. Available at: http://www.epa.gov/ safewater/security/secfs.html. 13. Burkle FM. Mass casualty management of a large-scale bioterrorist event: an epidemiological approach that shapes triage decision. Emerg Med Clin North Am. 2002;20:409-36. 14. Public Health Response to Biological and Chemical Weapons:WHO Guidance. World Health Organization. Available at: http://www. who.int/csr/delibepidemics/biochemguide/en/. 15. Kaufmann AF, Meltzer MI, Schmid GP. The economic impact of a bioterrorist attack: are prevention and postattack intervention programs justifiable? Emerg Infect Dis. 1997;2(3). Available at: http://www.cdc.gov/ncidod/EID/vol3no2/downkauf.htm. 16. Burrows WD, Renner SE. Biological warfare agents as threats to potable water. Environ Health Perspect. 1999;107:975-84.

INTENTIONAL CONTAMINATION OF WATER SUPPLIES 907

chapter 186

Food Supply Contamination Marc C. Restuccia

DESCRIPTION OF EVENT Despite the many improvements made in overseeing the nation’s food supply, foodborne illness remains a serious cause of morbidity and mortality throughout the world, including the United States. Many factors contribute to an ideal chain for amplification of foodborne pathogens, including the following: growth of modern mass production farms; the scale of modern water supplies; importation of food from other countries, which may lack the strict food handling and shipping guidelines present in the United States; adoption of immense food and processing plants; and distances, sometimes quite lengthy, that food is transported to consumers. The scale of the problem is not known with great accuracy.1 It is estimated that millions of people are affected worldwide. The majority suffer only temporary discomfort. However, for the young, the very old, patients with concomitant systemic illness, and, increasingly, for the immunocompromised (cancer patients, AIDS patients, patients who have had organ transplants), foodborne illness can be fatal. In the United States, approximately 76 million people suffer foodborne illnesses every year, and approximately 5000 deaths are attributable to this annually.2 Foodborne illnesses are virtually always the result of human actions (or omissions). They can be categorized as those seen routinely in daily life or as intentional attacks on the food chain for a given population. Each will be described separately.

Typical Food Poisoning Improper handling, leading to fecal contamination of food, is the usual cause of most foodborne illnesses. Typical agents causing the illness include bacteria, viruses, parasites, and toxins. Recently, a newly described class of agents, prions, has been implicated in causing human illness, namely transmissible spongiform encephalopathies. Infected beef cattle have been discovered in several countries. Documented cases of human illness have been described in the United Kingdom. These discoveries have devastated the cattle industries in both Britain and America and have led to the banning of British and American food imports. 908

In addition, many people around the world have considered changing their dietary habits, with a significant decrease in beef consumption. One cause of food supply contamination may be seen when the food supply chain is disrupted by a natural event. Scenarios such as an earthquake, tornado, hurricane, or flood contaminating foods during production, processing, transportation, or preparation would have severe consequences on the affected population. Fortunately, in such an event, unaffected areas of the state, region, country, or world could supply untainted food to the stricken area or region. The diagnosis of foodborne illness in the typical scenario is difficult. Unless multiple persons present with symptoms and a clearly identifiable source is determined, an individual healthcare provider may have difficulty in identifying a foodborne epidemic. The incubation period can range from a few hours, in the case of bacterial toxins, to days, as with many bacterial, viral, parasitic, and protozoan agents, to years with prion-induced illness. Multiple other causes of gastrointestinal dysfunction may mimic foodborne illness, making the diagnosis exceedingly difficult. In the case of typical foodborne illnesses, if multiple persons are affected and have a common point in their history, such as attending a particular wedding, eating at a specific restaurant, or buying a specific food item at a particular food market, the diagnosis may quickly become evident. If patients present at multiple emergency departments, physicians’ offices, and urgent care facilities, the appropriate questions may not be asked or accurately answered, and the diagnosis may not be made in a timely manner. The typical signs and symptoms of foodborne illness—nausea, vomiting, diarrhea, abdominal pain, fever, and dehydration—may be seen with many non-foodborne illnesses and require an astute clinician to make the connection.

Intentional Attack on the Food Supply In the current climate of worldwide terrorist activities, the potential for an individual or group to deliberately contaminate a population’s food supply cannot be discounted. Due to this concern, congress enacted the

Public Health Security and Bioterrorism Preparedness and Response Act of 2002. The Food and Drug Administration (FDA) was charged with developing guidelines to ensure the safety of food produced in the United States and that which is imported from outside U.S. borders. These regulations, currently still being formulated, may be viewed on the FDA’s Web site. In addition, when the Department of Homeland Security was created, it was recognized that U.S. agriculture and food industries had to be included in the list of critical parts of society’s infrastructure needing protection.3 The expanding aggregation of growers, suppliers,and long lines of transportation,often stretching across international boundaries, made this chain of supply uniquely susceptible to intentional contamination. Although never actually experienced by a society, warring nations historically have sought biologic weapons to sabotage an opposing nation’s food supply.4 A terrorist seeking to sabotage a nation’s food supply, especially in a highly industrialized nation like the United States, has many potential targets for food contamination. Crops, livestock, fertilizer, cattle feed, products in the food processing and distribution chain, storage facilities, transport modes, and food and agricultural research laboratories all provide potential sites for such an act of terror. As the General Accounting Office (GOA) noted in its 2003 report, individuals or groups seeking to cause economic disruption may well target livestock and crops.3 Conversely, if such groups seek to inflict human illness, they might contaminate finished food products at the processing stage, the distribution or transportation stage, or potentially at the site of consumption. An example of the latter was a cult in the 1980s which, seeking to sway a local election, contaminated a local restaurant’s salad bar with Salmonella.5 This act would, the cult envisioned, sicken enough of the local populace so as to render them unable to vote, allowing the cult to gain a majority in the election. The GAO’s report3 noted that there are significant gaps in federal controls for protecting agriculture and the food supply. These gaps include inadequate education of border inspectors on foot-and-mouth disease,inadequate numbers of inspectors to handle the magnitude of international passengers, and inadequate scanning technology or inconsistency in its use at cargo and bulk mail facilities.3 The potential costs of a bioterrorist attack on the food supply, especially if it involved livestock, would be much greater than simply the cost of the livestock and disposal of the animals.4 As was seen in Great Britain with the outbreak of foot-and-mouth disease (a nonterrorist incident), the loss of confidence in British food suppliers and the loss of tourism income multiplied the loss to the U.K.’s economy significantly. In the case of a terrorist-sponsored food contamination attack, assuming that the terrorists were seeking to maximize the impact, the economic losses and disruption could be magnified many times. Lastly, the mere threat or suggestion of a biologic attack on the food supply would be sufficient to seriously disrupt the economy and the lives of the population targeted. Lack of confidence in the safety of the food available would have unimaginable consequences for the area targeted.

In the event of a contamination of the food supply, the speed at which it would be recognized would vary depending on the agent(s) used. For long-incubating agents, such as bovine spongiform encephalopathies (mad cow disease), the first indication would be positive test results of the disease in sample livestock. It would not, however, appear in the human population at risk for years. With other agents targeted at the human population and introduced at later stages of the food production chain, such as the Salmonella attack previously described, it would take only hours to a few days for the population at risk to show signs and symptoms of food poisoning. Such signs and symptoms would mirror those of a typical foodborne illness event, only potentially magnified many times. It is entirely conceivable that not only would healthcare facilities and providers be overwhelmed with the numbers and severity of patients, but it is also extremely likely that the healthcare providers also would be stricken. A calculated terrorist act might very well first target the healthcare infrastructure to maximize the disruption and loss of life and productivity of the stricken populace.

PREINCIDENT ACTIONS Planning for the possible contamination of any part of the food supply chain, whether due to deliberate acts of terrorism or simply to human carelessness, must be done in advance of the event. Developing a plan for such a situation must include the following: rapid identification of the altered food supply, limiting its health and economic impact, treatment of affected persons, and identification of alternative sources of noncontaminated food. Adequate numbers of unaffected public safety and healthcare workers need to be available to identify the outbreak, limit its expansion, maintain public safety, and treat victims. Local, state, and federal officials need to identify beforehand those links in the food supply chain that are particularly vulnerable to contamination and implement policies and plans for prevention. Education of the entire population would be beneficial. Farmers, distributors, retailers, and consumers need to be informed about the potential for foodborne illnesses, recognizing signs and symptoms, identifying when the food supply chain is compromised, and acting decisively if such a situation arises. Legislators at local, state, and federal levels need to understand the vulnerability of the food supply and be proactive in initiating legislation, including funding. This legislation would be to protect the food supply, treat the victims, and limit the economic devastation of any disruption in the supply. Syndromic surveillance is a fairly new method of rapidly tracking and identifying disease trends. It allows cities, regions, states, and even wider communities to share, via computer, the background health of a population. An example would be a surveillance system that receives data on symptoms and diagnoses of patients admitted to the area emergency departments on a daily basis. This system, in theory, would quickly identify unusual disease clusters and alert boards of health, triggering a preplanned FOOD SUPPLY CONTAMINATION 909

response. This powerful tool has implications beyond that of food supply contamination and could well be invaluable in any disease outbreak or bioterrorist attack. Every hospital, locality, state, and nation should have predeveloped disaster plans to cover the eventuality of a food supply disruption. These should include access and distribution of needed medications and methods for communicating with local boards of health, public safety agencies, the medical community, and especially the public. Identification of alternative food supplies should be part of the plan. Although state and federal assistance can be expected, such responses will take some time and each of the aforementioned entities should have a detailed plan for dealing with the first few hours of the disaster, possibly even the first 3 days. Greater state and federal oversight of the food supply, as previously mentioned, is critical to prevent and limit the impact of a widespread foodborne illness. Improved inspection of all food products, during both production and shipping (potentially over international borders), is desirable. Rapid containment of such an outbreak will limit its progression, minimize its economic impact, and restore the public’s confidence in the food supply.

POSTINCIDENT ACTIONS After an outbreak of foodborne poisoning, a high degree of suspicion is necessary, especially on the part of medical professionals, to determine whether a cluster of illnesses is something out of the ordinary. Open lines of communication and the use of tools, such as syndromic surveillance, will be essential for early identification of the problem, limitation of a burgeoning outbreak, and prompt and appropriate treatment of victims. Consideration of the impact on critical societal elements, such as police, fire, and healthcare, must be made along with restoration of more normal functioning of the area affected. Early notification and clear lines of communication will be vital in controlling the situation.

MEDICAL TREATMENT OF CASUALTIES For many people suffering from foodborne illness, the treatment is primarily supportive. With some diseases, the addition of appropriate antibiotics can be lifesaving or at least shorten the duration of the illness.

UNIQUE CONSIDERATIONS The major difficulty in determining whether a food supply contamination has occurred will be the way patients present. Early on,many medical practitioners generally will see a few cases each of what appears to be viral gastroenteritis. Only if the healthcare community, food supply industry, and governmental agencies are communicating and ready to act will such an event be identified and addressed before serious health and economic consequences occur. 910 OTHER EVENTS, COMBINATION EVENTS

PITFALLS • Failure to have a disaster plan in place that specifically details the steps to take in the event of a food supply contamination • Failure to communicate among the healthcare community and boards of health regarding new trends in disease appearance • Failure to protect the healthcare community and public safety agencies from being ravaged by an outbreak • Failure to identify alternative means of feeding the population if the primary food supply is contaminated or unavailable • Failure of legislators, at all levels, to be proactive in preventing and limiting the effects of an outbreak

CASE PRESENTATION Bedford Falls is a fairly isolated town located on the coast of New England. Recently a group of people advocating an anarchistic form of government have begun moving into town and buying property. The locals are increasingly uneasy with the influx of newcomers. As their ranks swell, the newcomers begin asserting political power, with their members winning seats on governing boards and committees. Alarmed, the locals schedule a referendum that would effectively remove the newcomers from these positions of authority. A bitter, often acrimonious debate between the groups ignites. One week before the vote on the referendum, many of the longtime residents present to the local emergency department (ED) and physicians’ offices complaining of vomiting, diarrhea, and abdominal pain. The director at the local ED,remembering a Salmonella outbreak in the past decade under similar circumstances, becomes suspicious. When multiple stool cultures from those affected return as being positive for Salmonella, the ED director contacts the local authorities and board of health. The police chief immediately arrests the newly elected selectman, the representative of the school board, and other members of the anarchist group, charging them with deliberate food poisoning intended to influence the upcoming vote. The head of the board of health contacts the state and the Centers for Disease Control and Prevention for assistance. By the time help arrives,25 local residents have fallen ill, virtually all of them longtime residents opposing the new group. Prompt attention to medical care for those who are ill is instituted, and a full investigation is commenced. Investigators quickly determine that all those who have fallen ill ate at the same restaurant, catering mainly to locals and infrequently visited by members of the anarchist group. All of the ill patients had consumed the same batch of egg salad. Examination of the restaurant’s food processing areas reveals multiple positive cultures for Salmonella species indistinguishable from those infecting the victims. Further investigation reveals, however, that the egg salad in question was inadvertently left outside the refrigerator for 24 hours before being mixed with fresh egg salad served to the restaurant’s patrons. Fortunately, all the victims recover after 5 to 7 days without serious sequelae. The police chief releases the suspects and alerts the town’s attorney that she may expect multiple legal cases from the incident. The referendum vote proceeds as scheduled.

REFERENCES 1. Keene WE. Lessons from investigations of food borne disease outbreaks. JAMA. 1999;181:1845-7. 2. Bashai WR, Sears CL. Food poisoning syndromes. Gastroenterol Clin North Am. 1993;3:579. 3. General Accounting Office. Bioterrorism: A Threat to Agriculture and the Food Supply. Available at: http://www.gao.gov/new.items/ d04259t.pdf.

4. Cain S. Agroterrorism. A Purdue Extension Backgrounder. Available at: http://www.ces.purdue.edu/eden/disasters/agro/ Agroterrorism.doc. 5. wbur.org. Bioterrorism in History: 1984: Rajneesh Cult Attacks Local Salad Bar. Available at: http://www.wbur.org/special/specialcoverage/feature_bio.asp.

FOOD SUPPLY CONTAMINATION 911

chapter 187

Mass Gatherings Katharyn E. Kennedy

DESCRIPTION OF EVENT Mass gatherings may be defined as events with a large number of individuals gathered together in a specific place for a specific purpose.1 Thousands of such events take place worldwide each year. In the United States, 5.5 million attend the National Association for Stock Car Auto Racing (NASCAR) events. As many as 65 million attend National Basketball Association (NBA), National Football League (NFL), and/or National Collegiate Athletic Association (NCAA) events. Other such gatherings include leisure events (fairs, sporting events, and concerts), religious festivals, parades, demonstrations, and public disorder. Medical care of some sort has been provided for such gatherings for the last 30 years in both the United States and Europe. Event organizers everywhere need to take responsibility for the safety and well-being of the participants at an event. Various numbers have been used to define a mass gathering—groups greater than 1000 have been used,2 although many researchers use numbers greater than 25,000.3 Considerable variation exists in the type of medical care provided to both participants and spectators at these gatherings. General standards have been proposed for the provision of primary care, emergency and disaster care, and evacuation. Both the American College of Emergency Physicians (ACEP)4 and the National Association of Emergency Medical Service Physicians (NAEMSP)5 have addressed the previous lack of guidelines and standardized care. A survey in 19986 showed that only six U.S. states provided regulatory guidance for the provision of care at mass gatherings, although many are starting to address this omission. A number of disasters have occurred at gatherings throughout the world, in particular at soccer events (Table 187-1). Terrorist threats have also become an unfortunate reality, as shown by the bombing at Centennial Park during the 1996 Olympics in Atlanta, Ga.

PREINCIDENT ACTIONS Mass Gatherings Overall At organized mass gatherings, predictable medical problems and an unpredictable wide variation in medical care 912

exist worldwide. Preplanning and prediction of resource requirements, based on careful needs assessment of anticipated medical care usage and public health risks, may lead to a standardized optimal provision of medical care (Box 187-1).7 Provision of medical care is the responsibility of the event planners. Public health officials need to be involved early in the planning process, especially for large events, such as the Olympics, world fairs, and pilgrimages. The local health department should be involved in the overseeing of the preparation, storage, and serving of food and sanitation requirements. Once identified, those providing medical care at mass gatherings need to liaise with local emergency medical services (EMS), fire, and law enforcement officials. Ground and building plans, close estimates of possible attendance, and identification of any specific hazards should be shared among these providers. Estimates of attendance may be gleaned from advanced ticket sales or from attendance at previous similar events. However, previous history is notoriously unreliable, as demonstrated at the papal mass in Denver (1993) where 250,000 were predicted but 500,000 turned up. Ticket sales on the day of play may have contributed to crowds rushing into soccer stadiums just before kick-off in both England in 1989 and Africa in 2001, with disastrous consequences (see Box 187-1). The type of medical care to be provided at the event needs to be considered beforehand (Table 187-2).8–12 Primary medical care, such as first aid, emergency care, and preparation for a possible disaster, should be addressed. Staffing levels and type of staffing also need to be anticipated. Recommended ratios include 1 to 2 physicians per 50,000 attendees, 2 paramedics or 1 paramedic and 1 emergency medical technician per 10,000 attendees, and 1 basic first-aid provider per 1000 participants at the event.13 On-site physicians have been shown to reduce ambulance transfers to local hospitals by as much as 89%,14 significantly lessening the impact of an event on local EMS services and hospitals. Physician presence should be strongly encouraged at events where significant trauma may occur, where there is a long distance to definitive care, or to enhance an anticipated disaster response. Multiple variables interact to make planning for a mass gathering event challenging. An understanding of these may allow for a more efficient

TABLE 187-1 MAJOR SOCCER DISASTERS DATE 1985

DISASTER May 11 May 26 May 29

1988

March 12

1989

April 15

1992 1996

May 5 October 16

2001

April 11 May 9

Bradford, England: 56 burned to death, 200 injured due to a fire at Bradford soccer stadium. Mexico City, Mexico: 10 trampled to death and 29 injured forcing their way into a match. Brussels, Belgium: British soccer fans attack rival Italian supporters at Heysel Stadium.A concrete retaining wall collapses, resulting in 39 deaths and more than 400 injured. Katmandu, Nepal: 80 fans seeking shelter during a violent hailstorm are trampled to death. Sheffield, England: 96 died at Hillsborough Stadium. Many are crushed to death when a barrier collapses on an overcrowded area. Bastia, Corsica: 17 killed when grandstand collapses. Guatemala City: 84 killed and 147 injured by stampeding fans at Mateo Flores National Stadium. Johannesburg, S.Africa: 43 die, 250 injured at Ellis Park Stadium due to crush as crowds push into an already overcrowded stadium. Accura, Ghana: More than 120 killed in a stampede at a soccer match.

BOX 187-1 REQUIREMENTS FOR MEDICAL CARE AT MASS GATHERINGS • Identification of those providing care • Physician medical oversight • Identification of level of care needed, personnel to pro• • • • • • •

vide care, and appropriate equipment needs Public health issues Treatment facilities and access to care Transportation of injured Emergency medical aspects Communication Command and control Documentation

Adapted from data from NAEMSP.

and effective planning process. However, the unexpected can be expected. Environmental factors play a role in anticipating medical usage at events. Heat-related illnesses are a factor in outdoor concerts, papal visits, and political demonstrations. Thirty-one percent of physician encounters recorded at the 1996 California AIDS ride were for heatrelated problems.15 The Denver papal visit resulted in an unanticipated 21,000 patient encounters at a mainly youthful gathering, due in part to the 14-mile walk and high temperatures.3 Preplanning in the form of educational packages that addressed measures to prevent heatrelated illnesses given to those who purchased advance tickets for the Atlanta Olympics in 1996 might have led to a decrease in the number of patient encounters for this problem despite the high heat and humidity.16 Cold weather events generally lead to lower medical usage rates by participants and spectators.17 Alcohol and illicit drug usage may increase the number of patient encounters. Historically, the consumption rate of alcohol and drugs may be higher at music festivals, rock concerts, and raves. Open-air music events in the

United Kingdom have resulted in a primary diagnosis of alcohol intoxication in 4% of patient encounters.18 Banning the consumption of alcohol at Wembley Stadium led to a 50% reduction in alcohol-related problems. Anticipating medical usage rates may allow for more appropriate staffing levels. However, a wide variation in usage rates has been reported. One study has shown that the overall medical usage rate decreases with overall crowd size. Patient encounters at events with more than 1 million participants average 10 per 10,000 patient encounters. Events with lower numbers average 41 per 10,000 spectators.1 The medical usage rate can vary even within an event itself. At the Los Angeles Olympics, soccer events had usage rates of 68 per 1000 and rowing and canoeing 6.8 per 1000. Other variables to consider include ages of attendees; event duration and time of occurrence; mobile versus stationary event; event type; presence of fireworks, torches, or bonfires; outdoor versus indoor event; and the physical plant and location. Attendance at “on-off” events can be very difficult to estimate, and advance ticket sales can help considerably. Anticipated crowd demographics may be useful in the preplanning stage. Older groups may be expected at papal visits, classical music concerts, and large sporting events.19 Younger age groups frequently attend rock concerts and auto-racing events.20 The needs of children also must be considered. Most children present with minor injuries, but medical teams need to be prepared to deal with serious medical emergencies and trauma. Overall medical usage at a children’s fair was 19.2/10,000, and one-half of those who presented were younger than 14 years old. Protocols need to be in place for the provision of care to minors who present without an accompanying adult.11 Crowd “mood” is an unpredictable variable. Certain types of music, known team rivalry, and religious furor may lead to disruptive behavior and an increase in medical usage rates. Crowded events may lead to a “too-close-for-comfort” feel among event-goers. Environmental conditions, MASS GATHERINGS 913

TABLE 187-2 ANTICIPATING MEDICAL NEEDS AT MASS GATHERINGS TYPE OF EVENT

INJURIES TO BE EXPECTED

Political events: Religious events:

Minor and major trauma Minor injuries, heat-related problems, cardiac problems Drug/alcohol use, minor trauma Minor trauma, heat-related problems, and cardiac issues Severe trauma, heat- and alcoholrelated problems

Sports/musical events: Sporting events: Auto racing:

such as inclement weather, squalid conditions, poor sanitation, and lack of access to drinking water, may lead to ugly crowd dynamics. Despite the many variables to be considered, it has been shown that event type and temperatures are the variables that best predict medical usage rates.1,9,21 After the anticipated usage rates and staffing levels have been addressed, the positioning, number, and type of aid stations should be considered. Fixed events at stadiums may have areas specially designed and designated for medical care. For other events, aid station locations should be no more than a 5-minute walk for attendees. Stations should be clearly visible, and the locations should be known to participants and other event personnel. These areas need to be adequately and appropriately staffed before the anticipated start of the event and remain so until the event is completed. Consideration needs to be given to providing medical care in the crowd for occurrences such as cardiac arrests or lower extremity fractures, including how to transport these patients back to aid stations. Thought needs to be given regarding provision of ambulances for hospital transport and access and egress for these vehicles. The organizers of medical care need to know the capabilities of local hospitals and should liaise with hospital personnel before the event. Attention to the location, staffing, and communication needs of a medical command center should be addressed. Communication needs should be considered for event medical providers; other event planners; and local EMS, police, and fire personnel. Back-up communication in the form of handheld devices or cell phones should be decided on, and medical personnel must be able to connect with local dispatch centers. An incident command structure for medical personnel may be used. The event medical officer oversees all aspects of medical care provided at the site. The event triage officer conducts and directs medical assessment of casualties at designated treatment areas or while roving through the crowds and transporting patients to a central area.The event treatment officer oversees treatment to the sick and injured. The event transport officer directs transport to other facilities, and the logistics officer provides the necessary support for EMS at the event. Consideration may be given to the need for hazardous materials teams, decontamination, wilderness medicine, or use of amateur radio groups. 914 OTHER EVENTS, COMBINATION EVENTS

All patient encounters should be documented. Use of NCR (noncarbon record) paper will facilitate a copy accompanying a patient who needs transport to a medical facility. Records are needed for medical and legal reasons and also may be useful for research purposes.

Concerts/Sports Gatherings The medical usage rate may vary by type of music, with rhythm/blues having rates of 1.3/10,000 and gospel/ Christian 12.6/10,000. The overall median usage for concerts is 2.1/10,000.19 Rock concerts typically have rates 2.5 times that of other concerts. The anticipated audience participation in “moshing,” crowd surfing, and stage diving may lead to a dramatic increase in medical incidents.22 Other problems encountered include minor trauma and ethanol or illicit drug intoxication.23 Surgical problems may be caused by falls; assaults; being crushed against barriers; and assorted “missiles” causing head injuries. Severe trauma may occur in up to 1.4% of attendees at rock concerts. Medical issues include headache, syncope, asthma, and hypoglycemia. Cardiac arrest is uncommon, with a rate of 0.01 to 0.04/10,000. Asthma may be very common at rodeos.24 The ultimate sporting event is probably the Olympics. Planning for the medical care of both spectators and participants begins as soon as the host city has been announced. Apart from routine medical care, there exists a potential for transmission of infectious diseases, risk of injury from crowd crushes, and now the very real risk of terrorist activity or political protests. Extensive planning at local, state, and federal levels is vital to ensure the health and safety of all concerned.25–27 At the 1996 Atlanta games, specialized incident assessment teams were set up to analyze terrorist risks and to address issues such as stockpiling antibiotics and antidotes. Medical providers of all levels received training in awareness of chemical, biologic, and radiologic weapons. 28 Local hospitals were updated to include mass decontamination units. Local EMS providers were given uniform operational plans and procedures, enhanced communications were agreed on, protocols were developed for the management of heat-related illnesses, and guidelines for response to mass casualties were issued. Public health initiatives to address heat-related illnesses included a media campaign; packets sent to ticket purchasers; shelters; and provision of water, wide-brimmed hats, sunscreen, and water misters at the most crowded sites. These, plus the cooler-than-normal temperatures, may have led to a decrease in the expected number of hyperthermia victims.

Marathons More than 300 marathons are staged each year, along with countless half marathons, triathlons, and 5K or 10K events. Preincident considerations include course layout, number of runners, climate, and medical team experience. Earlier start times and the addition of half marathons have led to a decreased risk of injury.29,30 Encouraging runners to seek help early has also reduced

serious medical problems.31 Educating runners before the event on issues such as dehydration, low blood sugar, exhaustion, blisters, the importance of good preparation and training, and the use of energy drinks may lessen the need for medical intervention. Runners with a history of asthma are encouraged to carry their inhalers and not to run if they feel ill. Accessible, visible first-aid stations along the route, use of mobile paramedic teams, and a medical control center should provide adequate medical coverage. Radio communication is essential between medical providers, and a treatment tent at the finish line should include paramedic/triage teams, massage therapists, and podiatrists. The use of computer tracking chips may be used to identify how many runners use medical treatment and help in the planning of the provision of care and supplies in the future.

Pilgrimages Millions of people perform pilgrimages every year. The Muslim pilgrimage, the Haji, to the Holy Land of Makkah (Mecca) in Saudi Arabia may have up to 2.5 million participants from 140 countries for a period of 5 to 7 days. The pilgrimage involves a 24-mile round trip from Makkah through the plains of Arafat. Many of the pilgrims are elderly, come from poor countries, live in tents in extreme conditions, and perform physically exhausting religious rituals. In India, millions of pilgrims visit Lord Ayyappa at Sabarimala each year. This occurs over a 41-day period and involves a 90-minute trek uphill to the temple. Many other pilgrimages on a smaller scale take place throughout the world. Several of the problems encountered may be anticipated. Many of the participants are not in good health and may have chronic medical problems. Heat exhaustion is common during the hot cycle of the Haji. Cases of heat stroke doubled from 1980 to 1981. This may be overcome by the education of pilgrims before and during the event. Infectious disease outbreaks are also common. These include meningococcal meningitis; gastroenteritis; hepatitis A, B, and C; and various zoonotic diseases. The implementation of vaccination policies, infection control policies, and public health initiatives are proving successful in addressing these problems.32 Pilgrims need proof of appropriate vaccinations to obtain a visa for travel to Saudi Arabia. Face mask use is encouraged to reduce the spread of respiratory infections. Head shaving by men, at completion of the pilgrimage, has been associated with the transmission of bloodborne diseases as illegal barbers reuse razors several times. The ritualistic slaughter of thousands of sheep during the ending ceremony may led to outbreaks of Rift Valley fever. This has led to the banning of importation of sheep from countries where this fever is endemic. There is strict surveillance and supervision of accredited slaughterhouses. Free medical care is provided at the holy site in Makkah. In 1997 and 1998 a “treat and release” program was commenced, leading to a 73% reduction in ambulance transports.33 In India at Sabarimala, a medical center is provided at the site. Typically 8000 pilgrims receive medical care over the 41-day period.

POSTINCIDENT ACTIONS In the wake of various disasters at mass gatherings, it is vital to learn from previous mistakes. The European Convention on Spectator Violence and Misbehavior met in 1985 to address issues rising largely from the Heysel Stadium disaster. It identified the need for police and sports authorities to cooperate in ensuring segregation of rival supporters, controlling access to stadiums, and banning the consumption of alcohol. After the 1989 Hillsborough disaster in England, the Gibson Report recommended medical care at stadiums for the first time. All-seats stadiums were to be phased in, leading to safer stadiums with greater attendance. The Boston Marathon has instituted a postevent clinic that is open for 3 days after the event to meet the delayed medical needs of runners.

MEDICAL TREATMENT OF CASUALTIES In general, most participants require minor medical interventions that may be addressed by first responders or paramedics.8 Paramedics may use triage protocols to identify casualties who should be transported to a hospital after initial stabilization rather than waiting for treatment by an on-site physician.34 At rock concerts, 1.4% of attendees may experience severe trauma. Minor trauma results from falls, assaults, being crushed against barriers, and head injuries from assorted “missiles.”Anticipated medical problems include headaches, syncope, hyperventilation, asthma, epilepsy, and hypoglycemia. At the Atlanta Olympics, most of the injuries compromised sprains or strains (13%) and contusion abrasions (7%). Bronchitis was common (9%), and heat cramps/dehydration accounted for 7% of those seeking medical care.26 In addition, three cardiac arrests were reported; the provision of defibrillators at mass gatherings is an important consideration.35 Hyponatremia is increasingly prevalent among marathon runners. It is defined as a serum sodium level of less than 136 mmol/L and is commonly caused by overhydration. Mild cases may be treated by fluid restriction and consumption of salty foods until urination resumes. In moderate cases the patient’s sodium level may need to be checked hourly and, in critical cases, intravenous access will be required and diuretics and 3% saline may be administered. Complications such as seizures, pulmonary edema, and coma should be treated appropriately. Runners should be encouraged to replace only 16 ounces of fluid along with salt for every pound of weight lost. Exercise-associated collapse may occur at the finish due to venous pooling. This may be treated by laying the patient supine with the legs elevated and rehydrating with oral electrolyte/carbohydrate solution. Dehydration should be assessed clinically and treated with oral fluids. Heatrelated illnesses are addressed in the usual fashion. Hypoglycemia is treated with oral or intravenous glucose replacement. MASS GATHERINGS 915

Many pilgrims are in poor health before the event and may need more than minor first aid. Many suffer from heat-related illnesses or infectious diseases. Provision of free medical care and on-site medical facilities with capabilities of providing even an intensive care unit level of care may meet these needs. Disasters do occur at mass gatherings, and appropriate medical care needs to be available. Frequently, the cause of death is traumatic asphyxia,36 for which rapid interventions may make a difference.

UNIQUE CONSIDERATIONS Every mass gathering should be considered a unique event. Careful and exhaustive preplanning may reap many benefits. It is important for those providing medical care at the event not to do so in a vacuum. Local EMS providers may well be needed and certainly will be required if a mass casualty event occurs. Mass gatherings occurring in urban settings will have different characteristics and requirements from those in more rural or remote settings. Even though it may be difficult to predict all the medical needs of the crowd, prior studies have started to use a more scientific approach to addressing these needs. Event type, duration, expected attendance, and weather conditions need to be taken into careful consideration in the planning process.

PITFALLS • Lack of legislation regulating minimum standards for provision of medical care at mass gatherings • Lack of a coordinated, integrated preplanning process • Lack of funding to provide needed public health initiatives and medical resources • Failure to identify a medical director for the event • Failure to learn from previous experiences • Underestimating expected attendance • Failure to consider all variables,such as crowd size,demographics, event duration, and environmental factors

CASE PRESENTATION Always eager for a challenge, many months previously you accepted the position of medical director to oversee medical care at a large open-air concert to be held in your city to celebrate its 250th anniversary. Fifty thousand spectators are anticipated based on advance sales. You have spent many hours in meetings with all the key players arranging appropriate medical care for this event. On the morning of the event, the temperature has already risen 10 degrees above average and the humidity is climbing. An hour into the event,it becomes apparent that many people have forged tickets, and the crowd is now estimated at 75,000. Shortly before the much anticipated heavy metal band is due to play, you receive a call on your radio that the crowd is getting unruly in the mosh pit, and your paramedics are concerned that people will be crushed.... 916 OTHER EVENTS, COMBINATION EVENTS

• Failure to consider and prepare for a terrorist or mass casualty event • Inability to allow capacity crowd ingress to a stadium in a 1-hour period • Failure to consider ambulance access and egress at an event • Lack of training of security personnel, leading to failure to recognize and control potentially dangerous situations

REFERENCES 1. Michael JA, Barbera JA. Mass gathering medical care: a twenty-five year review. Prehospital Disaster Med. 1997;12(4):305-12. 2. Rose W, Laird S, Prescott J, et al. Emergency medical services for collegiate football games. A six and one-half year review. Prehospital Disaster Med. 1992;7:159-9. 3. De Lorenzo RA. Mass gathering medicine: a review. Prehospital Disaster Med. 1997;12(1):68-72. 4. Leonard RB, Petrilli R, Noji EK, et al. Provision for Emergency Medical Care for Crowds. Dallas:ACEP Publications; 1990:1-25. 5. Jaslow D,Yancy A, Milsten A. Mass gathering medical care. Prehosp Emerg Care. 2000;4(4):359-60. 6. Jaslow D, Drake M, Lewis J. Characteristics of state legislation governing medical care at mass gatherings. Prehosp Emerg Care. 1999;3(4):316-20. 7. Jaslow D, Yancy A, Milsten A. Mass Gathering Medical Care: The Medical Director’s Checklist for the NAEMSP Standards and Clinical Practice Committee. Lenexa, Kan: National Association of Emergency Medical Services Physicians; 2000. 8. Varon J, Fromm RE, Chanin K, et al. Critical illness at mass gatherings is uncommon. J Emerg Med. 2003;25(4):409-13. 9. Arbon P, Bridgewater F, Smith C. Mass gathering medicine: a predictive model for patient presentation and transport rates. Prehospital Disaster Med. 2001;16(3):109-16. 10. Zeitz KM, Schneider DP, Jarrett D, et al. Mass gathering events: retrospective analysis of patient presentations over seven years at an agricultural and horticultural show. Prehospital Disaster Med. 2002;17(3):147-50. 11. Thierbach AR,Wolcke BB, Piepho T, et al. Medical support for children’s mass gatherings. Prehospital Disaster Med.2003;18(1):14-9. 12. Milsten AM, Maguire BJ, Bissell RA. Mass-gathering medical care: a review of the literature. 2002;17(3):151-62. 13. Football Licensing Authority: Guide to Safety at Sports Grounds. 4th ed. London:The Stationery Office; 1997. 14. Grange JT, Baumann GW, Vaezazizi R. On-site physicians reduce ambulance transports at mass gatherings. Prehosp Emerg Care. 2003;7(3):322-6. 15. Friedman LJ, Rodi SW, Krueguer MA, et al. Medical care at the California AIDS Ride 3: experiences in event medicine. Ann Emerg Med. 1998;31(2):219-23. 16. Centers for Disease Control and Prevention. MMWE: Prevention and management of heat-related illness in many spectators and staff during the Olympic Games—Atlanta, July 6-23, 1996. JAMA. 1996;45(29):631-3. 17. Eadie JL. Health and safety at the 1980 Winter Olympics, Lake Placid, New York. J Environ Health. 1981;43(4):178-87. 18. Hewitt S, Jarrett L, Winter B. Emergency medicine at a large rock festival. J Accid Emerg Med. 1996;13(1):26-7. 19. Grange JT, Green SM, Downs W. Concert medicine: spectrum of problems encountered at 405 major concerts. Acad Emerg Med. 1999;6(3):202-7. 20. Nardi C, Bettini M, Brazoli C, et al. Emergency medical services in mass gatherings: the experience of the Formula 1 Grand Prix ‘San Marino’ in Imola. Eur J Emerg Med. 1997;4(4):217-23. 21. Milsten AM, Seaman KG, Liu P, et al. Variables influencing medical usage rates, injury patterns, and levels of care for mass gatherings. Prehospital Disaster Med. 2003;18(4):334-46. 22. Janchar T, Samaddar C, Milzman D. The mosh pit experience: emergency medical care for concert injuries. Am J Emerg Med. 2000;18(1):62-3.

23. Erickson TB, Koenigsberg M, Bunney E, et al. Prehospital severity scoring at major rock concert events. Prehospital Disaster Med. 1997;12(3):195-9. 24. Fromm RE, Varon J. Frequency of asthma exacerbations at mass gatherings. Chest. 1999;116(4):251S. 25. Meehan P, Toomey KE, Drinnon J. Public health response for the 1996 Olympic Games. JAMA. 1998;279(18):1469-73. 26. Wetterhall SF, Coulombier DM, Herndon JM, et al. Medical care delivery at the 1996 Olympic Games. JAMA. 1998;279(18):1463-8. 27. Flynn M. More than a sprint to the finish: planning health support for the Sydney 2000 Olympic and Paralympic Games. ADF Health. 2000;1:129-32. 28. Sharp TW, Brennan RJ, Keim M, et al. Medical preparedness for a terrorist incident involving chemical or biological agents during the 1996 Atlanta Olympic Games. Ann Emerg Med. 1998;32(2):214-23. 29. Crouse B, Beattie K. Marathon medical services: strategies to reduce runner morbidity. Med Sci Sports Exerc. 1996;28(9):1093-6. 30. Roberts WO. A 12-year profile of medical injury and illness for the Twin Cities Marathon. Med Sci Sports Exerc. 2000;32(9):1549-55.

31. Ridley SA, Rogers PN, Wright IH. Glasgow marathons 1982-1987. A review of medical problems. Scott Med J. 1990;35(1):9-11. 32. Memish ZA. Infection control in Saudi Arabia: meeting the challenge. Am J Infect Control. 2002;30(1):570-65. 33. Al-Bayouk M, Seraj M, Al-Yamani I, et al. Treat and Release: A New Approach to the Emergency Medical Needs of the Oldest Mass Gatherings—The Pilgrimage. Presented at: 11th World Congress on Emergency and Disaster Medicine. Free Paper Session Topics and Abstracts, May 10-13, 1999, Osaka, Japan, 2002. 34. Salhanick SD, Sheahan W, Bazarian JJ. Use and analysis of field triage criteria for mass gatherings. Prehospital Disaster Med. 2003;18(4):347-52. 35. Crocco TJ, Sayre MR, Liu T, et al. Mathematical determination of external defibrillators needed at mass gatherings. Prehosp Emerg Care. 2004;8(3):292-7. 36. Orue M, Pretell R. Mass Casualty in a Pop Music Concert Instead of Being a Programmed Event: Home Fair 1997, Lima, Peru. Available at: http://pdm.medicine.wisc.edu/moncerrat.htm.

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chapter 188

Ecological Terrorism* George A. Alexander

DESCRIPTION OF EVENT Ecological terrorism or ecoterrorism may be defined as the use of force directed at the environment or ecosystem to terrorize, frighten, coerce, or intimidate governments or societies.1 The scenario of a terrorist or rogue nation group using nuclear, radiologic, biologic, or chemical agents or weapons as a means of ecoterrorism is plausible. Radiologic agents can be obtained readily through legal and illegal means. Chemical and biologic agents are easy and cheap to develop and use. In addition to the devastating human effects of such agents, they can have destructive environmental consequences. For these reasons, global terrorists are more likely to resort to ecological terrorism. Ecological terrorism may occur as a result of sabotage or attack on commercial nuclear power reactors, spent fuel storage depots, or nuclear fuel reprocessing facilities. There are 107 nuclear power plants in the United States and more than 429 nuclear power plants worldwide.2 The 1986 Chernobyl nuclear power plant accident in the former Soviet Union serves as a harsh reminder of potential scenarios in which terrorists could engage in ecological terrorism by trying to release radioactive nuclear materials into the environment. As a result of the Chernobyl accident,28 people died acutely from radiation exposure, 134 patients suffered from acute radiation syndrome, hundreds of thousands of people were evacuated, and almost as many people were involved in the cleanup efforts.3 The extensive atmospheric fallout caused considerable concern far from the accident site. Within 10 days after the accident, elevated levels of radioactivity were reported from Israel, Kuwait, Turkey, Japan, China, the United States, and Canada.4 In addition, radioactive fallout contaminated large forested areas in Europe.5 A large radiologic dispersal device (RDD) also has the potential to contaminate the environment or ecosystems. The environmental hazards from dispersal of highly radioactive fuel in a large RDD would be similar to

*The views expressed in this chapter are those of the author and do not necessarily represent the official policy or position of the National Cancer Institute, the National Institutes of Health, or the Department of Health and Human Services.

918

that which occurred at Chernobyl, but on a smaller scale.6 Radioactive gases, liquids, and particulates would cause considerable environmental contamination. The areas of risk from radioactive contamination can extend many miles away from the explosion site. Biologic pathogens may be used to perpetrate ecological terrorism. For example, Bacillus anthracis, the organism that causes anthrax, is very stable because of its ability to sporulate. This characteristic makes it attractive for terrorists to use anthrax spores to contaminate the environment. Dormant spores are known to have survived in some archaeological sites for perhaps hundreds of years.7 An aerosol release of anthrax spores in parks,playgrounds, or sports fields using a portable crop duster sprayer would contaminate these areas and may infect unsuspecting people who come in contact with the spores. A public acknowledgment of such a release by a terrorist group would cause widespread distress, panic, and fear. During the Gulf War of 1990, the Iraqis deliberately released oil from Kuwaiti oil fields with the intention of polluting and contaminating Saudi Arabian waters and coastlines. These acts were tantamount to ecological terrorism.1 Approximately 400 miles of Persian Gulf shoreline were contaminated with oil.8 The environmental consequences of these oil spills will adversely affect these shorelines and coastal waters for years to come. Similar acts of oil dispersal on land resulted in much larger oil-polluted areas in Kuwait. The burning of Kuwaiti oil fields by the Iraqis was another form of ecological terrorism. More than 700 oil wells in Kuwait burned for about 10 months.9 These fires consumed up to 6 million barrels of oil per day and engulfed the entire region with massive clouds of smoke.10 These acts of ecological terrorism resulted in a level of environmental pollution exceeding that of any other previous manmade disaster.11 The long-term environmental impact of this ecological catastrophe is unknown.12 The estimated deaths of more than 10,000 people and morbidity of approximately 200,000 persons from the accidental release of methyl isocyanate in Bhopal, India, in 198413 serve as a bleak reminder of potential scenarios in which terrorists could engage in ecological terrorism by attempting to release toxic industrial chemicals into the environment.1 Unlimited possibilities of threats

exist from chemical ecoterrorism. An estimated 70,000 chemicals are used commonly worldwide, and an additional 200 to 1000 new synthetic chemicals are marketed by the chemical industry each year.9

PREINCIDENT ACTIONS The first challenge for medical and public health providers in preparing for ecological terrorism is to make an assessment of potential environmental targets and ecological threats from nuclear, radiologic, biologic, and chemical agents. Medical response plans for a variety of likely targets should be developed. These should contain descriptions of the types of possible ecological terrorism, including the identification of anticipated hazards and the response actions that can be taken to minimize them. The medical resources needed for each threat situation and a plan for augmenting those resources should be specified. Consultation should be sought with specialists who have experience in the management of terrorist threats. Management response plans should be scenario-based according to the particular type or category of agent. Planning should be coordinated with local and state hazardous material response teams and medical and environmental laboratories.

POSTINCIDENT ACTIONS Awareness of ecological terrorism is the second challenge and should focus on recognizing that an act of terrorism has occurred. Early detection of an ecological hazard should be the goal to prevent or reduce adverse human and environmental health risks. Any assessment of potential hazards or risks from chemical or radiologic exposures should consider not only the innate toxicity of the substance, but also the nature of the exposure. Once aware of the threat, executing a credible medical response to any attack is the third challenge. An ecological risk assessment should be performed to estimate the probability that untenable ecological health effects may occur in populations as a result of exposure to a specified hazard. The basic elements of an ecological risk assessment should include defining the problem, obtaining the necessary information/data, assessing the hazard potential, assessing the exposure potential, integrating the hazard and exposure assessment (risk characterization), and summarizing and presenting the results.14

ders. A latent period may occur between release of the agent and the development of symptoms associated with illness. Symptoms of acute disease may be seen within minutes or hours, whereas chronic exposure can be insidious and continue undetected until large numbers of people develop catastrophic illness. Several months may pass without people knowing they have been exposed and are at risk. The long-term effects of these exposures may be the most important consideration, particularly if there are no acute effects.15 The clinico-pathologic effects of the terrorist weapons previously mentioned are well known. Certain syndromes with specific symptomatology may arise as the focus of a known or suspected incident. Acute radiation syndrome is associated with nuclear or radiologic incidents. Specific biologic syndromes are associated with a variety of infectious disease agents. Chemical syndromes also exist for numerous toxic chemical agents.

UNIQUE CONSIDERATIONS As already indicated, the medical, public health, and environmental consequences of ecological terrorism require specialized considerations. Emergency responders and healthcare providers should apply similar medical and public health management principles regardless of the ecological threat. Exposure to pollutants from ecological terrorism may or may not result in acute illness requiring the treatment of large numbers of people. In fact, after exposure to any terrorist ecological hazard, people may present with nonspecific symptoms such as headache, fatigue, skin rashes, fever, eye and respiratory irritation, gastrointestinal problems, tiredness, and poor concentration. Depending on the agent involved, evacuation from the scene of a terrorist toxic release contaminating the environment may need to be made immediately after the release. Unfortunately, the information needed to fully evaluate the risk and on which to base an evacuation decision may not be available. In this situation, a health risk assessment should be considered to help decide whether evacuation is necessary immediately after the terrorist release or to predict long-term health consequences. The health risk assessment includes hazard identification, dose-response assessment, exposure assessment, and risk characterization.1

PITFALLS MEDICAL TREATMENT OF CASUALTIES Management of specific human injuries associated with various forms of ecological terrorism is beyond the scope of this chapter and is readily available elsewhere in this book. An intentional release of nuclear, radiologic, biologic, or chemical agents or weapons into the environment has the potential to cause a major public health disaster. Such incidents pose special features that require specific considerations by emergency respon-

Obstacles to the provision of optimal medical and public health management include the following: • Lack of adequate preparedness, emergency response, and recovery planning for possible ecological terrorist attacks before they occur • Lack of coordination with local and state medical, public health, and environmental response agencies • Lack of consultation with health professionals who have expertise to manage specific types of ecological terrorism ECOLOGICAL TERRORISM 919

• Lack of recognition that reporting of nonspecific symptoms among an affected population may be associated with various forms of ecological terrorism • Lack of involvement of behavioral and social health professionals to address the psychosocial consequences of ecological terrorism

CASE PRESENTATION While walking past a television in your emergency department, you see a news alert that a series of explosions occurred about 20 minutes ago at a nuclear power plant located 5 miles south of your 120-bed community hospital. An aerial view from a news helicopter shows a fire involving the containment structure with a gigantic plume that is reported to be moving horizontally in a northeast direction toward a populated city 10 miles away. More than 500 workers were on-site at the time of the explosion. Hundreds of additional personnel have been called in for rescue, plant control, and firefighting operations. An anonymous caller has just contacted the local newspaper and is reported to have said that the power plant explosion was no accident. The plant was sabotaged to pollute the air, land, and waters of America. The governor of your great agricultural state declares a state of emergency and appeals to the public to remain calm. One hour later, three patients with serious trauma injuries, including thermal burns, are brought to the hospital by ambulance. After another 30 minutes, five rescue workers arrive complaining of nausea and vomiting.

REFERENCES 1. Alexander GA. Ecoterrorism and nontraditional military threats. Mil Med. 2000;165:1-5. 2. King G. Dirty Bomb: Weapon of Mass Disruption. New York: Penguin Group; 2004.

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3. Soloviev V, Ilyin LA, Baranov AE, et al. Radiation accidents in the former U.S.S.R. In: Gusev I, Guskova AK, Mettler FA Jr, eds. Medical Management of Radiation Accidents. 2nd ed. Boca Raton, Fla: CRC Press; 2001:157-94. 4. Guskova AK, Gusev IA. Medical aspects of the accident at Chernobyl. In: Gusev I, Guskova AK, Mettler FA Jr, eds. Medical Management of Radiation Accidents. 2nd ed. Boca Raton, Fla: CRC Press; 2001:195-210. 5. Linkov I, Morel B, Schell WR. Remedial policies in radiologicallycontaminated forests: environmental consequences and risk assessment. Risk Anal. 1997;17:67-75. 6. National Council on Radiation Protection and Measurement. Management of Terrorist Events Involving Radioactive Material. Report No. 138. Bethesda, Md: National Council on Radiation Protection and Measurement; 2001. 7. Knobler SL, Mahmoud AAF, Pray LA, eds. Biological Threats and Terrorism: Assessing the Science and Response Capabilities. Washington, DC: National Academy Press; 2002. 8. Overton EB, Sharp WD, Roberto P. Toxicity of petroleum. In: Cockerham LG, Shane BS, eds. Basic Environmental Toxicology. Boca Raton, Fla: CRC Press; 1994:133-56. 9. Moeller DW. Environmental Health. Cambridge, Mass: Harvard University Press; 1997. 10. Warner F. The environmental consequences of the Gulf War. Environ. 1991;33:5-7. 11. Johnson DW, Kilsby CG, McKenna DS, et al. Airborne observations of the physical and chemical characteristics of the Kuwait oil smoke plume. Nature. 1991;353:617-21. 12. Small RD. Environmental impact of fires in Kuwait. Nature. 1991;350:11-12. 13. Murthy RS. Bhopal gas leak disaster: impact on mental health. In: Havenaar JM, Cwikel JG, Bromet EJ, eds. Toxic Turmoil: Psychological and Societal Consequences of Ecological Disasters. New York: Kluwer Academic/Plenum Publishers; 2002:129-48. 14. Rodier DJ, Zeeman MG. Ecological risk assessment. In: Cockerham LG, Shane BS, eds. Basic Environmental Toxicology. Boca Raton, Fla: CRC Press; 1994:581-604. 15. Hyams KC, Murphy FM, Wessely S. Responding to chemical, biological, or nuclear terrorism: the indirect and long-term health effects may present the greatest challenge. J Health Polit Policy Law. 2002;27:273-91.

chapter 189

Computer and Electronic Terrorism and EMS M. Kathleen Stewart and Charles Stewart

DESCRIPTION OF EVENT Every machine connected to the Internet is potentially a printing press,a broadcasting station,and a place of assembly. With the advent of the Internet, a terrorist group can disseminate its information undiluted by the media and untouched by government censors.1 It should come as no surprise, then, that these same terrorists have used the Internet to spread instructions, propaganda, and plans for both devices such as improvised explosives and attacks. This use of computers for terrorism is both real and a true threat to societies.2 Unfortunately, actual terrorist use of computers, networks, information architectures, and the Internet has been largely ignored by the media in favor of a headlinegrabbing “cyber attack” or “cyberterrorism.”The reality of our weaknesses and vulnerabilities is both more chilling and far less reassuring. Three major venues of attack that would affect emergency medical services (EMS) are a “viral” attack, a denial of service attack, and a “social engineering” attack to retrieve secure or restricted data for nefarious purposes.

Viruses/Worms Malignant computer programs are often called viruses because they share some of the traits of biologic viruses. The computer virus requires a functioning “host machine” to replicate, works only with the proper “host,” and passes from computer to computer like a biologic virus passes from person to person. There are other similarities. A biologic virus is a fragment of deoxyribonucleic acid (DNA) inside a protective jacket. A computer virus must piggyback on top of another program, document, or e-mail to get into the computer, and it often must disguise itself from antiviral software with a surrounding innocuous package, like its biologic counterpart. People create computer viruses. A person has to write the code for the virus and test it to make sure that it functions as intended and spreads as designed. A computer that has an active copy of a virus is considered infected. The way that the virus is activated

depends on the design (coding) of the virus. Some viruses become active if the user simply opens an infected document. Others require specific actions on the part of the user. Traditional computer viruses were first noted in the 1980s. During that decade, computers were not only found in large centralized areas, but also small businesses and homes because of the availability of small computers—the advent of the personal computer, or PC. The first viruses were “Trojan horse” viruses. A Trojan horse is a malignant computer program that claims to do one thing (often a game or a utility) but actually does something else instead, such as erase your disk. A Trojan horse program has no way to replicate automatically. Another early virus was the boot sector virus. The boot sector is a small program that initializes the computer and the process of loading the operating system, thus “booting” it into the memory. By putting code in the boot sector, the virus guarantees that it will be loaded into memory immediately and will be able to run whenever the computer is on. Modern viruses are much more insidious in their invasions. Attachments that come as word files (.doc), spreadsheets (.xls), and images (.gif and .jpg) can contain viral attachments. Even opening a contaminated Web site may download a viral program. A file with an extension such as .exe, .com, or .vbs is executable and can do any damage the designer wants. Many viruses disguise themselves by doubling the suffix of the program name, such as stuff.gif.vbs. Once the virus is active on the computer, it can copy itself to files, disks, and programs as they are used by the computer, whether automatically or by the computer user. The big difference between a computer virus and other programs is that the computer virus is specifically designed to make a copy of itself. When the viral programs are executed, the virus examines the hard drives to see whether there is a susceptible program on the disk. If found, the virus adds the viral code to the program or replaces the program or file with its own code. The virus has now reproduced itself so that two or more programs are infected. Every time the user runs any infected program, the virus has the chance to reproduce 921

by attaching to other programs, and the cycle continues. This replication often occurs without the knowledge of the computer user (sometimes the programs infected are system programs that the user doesn’t control). A virus often contains a “payload,” or an additional program that the virus will carry out in addition to replicating itself. Payloads vary from trivially annoying to destructive. Some nondestructive and nontrivial payloads include logging programs that record every keystroke typed in, programs that automatically send e-mail to every address in the computer,and programs that open portals for strangers to examine and use your computer. If the payload is well designed, the user may not even be aware that the computer is infected. Public machines, nonsecure business or official machines, and some secure systems can be used as remote intelligence gathering devices. Locating the offending program is often difficult because many of the keylogging programs are titled or disguised as necessary system files or folders. A worm is simply a virus that has the ability to copy itself from machine to machine. A copy of the worm looks around and infects other machines with the same security defect through any available computer network. Using the networks and the Internet, worms can infect other machines incredibly quickly. Modern computer viruses can be found in programs available on floppy disks, CDs, and DVDs; can be hidden in multiple kinds of e-mail attachments; and can be found in material that is downloaded from the Internet.3,4 Examples of Recent Destructive Viruses/Worms Code Red (now with multiple variants) first appeared in July 2001 and ultimately infected more than 300,000 computers in the United States.5 The worm exploited a security opening in Microsoft’s IIS Web servers. No one knows where this worm originated or by whom it was written. The worm was time sensitive, based on dates. From days 1 to 19 of the month, the worm would propagate. From days 20 to 27, it would launch a denial of service attack against a particular site. From the 27th through the end of the month, the worm would “sleep” in the computer.6 Some variants have opened covert access ports (back doors) in operating systems that allow other intrusions. The concept of the covert access port (back door) is important. These covert ports of entry allow a malicious programmer remote access and even control of programs running on the affected computer. The access may be gained by contaminating programs with a virus, as part of the “remote help” services in some operating systems or by being built into a program by the designer or a programmer (either disgruntled or operating under instructions). Even though Microsoft provided a patch for Code Red, many system administrators did not obtain or apply the patch to their systems. These unprotected computers remain vulnerable to this virus. The newer intrusions using similar exploits may have a more malignant purpose: For example, the Nimda worm appeared 1 week after the Sept. 11, 2001, terrorist attacks on the United States 922 OTHER EVENTS, COMBINATION EVENTS

and targeted the financial sector.7 A more “intelligent” worm, Nimda could replicate itself in several ways: by infecting e-mail programs, by copying itself onto the computer servers, or by affecting users who downloaded infected pages from the infected Web servers. The Nimda affected millions of computers and brought the Internet to a crawl. The Nimda worm replicated itself much faster than the Code Red worm did and caused billions of dollars in damage.8 The Slammer worm, or Sapphire worm as it is also known, surfaced Jan. 25, 2003, on Super Bowl weekend.9 The Slammer exploited a vulnerability in the servers delivering Web pages to users. It was the fastest cyber attack in history. The number of Slammer infections doubled every 8.5 seconds, and the Slammer did more than 90% of its damage in the first 10 minutes of its release. Slammer incapacitated parts of the Internet in Korea and Japan; disrupted phone service in Finland; and markedly slowed airline reservation systems, credit card networks, and ATM machines in the United States.8 Slammer could have been much more destructive had it been properly programmed. When the next “new, improved Slammer” is released, it could do much more damage. It could even affect phone and other trunking communication systems (including some radio links) for a city or larger region of the country. Although control systems are unlikely to be directly damaged by an Internet virus like Slammer, the denial of service to control points for water distribution systems, railroad switch points, power grids, chemical plants, and telephone systems may cause widespread nondestructive failures. Since the “mapping” (remote identification) of the covert access points previously described, terrorists may well have targeted specific weak spots for harassment. Any of the modern viruses/worms could be redesigned to destroy, or at least severely cripple, the 911 emergency response system in the United States. They could also cripple or destroy electrical power, transportation, and telecommunications systems, as well as disrupt water supplies and perhaps our defense systems.

Social Engineering Attacks “Social engineering” is the exploitation of the “weakest link” in the security chain of an organization—the human.10 The aim is to trick people into revealing passwords or other information that compromises a target system’s security. The infamous Kevin Mitnick, for example, conducted most of his corporate intrusions by using the telephone, relying on the gullibility and friendly helpfulness of real people to gain access to corporate networks.11 Hackers may call an organization and pretend to be users who have lost their password or show up at a site and simply wait for someone to hold a door open for them.12,13 Techniques to mitigate a social-engineering attack include the following: • Activate caller ID at work. Match the name given by the caller with the number and extension. • Set your organization’s outbound caller ID to display only the front desk’s phone number, not individual phone extensions.

• Implement an organizational call-back policy. If someone calls asking for information about the organization, say you’ll call them back, then look up and dial the number or go through their company’s switchboard operator. • Be mindful of information posted in out-of-the-office messages. • Never allow another person to piggyback his or her physical access into a secured room or facility on your security ID card—even if the person apparently has his or her own card. • Confront strangers. Ask whether you can take them to someone’s office or help escort them outside. If they balk, contact security. • Get to know your information technology (IT) support staff. • Never write down your network password on a sticky note or tape it to the bottom of your keyboard. “Crackers” (experts at finding and cracking passwords) know where to look. • Beware of e-mail that asks for verification of your password. This is often a practice called “phishing” that solicits passwords for illicit use. • Periodically perform a Google search on your organization and scrutinize whether sensitive information is available outside your organization’s firewall. • Institute a security alert system. Have anyone who receives a suspicious phone call report it to a simple e-mail address, something like [email protected]. If someone calls saying he or she from IT and asks for your network password, say “no,” hang up, and contact IT and security.

Denial of Service Attack A denial of service (DoS) attack is not a virus but a method hackers use to prevent or deny legitimate users access to a computer or servers. The loss of service may be as simple as the inability of a particular network service to use e-mail or the loss of all network connectivity and services for every computer attached to the Internet in any way. The most common DoS attack is simply to send more traffic to a network address than the programmers who planned its data buffers anticipated someone might send. The attacker may be aware that the target system has a weakness that can be exploited, or the attacker may simply try the attack in case it might work. For example, a terrorist creates a computer program that automatically calls 911. The 911 operator answers the telephone but discovers it is a prank call. If the program repeats this task continuously, it prevents legitimate customers from using 911 because the telephone line is busy. This is a denial of service. Many DoS attack tools are also capable of executing a distributed DoS (DDoS) attack. For example, imagine the terrorist now plants his or her program onto many computers on the Internet and has them all call 911 at once. This would have a bigger impact because there would be more computers calling the 911 operators. It would also be more difficult to locate the attacker, since the program is not running from the attacker’s com-

puter; the attacker is only controlling the computer that secretly had the program installed. This is a DDoS attack. A DoS attack can also destroy programming and files in a computer system. In the worst case, an Internet-connected site can be forced to cease operation. If this is a critical control system, the organization will lose the use of the control functions that are connected to the Internet. How Can Antivirus Software Help Against a DoS Attack? Using a virus, the DoS attack tools can be secretly installed onto a large number of innocent computer systems. Systems that unknowingly have DoS attack tools installed are called Zombie agents, or Drones. These “Zombie” systems can be centrally managed by a hacker to initiate DoS attacks at targeted computers. Zombies are not the victims of the DoS attack, but they are used to perform the actual attack. Antivirus software detects viruses that can inject the DoS agents, but it does not detect the DoS attacks. By extracting a pattern or a signature from known Zombie agents, antivirus products can detect malevolent software on the compromised system. Antivirus software may also detect when a hacker is secretly installing Zombie agents.14 It is difficult to trace the origin of the request packets in a DoS attack, especially if it is a DDoS attack. It is impossible to prevent all DoS attacks, but there are precautions server administrators can take to decrease the risk of being compromised by a DoS attack. These precautions are beyond the scope of this chapter. By keeping the antivirus software up-to-date and using good computing practices previously listed, the IT service can keep the system from becoming a Zombie and aiding a DoS attack.

PREINCIDENT ACTIONS A significant protection is to install a commercial virus protection program on all computers and to update this virus protection frequently, almost “religiously.” Set up a schedule to perform operating system updates and run a virus scan. If a virus is found, eliminate it. Each virus is tailored for a specific operating system and/or program. If the computer is using a variation of Windows (e.g.,Windows 98, 2000, or XP), then a virus tailored for Unix will not affect this computer. Likewise, if the computer uses Linux, a Windows virus will not affect the computer. Some viruses are built to exploit known weaknesses in popular programs. If Microsoft Outlook, for example, is the target of such a virus, then computer users who do not use Outlook as their e-mail program will not be troubled by the virus. • Have the virus protection set to scan each document before it is opened. • Don’t open any file or attachment unless you were expecting that file from someone you know and trust. The file will execute as soon as it is open, and if it contains a harmful or destructive virus/worm, you have COMPUTER AND ELECTRONIC TERRORISM AND EMS 923

• •

•

•

just infected your system and anyone else you may e-mail. Don’t use macros in application programs unless they come from a known source. Macros are common ways to introduce viruses into systems. Ensure that the system administrator has a solid backup plan that can rapidly restore the operating system and essential programs in an emergency. Make sure that he or she keeps these backup copies readily available and updated to reflect new operating system and program updates. Essential operating systems, such as dispatch centers, should have an expert evaluate their computers for the presence of covert back doors that allow other intrusions. Ensure that all available updates for the operating system have been applied and that security services within the operating system have been properly activated.

POSTINCIDENT ACTIONS • Essential operating systems should require that known uninfected working copies of all necessary software be immediately available should a disruption occur. Trained personnel able to “revive” the computer system should be on-duty, in-house 24 hours a day every day for just this type of problem. • Perhaps the most important action is to report any suspicious e-mail or unusual computer activity to the person in charge, the system administrator, or other designated person. Establish an on-call pointof-contact with your Internet service providers and appropriate law enforcement officials should you discover a launching of a cyber attack by either someone in your organization or an external operator. Attacks on the Web site of the city of Mountain View, Calif., were discovered by astute and observant local operators (described later in this chapter).

MEDICAL TREATMENT OF CASUALTIES Direct medical casualties from a “cyber” attack would not be expected. The only direct casualties that would result would be those deprived of services due to an inability to dispatch emergency vehicles or to communicate with those vehicles. Medical care would consist of treatment of the underlying illness that originally prompted the call for help. In addition, some institutions use an Internetbased patient care and tracking system. In the event of an attack, these systems may be rendered inoperable or, worse, made to give inaccurate data. All medical facilities that rely on computer and Internet-based systems should have adequate backups in place.

UNIQUE CONSIDERATIONS Our Internet-enabled (net-centric) society is easy prey for two reasons. First, the growing technologic sophistication 924 OTHER EVENTS, COMBINATION EVENTS

of terrorists includes not only weapons of mass destruction and casualties, but a growing use of computers. Secondly, our own economic and technologic systems have an increasing vulnerability to carefully timed attacks as we increase our dependence on computers to include those that are critical to safety.15 The entire critical infrastructure of the United States, including electrical power, telecommunications, healthcare, transportation, water, and the Internet, is vulnerable to a cyber attack. Many control systems, communication systems, and dispatch systems are now connected to the Internet and thus potentially open to intrusion. This does not include the possible effects that a cyber attack could cause to the finance sector or national defense.

PITFALLS • Do not use weak passwords, such as “admin,”“administrator,” or “password.” • Do not leave passwords on sticky notes or taped to computers or desks. • Do not give out passwords in e-mail or on the phone— ever. • Ensure that virus protection is updated frequently (set virus protection software to automatic updates for the most rapid protection). • Do not use wireless networking for secure communications.

CASE PRESENTATION During the summer of 2001, the IT coordinator for the Web site of the city of Mountain View, Calif., noticed a suspicious pattern of computer intrusions. During a subsequent Federal Bureau of Investigation probe, investigators found that several other U.S. city/municipal government computer sites had had the same intruders. These computer intrusions apparently originated from the Middle East and Southern Asia. The invaders were looking up information about the cities’ utilities, government offices, and their emergency systems.6 This computer intrusion took on new importance when several computers were seized from Al-Qaeda operatives after the Sept. 11 attacks. Officials discovered a broad pattern of surveillance of U.S. infrastructure on these computers.8

REFERENCES 1. Conway M. Reality bytes: cyberterrorism and terrorist ‘use’ of the Internet. Available at: http://www.firstmonday.dk/issues/issue 7_11/conway/. 2. Institute for Security Technology Studies at Dartmouth College Technical Analysis Group. Examining the cyber capabilities of Islamic terrorist groups. Available at: http://www.ists. dartmouth.edu/TAG/ITB/ITB_032004.pdf. 3. Scandariato R, Knight JC. An automated defense system to counter Internet worms. Available at: http://dependability.cs.virginia.edu/ publications/2004/scandariat 4. Meinal C. How hackers break in. Sci Am. 1998;279:98-105. 5. Carnegie Mellon Software Engineering Institute. CERT Advisory CA-2001-19 “Code Red” worm exploiting buffer overflow in IIS

6. 7. 8. 9. 10.

indexing service DLL. Available at: http://www.cert.org/advisories/CA-2001-19.html. Frontline. Cyberwar! The warnings? Available at: http://www.pbs. org/wgbh/pages/ frontline/shows/cyberwar/warnings/. Carnegie Mellon Software Engineering Institute.CERT Advisory CA-2001-26 Nimda worm. Available at: http://www.cert.org/advisories/CA-2001-26.html. Frontline. Cyberwar! Introduction. Available at: http://www.pbs. org/wgbh/pages/frontline /shows/cyberwar/etc/synopsis.html. Moore D, Paxson V, Savage S, Shannon C, Staniford S,Weaver N. The spread of the Slammer/Sapphire worm. Available at: www.cs. berkeley.edu/~nweaver/sapphire/. Arthurs W. A proactive defence to social engineering. Available at: http://www.sans.org/rr/papers/51/511.pdf.

11. Gragg D. A multi-level defense against social engineering. Available at: http://www.sans.org/rr/papers/51/920.pdf. 12. Allen M. The use of ‘social engineering’ as a means of violating computer systems. Available at: http://www.sans.org/rr/papers/ 51/529.pdf. 13. Gulati R. The threat of social engineering and your defense against it. Available at: http://www.sans.org/rr/papers/51/1232.pdf. 14. Orvis WJ, Krystosek P, Smith J. Connecting to the Internet securely; protecting home networks. Available at: vialardi.org/ VdSF/pdf/Websecurity.pdf. 15. Greenwell WS. Learning lessons from accidents and incidents involving safety-critical software systems [master’s thesis presentation].Available at: www.cs.virginia.edu/colloquia/event310.html.

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chapter 190

VIP Care Lynne B. Burnett

DESCRIPTION OF EVENT Everyone is created equal. That famous sentiment expressed by Thomas Jefferson, a belief central to the American social and political systems, seemingly calls into question the need for a chapter concerning the care of VIPs—very important persons. Especially in the setting of a disaster, is it proper to deal with VIPs differently than other patients? A response in the affirmative or negative may be equally correct, the validity of each contingent on the specific situation being addressed. Within the medical context, a VIP has been variously defined as any patient who can exert unusual influence on the treating staff,1 and more broadly, as “anyone whose presence in the hospital, by virtue of fame, position, or claim on the public interest, may substantially disrupt the normal course of patient care.”2 Included would be those with public, financial, or political influence, as well as individuals with unusual professional influence,1 ranging from the president of the United States or another major political figure to the king of the Gypsies, a famous actor, a well-known sports figure, a chair of the hospital board,2 and many others. Although it is true that any of the aforementioned persons could potentially disrupt the normal course of patient care in the everyday activities of a hospital, the degree to which they would have such an effect in a disaster would, in large part, be a function of the importance of their role within society.

PREINCIDENT ACTIONS Healthcare organizations must have a disaster plan for incidents of a magnitude that can be expected to overwhelm the standard operating procedures of the emergency department and hospital. Such a document should include a written plan for treatment of VIP patients and should address, at minimum, the following2: • Which hospital personnel are to be notified of a VIP’s impending arrival? In what sequence? • What is the plan for security during the hospitalization of the VIP? • Who decides whether a command center needs to be established? What will be the makeup of its staff? What is the function of the center? 926

• How will the press receive necessary information? • What type of care will other patients receive? If the VIP is a primary person protected by the U.S. Secret Service, and time so permits, an advance team will assess hospital capabilities, choosing one or more to receive the VIP, while also selecting travel routes that are safest and most secure.3 Advanced planning also entails working with local emergency medical services (EMS) systems, hospitals, and trauma centers on various “what if” scenarios to ensure preparation for the visit4; for example, if the president or vice president is to be more than 20 minutes from a trauma unit, capability for helicopter evacuation is a priority. Decisions are made as to what doors, corridors, and elevators can and should be sealed and which areas can and should be evacuated, if such becomes necessary. If possible, one elevator is selected for movement of the VIP and, following an electronic sweep, continuously guarded. Clinical condition permitting, it is best to have the VIP patient stay in a room (or suite of rooms) in the safest area of the hospital, where equipment may be brought.5 The hospital should be prepared to provide the VIP’s security detail a complete personnel roster with the Social Security number and date of birth of all employees.5

POSTINCIDENT ACTIONS Consistent with the planned response, the emergency department (ED) and hospital must be quickly secured, appropriate to the anticipated level of need or threat as well as the demands imposed by the disaster itself. In an assassination attempt, the VIP’s security detail has no way of knowing the extent of the plot and who may be involved.2 In such a circumstance, it may be necessary to grant them control over the hospital environment. In the unlikely event that the hospital must be closed for security reasons, notification of EMS dispatch is essential. Presentation of a VIP often engenders crowd control problems, not only from the media or well-wishers, but also chiefs of service, other medical staff members, administrators, nurses, and other hospital personnel who want to see the VIP or observe what is going on.2 The problem of too many hands, rather than not enough,

makes control of access essential and problematic.2 Hospital security officers must often play a role in keeping unnecessary hospital personnel out of the VIP’s area, as well as ensuring the VIP’s safety. Restricting access may best be accomplished by placing a senior emergency medicine physician in a strategic location, in case security is unable to identify who should be allowed access to the emergency department or is hesitant to bar senior physicians or administrators. If the VIP patient is hospitalized, a list of those allowed access to the VIP should be generated and updated daily, with some means that will limit access only to those so authorized (e.g., frequently changed coded pins).5 Care of a VIP entails a need to coordinate and organize, lest chaotic care and diffusion of responsibility result.6 Clinical and administrative responsibilities should be separated.2 In the ED, the patient’s condition will be the determinative factor as to whether a senior emergency medicine physician assumes clinical control, delegating administrative control to a more junior physician or charge nurse, or vice versa. Another consideration the hospital must address is the immense media interest generated by a disaster, which is then magnified by involvement of a VIP. The media policy should ensure that the release of information is well controlled and that the VIP patient’s privacy is appropriately protected.2 The goal should be the orderly flow of accurate, timely information and the provision of a forum in which reporters’ questions may be asked and answered. Consideration should be given to establishment of a press area at a site separate from the hospital. A single physician, who is knowledgeable, should be designated to serve as spokesperson. All other hospital staff should be instructed not to talk with the media and should be cautioned about hallway or elevator conversations.

MEDICAL TREATMENT OF CASUALTIES One of the first considerations in disaster medical care is triage, with establishment of priority for care. When a VIP is among many patients, determination of who will be treated first has medical, practical, and moral facets. Triage was developed to meet the needs of the military in time of war; thus, priority for care went to soldiers with minor conditions over those more seriously ill or injured. Such an approach has been extended from soldiers to, for example, medical personnel with minor injuries, so that they could care for other patients in earthquakes.7 It is considered ethically justifiable for a person to receive priority for treatment based on social utility only if his or her contribution is indispensable to attaining a major social goal.7 Thus, someone who achieved VIP status because of fame as an actor would be triaged as would anyone else, based on the disaster triage8 factors of medical condition and the availability of personnel and equipment to meet the actor’s specific needs, within the context of caring for the needs of everyone else. In contradistinction would be the VIP who is a government official and whose leadership is needed to respond to the

crisis or whose death would significantly affect the resolve of the community, state, or nation. Such a VIP fulfills the criterion of a “mission-essential” role and thus would be triaged,per the military approach,as highest priority irrespective of the severity of the physiologic insult. A VIP syndrome has been described in which treating staff alter their usual operating procedures because a patient’s power and influence cause them to lose their objectivity and thereby the ability to make the cool, rational, detached decisions necessary for good medical care. VIP syndrome may prompt decisions to do fewer tests, diagnostic procedures, or therapeutic maneuvers to save the patient from pain9 or embarrassment. Spouses of physicians, for example, are less likely to have a pelvic examination than are other patients.10 The result may be a missed diagnosis.9 On the other hand, if too aggressive of an approach is used, the patient may unnecessarily undergo painful and potentially dangerous procedures. Treat the VIP first as a patient and secondarily as a VIP,2 evaluating him or her in a standard manner, including any embarrassing invasive procedures. “There is nothing biologically different from a pope or president, and there is no need to alter one’s thinking in caring for them.”9 To facilitate an orderly and uneventful transfer of care, it is essential that there be coordination between emergency physicians and specialists who will care for the patient in the hospital,7 bringing up yet another “syndrome” that has been identified in the care of a VIP patient. The “chief syndrome”occurs when senior physicians who do not routinely work in the ED respond because the patient is a VIP and intervene in an uncoordinated manner, upsetting the fashion in which the emergency team normally works together.2 It is essential that healthcare providers function in familiar roles. The attending physician must take command and explain that the care given will be identical to that of all other patients with a similar condition because,“Usual medical care is correct care.”9 Consults should be obtained as appropriate, but at all times it should be clear which physician is responsible for the patient’s clinical care,2 whether it be an emergency medicine attending physician, trauma surgeon, or other specialist.

UNIQUE CONSIDERATIONS The VIP may be traveling with a physician.2 If the VIP is a primary protectee of the U.S. Secret Service, it is the responsibility of the Secret Service to protect and, if necessary, rescue the principal. Meanwhile, the White House Medical Unit (WHMU), in conjunction with first responders who may be on-scene, have the responsibility to evaluate, resuscitate, and evacuate the patient to a suitable site for definitive care.11 The WHMU, all of whose members are military personnel, is a team consisting of a physician and emergency or critical care nurse who accompany primary protectees at all times for provision of initial medical care.3 Physicians who have completed Advanced Cardiac Life Support (ACLS) and Advanced Trauma Life Support (ATLS)5 represent the specialties of family medicine, internal medicine, or emergency medicine. All WHMU personnel, whether officer or enlisted VIP CARE 927

status, have completed chemical, biological, radiological, nuclear, and explosive (CBRNE) training, and some of the physicians have completed tactical medicine courses to support SWAT teams. In a life-threatening situation, the attending physician in the hospital bears the responsibility for patient care decisions,2 but diplomacy, collegiality, and good judgment are always required concerning participation by the VIP’s physician in patient care. For example, the physician in the ED may be an internist who is called on to provide initial care to an injured VIP who is accompanied by a board-certified emergency physician. Conversely, the ED physician who may be board-certified in emergency medicine may be responsible for providing emergent obstetric (OB) care to a VIP in the company of a family physician with considerable OB experience. If the VIP is the president of the United States, among the myriad factors needing to be addressed may be the issue of whether the president is capable of making the decisions necessary to fulfill the responsibilities of office. Carried in the “Football,” the briefcase in the custody of a military aide who is always near the president, are the codes necessary to launch a nuclear war. Also contained therein is an “emergency action plan” for devolution of presidential powers to the vice president, including the requisite paperwork for its emergency execution.11 The 25th amendment to the U.S. Constitution sets forth the mechanism whereby the vice president may assume presidential powers and duties as acting presi-

dent. In such a situation, the White House physician plays a critical role in the constitutional process of deciding whether the president is, on the basis of medical judgment, fit to govern.5 Even though the White House physician has an obligation to preserve the confidentiality of the president’s condition, that may, and in fact must, be broken “if the health of the president interferes with his or her ability to do the job.”11 “Impairment is a medical judgment, disability is a political decision”11; thus the findings and opinion of the White House physician are reported to a classified group of White House and Cabinet officials5 who make the final decision, if the president is unable to do so or if there is a question about the president’s decision.

PITFALL • Not providing medical treatment to the VIP like any other patient—too much, too little. REFERENCES 1. Strange RE. The VIP with illness. Mil Med. 1980;45(7):473-5. 2. Smith MS, Shesser RF. The emergency care of the VIP patient. New Engl J Med. 1988;319(21):1421-3. 3. NurseZone.com. Nurses a heartbeat away from the president. Available at: http://www.nursezone.com/Stories/SpotlightOn Nurses.asp?articleID=5067.

CASE PRESENTATION It will be a first for your town. Even though the governor has visited on a few occasions, the president of the United States has never done so—nor has the vice president for that matter—and now all three of them will be at a campaign function together at the high school gymnasium. Your hospital has 84 beds and even though it well serves many of the medical needs of the local residents, the Secret Service made it clear that any situation necessitating critical medical care for its protectees will result in aeromedical evacuation to the trauma center some 30 minutes away. The snowstorm rapidly approaching from the southeast has prompted a change in plans, however, and your hospital is informed that it is now the primary receiving hospital. The Secret Service agent assigned to the ED provides you with the following situation report: the president and governor are on a campaign bus en route to join the vice president, who has just come from the northern part of the state via another campaign bus, and the first lady, who has just flown in from Washington. Since the snowstorm has slowed the president’s bus motorcade, the vice president and first lady are starting the rally in the company of the mayor. The big question on the mind of most folks that day is the effect the weather will have on the number of people attending the event. That is not the question on the mind of the young fellow in the red hat who finds a place in the front, close to the stage. As the vice president begins to speak, someone in a red hat is seen leaping onto the stage, yelling that he has a bomb and that he is going to kill every928 OTHER EVENTS, COMBINATION EVENTS

one. As the Secret Service tackle him, the first lady falls off the stage, striking her head. She begins seizing, vomits, and aspirates significantly. Although not hurt, the vice president falls into a chair, his fist clenched over his sternum in the classic “neck tie sign.” The crowd, which is large despite the weather, begins to run from the building in panic on seeing the altercation on stage and hearing the screaming threats of the man in the red hat. Several people are trampled by the hundreds of onlookers attempting to escape the reach of the nonexistent bomb. The Secret Service informs you that the vice president and first lady are en route to your hospital. Your EMS system relays this information to the base station, plus the fact that the mayor and 27 other citizens of your fair community are to be transported to your facility. While the Secret Service is awaiting the arrival of the vice president and first lady and confirming the rooms that can be used by the president during his wife’s hospitalization, they are contacted by their command post and are told the president’s bus, driving fast in the snowstorm to get to the hospital at the direction of the president, has gone off an embankment and rolled over several times. The president, governor, and approximately 15 occupants of the bus (driver, Secret Service personnel, White House physician, governor’s security officers, presidential staff, campaign aides) are injured and will be transported to your hospital. Fixing his gaze as he walks toward you at a fast clip, someone who carries himself with an air of authority says, “You’re the doctor in charge...?”

4. Clark AA. All the president’s medics. J Emerg Med Serv. 1992;17(8):57-8, 62. 5. Nelsen V. VIP protection and executive protection in hospitals. J Healthc Protect Manage. 1989;6(1):56-68. 6. O’Leary DS, O’Leary MR. Care of the VIP patient. New Engl J Med. 1989;320(15):1016. 7. Beauchamp TL, Childress JF. Justice. In: Principles of Biomedical Ethics. 5th ed. New York: Oxford University Press Inc; 2001:225-82.

8. Hogan DE, Lairet J. Triage. In: Hogan DE, Burstein JL, eds. Disaster Medicine. Philadelphia: Lippincott Williams & Wilkins; 2002:10-5. 9. Block AJ. Beware of the VIP syndrome. (When status of a person affects medical care decisions) [editorial]. Chest. 1993;104(4):989. 10. Diekema DS. It’s wrong to treat VIPs better than other patients. ED Manag. 2000;12(8):92-3. 11. Murray FJ. President’s top doctor haunted by possibility of threats, errors. The Washington Times. April 16, 2000.

VIP CARE 929

I N D E X

ABA. See American Burn Association ABCDDs (airway, breathing, circulation, decontamination, and drugs), 551, 554 ABCs (airway, breathing, circulation), 412, 515 ABS-Avalanche Airbag System, 514 Absorbed dose, 401, 518 AC. See Hydrogen cyanide Accidental Death and Disability: The Neglected Disease of Modern Society, 21, 27 ACEP. See American College of Emergency Physicians Acetones, 430 Acetylcholines, 563, 702 ACLS. See Advanced Cardiac Life Support “Action with Respect to Threats to the Peace, Breaches of the Peace, and Acts of Aggression,” 104 Acute Care Centers (ACCs), 187, 193, 197 Acute lymphocyte count (ALC), 522 Acute radiation syndrome (ARS), 520, 521, 525–526, 530, 530t, 531f, 546, 775 Acute renal failure (ARF), 817 Acute respiratory infections (ARIs), 506 Acute stress disorder (ASD), 351 Acyclovir, 535 ADEPT. See Automated Disaster and Emergency Planning Tool ADS. See Autonomous detection systems Advanced Burn Life Support, 790, 791b Advanced Cardiac Life Support (ACLS), 170, 515, 927 Advanced Pediatric Life Support, 170 Advanced Trauma Life Support, 170, 927 AEL See Authorized equipment list Afghanistan, 49, 102, 106–107 AFIP. See Armed Forces Institute of Pathology Aflatoxin attacks (Aspergillus species) case presentation for, 723 considerations for, 723 description of events during, 722, 723f medical treatment of casualties from, 723 pitfalls of, 724 postincident actions after, 723 preincident actions before, 722–723 AFMIC. See Armed Forces Medical Intelligence Center AFRATs. See U.S.Air Force Radiation Assessment Teams Africa, 44, 239, 668, 718 African Americans, 556 AFRRI. See Armed Forces Radiobiological Research Institute Afterdamp, 853–854 Agency for Healthcare Research and Quality (AHRQ), 10, 97, 109, 194, 409 Agency for Toxic Substance and Disease Registry (ATSDR), 97, 248, 409, 570 Agent 15, 424 Agricultural Research Service, 10 Agriculture, 457 AHJ. See Authority having jurisdiction AHRQ. See Agency for Healthcare Research and Quality

AIDS/HIV, 44, 47, 56–57, 239, 242, 304 Air show disasters case presentation for, 836 considerations for, 836–837 description of events during, 834, 835t medical treatment of casualties from, 835, 836t pitfalls of, 837 postincident actions after, 834–835 preincident actions before, 834, 836b Aircraft crashes case presentation for, 832 considerations for, 832 description of events during, 829 medical treatment of casualties from, 830–832, 831t, 832t pitfalls of, 832–833 postincident actions after, 830, 830b preincident actions before, 829–830 crashes into high-rise building case presentation for, 866 considerations for, 866 description of events during, 864 medical treatment of casualties from, 866–867 pitfalls of, 866 postincident actions after, 865–866 preincident actions before, 864–865 hijacking case presentation for, 862 considerations for, 863 description of events during, 860, 861t medical treatment of casualties from, 861–862 pitfalls of, 863 postincident actions after, 861 preincident actions before, 860–862 Airliner crash, into nuclear power plant case presentation for, 871 considerations for, 871 description of events during, 869–870 medical treatment of casualties from, 870 pitfalls of, 871 postincident actions after, 870, 870t preincident actions before, 870 Airport rescue firefighting (ARFF), 830 Air-purifying respirators (APRs), 249–251, 250f Airway, breathing. See ABCs; ABCDD Alabama, 87 Alanine aminotransferase (ALT), 669, 696 Alaska, 509 Albania, 241 ALC. See Acute lymphocyte count Aleutian Islands, 492 Alibek, Ken, 425, 617 ALT. See Alanine aminotransferase Aluminum, 752 AMA. See American Medical Association Amatoxins, 596 Amenemhet II (Pharaoh), 27 America Online, 130 American Academy of Emergency Medicine, 64 American Blood Centers, 242

American Board of Emergency Medicine, 27 American Board of Medical Specialties, 27 American Burn Association (ABA), 790 American College of Emergency Physicians (ACEP), 27, 64, 298, 883, 912 policy statements of, 28, 187 Section of Disaster Medicine, 28 American College of Physicians, 64 American College of Radiology, 533 American Hospital Association, 183, 194 American Medical Association (AMA), 13–14, 64 American National Standard, 30 American Public Health Association (APHA), 9–10 American Red Cross (ARC), 8, 11, 20, 80, 100, 185 Disaster Relief Services, 200–201 American Samoa, 23, 318 American Society for Testing and Materials (ASTM), 110 American Veterinary Medical Association, 266 Americium-241, 541 AmeriCorps, 86 Amherst, Sir Jeffrey, 424 AMIA. See Argentine Israeli Mutual Association Aminoglycosides, 645, 702 Ammonia, 550, 563, 789 Amoxicillin, 535, 645 Amphotericin B, 731 Ampicillin, 645 Anatoxin-a(s), 596 Anemia, 54 Anesthetic-agent attacks case presentation for, 603 description of events during, 600 medical treatment of casualties from, 603 pitfalls of, 603 postincident actions after, 602–603 preincident actions before, 602 properties of, 600–602 Anfal Operations, 722 Angola, 43, 47, 303 Animal and Plant Health Inspection Service (APHIS), 10 Animals current practices with, 265–267, 267b, 267t historical perspectives on, 264–265 pitfalls with, 267–268 Annals of Emergency Medicine, 215 Anthrax. See Bacillus anthracis Anthrax Vaccine Absorbed (AVA), 147 Anti-Bioterrorism Initiative, 309 Antibiotics, 614, 651, 654, 669, 672, 702 Anticholinesterases, 563 Antidotes, 12 Antimuscarinic agent attacks case presentation for, 583 considerations for, 584, 584f description of events during, 582 medical treatment of casualties from, 583–584

931

Antimuscarinic agent attacks (Continued ) pitfalls of, 584 postincident actions after, 583 preincident actions before, 582–583 Antitoxins, 703 Antivirals, 683 Antivirus softwares, 923 Antony, Marc, 302 Anxiety, 18 APF. See Assigned protection factor APHA. See American Public Health Association APHIS. See Animal and Plant Health Inspection Service Appalachian Mountains, 509 Appropriations Act (Public Law 105-119), 21 APRs. See Air-purifying respirators Aquinas, Saint Thomas, 69 ARC. See American Red Cross Arenaviruses. See Viral hemorrhagic fevers ARF. See Acute renal failure ARFF. See Airport rescue firefighting Argentina, 653, 668 Argentine Israeli Mutual Association (AMIA), 738 ARIs. See Acute respiratory infections Arkia Airlines, 830 Armageddon syndrome, 399–400 Armed Forces Institute of Pathology (AFIP), 100, 835 Armed Forces Medical Intelligence Center (AFMIC), 355, 356t Armed Forces Radiobiological Research Institute (AFRRI), 100, 522, 530, 533, 534 Armenia, 239t, 240, 310, 479–482 Army Soldier and Biological Chemical Command (SBCCOM), 110, 195 ARPANET, 130 Arrhythmias, 500 ARS. See Acute radiation syndrome ASBESTOS (evaluation of chemical casualties), 552t, 554 ASD. See Acute stress disorder Asia, 26, 44, 102, 216, 668 Aspartate aminotransferase (AST), 669 Aspergillus flavus, 722 Aspergillus parasiticus, 722 Aspergillus species. See Aflatoxin attacks ASPHEP. See Office of the Assistant Secretary for Public Health Emergency Preparedness Asphyxiation, 514 Assigned protection factor (APF), 248 Association of Public Health Laboratories, 645 Association of State and Health Officials (ASTHO), 141 Assyrians, 605 AST. See Aspartate aminotransferase Asteroid/meteoroid impacts considerations for, 841 description of events during, 838, 839t medical treatment of casualties from, 840–841 pitfalls of, 841 postincident actions after, 840 preincident actions before, 838–840 ASTM. See American Society for Testing and Materials ATF. See Bureau of Alcohol,Tobacco and Firearms Atlanta Centennial Olympics bombing, 284, 287–288, 343, 361, 496, 577, 813 Atropines, 566–567, 582 ATSDR. See Agency for Toxic Substance and Disease Registry 932 INDEX

Augustus, Emperor, 26 Aum Shinri Kyo cult, 35, 80, 284, 384, 416, 425, 518, 549–550 Australia, 765, 801–802, 801t Austria, 778 Authority having jurisdiction (AHJ), 203 Authorized equipment list (AEL), 408 Automated Disaster and Emergency Planning Tool (ADEPT), 167, 172 Automatic aid, 204 Autonomous detection systems (ADS), 610 AVA. See Anthrax Vaccine Absorbed Avalanche Ball, 514 Avalanches case presentation for, 516 considerations for, 515 description of events during, 514 medical treatment of casualties from, 515 pitfalls of, 515–516 postincident actions after, 514–515 preincident actions before, 514 AvaLung (artificial air pocket device), 514 Avianca Flight 52, 829 Aviation and Transportation Security Act, 860 Azithromycins, 734, 883 Aztreonam, 614

Baccharis megapotamica, 714 Bacillus anthracis (anthrax), 11, 17, 136, 145, 147, 304–305, 325, 344, 369–370, 375, 418–420, 418t, 419t, 425, 573, 605 attacks case presentation for, 613 considerations for, 613 description of events during, 608 medical treatment of casualties from, 610–611, 610t, 611t, 612t pitfalls of, 613 postincident actions after, 612–613 preincident actions before, 611 Bacillus cereus, 15 BAL. See British anti-lewisite Bali, 383, 765 Balkan Wars, 49 Balkans, 43 Baltimore, 778, 803–804, 862 Baltimore Washington International Airport, 862 Bandelier National Monument, 800 Bangladesh, 305, 327, 475 Bar codes, 294, 294b Barbera, Joe, 206–207 Barton, Clara, 20, 297 Basal Convention, 239 BAT. See Biodosimetry Assessment Tool Battle of Stalingrad, 617 Becquerel, Henri, 519 Beef, ground, 372 Beirut bombings, 746 Bejerot, Nils, 888 Belgium, 327, 548, 737 Bellevue Hospital, 229 Beltway snipers, 389, 811 Benzodiazepines, 567 Beriberi, 54 Berkeley Hills Tunnel Fire, 800 BERM. See Bioterrorism and Epidemic Outbreak Response Model BGPC. See Blood-gas partition coefficient Bhopal, India, 35 Bible, 4, 27 Bilboa, 878 Binarization, 430 Biodefense Clinical Research Branch, 98

Biodosimetry Assessment Tool (BAT), 522, 530, 533, 534, 536 Bioengineered pathogens, 428 Biologic agents, 710 introduction to, 605–606, 606t surveillance of, 606, 607t Biologic response modifiers (BRMs), 425, 427–428 Biologic weapons, 13. See also Quarantines conclusions on, 431 future of, 425–428 historical perspectives on, 424–425 Biological and Toxin Weapons Convention, 145, 306, 424–425, 714, 722 Biological protective equipment, 251 BioPort Corporation, 147 Biopreparat, 425 Biotechnology, 431 Bioterrorism (BT), 17–18 current practices for, 416–422, 417t, 418t, 419t detection systems, 136–137 epidemics and, 68 historical perspectives on, 415–416, 416t measures for, 98 pitfalls of, 422 -related issues, 97 Bioterrorism and Epidemic Outbreak Response Model (BERM), 199 BITNET, 130 Black Bane outbreak, 608 Black Death, 882 Black powder, 749 Blackdamp, 853 Blackouts, 12, 38, 134. See also Power system failures Blast lung injury (BLI), 740–741 Blasts. See also Explosions descriptions of, 736–737 historical context of, 737–739, 739t medical treatment of casualties from, 739–743 pitfalls of, 743 BLI Severity score (BLISS), 741 Blizzards, 34 Blood donations, 242 Blood urea nitrogen (BUN), 658 Blood-gas partition coefficient (BGPC), 601 Body surface area (BSA), 797–798 Bolivia, 668 Bombs hydrogen, 399 lava blocks/, 502 pipe case presentation for, 815 clinical presentation of, 814 considerations for, 815 description of events during, 813–814 medical treatment of casualties from, 814–815 pitfalls of, 815 postincident actions after, 814 preincident actions before, 814 Bone marrow syndrome, 520 Boot sector virus, 921 Bores, 493 Bosnia, 102, 238, 240, 310 Boston News-Letter, 232 Botulism Immune Globulin Intravenous (BIG-IV), 147 Botulism. See Clostridium botulinum toxin Brazil, 35, 371, 519, 556, 885 Brentwood postal facilities, 425 Bridge collapses case presentation for, 848

Bridge collapses (Continued ) considerations for, 850 description of events during, 846–847 medical treatment of casualties from, 848 pitfalls of, 850 postincident actions after, 847–848 preincident actions before, 847 British Airtours Boeing 737 accident, 829 British anti-lewisite (BAL), 569 BRMs. See Biologic response modifiers Bromobenzylcyanide, 593 Brucella species (brucellosis), 148, 646 attacks case presentation for, 622 considerations for, 622 description of events during, 621 medical treatment of casualties from, 622 pitfalls of, 622 postincident actions after, 622 preincident actions before, 621 BSA. See Body surface area BT. See Bioterrorism Building(s) aircraft crashes into high-rise case presentation for, 866 considerations for, 866 description of events during, 864 medical treatment of casualties from, 866–867 pitfalls of, 866 postincident actions after, 865–866 preincident actions before, 864–865 collapses case presentation for, 844 considerations for, 843–844 description of events during, 842 medical treatment of casualties from, 843, 844t pitfalls of, 844–845 postincident actions after, 843 preincident actions before, 842–843 damaged, 217 explosions, high-rise Building(s) case presentation for, 772 considerations for, 772 description of events during, 770 medical treatment of casualties from, 771–772 pitfalls of, 772 postincident actions after, 771 preincident actions before, 770–771 BUN. See Blood urea nitrogen Bunyavirus. See Viral hemorrhagic fevers Bureau for Democracy, Conflict and Humanitarian Assistance (DCHA), 102 Bureau of Alcohol,Tobacco and Firearms (ATF), 71, 392 Bureau of Population, Refugees and Migration (PRM), 103–104 Bureau of Public Roads, 79, 112 Burkholderia mallei (Glanders), 148 attacks case presentation for, 649 considerations for, 649 description of events during, 647–648, 648t medical treatment of casualties from, 648–649 pitfalls of, 649 postincident actions after, 648 preincident actions before, 648 Burkholderia pseudomallei (melioidosis), 148 attacks case presentation for, 651

Burkholderia pseudomallei (melioidosis) (Continued) considerations for, 652 description of events during, 650–651 medical treatment of casualties from, 651 pitfalls of, 652 postincident actions after, 651 preincident actions before, 651 Burns, 402 current practices for, 790–793, 791b pitfalls of, 793–794 summary on, 794 unique considerations for, 793, 793t Bus accidents case presentation for, 827 considerations for, 827 description of events during, 826 medical treatment of casualties from, 827 pitfalls of, 827 postincident actions after, 826–827 preincident actions before, 826 Bush, George H.W., 393 Bush, George W., 386 Bush, John Ellis, 386 BWC. See Convention on the Prohibition of the Development, Production, Stockpiling and Use of Biological and Toxin Weapons and on Their Destruction BZ. See 3-Quinuclidinyl benzilate (QNB)

Caesar,Augustus, 302 CAK. See Cyanide antidote kit California, 9, 96, 109, 117, 141, 244, 393, 800–801 Call-Chronicle-Examiner, 232 Cambridge Dictionary, 5 CAMEO (computer-aided management of emergency operations), 130, 559 Cameroon, 503 Canada, 12, 28, 46, 141, 178–179, 200, 426, 544 Canadian International Development Agency (CIDA), 46 Cancers, 546 Capability Assessment for Readiness (CAR), 110 Carbamates, 563 Carbon dioxide, 854 Carbon monoxide poisoning, 499, 500–501 C4H10O. See Diethyl ether Carboxyhemoglobin, 831t Cardiovascular syndrome, 521 Caritas, 239 Carter, Jimmy, 29, 80, 90, 113, 183, 229 Case fatality rate (CFR), 54 Case identification, 13 Casualty Care Research Center, 298, 886 Catastrophic Incident Response Annex Supplement (CIRAS), 367 Cathay Pacific, 153 CATS. See Consequence Assessment Tools Set Cave Automated Virtual Environment, 323 CBC. See Complete blood count CBIAC. See Chemical and Biological Defense Information Analysis Center CBIRP. See Chemical and Biological Immediate Response Force CBRNE. See Chemical, biological, radiological, nuclear, and explosive sensors C/B-RRT. See Chemical Biological Rapid Response Team C/B-SMART. See U.S.Army Chemical and Biological Special Medical Augmentation Response Teams

CC Readiness Force (CCRF), 99 CC. See Commissioned Corps CDC. See Centers for Disease Control and Prevention CEEV. See Central European encephalitis virus Cefaclor (Ceclor CD), 239 Cefotetan, 614 Cefozolin, 614 Ceftazidimes, 614, 648, 651 Center for Research on the Epidemiology of Disasters (CRED), 327 Center for Risk Communication, 126 Center Polynesien de Prevention des Tsunamis, 493 Centers for Disease Control and Prevention (CDC), 10, 46 activities/roles of, 10–11, 71, 93, 97–98, 105, 109, 131, 304, 355–359, 357t–358t, 490, 678 Advisory Committee on Immunization Practices, 176–177 categories of, 605, 606t creation of, 90 preparedness guidelines of, 8, 13–14, 416, 417t Science and Technology Center at, 361 Central America, 275, 475 Central European encephalitis virus (CEEV), 663 Central Intelligence Agency (CIA), 71, 329, 585 Central nervous system (CNS), 521, 582, 589, 743 Cerebrovascular accident (CVA), 175 CERTs. See Community emergency response teams CEs. See Emergencies, complex Cesium, 467, 544 CF. See Complement-fixation CFR. See Case fatality rate CG. See Phosgenes Chain reactions, 519 Champion Trauma Scale, 285, 288 CHCl3. See Chloroform Chechnya, 102, 600 Chelation, 541–542, 873 Chemical agents, 406–407, 549 Chemical and Biological Defense Information Analysis Center (CBIAC), 407 Chemical and Biological Immediate Response Force (CBIRP), 100, 396, 407, 409 Chemical, biological, radiological, nuclear, and explosive sensors (CBRNE), 110, 157, 363–364, 407, 409 Chemical Biological Rapid Response Team (C/B-RRT), 396 Chemical disasters case presentation for, 553 current practices for, 550–553, 550b, 551b, 551f, 552t, 553b historical perspectives on, 548–550, 549b industrial considerations for, 561 description of events during, 556 medical treatment of casualties for, 559–560, 560b, 560t pitfalls of, 561 postincident actions after, 558–559, 558b, 559b, 560b preincident actions before, 556–558, 557t pitfalls of, 553–554 Chemical incidents, 12, 13, 371–372 Chemical Stockpile Emergency Preparedness Program (CSEPP), 11 INDEX 933

Chemical warfare. See Warfare Chemical Warfare Service, 406 Chemical weapons. See also Quarantines conclusions on, 431 future of, 428–431 historical perspectives on, 424–425 Chemical Weapons Convention (CWC), 406 Chemicals, toxic, 787–789 Chemistry, combinatorial, 431 CHEMPACK program, 96, 200, 309, 365, 413 Chernobyl Nuclear Power Plant, 385, 479, 518, 536, 544, 774–776, 918 Chest radiography (CXR), 695 CHF. See Congestive heart failure Chicago, 13, 24, 232 Chicago Daily Tribune, 125 Chikungunya virus attacks case presentation for, 679 considerations for, 679 description of events during, 678 medical treatment of casualties from, 679 pitfalls of, 679 postincident actions after, 678–679 preincident actions before, 678 Children, 546 current practices on, 52–53 disasters and, 51–58 historical perspectives on, 51–52 malnutrition amongst, 44, 54–55, 507 medical responses/treatments for, 55–56 mortality rates of, 52, 53–54, 330, 506 pitfalls of, 57–58 psychological support for, 57 sanitation and, 53–54 shelter and, 55 water and, 53, 305 Chile, 492, 493 China, 13, 26, 141, 179, 416, 556 Chlamydia psittaci (psittacosis), 148 attacks, 148 case presentation for, 655 considerations for, 655 description of events during, 653–654 medical treatment of casualties from pitfalls of, 655 postincident actions after, 654–655 preincident actions before, 654 Chloramphenicol, 633, 645 Chlorine, 548 Chlorine gas (Cl2), 573 1-Chloroacetophenone (CN), 593 O-Chlorobenzylidene malononitrile (CS), 593 Chlorobornanes, 429 Chloroform (CHCl3), 601 Chokedamp, 853 Cholera. See Vibrio cholerae CIA. See Central Intelligence Agency CIDA. See Canadian International Development Agency Cidofovir, 683 Ciprofloxacin, 648 CIRAS. See Catastrophic Incident Response Annex Supplement CISD. See Critical incident stress debriefing CISM. See Critical incident stress management Cities Readiness Initiative (CRI), 109 Citizens Corps, 86, 184 Civil Air Patrol, 185 Civil Defense Act, 79 Civil Military Operations Center (CMOC), 104 Civil Support Teams,Weapons of Mass Destruction (CST/WMD), 189, 529 934 INDEX

Civil unrest/rioting case presentation for, 889 considerations for, 891 description of events during, 889–890 medical treatment of casualties from, 891 pitfalls of, 892 postincident actions after, 891 preincident actions before, 890–891 Civil War, 27, 297, 354 CK. See Cyanogen chloride Clindamycins, 702 Clinton, Bill, 76, 80, 336 Clostridium botulinum toxin (botulism), 13, 17, 145, 147, 420–422, 424 attacks case presentation for, 703 considerations for, 703 description of events during, 701 medical treatment of casualties from, 702–703 pitfalls of, 703 postincident actions after, 702 preincident actions before, 701 Clostridium perfringens toxin, 15, 424 attacks case presentation for, 708 considerations for, 707 description of events during, 705–706 medical treatment of casualties from, 707 pitfalls of, 707 postincident actions after, 706–707 preincident actions before, 706 CMOC. See Civil Military Operations Center CMR. See Crude mortality rate CMRT. See Consequence Management Response Team CN. See 1-Chloroacetophenone CND. See Council of National Defense CNG. See Compressed natural gas CNS. See Central nervous system Coalition Provisional Authority (CPA), 48 Cobalt, 467 Coccidioides immitis (coccidioidomycosis), 509 attacks case presentation for, 728 considerations for, 728 description of events during, 725–726 medical treatment of casualties from, 727 pitfalls of, 728 postincident actions after, 727 preincident actions before, 726–727 Cockpit resource management, 220 Coconut Grove, 850 Code Red worm, 921 COG. See Council on Governments Cold War, 45, 399 Cold zones, 885 Colorado, 13, 26, 71, 75, 96, 110, 489, 510, 808 Columbia, 26, 505, 509, 885 Columbia (space shuttle), 4, 840–841 Columbine High School shooting, 71, 75, 808 Combat Trauma Patient Simulator, 324 Commissioned Corps (CC), 96 Committee on Research and Development to Improve Civilian Medical Response, 693 Common Era, 303 Common strategy, 860 Commonwealth of Northern Mariana Islands, 23 Communicable Disease Center, 90 Communication(s), 39, 90, 127, 458 devices, 134–135, 135t during disasters

Communication(s) (Continued ) current practices for, 229–230 historical perspectives on, 229 pitfalls/strategies for, 230–231 vehicles, mobile, 134–135 Communications-on-wheels (COWS), 40, 134 Community emergency response teams (CERTs), 30, 184, 198 Compartmentalization, 826 Complement-fixation (CF), 654, 741 Complete blood count (CBC), 571, 715 Complex emergencies. See Emergencies, complex Comprehensive emergency management (CEM), 108, 113 Comprehensive Environmental Response, Compensation, and Liability Act, 463 Compressed natural gas (CNG), 782 CompuServe, 130 Computed tomography (CT), 609, 861–862 Computer/electronic devices, 130 laptop as, 131–132, 132b PDAs as, 132–133, 133b tablet PC as, 132, 132b terrorism and case presentation for, 924 considerations for, 924 description of events during, 921–923 medical treatment of casualties from, 924 pitfalls of, 924 postincident actions after, 924 preincident actions before, 923–924 viruses/worms and, 921–922 Concepts of Operation of Health Service Support in an NBC Environment, 473 Concerts, 914 Condoms, 57 CONELRAD (Control of Electromagnetic Radiation), 233 Confined space, 269, 271–272, 739, 739t Congestive heart failure (CHF), 54 Congo, Democratic Republic of, 43, 44, 47, 688 Congressional Act of 1803, 28 Connecticut, 12, 13 Conotoxins, 710–711 CONPLAN. See U.S. Governmental Interagency Domestic Terrorism Concept of Operations Plan Consequence Assessment Tools Set (CATS), 559 Consequence management, 391 Consequence Management Response Team (CMRT), 104 Contamination, 465, 876–877 Continuous quality improvement (CQI), 169–170 CONTOMS. See Counter Narcotics and Terrorism Operational Medical Support Contract tracing, 13 Controlled Substance Act, 585 Convention on the Prohibition of the Development, Production, Stockpiling and Use of Biological and Toxin Weapons and on Their Destruction (BWC), 415 “Convention on the Prohibition of the Development, Production, Stockpiling and Use of Chemical Weapons and on Their Destruction,” 406 Convergence, 30 Convergent volunteerism, 864 Coronary heart diseases, 7 Coronavirus species, 695

Corps of Vigiles, 26 Council of National Defense (CND), 112 Council of State and Territorial Epidemiologists, 645 Council on Foreign Relations, 32 Council on Governments (COG), 186 Counter Narcotics and Terrorism Operational Medical Support (CONTOMS), 298, 886 “Countering Agricultural Bioterrorism,” 264 Coupled human-environment system, 328 Courts, 72–73, 76 Covello,Vincent, 126 COWS. See Communications-on-wheels Coxiella burnetii (Q fever), 148 attacks case presentation for, 625 considerations for, 626 description of events during, 624–625 medical treatment of casualties from, 625 pitfalls of, 626 postincident actions after, 625 preincident actions before, 625 CPA. See Coalition Provisional Authority CQI. See Continuous quality improvement CR. See Dibenz-1:4-oxazepine CRAMS and Triage Index, 285 Creatine kinase, 696 CRED. See Center for Research on the Epidemiology of Disasters Crew resource management (CRM), 220 Crew Training Common Strategy, 860 CRI. See Cities Readiness Initiative Crimean-Congo hemorrhagic fever, 668 Crisis management, 391 Crisis Management Group, 394 Crisis Relocation Planning (CRP), 113 Critical incident stress debriefing (CISD), 24, 887 Critical Incident Stress Foundation, 351, 352 Critical incident stress management (CISM), 61–62, 61t Cronkite,Walter, 124 CRP. See Crisis Relocation Planning CRS. See Cutaneous radiation syndrome Crude mortality rate (CMR), 256, 329–330, 506 Cruise ships, infectious disease outbreaks on case presentation for, 884 considerations for, 884 description of events during, 882 medical treatment of casualties from, 883–884 pitfalls of, 884 postincident actions after, 883 preincident actions before, 882–883 Crush injuries, 272 Crush Syndrome, 272, 482 introduction to case presentation for, 819 considerations for, 819 description of events during, 817 medical treatment of casualties from, 818–819 pitfalls of, 819 postincident actions after, 818 preincident actions before, 817–818 Cryptosporidium parvum (cryptosporidiosis), 149 attacks case presentation for, 734 considerations for, 735 description of events during, 733–734 medical treatment of casualties from, 734–735 pitfalls of, 735

Cryptosporidium parvum (cryptosporidiosis) (Continued ) postincident actions after, 734 preincident actions before, 734 CS. See O-Chlorobenzylidene malononitrile CSEPP. See Chemical Stockpile Emergency Preparedness Program CST/WMD. See Civil Support Teams,Weapons of Mass Destruction CT. See Computed tomography C2HBrCIF3. See Halothane Cuban Missile Crisis, 79 Curie, Marie, 465 Curium, 541 Cutaneous radiation syndrome (CRS), 522 CVA. See Cerebrovascular accident CWC. See Chemical Weapons Convention CX. See Phosgene oxime CXR. See Chest radiography Cyanide, 161 attacks case presentation for, 579 considerations for, 579–580 description of events during, 576 medical treatment of casualties from, 578, 580t pitfalls of, 580–581 postincident actions after, 577–578 preincident actions before, 576, 577b Cyanide antidote kit (CAK), 578 Cyanogen chloride (CK), 576, 580 Cyclones, 34 case presentation for, 478 considerations for, 477 description of events during, 475, 476t medical treatment of casualties from, 477 pitfalls of, 477–478 postincident actions after, 477 preincident actions before, 476–477 Cytokines, 428, 535 Czechoslovakia, 424

DACs. See Disaster assistance centers DALYs. See Disability adjusted life years Damages, 473–474 DARPA. See Defense Advanced Research Projects Agency DART. See Disaster assistance response team DCHA. See Bureau for Democracy, Conflict and Humanitarian Assistance DCO. See Defense coordinating officer Deaths, 7 excess, 47 rates, crude, 329–330 Decontamination, 40, 87, 280–281, 412, 447–448, 550, 577 chemical, 459–460, 559 current practices for, 461–463, 462f pitfalls of, 463–464 radiation current practices for, 465–470 historical perspectives of, 465 hospital, 466–467 pitfalls of, 470 of PPEs, 468–469 Defense Advanced Research Projects Agency (DARPA), 10 Defense Against Weapons Of Mass Destruction Act, 80, 336, 343 Defense Civil Preparedness Agency, 112–113 Defense coordinating officer (DCO), 395–396, 395f Defense Intelligence Agency (DIA), 355

Deforestation, 44 Dehydration, 15, 53, 354 Delaware, 26 DEMPS. See Disaster Emergency Medical Personnel System Dendrimers, 430 Dengue fever, 675, 676 Denial of service attack (DoS), 923 Denton Amendment, 104 Denver, 13 Department of Health (DOH), 92 der Heide,Auf E., 31, 32, 216, 219–220 Detroit Free Press, 127 DFA. See Direct fluorescent antibody DHHS. See U.S. Department of Health and Human Services DHS. See U.S. Department of Homeland Security DIA. See Defense Intelligence Agency Diagnostic and Statistical Manual of Mental Disorders (DSM-III), 59 Diagnostic peritoneal lavage (DPL), 747 Diaphoresis, 564 Diarrhea, 18, 34, 53, 56, 354 Dibenz-1:4-oxazepine (CR), 593 DIC. See Disseminated intravascular coagulation Diethyl ether (C4H10O), 601 Diethylenetriamine pentaacetic acid (DTPA), 530 Diphosgenes (DP), 573 Diphtheria, 7 Direct fluorescent antibody (DFA), 687, 734 Directed-energy weapons considerations for, 443, 443t description of events for, 441–442 medical treatment of casualties from, 442–443, 443f pitfalls of, 444 postincident events for, 442, 442f preincident events for, 442 Director of military support (DOMS), 395 Dirty bomb. See Radiologic dispersal devices Disability adjusted life years (DALYs), 44 Disaster(s), 3, 9 accidental v. intentional current practices of, 370–372 historical perspectives on, 369–370 pitfalls of, 372 assistance, 184–190 CDC’ preparedness guidelines for, 8 containment of, 87 cycles, 3, 4f declaration process, 189–190 definition of, 4–5, 9, 164–165, 473 direct/indirect effects of, 317 education/research, 322–325 emergency medicine in MCIs/, 63–69 informatics/telecommunications in, 130–137 large-scale, 16–17 manmade, 3–4, 12, 350 planning, 90–93, 91t policies, 9 psychological impact of current practices for, 59–62, 60t, 61t historical perspectives on, 59 pitfalls of, 62 public health and, 7–18 small-scale, 16 supplies, 40 zones current practices for, 304–306 historical perspectives on, 302–304 pitfalls of, 306 INDEX 935

Disaster assistance centers (DACs), 318 Disaster assistance response team (DART), 103, 104 Disaster Emergency Medical Personnel System (DEMPS), 99 Disaster Epidemiology Research Center, 46 Disaster management, 20–24 conclusions on, 207 current practices for, 204–206, 205b, 206b historical perspectives on, 203–204 logistics/operations of, 203–207, 205b, 206b pitfalls of, 206–207, 206b Disaster Management Committee, 30 Disaster Medical Assistance Teams (DMATs), 5, 22, 28, 30 activities of, 95, 99, 201, 205, 218 immunity statutes for, 77–78 Disaster medicine, 3, 5–6. See also Emergency medicine Disaster Mitigation Act (2000), 140 Disaster Mortuary Affairs Response Teams (DMARTs), 261 Disaster Mortuary Operations Response Teams (DMORTs), 95–96 development of, 260–261, 261b guidelines by, 542–543 Disaster Portable Morgue Units (DPMUs), 261, 262f Disaster Relief Acts, 79, 113 Disaster Research Center (DRC), 26, 110 Disaster Research Plans, 407 Disaster responses, 317 facility considerations during, 88 federal, 95–101, 97b international, 102–107, 104b, 104t, 106b local, 84–88, 85t, 86t public welfare issues during, 88 scene operations during, 87 scene safety during current practices for, 216–219, 216b, 218b damaged buildings and, 217 falling/flying debris in, 216–218 geographical scale/surroundings of, 216, 216b HazMat and, 217 historical perspectives on, 215 personnel/volunteers and, 218–219 pitfalls of, 222 PPEs and, 217–218, 218b safety management cycle at, 219–222, 219f weather and, 217 special teams at, 30–31 summary on, 88 in U.S., 79–83 Disaster victim identification (DVI), 261 Disaster Victim Identification Guide, 261 Disasters, natural, 3–4, 12, 350, 474–475 Discrimination, 40 Disease and non-battle injury (DNBI), 354 Diseases, 4, 7, 46. See also Cruise ships; specific diseases control of, 47 dirty hands, 53 infectious, 7, 12, 369 outbreaks, 370–371 target, 242 Disseminated intravascular coagulation (DIC), 669 District of Columbia, 23 D-lysergic acid diethylamide (LSD), attacks case presentation for, 587 considerations for, 587 description of events for, 585–586 medical treatment of casualties for, 587 936 INDEX

D-lysergic acid diethylamide (LSD), attacks (Continued ) pitfalls of, 587–588 postincident actions after, 587 preincident actions for, 587 DMATs. See Disaster Medical Assistance Teams DMORTs. See Disaster Mortuary Operations Response Teams DNBI. See Disease and non-battle injury DOC. See U.S. Department of Commerce Doctors without Borders (Médicins sans Frontières), 105, 239–240, 302, 305 DOD. See U.S. Department of Defense DOE. See U.S. Department of Energy DOH. See Department of Health DOJ. See U.S. Department of Justice DOMS. See Director of military support DoS. See Denial of service attack DOS. See U.S. Department of State Dose equivalent, 401 DOT. See U.S. Department of Transportation Doxycyclines, 648, 654–655 DP. See Diphosgenes DPL. See Diagnostic peritoneal lavage DPMUs. See Disaster Portable Morgue Units DRC. See Disaster Research Center Drones, 923 Drug(s) donations current practices of, 240–242, 241b, 241t historical perspectives of, 238–240, 239t introduction to, 238 dumping, 238 investigational new, 98 usage of, 66, 275 Dryvax. See Vaccinia virus DSM-III. See Diagnostic and Statistical Manual of Mental Disorders DTPA. See Diethylenetriamine pentaacetic acid Duke University Hospital, 120, 121t–122t, 275 Dunant, Henry, 305 Durham County, North Carolina, 115 DVA. See U.S. Department of Veterans Affairs DVI. See Disaster victim identification Dysrhythmias, 500

Earthquake(s), 3, 29, 34–35, 56, 102, 117, 141, 239t, 240 Alaska, 79, 183 Athens, 57 description of events during, 479 Hanshin, 57 Indian Ocean, 4 Iran, 141 Loma Prieta, 57, 184, 204, 243, 318 medical treatment of casualties from, 481–482 Northridge, 35, 141, 244, 328, 509 pitfalls of, 482 postincident actions after, 480–481 preincident actions before, 480 San Francisco, 112, 232, 242, 510, 687 Turkey, 102, 103, 230 Earthquake Hazards Act (1977), 336 Earthquake Preparedness Guidelines for Hospitals, 208–209 EAS. See Emergency Alert System East Germany, 544 East Timor, 43 Eastern equine encephalitis (EEE), 661

Ebola fever, 17, 148, 605, 671 EBWs. See Enhanced blast weapons EC. See Environment of Care ECBC. See Edgewood Chemical Biological Center Ecuador, 885 Edema factor (EF), 608 Edgewood Chemical Biological Center (ECBC), 409 EDs. See Emergency departments EEE. See Eastern equine encephalitis EF. See Edema factor Egypt, 27, 608, 668 EIA. See Enzyme immunoassays EIS. See Epidemic Intelligence Service EISOs. See Epidemic Intelligence Service Officers El Niño, 114 Electromagnetic pulse (EMP), 528, 893–894 Eli Lilly, 239 ELISA. See Enzyme-linked immunosorbent assay Elo, Olavi, 232 EM. See Emergency management EM. See Emergency medicine EMAC. See Emergency Management Assistance Compact EMAP. See Emergency Management Accreditation Program EMAs. See Emergency Management Agencies Emergencies, complex (CEs), 102 chronic/smoldering country model and, 44 current practices in, 45–46 definition of, 43 developed/developing country model and, 44 epidemiological models and, 44 evolution of intervention in, 45 food programs and, 46–48, 103 health interventions in, 47 historical perspectives on, 44 major characteristics of, 43–44 medical personnel in, 48 multinational model response in, 45–46 pitfalls of, 49 unilateral model response in, 48–49 Emergency Alert System (EAS), 233 Emergency departments (EDs), 127, 211 assessments/treatments by, 792–793 design of conclusions on, 449 current practices on, 445–448 historical perspectives on, 445 pitfalls of, 448–449 Emergency management (EM). See also Comprehensive emergency management offices, 84 phases of, 317 programs, 407 concepts/principles/systems of, 108–109 domestic preparedness as, 109–110 federal, 109–110 military medical educational resources as, 110 standards for, 110 summary on, 110–111 university, 110 Emergency Management Accreditation Program (EMAP), 110 Emergency Management Agencies (EMAs), 11, 80, 84, 113, 318. See also State Emergency Management Agencies current practices of, 90–92, 91t requests for, 204

Emergency Management Assistance Compact (EMAC), 30, 80, 92, 183, 189, 384 Emergency Management Institute (EMI), 198 Emergency Management Strategic Healthcare Group (EMSHG), 99, 120 Emergency Medical Response Teams (EMRTs), 99 Emergency Medical Services (EMS), 11, 84, 90, 125. See also Tactical Emergency Medical Support current practices of, 22–24, 23t historical perspectives on, 20–22 liability issues regarding, 71 civil legal, 75 historical perspectives on, 72 laws and, 72–74 pitfalls of, 78 regulatory violations as, 74 responders legal obligations of, 75–76 legal protections for, 76–78 state created/enhanced danger doctrines as, 76 local/state, 92 personnel, 161–162, 215 pitfalls of, 24–25 roles of, 20–25, 28, 52, 274 Emergency medical technicians (EMTs), 12, 175, 274–275 Emergency Medical Treatment and Labor Act (EMTALA), 175–176, 202, 288 Emergency medicine (EM). See also Disaster medicine current practices of, 29–30, 30f in disasters/MCIs, 63–69 evolution of, 3, 26–28, 27t future directions for, 31 general concepts/definitions of, 30–31, 31b, 32t historical perspectives on, 26–27 pitfalls of, 31–32, 32b role of, 26–32, 27t Emergency Operations Center (EOC), 38, 38b, 109, 188, 204, 208, 229, 394 Emergency Operations Plan (EOP), 90 Emergency Planning and Community Right to Know Act (EPCRA), 90, 158 Emergency planning zones (EPZs), 114 Emergency preparedness liaison officer (EPLO), 396 Emergency Responder Guidelines, 22, 23t Emergency Responder Injuries and Fatalities, 216 Emergency Responders; Drastically Underfunded, Dangerously Unprepared, 32 Emergency Response Guidebook, 2000, 220, 804 Emergency Support Functions (ESFs), 82, 189 identification of, 99–100 #8 — Public Health and Medical Services, 9 #6 — Mass Care, 185 Emergency System for the Advance Registration of Volunteer Health Professionals (ESAR-VHP), 187, 200 EMI. See Emergency Management Institute EMIT. See Enzyme multiplied immunoassay technique EMP. See Electromagnetic pulse EMRTs. See Emergency Medical Response Teams EMS. See Emergency Medical Services EMSHG. See Emergency Management Strategic Healthcare Group

EMT-paramedic (EMT-P), 175 EMTs. See Emergency medical technicians England, 27, 255, 369, 544 Enhanced blast weapons (EBWs), 761 Enterotoxins, 698 Environment, 10, 14–15 Environment of Care (EC), 110, 186–187 Environmental Protection Agency (EPA), 10, 81, 105 Enzyme immunoassays (EIA), 684 Enzyme multiplied immunoassay technique (EMIT), 587 Enzyme-linked immunosorbent assay (ELISA), 618, 665, 672, 674, 678 EOC. See Emergency Operations Center EOD. See Explosive ordinance disposal EOP. See Emergency Operations Plan EPA. See Environmental Protection Agency EPCRA. See Emergency Planning and Community Right to Know Act Epibatidines, 596 EpiCentre. See European Expert Group in Practical Epidemiology Epidemic Intelligence Service (EIS), 359 Epidemic Intelligence Service Officers (EISOs), 18 Epidemics, 3–4, 44, 46, 68 Epidemiologic Exchange (Epi-X), 97–98 Epidemiology, disaster, 17 applications of, 327–331, 328b, 329b, 330t current practices of, 327–331, 328b, 329b, 330t historical perspectives of, 327 pitfalls of, 330 EPLO. See Emergency preparedness liaison officer EPZs. See Emergency planning zones Eritrea, 239 ESAR-VHP. See Emergency System for the Advance Registration of Volunteer Health Professionals Escherichia coli, 149, 486, 490, 507, 605 O157-H7 (hemorrhagic E. coli) attacks case presentation for, 659 considerations for, 659 description of events during, 657–658, 658t medical treatment of casualties from, 659 postincident actions after, 658–659 preincident actions before, 658 ESF-8. See Emergency Support Functions Ethiopia, 47, 239t, 549 Ethylenediamine tetraacetic acid, 542 European Expert Group in Practical Epidemiology (EpiCentre), 46 European Society of Emergency Medicine (EuSEM), 64 European Union Commission on Preparedness and Response to Biological and Chemical Agent Attacks, 648 Evacuations, 175 Evidence Response Teams, 394 Expeditionary Medical Support, 100, 396 Explosions. See also Blasts; Improvised explosive devices conventional case presentation for, 747 considerations for, 747 description of events during, 745 medical treatment of casualties from, 746–747 pitfalls of, 748 postincident actions after, 745–746 preincident actions before, 745

Explosions. See also Blasts; Improvised explosive devices (Continued ) fireworks case presentation for, 751 considerations for, 751–752 description of events during, 749 medical treatment of casualties from, 750–751 pitfalls of, 752 postincident actions after, 749–750 preincident actions before, 749 high-rise building case presentation for, 772 considerations for, 772 description of events during, 770 medical treatment of casualties from, 771–772 pitfalls of, 772 postincident actions after, 771 preincident actions before, 770–771 hospital case presentation for, 768 considerations for, 768–769 description of events during, 767 medical treatment of casualties from pitfalls of, 769 postincident actions after, 767–768 preincident actions before, 767, 768t liquefied natural gas case presentation for, 782 considerations for, 782 description of events during, 781 medical treatment of casualties from, 782 pitfalls of, 782 postincident actions after, 782 preincident actions before, 781–782 at mass gatherings case presentation for, 765 considerations for, 765–766 description of events during, 764 medical treatment of casualties from, 765 pitfalls of, 766 postincident actions after, 765 preincident actions before, 764–765 nuclear power plant case presentation for, 776 considerations for, 777 description of events during, 774 medical treatment of casualties from, 775–776, 776t pitfalls of, 777 postincident actions after, 775 preincident actions before, 774–775 at nuclear waste storage facilities case presentation for, 876 considerations for, 876–877 description of events during, 875 medical treatment of casualties from, 876, 876t pitfalls of, 877 postincident actions after, 875–876 preincident actions before, 875 petroleum distillation/processing facility case presentation for, 789 considerations for, 789 description of events during, 786–787 hazards from, 787, 788t medical treatment of casualties from, 787–789 pitfalls of, 789 postincident actions after, 787 preincident actions before, 787 tunnel INDEX 937

Explosions. See also Blasts; Improvised explosive devices (Continued ) case presentation for, 780 considerations for, 780 description of events during, 778 medical treatment of casualties from, 779–780 pitfalls of, 780 postincident actions after preincident actions before, 778–779 Explosive ordinance disposal (EOD), 412 Explosives, 736 Exposure management, 13 External irradiation, 520 Exxon Valdez oil tanker spill, 317, 878 Eye wear, 217–218

FAA. See Federal Aviation Administration Fairfax County Virginia International Search and Rescue Team 1, 103 Family Assistance Core Group, 96 Famines, 26 case presentation for, 508 considerations for, 508 description of events during, 506 medical treatment of casualties from, 507–508 pitfalls of, 508 postincident actions after, 507 preincident actions before, 507 FAO. See Food and Agriculture Organization FARC. See Revolutionary Armed Forces of Columbia FAST. See Focused abdominal sonography for trauma FBI. See Federal Bureau of Investigation FCC. See Federal Communications Commission FCDA. See Federal Civil Defense Administration FDA. See U.S. Food and Drug Administration Federal Aviation Administration (FAA), 233–234, 325 Federal Bureau of Investigation (FBI), 10, 71, 84, 339, 392 Hostage Rescue Team, 885 Federal Civil Defense Act (1950), 112, 393 Federal Civil Defense Administration (FCDA), 112 Federal Communications Commission (FCC), 233 Federal coordinating centers, 37, 96 Federal coordinating officer (FCO), 396 Federal Disaster Act (1950), 112–113 Federal Disaster Assistance Administration, 29, 183 Federal Emergency Management Agency (FEMA), 9, 22, 876 assistance programs by, 318–319 authority of, 13, 336 creation of, 80, 90, 113, 229, 233 drills, 13 Higher Education Project, 110 Mobile Operations Division, 206, 206b Mutual Aid Agreements for Public Assistance, 186 roles of, 28–29, 71, 82, 95, 125, 131, 183–184, 318 Federal Emergency Medical Treatment Active Labor Act, 845 Federal Insurance Administration, 29, 114 Federal Medical Contingency Stations, 187 Federal Occupational Health, 98 938 INDEX

Federal Radiological Emergency Response Plan (FRERP), 9, 80, 319, 528 Federal Register, 178 Federal Response Plan (FRP), 9, 80, 92, 269 for a Catastrophic Earthquake, 336 Federal Tort Claims Act (FTCA), 77 FEMA. See Federal Emergency Management Agency Fentanyl, 429, 589–590, 590t Fermi, Enrico, 520 Ferrofluids, 430 FEST. See Foreign Emergency Support Team FFP. See Food For Peace Program Field evaluation teams (FETs), 175–176 Field Management of Chemical and Biological Casualties Courses, 409 File repositories (FTP sites), 130 Filo virus. See Viral hemorrhagic fevers Fire Department of New York, 21 Firedamp, 853 Fires, 34 current practices for, 790–793, 791b forest/wilderness case presentation for, 802 considerations for, 802 description of events during, 800 medical treatment of casualties from, 801–802, 801t pitfalls of, 802 postincident actions after, 801 preincident actions before, 800–801 pitfalls of, 793–794 structural case presentation for, 798 considerations for, 798 description of events during, 796 medical treatment of casualties from, 797–798 pitfalls of, 798 postincident actions after, 797 preincident actions before, 796–797 summary on, 794 tunnel case presentation for, 805 considerations for, 805 description of events during, 803–804 medical treatment of casualties from, 805 pitfalls of, 805–806 postincident actions after, 805 preincident actions before, 804–805 unique considerations for, 793, 793t FIRESCOPE (Firefighting Resources Organized for Potential Emergencies), 30, 79, 208, 336 Fireworks case presentation for, 751 considerations for, 751–752 description of events during, 749 medical treatment of casualties from, 750–751 pitfalls of, 752 postincident actions after, 749–750 preincident actions before, 749 Flash blindness, 402 Flashbacks, 59–60 Flashovers, 160 Flexner Report, 274 Flood Control Act (1936), 112, 203 Floods, 12, 26, 34–35, 99, 114, 265, 318, 475 case presentation for, 491 considerations for, 490 description of events during, 489 hazards maps, 489 medical treatment of casualties from, 490

Floods (Continued ) pitfalls of, 490–491 postincident actions after, 489–490 preincident actions before, 489 Florida, 11, 26, 244, 324, 369, 384–385, 661 Florida Hospital Ormond Memorial, 384–385 Fluconazole, 535 Fluoroquinolone, 535 Focused abdominal sonography for trauma (FAST), 861–862 Food(s) displaced populations and, 314, 315, 315t programs, 46–48, 103 protection of, 10, 457 ready-to-use therapeutic, 508 safety threats, 10, 149 services, 40 storage of, 15 supply contamination case presentation for, 910 considerations for, 910 description of events during, 908–909 medical treatment of casualties from, 910 pitfalls of, 910 postincident actions after, 910 preincident actions before, 909–910 tampering, 722 Food and Agriculture Organization (FAO), 105 Food For Peace Program (FFP), 103 Food Safety Inspection Service (FSIS), 10 Foreign Emergency Support Team (FEST), 104 Fort McHenry Tunnel, 803–804 France, 778 Francisella tularensis (tularemia), 17, 145, 147, 360, 421, 425 attacks case presentation for, 620 considerations for, 619 description of events during, 617–618 medical treatment of casualties from, 619 pitfalls of, 619–620 postincident actions after, 618–619 preincident actions before, 618 French Polynesia, 493 FRERP. See Federal Radiological Emergency Response Plan Frisch, O.R., 520 Frostbites, 15, 499 FRP. See Federal Response Plan FSIS. See Food Safety Inspection Service FTCA. See Federal Tort Claims Act FTP sites. See File repositories Fujita-Pearson Tornado Scale, 484, 484t Fullerenes, 430

Galeras Volcano, 505 Gamma rays, 518, 524, 775 GAO. See General Accounting Office Gas chromatography/mass spectrometry (GCMS), 411 Gastroenteritis, 18, 53 Gastrointestinal syndrome, 520–522 Gastrointestinal tract (GI), 597, 715, 882 GCMS. See Gas chromatography/mass spectrometry GCS. See Glasgow Coma Scale Geiger counters, 466, 545 Gene therapies, 431 General Accounting Office (GAO), 335 General Services Administration (GSA), 29

Geneva Conventions, 45, 48, 63, 305 Geneva Protocol, 145, 549 Genocides, 43, 102 Genomics, 431 Geographical Resource Intranet Portal, 847 Georgia, 490, 661 Georgia (Russia), 239 Geospatial information systems (GIS), 131, 258 Gephardt, Dick, 125 Germany, 193, 255, 317–318, 430, 520, 548–549 GI. See Gastrointestinal tract Gilmore Report, 339, 343 GIS. See Geospatial information systems Giuffrida, Louis, 113 Glanders. See Burkholderia mallei Glasgow Coma Scale (GCS), 285, 756, 827 Global Alliance for Vaccines and Immunization, 304 Global Patient Movement Requirements Center (GPMRC), 96 Global Positioning System (GPS), 134, 879 Gorgas,William, 303 Government Accountability Office, 339, 343 GPMRC. See Global Patient Movement Requirements Center GPS. See Global Positioning System Grady Memorial Hospital, 284 Graniteville, South Carolina, 9 Great Britain, 102, 283, 647 Great Depression, 318 Great Fire of 1666 (London), 27 Great Plague, 605 Greater New York Hospital Association, 32 Greece, 302 Grenade attacks case presentation for, 815 clinical presentation of, 814 considerations for, 815 description of events during, 813–814 medical treatment of casualties from, 814–815 pitfalls of, 815 postincident actions after, 814 preincident actions before, 814 Group cohesion, 889 Group special mobile (GSM), 134 GSA. See General Services Administration GSM. See Group special mobile Guam, 23, 104, 318 Guarnieri bodies, 681 Guatemala, 327 Guide for the Selection of Personal Protective Equipment for Emergency First Responders, 16 Guide to Ship Sanitation, 883 Guiliani, Rudy, 126 Guillain-Barré syndrome, 149 Gunpowder, 749 Gunshot attacks/mass casualties case presentation for, 808 considerations for, 808–809 description of events during, 807 medical treatment of casualties from, 808 pitfalls of, 809 postincident actions after, 807–808 preincident actions before, 807

HA. See Humanitarian assistance HAART. See Highly active antiretroviral therapy HACC. See Humanitarian Assistance Coordination Center

Hahn, Otto, 520 Haiti, 26, 44, 46, 239t, 372 Hallucinations, 582 Halothane (C2HBrCIF3), 602 Hamburg, 317–318 HANs. See Health Alert Networks Hantavirus, 98, 148–149, 360 pulmonary syndrome attacks case presentation for, 692 considerations for, 691–692 description of events during, 690–691 medical treatment of casualties from, 691 pitfalls of, 691 postincident actions after, 691 preincident actions before, 691 Harris, Eric, 808 Hart Senate Office, 425 Harvey, John, 549 Hawaii, 509 Hazard(s), 474 definition of, 253 identification, 113–114, 114b impact/risks of, 119 probability of, 119–120, 120f profiling, 114–115 Hazard vulnerability assessment (HVA), 24–25, 29, 37, 117, 550 community conclusions on, 115–116 current practices of, 113–115, 114b historical perspectives on, 112–113 PPE and, 247 team membership, 113 Hazardous materials (HazMat), 11, 36, 87, 90, 204, 548 behavior, 279 definitions, 551b disaster responses/scene safety and, 217 incidents, 247–248, 278 conclusions on, 282 current practices on, 280–281 danger of, 279 historical perspectives, 279–280 occurrence of, 278 pitfalls of, 282 physiology/treatments for, 281 releases, 252 risks, 576 Hazardous Materials Response Teams, 394, 406 Hazardous Materials Response Unit (HMRU), 394 Hazardous Substances Emergency Events Surveillance (HSEES), 248, 550 Hazards Center. See National Hazards Research and Information Applications Center HazMat. See Hazardous materials HAZWOPER (hazardous waste operations and emergency response), 157, 252, 408 HCW. See Healthcare workers HDR. See Human daily rations Health assessments, 46–47 departments, 11, 14 interventions, 47 professionals, 10 reproductive, 44 service supports, 363–368, 366t Health Alert Networks (HANs), 97, 230 Health Disaster Management Guidelines for Evaluation and Research in the Ulstein Style, 473 Health information systems, 47

Health Insurance Portability and Accountability Act (HIPAA), 291 Health Resources and Services Administration (HRSA), 98, 109, 143, 187, 324, 409 Healthcare, 10 optimal, 65 practitioners/providers, 13, 52 remote areas and current practices of, 274–275, 276f historical perspectives on, 274 pitfalls, 275–276 summary on, 276–277 sources of, 46 systems, 12–13, 46–47 Healthcare facility (HCF) conclusions on, 122–123 current practices of, 118–122, 120f, 121t–122t historical perspectives on, 117–118, 118b pitfalls of, 122 Healthcare Sector Coordinating Council, 154 Healthcare workers (HCW), 176 Heat stroke, 15 waves case presentation for, 497 considerations for, 497, 497t description of events during, 496, 497f medical treatment of casualties from, 496–497 pitfalls of, 497–498 postincident actions after, 496 preincident actions before, 496 Heat index (HI), 496 HEAT. See Hospital Emergency Analysis Tool Heating-ventilation-air conditioning systems (HVAC), 38–39 HEICS. See Hospital Emergency Incident Command System Height-for-age (HFA), 54 Hemagglutinin, 426 Hematopoietic syndrome, 520 Hemolytic uremic syndrome (HUS), 657–658 Hemorrhagic E. coli. See Escherichia coli Hemorrhagic fevers. See Viral hemorrhagic fevers Hendra virus, 427 attacks case presentation for, 694 considerations for, 694 description of events during, 693 medical treatment of casualties from, 694 pitfalls of, 694 postincident actions after, 693–694 preincident actions before, 693 HEPA. See High-efficiency particulate Hepatitis A, 15, 53, 490 acute, 723 Herbicides, 549. See also Pesticides Herzegovina, 102, 238, 240, 310 HEU. See Uranium, highly enriched Heydrich, Reinhard, 424 HFA. See Height-for-age HI. See Heat index High-efficiency particulate (HEPA), 251, 672 Highly active antiretroviral therapy (HAART), 735 Highway Safety Act of 1966, 21 Hindenburg disaster, 232 HIPAA. See Health Insurance Portability and Accountability Act Hippocratic oath, 63 Hiroshima, 375, 399–400, 520, 528 INDEX 939

HIS. See Humanitarian information systems Hiscox Group, 885 Histoplasma capsulatum (histoplasmosis) attacks case presentation for, 730 considerations for, 730 description of events during, 729–730 medical treatment of casualties from, 730 pitfalls of, 730 postincident actions after, 730 preincident actions before, 730 HIV/AIDS, 44, 47, 56–57, 239, 242, 304 HMRU. See Hazardous Materials Response Unit Hoffman,Albert, 585 Holarctica (Type B), 617 Holland Tunnel, 804 Homeland Security Act of 2002, 11, 22, 29, 77, 81, 177, 309, 339 Homeland Security Council, 22 Homeland Security Exercise and Evaluation Program, 24 Homeland Security Presidential Directives, 80 −5 (HSPD), 9, 29, 82, 142, 309, 336, 364, 407 −3 (HSPD), 344–345 Honduras, 52 Hong Kong, 13, 179, 427, 510, 684 Hospital(s), 29–30, 384 capacity of, 34, 35t casualty distributions among, 40 conclusion on, 41 current practices of, 36 disaster preparedness of crime scene/evidence management during, 39–40 critical elements in, 38–40, 38b physical security in, 39 risk communications/media management during, 39 staff notification during, 39 disasters’ effect on, 34–35 evolving perspectives on, 35–36 explosions case presentation for, 768 considerations for, 768–769 description of events during, 767 medical treatment of casualties from pitfalls of, 769 postincident actions after, 767–768 preincident actions before, 767, 768t as first responders, 142–143 introduction to, 34 mass fatalities and, 40 mutual aid and, 186–188 organizations, 92 patients in admission/identification/tracking in, 40 emergency decontamination of, 40 personal protective equipment for, 40 pitfalls of, 40–41 planned innovation for, 41 power outages at case presentation for, 900 considerations for, 900 description of events during, 897 medical treatment of casualties from, 899–900 pitfalls of, 900 postincident actions after, 899 preincident actions before, 897–899 preparedness of critical elements in, 36–37 federal role in emergency, 37–38 philosophy, 37 940 INDEX

Hospital(s) (Continued ) public expectations of, 36 radiation decontamination in, 466–467 role of, 34–41 state, 92 surge capacity of, 36, 345 vulnerability of, 36 Hospital Council of Northern California, 208–209 Hospital Disaster Support Communications System, 231 Hospital Emergency Analysis Tool (HEAT), 37 Hospital Emergency Incident Command System (HEICS), 32, 38, 109, 188, 209, 212 ICS and, 212, 213f, 407 Hostage taking case presentation for, 887 considerations for, 887 description of events during, 885–886 medical treatment of casualties from, 887 pitfalls of, 888 postincident actions after, 886–887 preincident actions before, 886 Hot zones, 885 Housing and Urban Development, 29 HRSA. See Health Resources and Services Administration HSEES. See Hazardous Substances Emergency Events Surveillance HSPD. See Homeland Security Presidential Directives HUD. See U.S. Department of Housing and Urban Development Human daily rations (HDR), 106–107 Human Genome Diversity Project, 431 Human Genome Project, 431 Human stampedes case presentation for, 851 considerations for, 851–852 description of events during, 850–851 medical treatment of casualties from, 851 pitfalls of, 852 postincident actions after, 851 preincident actions before, 851 Humanitarian assistance (HA), 102 Humanitarian Assistance Coordination Center (HACC), 104 Humanitarian Charter and Minimum Standards (SPHERE Project), 47, 106, 170, 172 Humanitarian information systems (HIS), 136 Hungary, 722 Hurricane(s), 3, 11–12, 26, 29, 34 Andrew, 26, 57, 204, 216, 218, 264, 336, 388, 475, 477 Betsy, 79 Camille, 79 case presentation for, 478 Charley, 329, 385, 386 considerations for, 477 description of events during, 475, 476t Floyd, 57, 175, 264, 490 Frances, 385 Georges, 335 Gilbert, 318, 320 Gloria, 184 Hugo, 204, 320 Katrina, 26, 34, 490, 901 medical treatment of casualties from, 477 Mitch, 171, 303, 335, 475 pitfalls of, 477–478 postincident actions after, 477 preincident actions before, 476–477 HUS. See Hemolytic uremic syndrome

Hussein, Saddam, 428 HVA. See Hazard vulnerability assessment HVAC. See Heating-ventilation-air conditioning systems Hyalomma marginatum, 668 Hydrofluoric acid, 787–789 Hydrogen bomb, 399 fluoride, 503 Hydrogen cyanide (AC), 576, 580 Hydroxocobalamin, 578 Hyperarousal, 60 Hyperinflation, 317 Hyperkalemia, 817, 818 Hypertension, 598 Hypothermia, 15, 499–500, 515 Hypoxia, 515

IAPs. See Incident action plans IC. See Incident commander ICPs. See Incident command posts ICRC. See International Committee of the Red Cross ICS. See Incident Command System IDE. See Investigational device exemption ID-ME (immediate, delayed, minimal, expectant), 39 IDNDR. See International Decade of Natural Disaster Reduction IDPs. See Internally displaced persons IEMS. See Integrated Emergency Management System IFRC. See International Federation of the Red Cross IHS. See Indian Health Service IMA. See Israeli Medical Association IMARSAT (satellite phone service), 134 Imipenem, 648, 651 Immunizations, 145–146 Imo, 737 IMO. See International Maritime Organization Implosions, 737 Improvised explosive devices (IEDs), 410. See also Vehicle-borne improvised explosive devices conclusions on, 440 current practices for, 435–437, 436f historical perspectives on, 434–435, 435f pitfalls of, 438–440 victims of, 437–438 Improvised nuclear devices (INDs), 395, 400, 402 IMSuRT. See International Medical and Surgical Response Team Incidence, 330 Incident action plans (IAPs), 204, 211–212 Incident command posts (ICPs), 188 Incident Command System (ICS), 20, 21, 23–24, 30, 32, 413 administration/finance sections of, 211, 211b command functions of, 209, 210b concepts/principles of, 211–212, 211b current practices of, 209, 209f, 244 definitions of, 29 development of, 79, 108–109, 215, 336 HEICS and, 212, 213f historical perspectives on, 208–209 logistics sections of, 210, 210b operations sections of, 210 planning sections of, 210, 210f principles of, 188 summary on, 212–214 utilization of, 71–72, 124

Incident commander (IC), 230 Incident Management System/unified command structure (EM/UC), 382 “Incident of National Significance,” 9 Incident safety officers (ISOs), 215, 217–218 India, 9, 35, 102, 239, 371, 475, 556, 885 Indian Health Service (IHS), 98 Indian Ocean, 4, 270, 284 Indiana, 264 Indicators, 328 Indoles, 585 Indonesia, 9, 492 INDs. See Improvised nuclear devices INF-a. See Interferon-alpha Infants, malnutrition amongst, 44 Influenza, 370. See also Severe acute respiratory syndrome avian, 426 human, 426 pandemic (1917-1918), 26, 284 statistics, 354 virus attacks case presentation for, 685 considerations for, 685 description of events during, 684 medical treatment of casualties from, 685 pitfalls of, 685 postincident actions after, 685 preincident actions before, 684–685 Information technology (IT), 344, 411 INSARAG. See International Search and Rescue Advisory Group Integrated Emergency Management System (IEMS), 108, 113 Intelligence Hazard Mitigation Team, 318 Interagency OPSEC Support Staff (IOSS), 120, 122 Interferon-alpha (INF-a), 672 Interim Smallpox Response Plan and Guidelines, 145 Internally displaced persons (IDPs), 103, 313 International Centre for Diarrheal Diseases Research, 305 International City Management Association, 29 International Committee of the Red Cross (ICRC), 45, 105, 292, 305 International Council of Cruise Lines, 883 International Decade of Natural Disaster Reduction (IDNDR), 165, 232 International Dispensaries Association, 241–242 International Federation of the Red Cross (IFRC), 105, 106, 327 International Maritime Organization (IMO), 878 International Medical and Surgical Response Team (IMSuRT), 22, 104 International Partnership Against AIDS in Africa, 304 International Red Cross (ICRC), 64 International relief organizations (IROs), 45–46, 49 International Rescue Committee (IRC), 105 International Search and Rescue Advisory Group (INSARAG), 105 Internet, 130 Interpol (International Criminal Police Organization), 261 Interventions, 482 Investigational device exemption (IDE), 98 Iodine, 876 IOSS. See Interagency OPSEC Support Staff Iowa, 292 IRA. See Irish Republican Army

Iran, 102, 103, 141, 304, 430 Iran-Iraq War, 428, 570 Iraq, 48, 49, 424–425, 428–430, 668, 722. See also Kurds IRC. See International Rescue Committee Ireland, 377, 434 Irish Republican Army (IRA), 389 IROs. See International relief organizations ISAC (Informational Sharing and Coordination), 154 Ishii, Shiro, 424 Isolation, 150, 447–448, 452 ISOs. See Incident safety officers Isotopic dilution, 541 Israel, 64, 65, 324, 435 Israel Center for Medical Simulation, 324 Israeli Army Medical Corps, 65 Israeli Maccabiah Games, 847 Israeli Medical Association (IMA), 64 Israeli National EMS, 65 IT. See Information technology Italy, 548–549 Itraconazole, 731 Ixodes persulcatus, 663

Jamaica, 318, 320 Japan, 46, 239, 303, 375, 492, 520, 549–550 Japan Disaster Relief Medical Team, 303 Japan International Cooperation Agency (JICA), 46 Japan Meteorological Agency, 493 JDOMS. See Joint Director of Military Support Jenner, Edward, 147 Jerusalem Sbarro bombing, 284, 288 JFO. See Joint Field Office JICA. See Japan International Cooperation Agency JOC. See Joint Operations Command Johannesburg World Summit on Sustainable Development, 165, 166 Joint Chiefs of Staff, 100 Joint Commission on Accreditation of Healthcare Organizations (JCAHO), 29, 117, 215 requirements of, 37, 186–187 standards, 30, 31–32, 31b, 32t, 110 Joint Director of Military Support (JDOMS), 100 Joint Field Office (JFO), 82, 394 Joint Operations Command (JOC), 188, 392 Joint Task Force (JTF), 104 Joint Task Force-Civil Support (JTF-CS), 10, 100, 396 Joint Task Force-Consequence Management (JTF-CM), 100 Joint Terrorism Task Force (JTTF), 392–393 Jonestown, Guyana, 578 Jordan, 430 JTF. See Joint Task Force JTF-CM. See Joint Task Force-Consequence Management JTF-CS. See Joint Task Force-Civil Support Judges, 73 Junin fever, 17, 148, 667 Juries, 73–74

Kahn, A.Q., 518 Kansas, 484 Kazakhstan, 617 Kennedy, John Fitzgerald, 124, 233 Kentucky, 265

Kenya, 103, 104, 305, 376, 722 Kerry, John, 125 Kiebold, Dylan, 808 Kilotons (KT), 528 King, Rodney, 889, 891 Klebsiella, 486 Koch, Robert, 304, 608 Korea, 20–21, 27, 134, 668 Korean Airlines, 134 Korean War, 20–21, 27 Kosovo, 43, 44, 106, 241 KT. See Kilotons Kuala Lumpur, 887 Kurds, 43, 53, 722 Kuwaiti oil fields, 918 Kyasanur Forest disease, 676

La Conchita, California, 9 Laboratory Response Network (LRN), 97, 304, 618, 719 Lactate dehydrogenase, 696 Laden, Osama bin, 400 Laerdal SimMan model, 323 LAFD. See Los Angeles Fire Department Lahars, 503 LAIV. See Vaccine, live-attenuated coldadapted Lake Monoun, 503 Lake Nyos, 503 LAN. See Local area network Landslides, 34, 318 case presentation for, 512 considerations/pitfalls of, 511b, 512–513 description of events during, 509, 510f medical treatment of casualties from, 512 postincident actions after, 511–512, 511b preincident actions before, 510, 511f Laos, 424 Lapilli, 502 Larry, Dominique-Jean, 20, 27 Laser(s), 441 eye injuries, 442–443, 443f skin burns, 443 Lassa fever, 17, 148, 665 Law enforcement, 10 current practices of, 393–396, 394f, 395f historical perspectives on, 391–393 pitfalls of, 396–397 Lead federal agencies (LFAs), 100 Leahy,Thomas, 596 Lebanon, 354, 377, 434–435 Legionella pneumophila, 882–884 LEPC. See Local Emergency Planning Committees Leprosy, 452 Leptotrombidium, 629 LET. See Linear energy transfer Letgers, Llewellyn, 354 Lethal factor (LF), 608 Letterman, Jonathan, 297, 354 Leviticus, 452 Levofloxacins, 883 Lewinsky, Monica, 128 Lewisite (L), 569 LF. See Lethal factor LFAs. See Lead federal agencies Liberia, 43, 47 Life support programs, 21 Linear energy transfer (LET), 518 Liquefied natural gas explosions case presentation for, 782 considerations for, 782 description of events during, 781 INDEX 941

Liquefied natural gas explosions (Continued ) medical treatment of casualties from, 782 pitfalls of, 782 postincident actions after, 782 preincident actions before, 781–782 Lithuania, 239, 310 Live-attenuated vaccine strain (LVS), 618 Llewellyn, Craig, 354 Local area network (LAN), 133 Local Emergency Planning Committees (LEPCs) activities of, 20, 85, 91, 113, 119, 152, 154–155, 407 development of, 184, 189 London Bombings (July, 2005), 14 Los Angeles Fire Department (LAFD), 198 LRN. See Laboratory Response Network LSD. See D-lysergic acid diethylamide LVS. See Live-attenuated vaccine strain

MAC. See Mean alveolar concentration MACA. See Military assistance to civil affairs Macedonia, 44 Machupo virus, 667 MacIntyre,Anthony, 207 Madrid train bombings, 3, 374 Magen David Adom (MDA), 64–65 Magnesium, 752 MaHIM. See Medical and Health Incident Management Malaria, 44, 47, 242, 303–304 Malaysia, 492 Malnutrition amongst children/infants, 44, 54–55, 507 global acute, 331 protein, 47–48 Malvo, Lee Boyd, 389, 811 Management support units (MSUs), 96 Manchester International Airport, 829 Manhattan Project, 399 MAOIs. See Monoamine oxidase inhibitors Marathons, 914–915 Marburg fever, 17, 148, 671 Marconi, Signor, 124 Marine Expeditionary Brigade (MEB), 396 Marine Hospital Service. See U.S. Public Health Service Marine toxin attacks clinical features of, 711, 712, 712t introduction to, 710 pitfalls of, 712 Maritime disasters case presentation for, 880 considerations for, 880 description of events during, 878 medical treatment of casualties from, 879 pitfalls of, 880–881 postincident actions after, 879 preincident actions before, 878–879 Maryland, 324 MASS (move, assess, sort, and send), 39 Mass Care Emergency Support Function, 100 Mass casualties, gunshot attacks/ case presentation for, 808 considerations for, 808–809 description of events during, 807 medical treatment of casualties from, 808 pitfalls of, 809 postincident actions after, 807–808 preincident actions before, 807 Mass casualty incidents (MCIs), 284, 864–865 942 INDEX

Mass fatalities conclusions on, 263 current practices for, 260–261, 261b, 262f historical perspectives of, 260 incidents, 260 pitfalls of, 261–263 Mass gatherings case presentation for, 916 considerations for, 916 description of events during, 912, 913t explosions at case presentation for, 765 considerations for, 765–766 description of events during, 764 medical treatment of casualties from, 765 pitfalls of, 766 postincident actions after, 765 preincident actions before, 764–765 medical treatment of casualties at, 915–916 pitfalls of, 916 postincident actions after, 915 preincident actions before, 912–915, 913b, 914t Massachusetts, 12, 35, 661, 850 Material safety data sheets (MSDS), 130 Maternal and Child Health (MCH), 508 MCH. See Maternal and Child Health MCIs. See Mass casualty incidents MDA. See Magen David Adom Mean alveolar concentration (MAC), 601 Mean upper arm circumference (MUAC), 506 Measles, 7, 44, 56 Measures of effectiveness (MOEs) current practices for, 333–334, 334f historical perspectives on, 333 pitfalls of, 334 MEB. See Marine Expeditionary Brigade Media. See also Public information management communications, 127 formats, 234 local/national, 234–235 management, 39 relations current practices of, 233–236 historical perspectives on, 232 pitfalls of, 236 reports, 127 Mediasiatica, 617 Medical and Health Incident Management (MaHIM), 207, 407 Medical Emergency Radiological Response Team (MERRT), 99, 541 Medical intelligence current practices of, 355–360, 356t, 357t–358t, 359t definition of, 354 historical perspectives of, 354–355 pitfalls of, 360 Medical Management of Chemical/Biological Casualties, 409 Medical Management of Radiation Accidents, 403 Medical Management of Radiological Casualties: Handbook, 533, 536 Medical Research Institute for Chemical Defense (USAMRICD), 100 Medical Reserve Corps (MRC), 86, 184, 199 Medical screening examination (MSE), 176 Medical Severity Index of Disasters, 117 Medical Simulation Initiative, 324

Medical supplies, 308 current practices of, 309–310, 309t historical perspectives on, 309 pitfalls of, 310 summary on, 311 Medical Threat Assessment (MTA), 298, 890 Medical usage rate, 764 Medications, 10 Médicins sans Frontières [Doctors without Borders] (MSF), 105, 239–240, 302, 305 Meitner, Lisa, 520 Melioidosis. See Burkholderia pseudomallei Memoranda of Agreements (MOAs), 461 Memoranda of understandings (MOUs), 8, 196, 461 MEMS. See Modular Emergency Medical System Mental health, 10 disaster, 39 early intervention in, 16 problems, 15 public health and, 15–16, 15b Merck’s Mectizan Donation Program, 239 Meropenem, 648, 651 MERRT. See Medical Emergency Radiological Response Team MERS. See Mobile Emergency Response Support Mesa Redonda shopping explosion, 749–751 Mescalines, 585–586 Meselson, Matthew, 425 Meta-theoretical notion, 348 Methyl isocyanate (MIC), 560 METI HPS model, 323 Metropolitan Medical Response System (MMRS), 30, 85–86, 86t, 95–96, 109, 188–189, 199, 201 METTAG system, 292 Mexico, 98, 103, 239t, 556 MFF. See Mobile field force MIC. See Methyl isocyanate Michigan, 12, 372 Microimmunofluorescence (MIF), 654 Micronarization, 430 Microwave-radiation emitters, 442 Middle East, 668 Military biologic/chemical weapons and, 429 current practices of, 393–396, 394f, 395f historical perspectives on, 391–393 pitfalls of, 396–397 Military assistance to civil affairs (MACA), 395 Military Claims Act, 77 Military Support to Civil Authorities (MSCA), 100 Mining accidents case presentation for, 856 considerations for, 855 description of events during, 853–854 medical treatment of casualties from, 855 pitfalls of, 855 postincident actions after, 854–855 preincident actions before, 854 Minnesota, 900 Mitigation, 7, 22, 29, 108 concept/goals of, 139–140 conclusions on, 143 current practices of, 141–143, 142b definition of, 139, 317 historical perspectives on, 140–141 pitfalls of, 143 Mitnick, Kevin, 922 MKA. See Modified vaccinia virus Ankara MMRS. See Metropolitan Medical Response System

MMWR. See Mortality and Morbidity Weekly Report MOAs. See Memoranda of Agreements Mobile Air Transportable Telecommunications, 206 Mobile Emergency Response Support (MERS), 206, 231 Mobile field force (MFF), 890 Mobile Medical Monitor (M3), 294 Model Intrastate Mutual Aid Legislation, 189 Model State Emergency Health Powers Act (MSEHPA), 64, 93 A Model for Smallpox Vaccination Policy, 178 Modified vaccinia virus Ankara (MKA), 147 Modular Emergency Medical System (MEMS), 187, 197 Modular Emergency Medical System: Concept of Operations for the Acute Care Center, 187, 197 MOEs. See Measures of effectiveness Mohammed, Khalid Sheikh, 377 Molluscum contagiosum, 687 Monkeypox attacks case presentation for, 689 considerations for, 688 description of events during, 687–688 medical treatment of casualties from, 688 pitfalls of, 688 postincident actions after, 688 preincident actions before, 688 Monoamine oxidase inhibitors (MAOIs), 60, 60t Mont Blanc, 737 Morbidity-incidence rates, 46 Morgan, John, 283 Morrison, Herb, 232 Mortality. See also Mass fatalities amongst children, 52, 53–54, 506 excess, 331 rates, 46, 256 from blasts/explosions, 737–738 crude, 256, 329–330, 506 under-age-5, 330 Mortality and Morbidity Weekly Report (MMWR), 46, 97, 429 Moscow Theater siege, 385 Mosquitos, 15, 661, 678 Mount St. Helens, 224, 503, 509 Mountbatten, Lord, 377 MOUs. See Memoranda of understandings Mozambique, 47, 53, 303 MRC. See Medical Reserve Corps MSCA. See Military Support to Civil Authorities MSDS. See Material safety data sheets MSE. See Medical screening examination MSEHPA. See Model State Emergency Health Powers Act MSF. See Medicins sans Frontieres [Doctors without Borders] MSUs. See Management support units MTA. See Medical Threat Assessment M3. See Mobile Medical Monitor MUAC. See Mean upper arm circumference Mudslides. See Landslides Muhammad, John Allen, 389, 811 Multiple casualty incidents (MCIs) basic principles for, 64, 203 conclusions on, 69 current practices during, 66–68 definition of, 65 ethical issues and, 65–68 historical perspectives on, 63 medical organizations and, 64–65

Multiple casualty incidents (MCIs) (Continued ) pitfalls of, 68–69 solutions for, 69 triages during, 66–67 Multi-Tag system, 292 Multitank Ascania, 878 Murrah Federal Building, 34, 35, 80, 127–128, 215, 218, 243–244, 246, 387, 738, 759, 770 Mutual aid, 30 concept, 182 current practices for, 184–190 federal assets for, 189–190 historical perspectives on, 183–184 hospitals and, 186–188 local community assets for, 184–188 operational pitfalls for, 190 planning concerns for, 183 state assets for, 188–189 summary on, 190–191 Mycotoxins, 723 Myoglobins, 817 Myrothecium riridum, 714 Myrothecium verrucaria, 714

N-acetylcysteine (NAC), 723 NAEMSP. See National Association of EMS Physicians Nagasaki, 399–400, 520 Nairobi, 376, 759 Nalmefenes, 590 Nanoshells, 430 Nanotechnology, 430 NASA. See National Aeronautics and Space Administration NASCAR. See National Association for Stock Car Auto Racing National Academies’ Board on Agriculture and Natural Resources, 264 National Academy of Sciences-National Research Council (NAS-NRC), 21, 27 National Aeronautics and Space Administration (NASA), 838–840 National Association for Stock Car Auto Racing (NASCAR), 912 National Association of EMS Physicians (NAEMSP), 297, 912 National Basketball League (NBA), 912 National Capital Region Mutual Aid Act, 186 National Cemetery System, 99 National Center for PTSD, 16 National Childhood Vaccine Injury Act, 146 National Collegiate Athletic Association (NCAA), 912 National Commission on Terrorist Attacks (9-11 Commission), 31, 110 National Contingency Plan. See National Oil and Hazardous Substances Pollution Contingency Plan National Council on Radiation Protection and Measurements (NCRP), 532–533, 538, 542–543 National Defense Authorization Act (1994), 336 National Disaster Medical System (NDMS), 10, 11, 22, 28–29, 193, 446, 529 activities of, 37, 95, 125, 199, 219, 260, 407 creation of, 95–96 National Earthquake Hazards Reduction Program, 142 National Electronic Disease Surveillance System (NEDSS), 136, 304, 305

National Emergency Management Association, 29, 90, 183, 189, 251 National Fire Incident Command System, 30, 796 National Fire Prevention and Control Administration, 29 National Fire Protection Association (NFPA), 22, 110, 208, 408 monitoring, 217 Standards Council, 30, 79, 141, 252 National Flood Insurance Program. See Federal Insurance Administration National Football League (NFL), 912 National Governor’s Association (NGA), 80, 113 National Guard Bureau, 189 National Hazards Research and Information Applications Center (Hazards Center), 110 National Highway Safety Act (1966), 274 National Highway Traffic and Safety Administration (NHTSA), 21 National Incident Management System (NIMS), 29, 30–31, 82, 101, 109, 407 goals/principals of, 183, 188, 204, 229, 365 on intelligence, 140 National Institute for Allergy and Infectious Diseases (NIAID), 10, 98, 150 National Institute for Occupational Safety and Health (NIOSH), 157, 216, 222, 718 reports by, 246–247, 247b standards, 408 National Institute for Safety and Health, 16 National Institute of Justice (NIJ), 16, 408 National Institute of Standards and Technology (NIST), 10, 408 National Institutes of Health (NIH), 10, 98, 150 National Intelligence Estimates (NIE), 360 National Interagency Incident Management System (NIIMS), 21, 108–109, 336 National Library of Medicine, 158 National Library of Medicine (NLM), 409 National Medical Response Teams (NMRTs), 96, 407 National Memorial Institute for the Prevention of Terrorism Responder Knowledge Base, 408 National Mutual Aid, 190 National Oceanic and Atmospheric Administration (NOAA), 32, 130, 487, 489 Tsunami Hazard Mitigation, 493 National Oil and Hazardous Substances Pollution Contingency Plan, 80, 319 National Personal Protective Technology Laboratory, 408 National Pharmaceutical Stockpile (NPS), 11, 31, 37 National Priorities List, 409 National Radio Network, 231 National Response Plan (NRP), 9, 31, 183, 185, 309 activities of, 82, 84–85, 85t, 92, 96, 97b, 367 creation of, 104, 189, 205 Initial, 393 National Response Team (NRT), 30 National Science Advisory Board for Biosecurity, 97 National Security Council (NSC), 104–105 National Security Special Events (NSSE), 99 National Smallpox Vaccination Program (NSVP), 177 National Tactical Officers Association, 298 INDEX 943

National Transportation Safety Board (NTSB), 71, 325, 820, 826, 829–830 National Urban Search and Rescue Response Team, 265, 269 National Voluntary Organizations Active in Disaster (NVOAD), 86 National Weather Service (NWS), 87, 114, 233 alerts, 484, 499 Community Preparedness Program, 29 National Wildlife Coordinating Group, 208 Nation-states, 43 Native American Indians, 424 NATO. See North Atlantic Treaty Organization Natural Hazards Center (Boulder, Colorado), 26 NBA. See National Basketball League NBC (nuclear, biologic and chemical), 605 NBC-CREST model, 193 NBCCTS. See Nuclear Biological Chemical Casualty Training System NCAA. See National Collegiate Athletic Association NCRP. See National Council on Radiation Protection and Measurements NDMS. See National Disaster Medical System Near-Earth objects (NEO), 838–840 Nebraska, 484, 826 NEDSS. See National Electronic Disease Surveillance System Needs assessment. See also Rapid needs assessment current practices of, 224–227 historical perspectives on, 224 pitfalls of, 227–228 Neighborhood Emergency Help Center, 187 Nerve agents, 429, 548–549 case presentation for, 566b considerations for, 567 description of events during, 563–564 medical treatment of casualties from, 565–567, 566t pitfalls of, 567 postincident actions after, 564–565, 565t preincident actions before, 564 Neuromuscular junction (NMJ), 596 Nevada, 875 New Emergency Health Kit, 309 New England Journal of Medicine, 178 New Hampshire, 12, 203, 275 New Jersey, 12, 232, 377, 661 New Mexico, 520 New York, 8, 12, 18, 21, 205, 229, 377 New York City Department of Health and Mental Health, 18 New York Fire Department, 205, 392 New York Police Department, 21, 229, 385 New York Post, 125 New York State Department of Health (NYS DOH), 8 New York Times, 31 New York University Downtown Hospital, 35 New Zealand, 492 NEXRAD Doppler radar, 484 NFL. See National Football League NFPA 1600: Standard on Disaster/Emergency Management and Business Continuity Programs 2004 Edition, 30 NFPA. See National Fire Protection Association NGA. See National Governor’s Association NGOs. See Nongovernment organizations NHTSA. See National Highway Traffic and Safety Administration NIAID. See National Institute for Allergy and Infectious Diseases 944 INDEX

Nicaragua, 52, 303 Nicotinic agent attacks case presentation for, 598 considerations for, 598 description of events during, 596–597 medical treatment of casualties from, 597–598 pitfalls of, 598 postincident actions after, 597 preincident actions before, 597 NIE. See National Intelligence Estimates Nigeria, 224, 327, 885 Nigerian (Biafran War), 327 NIH. See National Institutes of Health NIIMS. See National Interagency Incident Management System NIJ. See National Institute of Justice NIMS. See National Incident Management System 9-11 Commission. See National Commission on Terrorist Attacks 911 operating systems, 175–176, 229 911 tactical model, 298 NIOSH. See National Institute for Occupational Safety and Health Nipah virus (nipah virus encephalitis), 149, 427 attacks case presentation for, 694 considerations for, 694 description of events during, 693 medical treatment of casualties from, 694 pitfalls of, 694 postincident actions after, 693–694 preincident actions before, 693 NIST. See National Institute of Standards and Technology Nitraoxanides, 735 Nitric acid, 430 Nitrogen, 854 mustards, 569 N2O. See Nitrous oxide Nitrous oxide (N2O), 601 Nixon, Richard M., 605, 653 NLM. See National Library of Medicine NMJ. See Neuromuscular junction NMRTs. See National Medical Response Teams Noble Training Center, 37–38 Nongovernment organizations (NGOs), 45–46, 49, 102, 107, 327 Nordic Society for Disaster Medicine, 473 North Atlantic Treaty Organization (NATO), 292, 593, 893 North Carolina, 57, 96, 115, 275, 369, 490 North Carolina Department of Agriculture and Consumer Services’Terrorism Threat Vulnerability Self Assessment Tool, 115 North Carolina State University, 264 North Dakota, 489 North Korea, 401 Northern Ireland, 377, 434 Northern Mariana Islands, 318 Nova Scotia, 737 Novicida, 617 NPS. See National Pharmaceutical Stockpile NRC. See U.S. Nuclear Regulatory Commission NRP. See National Response Plan NRT. See National Response Team NSC. See National Security Council NSSE. See National Security Special Events NSVP. See National Smallpox Vaccination Program

NTSB. See National Transportation Safety Board Nuclear Biological Chemical Casualty Training System (NBCCTS), 324 Nuclear detonations case presentation for, 531 considerations for, 530 description of events during, 528 medical treatment of casualties from, 529–530, 530t, 531f pitfalls of, 531 postincident actions after, 528–529 preincident actions before, 528 Nuclear disaster(s), 403 biologic effects of, 400–401, 517–519, 520f current practices for, 520–523, 521t historical perspectives on, 519–520 management current practices of, 400–401 historical perspectives on, 399–400 pitfalls of, 404 pitfalls of, 523 scenarios, 518 Nuclear fission, 519 Nuclear physics, 399, 400–401, 517–518 Nuclear power plant(s) airliner crash into case presentation for, 871 considerations for, 871 description of events during, 869–870 medical treatment of casualties from, 870 pitfalls of, 871 postincident actions after, 870, 870t preincident actions before, 870 explosions case presentation for, 776 considerations for, 777 description of events during, 774 medical treatment of casualties from, 775–776, 776t pitfalls of, 777 postincident actions after, 775 preincident actions before, 774–775 meltdown at case presentation for, 546 considerations for, 546 description of events during, 544–545, 545f medical treatment of casualties from, 545–546 pitfalls of, 547 postincident actions after, 545 preincident actions before, 545 Nuclear reactors, attacks on, 402–403 Nuclear waste storage facilities, explosions at case presentation for, 876 considerations for, 876–877 description of events during, 875 medical treatment of casualties from, 876, 876t pitfalls of, 877 postincident actions after, 875–876 preincident actions before, 875 Nuclear weapons. See also Quarantines detonation of, 401 effects of, 402 tactical, 402 Nunn-Lugar-Domenici legislation. See Defense Against Weapons Of Mass Destruction Act NVOAD. See National Voluntary Organizations Active in Disaster NWS. See National Weather Service NYC Mayor’s Voluntary Action Center, 243 NYS DOH. See New York State Department of Health

OA. See Open air Oak Ridge Institute for Science and Education, 158 OC. See Oleoresin capsicum Occupational Health Coordinating Group (OH-CG), 154 Occupational health services, 152–155, 153b Occupational Safety and Health Administration (OSHA), 71, 154–155, 157, 201 standards, 252, 408, 411 OCHA. See United Nations Office of the Coordinator for Humanitarian Assistance OCM. See Office of Crisis Management OCPM. See Office of Crisis Planning and Management ODP. See Office of Domestic Preparedness OEM. See Office of Emergency Management OEP. See Office of Emergency Preparedness OFDA. See Office of Foreign Disaster Assistance Office for Domestic Preparedness (ODP), 14, 22, 109 Equipment Grant Program, 23 Office of Biodefense Research, 98 Office of Civil Defense, 112–113 Office of Clinical Research, 98 Office of Crisis Management (OCM), 98 Office of Crisis Planning and Management (OCPM), 10 Office of Domestic Preparedness (ODP), 408, 413 Office of Emergency Management (OEM), 21 Office of Emergency Preparedness (OEP), 10, 11, 98 Office of Foreign Disaster Assistance (OFDA), 48, 102–103, 269 Office of Justice Programs (OJP), 10, 22 Office of Law Enforcement Standards (OLES), 408 Office of Peacekeeping and Humanitarian Affairs (PK/HA), 104 Office of Reconstruction and Humanitarian Assistance (ORHA), 48 Office of State and Local Domestic Preparedness, 343 Office of the Assistant Secretary for Public Health Emergency Preparedness (ASPHEP), 97 Ohio, 12, 110 Ohio State University, 110 Oil-for-Food program, 48 Oil-for-Medicine program, 48 OJP. See Office of Justice Programs Oklahoma, 34, 35, 80, 127–128, 215, 218, 243–244, 246, 484, 846–847 Oklahoma City Bombing, 34, 35, 80, 127–128, 215, 218, 243–244, 246, 387, 738, 759, 770 Oklahoma Department of Transportation, 847 Oklahoma I-40 bridge, 846 O’Leary, Dennis, 31 Oleoresin capsicum (OC), 593 OLES. See Office of Law Enforcement Standards Omsk Viral hemorrhagic fever, 675, 676 On-Site Operations Coordination Center (OSOCC), 105 OPCW. See Organization for the Prevention of Chemical Weapons Open air (OA), 739, 739t Operational debriefing, 169 Operations security (OPSEC) challenges of, 383–385 conclusions on, 390 crowd/information security/traffic and, 388–389

Operations security (OPSEC) (Continued ) dignitaries/press and, 386 evidence protection during, 388 foundation of, 382–383 integration of, 385 secondary devices/threats and, 389 sites, 386–388 Operations Support Directorate (OSD), 206 Opioid agent attacks case presentation for, 592 considerations for, 591–592 description of events for, 589 medical treatment of casualties from, 590–591 pitfalls of, 592 postincident actions after, 590 preincident actions before, 589=590, 590t OPSEC. See Operations security Oral rehydration therapy (ORT), 56, 507 Orange County Emergency Medical Services, 209 Oregon, 34 Organization for the Prevention of Chemical Weapons (OPCW), 406 Organofluorines, 429 Organophosphates, 563–564 ORHA. See Office of Reconstruction and Humanitarian Assistance Orientia tsutsugamushi (scrub typhus), attacks case presentation for, 630 considerations for, 630 description of events during, 629–620 medical treatment of casualties from, 630 pitfalls of, 631 postincident actions after, 630 preincident actions before, 630 ORT. See Oral rehydration therapy Orthogentic principle, 348 OSD. See Operations Support Directorate OSHA. See Occupational Safety and Health Administration OSOCC. See On-Site Operations Coordination Center OST3C (off-site triage, treatment and transportation center), 195, 197 Oxime, 566 Oxygen, 854

PA. See Protective antigen Pacific Coastal Ranges, 509 Pacific Islands, 492 “Pacific Settlement of Disputes,” 104 Pacific Tsunami Warning Center (PTWC), 493 PAHO. See Pan American Health Organization Pakistan, 401, 668 Palestine, 54 Palytoxins, 711 Pan American Health Organization (PAHO), 105, 172, 240–241, 241b, 241t, 308 Pan American Health Organization Meeting on Evaluation of Preparedness and Response to Hurricanes Georges and Mitch, 335 Panama Canal, 303 PAPRs. See Powered air-purifying respirators Papua New Guinea, 492, 495, 504 Paradigm shifts, 35 Paramyxoviridae, 693 Paromomycins, 734–735 Particle beam generators, 442 Pasteur, Louis, 304

Patient(s), 96, 324 autonomy/rights of, 65 in hospitals admission/identification/tracking in, 40 emergency decontamination of, 40 tracking systems current practices on, 291–294, 292f, 293f, 294f future of, 294–295 historical perspectives on, 291 pitfalls of, 295 Patrick, Bill, 653 PBIs. See Primary blast injuries PCR. See Polymerase chain reaction PDA. See Preliminary damage assessment PDDs. See Presidential Decision Directives Peace Corps, 86, 320 Peacekeeping, 104 Pellagra, 54 PEM. See Protein energy malnutrition Penicillin, 535, 702 Pennsylvania, 12, 115, 489, 544, 778 Pennsylvania Municipal Police Officer’s Education and Training Commission’s Vulnerability Assessment Worksheet, 115 Pentagon, 80, 90 PEP. See Prepositioned Equipment Program Pepolonnesian War, 424 Persian Gulf War, 48, 134, 238, 283 Personal digital assistant, 131, 132–133, 133b Personal flotation devices (PFDs), 878–879 Personal protection equipment (PPE), 12, 110, 175, 215, 408, 446 challenges/pitfalls of, 252–253 current practices for, 247–252, 249t, 250f, 270 disaster responses and, 217–218, 218b historical perspectives on, 246–247, 247b HVA and, 247 radiation decontamination of, 468–469 Peru, 509, 749–751 Pest control, 15 Pesticides, 372. See also Herbicides Petroleum distillation/processing facility explosions case presentation for, 789 considerations for, 789 description of events during, 786–787 hazards from, 787, 788t medical treatment of casualties from, 787–789 pitfalls of, 789 postincident actions after, 787 preincident actions before, 787 Peyotes, 585–586 PFDs. See Personal flotation devices PFO. See Principal federal official Pharmaceuticals, 11, 31, 37, 41, 308 companies, 239–240 current practices of, 309–310, 309t historical perspectives on, 309 pitfalls of, 310 summary on, 311 PHE. See Public health emergency Phenylethylamines, attacks case presentation for, 587 considerations for, 587 description of events for, 585–586 medical treatment of casualties for, 587 pitfalls of, 587–588 postincident actions after, 587 preincident actions for, 587 Philippines, 103, 376, 492, 509, 885 Phosgene oxime (CX), 569 Phosgenes (CG), 548, 569, 573–574 INDEX 945

Phosphates, 817 Physician Preparedness for Acts of Water Terrorism: An On-line Readiness Guide, 905 Pilgrimages, 915 PIO. See Public information officer Pipe bomb attacks case presentation for, 815 clinical presentation of, 814 considerations for, 815 description of events during, 813–814 medical treatment of casualties from, 814–815 pitfalls of, 815 postincident actions after, 814 preincident actions before, 814 PK/HA. See Office of Peacekeeping and Humanitarian Affairs Plagues, 3, 27, 148, 421, 605. See also Pneumonic Plague; Yersinia pestis Planning, 210, 210f, 474 disaster, 90–93, 91t mutual aid and, 183 preparedness and, 29 state programs/responses in, 90–93, 91t Plasmodium falciparum, 303 Plutonium, 467–468, 541 Pneumonic Plague, 13, 613, 615t Poison gases, 424 Polio, 146 Poliomyelitis, 7 Polymerase chain reaction (PCR), 610, 672, 674, 678, 784 Popular Front for the Liberation Of Palestine, 376 Population(s). See also Refugees displaced food/nutrition/water and, 314, 315, 315t hygiene/sanitation and, 314–315, 315t initial evaluations of, 314–316, 314t measles and, 314 medical care and, 316 priorities for, 313–314, 314b shelter and, 315, 315t protection measures, 559 Portsmouth, New Hampshire, 13 Posse Comitatus Act, 393 Posttraumatic stress disorders (PTSDs), 15–16, 51, 351, 887 prevention of, 60–61 treatments for, 59–60, 60t Potassium iodide, 530 Power system failures case presentation for, 895 considerations for, 895 description of events during, 893–894 medical treatment of casualties from, 895 pitfalls of, 895–896 postincident actions after, 895 preincident actions before, 894–895 Powered air-purifying respirators (PAPRs), 248 PPE. See Personal protection equipment PR. See Public relations Pralidoxime chloride (2-PAM chloride), 566 Pralidoximes, 567 Prednisone, 731 Preliminary damage assessment (PDA), 189 Preparedness, 108, 317 components of, 167–168 containment strategies and, 178 current practices for, 165–166, 225 customer focus and, 170 definition of, 164–165, 474 design/redesign and, 170 education/training for, 168 946 INDEX

Preparedness (Continued ) elements of, 166 emergency, 557–558, 557t empowerment/leadership and, 170–171 evaluation/monitoring for, 168–169 facility, 119, 120f functional approach to, 167, 168t future of, 172 guidelines, 8, 13–14 health objectives of, 166 historical perspectives on, 165 knowledge of variation and, 170 legislations for, 179–180 management, 169–170 pitfalls of, 171–172 planning and, 29 policy issues in, 174–180 process focus and, 170 program processes of, 166–167 SARS and, 178–179 smallpox vaccinations and, 176–178 Prepositioned Equipment Program (PEP), 413 Presidential Decision Directives (PDDs), 80, 104, 142 NSTC-7, 359 62, 392 39, 336, 361, 392 Prevalence, 330 Primary blast injuries (PBIs), 436, 736–737, 745–747 Prince of Wales Hospital, 179 Principal federal official (PFO), 24, 394, 394f Private voluntary organizations (PVOs), 102 PRM. See Bureau of Population, Refugees and Migration Proctor and Gamble, 153 Progressive collapse. See Buildings Project management, 169 Prophylaxis, 11–12, 535, 633, 655, 876 “Protecting Emergency Responders: Lessons Learned from Terrorist Attacks,” 246–247, 247b Protective antigen (PA), 608 Protein energy malnutrition (PEM), 47–48, 54–55 Proteus, 486, 630 Prueher, Joseph, 365 Prussian blue, 530 PSAP. See Public safety answering point Pseudocholinesterases, 565 Pseudomonas, 486 Psilocin, 585 Psilocybin, 585–586 Psittacosis. See Chlamydia psittaci PTSDs. See Posttraumatic stress disorders PTWC. See Pacific Tsunami Warning Center Public Assistance Program, 186 Public health achievements, 7 communications/education/training in, 13–14 conclusion on, 18 consequences/functions of, 167, 168t data systems within, 10, 17–18 definition of, 7 disasters and, 7–18, 9 environmental health/precautions and, 14–15 first responders and, 16–17 infrastructure, 10–11 introduction to, 4f, 7 medical services and, 11–13 mental health and, 15–16, 15b operation of, 9–10 recovery and, 8–9

Public health (Continued ) response cycles, 7–8 surveillance, 92 systems, 355–358 worker safety and, 16–17 Public Health and Medical Services Emergency Support Function, 100 Public health emergency (PHE), 93, 175–176 Public Health Emergency Fund, 96 Public Health Security and Bioterrorism Preparedness and Response Act (2002), 145, 339 Public Health Threats and Emergencies Act (2002), 96 Public information management conclusions on, 129 current practices of, 125–126, 344 disasters and, 124–125 effects of media reports on, 127 history of, 124 medical/EMS/fire models and, 126 pitfalls of, 128–129 Public information officer (PIO), 235, 386 Public relations (PR), 125 Public safety answering point (PSAP), 220–221, 229 Publick Occurrences, 232 Puerto Rico, Commonwealth of, 23 PVOs. See Private voluntary organizations Pythagoreans, 63

Q fever. See Coxiella burnetii Al-Qaeda, 376–378, 430, 518 QNB. See 3-Quinuclidinyl benzilate Quantum dots, 430 Quarantines, 150, 882 biologic/chemical/nuclear, 451 current practices for, 452–455, 454b, 455b pitfalls of, 457–458 protection of community assets during, 455–456, 456b history of, 451–452 Quecreek coal mine, 856 3-Quinuclidinyl benzilate (QNB), 582

Rabaul Volcano, 504 RACES (radio amateur civil emergency services), 231 Rad (radiation absorbed dose), 401, 518 Radiation, 870, 870t accidents, dispersed exposure case presentation for, 542 considerations for, 542–543 description of events during, 538, 539t medical treatment of casualties from, 539t, 540–542 pitfalls of, 543 postincident actions after, 540 preincident actions before, 538–540 accidents, isolated exposure, 403 case presentation for, 536 considerations for, 535 description of events during, 532 medical treatment of casualties from, 533–534, 535t pitfalls of, 536 postincident actions after, 533 preincident actions before, 532–533 alpha, 517, 524

Radiation (Continued ) beta, 517–518, 524 biology/physics of, 400–401, 517–518 disasters biologic effects of, 518–519, 520f current practices for, 520–523, 521t historical perspectives on, 519–520 pitfalls of, 523 scenarios, 518 equivalent, 518 incidents description of events during, 524 medical treatment of casualties from, 526 pitfalls of, 526 postincident actions after, 525–526 preincident actions before, 524 infrared, 443 injuries, acute, 530 neutron, 518 thermal, 402 Radiation Emergency Assistance Center/Training Site (REAC/TS), 158, 516, 533, 538, 541, 775 Radiation emission device (RED), 518–519 Radiation safety officer (RSO), 538 Radioactive contamination, 522 Radioactivity, 399, 401, 465, 519–520 Radiocesium, 524 Radiofrequencies (RFs), 135, 135t, 230–231 Radiofrequency identification chip (RFID), 294 Radiologic dispersal devices (RDDs), 400, 403, 518–519 case presentation for, 874 considerations for, 874 description of events during, 872–873 medical treatment of casualties from, 873 pitfalls of, 874 postincident actions after, 873 preincident actions before, 873 Radiological Emergency Preparedness (REP), 11 Radiological incidents, 12, 13, 371–372 Radios, 135, 135t, 230–231, 894 Radium, 465 RAM-W (Risk Assessment Methodology Water), 115 RAN. See Rapid needs assessment Rand Corporation, 216, 219, 222, 246–247, 247b Rapes, 44 Rapid assessments, 328–331, 328b, 329b, 330t Rapid needs assessment (RAN), 39 RDDs. See Radiologic dispersal devices RDECOM. See Research Development and Engineering Command Reactive Skin Decontaminant Lotion (RSDL), 412 REAC/TS. See Radiation Emergency Assistance Center/Training Site Reagan, Ronald, 134, 549 Recommendations for Using Smallpox Vaccine in a Pre-Event Vaccination Program, 177 Recommended Practice for Disaster Management, 208 Reconstruction Finance Corporation, 79, 112 Recovery activities/phases of, 29, 108, 317 current practices, 318–319 historical perspectives on, 317–318 horizontal/vertical mediation of, 317 pitfalls, 320–321 public health and, 8–9 /rescue workers, 10

Red Crescent Societies, 105, 327 Red Cross, 11, 20, 218, 242, 305. See also American Red Cross; International Committee of the Red Cross; International Federation of the Red Cross; International Red Cross Red Cross Movement, 46, 48, 106, 238 RED. See Radiation emission device Reed,Walter, 303 Refugees, 44, 53–54, 103–104. See also Populations Regional emergency support functions (RESFs), 186 Regional Radio Network, 231 Regional Response Coordination Center (RRCC), 82 Regionalization of Bioterrorism Preparedness and Response, 194, 196 Registered nurses (RNs), 175 Rem, 401, 518 REP. See Radiological Emergency Preparedness Research Development and Engineering Command (RDECOM), 409 Research Institute of Viral Preparations, 147 R-ESFs. See Regional emergency support functions Resilience, 302 Respirators APRs, 249–251, 250f atmosphere-supplying, 249 PAPR, 248 Respiratory agent attacks case presentation for, 574–575 considerations for, 575 description of events during, 573–574 medical treatment of casualties from, 574–575 pitfalls of, 575 postincident actions after, 574 preincident actions before, 574 Respiratory infections, 18 Responders. See also Personal protection equipment EMAs/liability issues regarding legal obligations of, 75–76 legal protections for, 76–78 emergency medical, 3, 16 first, 10, 28 hospitals as, 142–143 public health and, 16–17 worker health/safety and, 159 front line, 11 secondary, 162 Reuters News Agency, 428–429 Revised Trauma Score (RTS), 285, 288 Revolutionary Armed Forces of Columbia (FARC), 389 RFID. See Radiofrequency identification chip RFs. See Radiofrequencies Rhode Island Disaster Initiative (RIDI), 325 Rhode Island Hospital, 324, 445 Rhode Island nightclub fire, 35, 41 Rhode, Michael, 801 Ribavirin, 666, 669, 676, 694 Ribonucleic acid (RNA), 665, 671, 674 Ribosomal ribonucleic acid (rRNA), 718 Richmond Hill Hospital, 178 Ricin toxin, 424 Ricinus communis (castor beans) attacks and case presentation for, 720 considerations for, 720–721 description of events during, 718–719 medical treatment of casualties from, 720

Ricin toxin (Continued ) pitfalls of, 721 postincident actions after, 719–720 preincident actions before, 719 Rickettsia prowazekii (typhus fever), 148, 354 attacks case presentation for, 628 considerations for, 628 description of events during, 627 medical treatment of casualties from, 627–628 pitfalls of, 628 postincident actions after, 627 preincident actions before, 627 Rickettsia rickettsii (Rocky Mountain spotted fever), 687 attacks case presentation for, 633 considerations for, 634 description of events during, 632 medical treatment of casualties from, 633 pitfalls of, 634 postincident actions after, 633 preincident actions before, 632–633 Ridge,Tom, 367 RIDI. See Rhode Island Disaster Initiative Rifampin, 614 “Ring of Fire,” 492 Riot-control agent attacks case presentation for, 595 considerations for, 595 description of events during, 593 medical treatment of casualties from, 594–595 pitfalls of, 595 postincident actions after, 594 preincident actions before, 594 Risk, 579 assessments, 339 hazard, 119 management, 359–360, 359t, 556–557 perception, 328 Risk Management Series: Reference Manual to Mitigate Potential Terrorist Attacks Against Buildings, 115 RNA. See Ribonucleic acid RNs. See Registered nurses Robert T. Stafford Disaster Relief and Emergency Assistant Act, 9, 77, 80–81, 93, 184, 189, 203, 269, 309, 318, 336, 392 “Robinson Crusoe syndrome,” 220 Roche, 240 Rocket-propelled grenade attacks (RPGs), 830 case presentation for, 762 considerations for, 762 description of events during, 761 medical treatment of casualties from, 762 pitfalls of, 762 postincident actions after, 761–762 preincident actions before, 761 Rocky Mountain spotted fever. See Rickettsia rickettsii Rocky Mountains, 509 Rodents, 15, 304, 687 Roentgen,Wilhelm, 519 The Role of Emergency Physicians in Mass Casualty/Disaster Management, 28 Roundtable on the Media, Scientific Information and Disasters, 232 Royal Darwin Hospital, 765 Royal National Park, 802 RPGs. See Rocket-propelled grenade attacks RRCC. See Regional Response Coordination Center RRNA. See Ribosomal ribonucleic acid INDEX 947

RSDL. See Reactive Skin Decontaminant Lotion RSO. See Radiation safety officer RSSEV. See Russian spring-summer encephalitis virus RTS. See Revised Trauma Score Rubella, 7 Rudman,Warren B., 32 Russia, 147, 300, 303, 317, 385, 429, 591, 600, 663, 668 Russian Federal Security Service (FSB), 591 Russian spring-summer encephalitis virus (RSSEV), 663 Russo-Japanese War, 303 Rutherford, Ernest, 399 Rwanda, 43, 52, 102, 241, 508

Sacco Triage Method, 24, 198 Saffir-Simpson Hurricane Scale, 26, 475, 476t St. Joseph, Minnesota, 900 St. Luke’s International Hospital, 550 St.Vincent’s Catholic Medical Center, 35 Salk, Jonas, 146 Salmonella enteritidis, 644 Salmonella species (Salmonellosis), 15, 56, 149, 360, 370, 416, 490, 507 attacks case presentation for, 641 considerations for, 643 description of events during, 641–642 medical treatment of casualties from, 642 pitfalls of, 643 postincident actions after, 642 preincident actions before, 642 Salmonella typhi (typhoid fever), 15, 53 attacks case presentation for, 646 considerations for, 645–646 description of events during, 644–645 medical treatment of casualties from, 645 pitfalls of, 646 postincident actions after, 645 preincident actions before, 645 Salmonella typhimurium, 644 Salvation Army, 185, 200–201, 218 SAMHSA. See Substance Abuse and Mental Health Services Administration Samples, 331 San Francisco, 112, 232, 242, 510, 687 Sanchez, Enrique, 283 Sanders, et al. v. The Board of County Commissioners of the County of Jefferson Colorado, et al., 71–72, 75–76 Sanofi Aventis, 239 Santayana, George, 26 Sapphire worm, 921 SAR. See Search and Rescue Sarin, 35, 87, 127, 246, 384, 425, 549–550, 563 SARS. See Severe acute respiratory syndrome SARS-CoV attacks case presentation for, 697 considerations for, 697 description of events during, 695–696 medical treatment of casualties from, 696 pitfalls of, 697 postincident actions after, 696 preincident actions before, 696 Satitoxins, 710 Saudi Arabia, 434 SBA. See Small Business Administration SBCCOM. See Army Soldier and Biological Chemical Command 948 INDEX

Scandinavia, 668 SCBA. See Self-contained breathing apparatus Scholtz, Nicky, 887 Schrader, Gerhard, 549 Scotts Air Force Base, 96 Scrub typhus. See Orientia tsutsugamushi Scurvy, 54 SDDs. See Simple dispersal devices Search and Rescue (SAR), 9, 251. See also Urban search and rescue Seattle, 13, 24 Secretary’s Emergency Response Team (SERT), 97 SEL. See Standardized equipment list Selective serotonin-reuptake inhibitors (SSRIs), 60, 60t Self-contained breathing apparatus (SCBA), 159–161, 248, 281, 570 SEMS. See Standardized Emergency Management System Senior Corps, 86 September 11, 2001 events, 32, 35, 68, 229. See also World Trade Center SERC. See State Emergency Response Commission Serratia, 486 SERT. See Secretary’s Emergency Response Team Severe acute respiratory syndrome (SARS), 3, 12–13, 34. See also SARS-CoV attacks -associated coronavirus, 426–427 mini-epidemic (2003), 68 outbreaks of, 141, 178–179, 200, 246, 425 Sexually transmitted diseases (STDs), 47 Shigella, 15, 56, 490, 507 Shigella dysenteriae (shigellosis), attacks case presentation for, 640 considerations for, 640 description of events during, 638–639 medical treatment of casualties from, 639–640 pitfalls of, 640 postincident actions after, 639 preincident actions before, 639 Siege of Malaga, 297 Silica (silicon dioxide), 430 Simple dispersal devices (SDDs), 403 Simpson, O.J., 124 Simulation Technologies for Trauma Care (STATCARE), 324 Simulation Training in Emergency Preparedness, 324 Singapore, 13, 426, 765 Slammer worm, 921 Small Business Administration (SBA), 319 Smallpox (variola major virus), 7, 11, 17, 147–148 attacks case presentation for, 683 considerations for, 683 description of events during, 681 medical treatment of casualties from, 682–683 pitfalls of, 683 postincident actions after, 682 preincident actions before, 681–682 outbreaks, 369, 420 vaccinations, 176–178, 420 Smallpox Emergency Personnel Protection Act (2003), 177 Smallpox Vaccine Injury Compensation Table, 178 Sniper attacks case presentation for, 811 clinical presentation of, 810

Sniper attacks (Continued ) considerations for, 811–812 description of events during, 810 medical treatment of casualties from, 811 pitfalls of, 812 postincident actions after, 810 preincident actions before, 810 Snow, John, 322 SNR. See Syndrome-to-none ratio SNS. See Strategic National Stockpile Solid phase micro-extraction (SPME), 411 Somalia, 43, 44, 47, 52, 369 Soman, 563 South Africa, 885, 887 South Carolina, 275 South Dakota, 87 South Korea, 778 South Wales Fire and Rescue Service, 800 Soviet Union, 26, 306, 399, 425, 479, 663, 885 Spalling, 737 SPC. See Storm Prediction Center Special relationship doctrine, 75–76 SPHERE Project. See Humanitarian Charter and Minimum Standards SPME. See Solid phase micro-extraction Sports gatherings, 914 SPRINTs. See U.S. Navy Special Psychiatric Intervention Teams Srebrenica, 582 Sri Lanka, 240 SSRIs. See Selective serotonin-reuptake inhibitors Stachybotrys atra, 714 Stachybotrys chartarum, 714–715 Standard for Fire Department Safety Officer, 220 Standard for Professional Competence of Responders to Hazardous Materials Incidents, 280 Standard on Disaster/Emergency Management and Business Continuity Programs, 141 Standard on Protective Clothing for Emergency Medical Operations, 218 Standardized Emergency Management System (SEMS), 109 Standardized equipment list (SEL), 408 Staphylococcal enterotoxin B attacks case presentation for, 699 considerations for, 699–700 description of events during, 698 medical treatment of casualties from, 699 pitfalls of, 700 postincident actions after, 699 preincident actions before, 698–699 Staphylococcus aureus, 15, 698 Stare decisis, 73 START (simple triage and rapid treatment), 39, 87, 198, 285, 287, 818, 832, 847 STATCARE. See Simulation Technologies for Trauma Care State and Local Guide for All-Hazard Emergency Operations Planning, 485 State Emergency Management Agencies (SEMAs), 81, 85 State Emergency Response Commission (SERC), 91, 184 STDs. See Sexually transmitted diseases Steering Committee of the Task Force on Quality Control of Disaster Management, 473 Sterilization, 57 Stewart, Martha, 128 Stinkdamp, 853–854 Stockholm syndrome, 888

Storm Prediction Center (SPC), 484 Storms. See also Hurricanes;Typhoons winter case presentation for, 501 considerations for, 401 description of events during, 499 medical treatment of casualties from, 499–501, 500f pitfalls of, 501 postincident actions after, 499 preincident actions before, 499 Strategic National Stockpile (SNS), 11, 24, 37, 309, 529, 558 activities of, 92, 95, 96, 109, 365 assets of, 201 Working Group, 535, 542 Streptococcus, group A, 15 Strokes, 7 Strontium, 468 Structural collapses, introduction to case presentation for, 819 considerations for, 819 description of events during, 817 medical treatment of casualties from, 818–819 pitfalls of, 819 postincident actions after, 818 preincident actions before, 817–818 Submarine/surface vessel accidents case presentation for, 859 considerations for, 859 description of events during, 857–858 medical treatment of casualties from, 858–859 pitfalls of, 859 postincident actions after, 858 preincident actions before, 858 Substance Abuse and Mental Health Services Administration (SAMHSA), 98–99 Subway derailments case presentation for, 824 considerations for, 824 description of events during, 823 medical treatment of casualties from, 824 pitfalls of, 824–825 postincident actions after, 823 preincident actions before, 823 Sudan, 44, 47, 52, 102, 239, 239t, 240–241, 306, 310 Suicide bombers, 377–378 case presentation for, 756 considerations for, 755–756 description of events during, 754 medical treatment of casualties from, 755 pitfalls of, 756 postincident actions after, 755 preincident actions before, 755 Sulfur dioxide, 550 Sulfur mustards, 430, 546, 569 Sulfuric acid, 430, 550 SUMA (Humanitarian Supply Management System), 172, 240–241, 241b, 241t Summit Venture, 846 Sunshine Skyway collapse, 847 Surge capacity conclusions on, 202 current practices for, 195–202, 196t, 198t, 199t definition of, 193 facilities for, 196–198 of hospitals, 36, 345 legal/policy issues on, 201–202 medications/supplies for, 200–201 personnel for, 198–200, 198t, 199t projections for, 193–195, 194t, 195f

Surgery, 27 Surveillance current practices for, 256–258, 256b, 258t, 331 historical perspectives on, 255–256 pitfalls of, 258–259 public health, 92 syndromic, 17–18 Sustainable development, 317 SWAT (special weapons and tactics), 860 Syndrome-to-none ratio (SNR), 18 Syndromic surveillance, 17–18, 909

Tabun, 563 Tachycardias, 817, 818 Tacoma Narrows Bridge, 846 Tactical Emergency Medical Support (TEMS), 885 current practices of, 298–301, 300f historical perspectives on, 297–298, 298t pitfalls of, 301 Taiwan, 103, 179, 426 Tajikstan, 509 Tanzania, 104, 239t, 376 TARUs. See Technical assistance response units TBE. See Tick-borne encephalitis TBSA. See Total body surface area TCAs. See Tricyclic antidepressants Technical assistance response units (TARUs), 96 Technical Escort Unit (TEU), 396, 409 Technical Support Working Group (TSWG), 408–409 Telecommunications conclusions on, 137 current practices in, 131–137 historical perspectives on, 130–131 Telephones, 134, 211 Televisions, 126, 136, 232 Tennessee, 274 Terrorism, 4, 8. See also Bioterrorism; Suicide Bombers;World Trade Center computer/electronic case presentation for, 924 considerations for, 924 description of events during, 921–923 medical treatment of casualties from, 924 pitfalls of, 924 postincident actions after, 924 preincident actions before, 923–924 ecological case presentation for, 920 considerations for, 919 description of events during, 918–919 medical treatment of casualties from, 919 pitfalls of, 919–920 postincident actions after, 919 preincident actions before, 919 lessons learned from current practices on, 339 historical perspectives of, 335–336, 337t–338t pitfalls of, 339–345, 340t–341t, 342t–343t multimodality, layered attacks as categorization/modes of, 374–376 historical perspectives, 0 medical management of, 379–380 notion of, 374 pitfalls of, 378–379

Terrorism, 4, 8. See also Bioterrorism; Suicide Bombers;World Trade Center (Continued ) premeditated/noncombatant targets of, 374 psychology of conclusions on, 353 current perspectives on, 348–351 historical perspectives on, 347–348 pitfalls of, 351–352 secondary explosive devices and, 219 Terrorism Incident Annex, 319 Terrorism Insurance Risk Act (2002), 140–141 Terrorism Threat Integration Center, 339 Tetanus, 7 Tetracyclines, 645, 654–655 Tetrodotoxins, 711 TEU. See Technical Escort Unit Texas, 35, 324, 328, 475, 484, 489 Texas Engineering Extension Services, 324 Texas Medical Center, 489 Textbook of Military Medicine, 406 Thailand, 9, 52, 650 Thermoregulation, 54 Third World, 518 Three Mile Island, 869–870 Thrombotic thrombocytopenic purpura (TTP), 657 Tick-borne encephalitis (TBE), virus attacks case presentation for, 664 considerations for, 664 description of events during, 663 medical treatment of casualties from, 663–664 pitfalls of, 664 postincident actions after, 663 preincident actions before, 663 Ticks, 663–664 TIVR. See Total-immersion virtual reality TMX/SMX. See Trimethoprim/sulfamethoxazole TNT (trinitrotoluene), 399, 403 Tobacco, 7, 87 Tokyo, 35, 87, 127, 246, 284, 518 Top Officials (TOPOFF1/2/3), 13, 24 “Tornado Alley,” 484 Tornadoes, 34, 244, 264–265 case presentation for, 487 considerations for, 487 description of events during, 484–485, 484t medical treatment of casualties from, 486 pitfalls of, 487 postincident actions after, 486 preincident actions before, 485–486, 485t Toronto, 13, 34, 178–179, 200 Total body surface area (TBSA), 791b Total suspended particles (TSPs), 503 Total-immersion virtual reality (TIVR), 323 Toxicokinetics, 551 Toxins, 148, 429–430, 434, 560, 560b, 710. See also specific toxins Toxophenes, 429 Train derailments case presentation for, 821 considerations for, 821 description of events during, 820 medical treatment of casualties from, 821 pitfalls of, 821 postincident actions after, 820–821 preincident actions before, 820 Transmission control, 13 Transportation Security Administration (TSA), 860 INDEX 949

Trauma, 44 care, 21 centers, 12, 445 systems development, 92 Triage(s), 5–6, 24, 578. See also OST3C areas, alternate, 39 concepts, 27 current practices for, 284–289, 284b, 285b, 287t during disasters, 5–6, 24, 558–559 efficacy, 738 historical perspectives on, 283–284 during MCIs, 66–67 medical, 411–412 pitfalls of, 289 systems, 32, 39 tags, 291–294, 292f, 293f, 294f treatment, 791b of victims, 87 Triage Scoring System, 283 Tricothecenes, 714, 715t Tricyclic antidepressants (TCAs), 60, 60t TRIGA (Training Research Isotopes, General Atomics) nuclear reactors, 544–545 Trimethoprim/sulfamethoxazole (TMX/SMX), 645, 648–649, 651 Trinitrotoluene (TNT), 434, 528 Tritium, 468 Trojan horse virus, 921 Tropical storm Allison, 35 Truman, Harry S., 112, 233 TSA. See Transportation Security Administration TSPs. See Total suspended particles Tsunami Warning System in the Pacific (TWSP), 493 Tsunamis, 3, 4, 9, 12, 26, 56, 216, 270 case presentation for, 495 considerations for, 494 description of events during, 492 medical treatment of casualties from, 494 pitfalls for, 494 postincident actions after, 493–494 preincident actions before, 493 wave train of, 492 TSWG. See Technical Support Working Group “T2 After Action Summary Report,” 24 T-2 toxin (trichothecene mycotoxins), 424 attacks case presentation for, 716 considerations for, 716 description of events during, 714–715, 715t medical treatment of casualties from, 715–716 pitfalls of, 716 postincident actions after, 715 preincident actions before, 715 Tuberculosis, 44, 47, 242, 304, 646 Tularemia. See Francisella tularensis Tunguska explosion, 839 Tunnel(s) explosions case presentation for, 780 considerations for, 780 description of events during, 778 medical treatment of casualties from, 779–780 pitfalls of, 780 postincident actions after preincident actions before, 778–779 fires in case presentation for, 805 considerations for, 805 description of events during, 803–804 950 INDEX

Tunnel(s) (Continued ) medical treatment of casualties from, 805 pitfalls of, 805–806 postincident actions after, 805 preincident actions before, 804–805 Turkey, 102, 103, 230, 303 Tutsis, 52 Tuzla, 582 TWA Flight 800, 832 Two-hat syndrome, 190 TWSP. See Tsunami Warning System in the Pacific Tympanic membrane, 747 Typhoid fever. See Salmonella typhi Typhoons, 34 case presentation for, 478 considerations for, 477 description of events during, 475, 476t medical treatment of casualties from, 477 pitfalls of, 477–478 postincident actions after, 477 preincident actions before, 476–477 Typhus fever. See Rickettsia prowazekii

UCS. See Unified Command System UHFs. See Ultra high frequencies Ukraine, 544 Ultra high frequencies (UHFs), 135, 230–231 UNDAC. See United Nations Disaster Assessment and Coordination UNDMTP. See United Nations Disaster Management Training Programme UNDP. See United Nations Development Program UNHCR. See United Nations High Commissioner for Refugees UNICEF. See United Nations Children’s Fund Unified Command System (UCS), 23, 407 Uniformed Services University, 298, 354, 886 Union Carbide factory, 35 United Airlines Flight 232, 832 United Kingdom, 13 United Nations (UN), 4–5, 347 agencies/organizations, 45–46, 49, 102, 105–106 Charter, 45–46, 48, 104 General Assembly, 105, 165 interventions by, 45 Resolutions, 105 Security Council, 45–46 United Nations Children’s Fund (UNICEF), 46, 105 United Nations Conference on the Human Environment (Stockholm, 1972), 166 United Nations Development Program (UNDP), 105 United Nations Disaster Assessment and Coordination (UNDAC), 105 United Nations Disaster Management Training Programme (UNDMTP), 4–5 United Nations Emergency Relief Coordinator, 105 United Nations High Commissioner for Refugees (UNHCR), 44, 105, 313 United Nations Office of the Coordinator for Humanitarian Assistance (OCHA), 46, 105 United Nations Programme on HIV/AIDS, 304 United States (U.S.), 102, 274, 399 disaster responses by, 26, 79–83 current concepts of, 80–82, 82t early years of, 79

United States (U.S.) (Continued ) federal level management of, 81–82, 82t federal/state, 80 historical perspectives of, 79–80 international, 102–105, 103b, 104t lower level management of, 81 new millennium, 80 state level management of, 81 summary on, 82–83 embassies, 104, 376 government agencies, 185 medical disaster responses in, 5, 12, 38 policies of, 336, 337t–338t, 424 Unit 731, 424 University Association of Emergency Medicine, 28 University Hospital Center of Rijeka, 240 University of California, Davis, 266 University of California, Irvine, 310 University of Chicago, 520 University of Colorado, 110, 131 University of Delaware, 110 University of Louvain, 327 University of Michigan, 323 University of Missouri-Rolla, 323 University of North Texas, 110 University of Padova, 323 University of Texas, 297 “Unlimited National Emergency,” 335–336 Uranium, 468, 541 Uranium, highly enriched (HEU), 519 Urates, 817 Urban search and rescue (US&R), 30, 204–205 current practices of, 269–273, 270b, 270t historical perspectives on, 269, 270b pitfalls of, 273 Task Force, 269, 270–273, 270t U.S.Agency for International Development (USAID), 46, 48, 102–103, 104 U.S.Air Force, 96, 100, 393 U.S.Air Force Radiation Assessment Teams (AFRATs), 100, 396 U.S.Air National Guard, 92, 100 U.S.Army, 10, 11, 393, 430, 617 Center for Health Promotion and Preventive Medicine, 251 Civil Affairs, 99–100 Europe, 261 52nd Ordinance Group, 396 Medical Intelligence Office, 355 National Guard, 92 Surgeon General, 355 U.S.Army Chemical and Biological Special Medical Augmentation Response Teams (C/B-SMART), 100, 257 U.S.Army Medical Research Institute of Chemical Defense (USAMRICD), 110, 409 U.S.Army Medical Research Institute of Infectious Diseases (USAMRIID), 10, 100, 110, 665, 678 U.S.Attorney General, 21–22 U.S. Coast Guard (USCG), 10, 81, 393 U.S. Congress, 21, 112 U.S. Constitution, 75 U.S. Department of Agriculture (USDA), 10, 103, 319 U.S. Department of Commerce (DOC), 10, 319 U.S. Department of Defense (DOD), 10, 48, 298, 343, 529 Defense Civil Preparedness Agency of, 29 ESSENCE system of, 136 missions of, 103–104, 104t, 107 roles of, 99–100, 103

U.S. Department of Energy (DOE), 10, 529 U.S. Department of Health and Human Services (DHHS), 10, 86, 93, 96–99, 97b, 109, 558 authority of, 145, 187, 344 Medical Reserve Corps, 125 U.S. Department of Health, Education, and Welfare, 90, 570 U.S. Department of Homeland Security (DHS), 9, 11, 22, 31, 558 creation of, 29, 145 Emergency Preparedness and Response Directorate, 95 functions of, 81–82, 91, 95–96, 109 management by, 37–38 U.S. Department of Housing and Urban Development (HUD), 183, 319 U.S. Department of Interior, 298 U.S. Department of Justice (DOJ), 10, 11, 13, 339, 343, 392, 408 U.S. Department of State (DOS), 48, 103–104, 107 U.S. Department of Transportation (DOT), 10, 21, 71, 220, 550 U.S. Department of Veterans Affairs, 413 U.S. Department of Veterans Affairs (DVA), 99 U.S. Federal Aviation Regulations, 829–839 U.S. Food and Drug Administration (FDA), 10, 98 U.S. Forest Service, 336 U.S. Geological Survey, 105, 114 U.S. government (USG), 102, 107 U.S. Governmental Interagency Domestic Terrorism Concept of Operations Plan (CONPLAN), 9, 344, 392–393 U.S. Marine Corps, 100, 393 U.S. National Guard, 10, 81, 92, 188–189, 529 U.S. Navy, 37, 100, 294, 393 U.S. Navy Special Psychiatric Intervention Teams (SPRINTs), 100 U.S. Northern Command (USNORTHCOM), 100, 396 U.S. Nuclear Regulatory Commission (NRC), 869–870, 875, 876 U.S. Occupational Safety and Health Administration, 22 U.S. Park Police, 298 U.S. Postal Service, 304 U.S. Public Health Service (USPHS), 10–11, 96 U.S. Secret Service (USSS), 10 U.S. Secretary of State, 104 U.S. See United States U.S. Surgeon General, 86, 99, 184 U.S.Weather Bureau, 233 USA Freedom Corps, 86, 184 USA Patriot Act, 145 USAID. See U.S.Agency for International Development USAMRICD. See U.S.Army Medical Research Institute of Chemical Defense USAMRIID. See U.S.Army Medical Research Institute of Infectious Diseases USCG. See U.S. Coast Guard USDA. See U.S. Department of Agriculture USPHS. See U.S. Public Health Service US&R. See Urban search and rescue USS Cole, 80 USSS. See U.S. Secret Service Utstein method, 24 Uzbekistan, 617

VA. See Veterans Administration Vaccinations, 7, 141, 176–178, 420, 688 Vaccine Adverse Events Reporting System, 146

Vaccine immune globulin (VIG), 682 Vaccine, live-attenuated cold-adapted (LAIV), 685 Vaccines, 10, 682, 719 biological agents of, 146 category A as, 147–148 category B as, 148–149 category C as, 149 characteristics of, 146 future efforts on, 150 historical background on, 145 immunity and, 145–146 isolation/quarantines and, 150 miscellaneous agents of, 149 Vaccinia virus (Dryvax), 688 Varicella Zoster Virus (VZV), 687 Variola major virus. See Smallpox Vascular leak syndrome, 718 VEE. See Venezuelan equine encephalitis Vehicle-borne improvised explosive devices (VBIEDs), 435 case presentation for, 758 considerations for, 758 description of events during, 757 medical treatment of casualties from, 758–759 pitfalls of, 758 postincident actions after, 758 preincident actions before, 757–758 Vendor management inventory (VMI), 96 Venezuela, 239t, 509–510, 510f, 668, 885 Venezuelan equine encephalitis (VEE), 661 Vermont, 12 Very high frequencies (VHFs), 135, 230–231 Vesicant agent attacks case presentation for, 571 considerations for, 571 description of events during, 569 medical treatment of casualties from, 570––571 pitfalls of, 571 postincident actions after, 570 preincident actions before, 569–570 Vesicles, 569 Vessel Sanitation Program (VSP), 883 Veterans Administration (VA), 10 Veterans Benefits Administration, 99 Veterans Health Administration (VHA), 99, 120, 413 Veterans Integrated Service Networks (VISNs), 99 Veterinary Medical Assistant Teams (VMATs), 265–266 VHA. See Veterans Health Administration VHFs. See Very high frequencies Vibrio cholerae (cholera), 15, 53–54, 56, 149 attacks considerations for, 636–637 description of events during, 635–636 medical treatment of casualties from, 636 pitfalls of, 637 postincident actions after, 636 preincident actions before, 636 Vietnam, 13, 20–21, 27, 124, 351, 426, 434 Vietnam War, 13, 20–21, 27, 124, 351, 813 VIG. See Vaccine immune globulin VIPs (very important persons), care of case presentation for, 928 considerations for, 927–928 description of, 926 medical treatment of, 927 pitfalls of, 928 postincident actions for, 926–927 preincident actions for, 926

Viral encephalitides (alphaviruses), 148 attacks case presentation for, 662 considerations for, 662 description of events during, 661 medical treatment of casualties from, 661–662 pitfalls of, 662 postincident actions after, 661 preincident actions before, 661 Viral hemorrhagic fevers arenaviruses attacks as, 17, 148, 304, 421 case presentation for, 667 considerations for, 666–667 description of events during, 665–666 medical treatment of casualties from, 666 pitfalls of, 667 postincident actions after, 666 preincident actions before, 666 Bunyavirus attacks as case presentation for, 670 considerations for, 670 description of events during, 668–669 medical treatment of casualties from, 669–670 pitfalls of, 670 postincident actions after, 669 preincident actions before, 669 Crimean-Congo, 668 Filo virus attacks as, 17, 148, 668 case presentation for, 673 considerations for, 672–673 description of events during, 671–672 medical treatment of casualties from, 672 pitfalls of, 673 postincident actions after, 672 preincident actions before, 672 Flavivirus attacks as case presentation for, 676 considerations for, 676 description of events during, 674–675 medical treatment of casualties from, 676 pitfalls of, 676 postincident actions after, 676 preincident actions before, 675–676 Rift Valley as, 668–669, 670 Virgin Islands, 23, 318 Virginia, 103, 274 Virginia Task Force 1. See Fairfax County Virginia International Search and Rescue Team 1 Virtual private network (VPN), 133 Virtual reality (VR), 323 VISNs. See Veterans Integrated Service Networks Vitamin A, 48 VMI. See Vendor management inventory VOAD. See Voluntary Organizations Active in Disasters Volcano eruptions, 224 case presentation for, 505 considerations for, 504 description of events during, 502–503 medical treatment of casualties from, 504 pitfalls of, 504 postincident actions after, 504 preincident actions before, 503–504 Voluntary Organizations Active in Disasters (VOAD), 243 Volunteer Protection Act, 1977 (VPA), 76–77 Volunteers current practices for, 244 historical perspectives of, 243–244 management of, 238, 242–244 scene safety for, 218–219 INDEX 951

VPN. See Virtual private network VR. See Virtual reality VSP. See Vessel Sanitation Program Vulnerability analyses, 328 VZV. See Varicella Zoster Virus

WADEM. See World Association for Disaster and Emergency Medicine War of Italian Unification, 305 Warfare chemical current guidelines/standards for, 407–409 current practices for, 407 historical perspectives on, 406 pitfalls of, 413–414 responses to, 409–413, 410f fourth generation, 363 conclusions on, 367–368 historical perspectives, 0 “outside the box” and, 364–367, 366t Washington, 13, 24, 305 Washington, D.C., 13 Washington Hospital Center, 445 Wasting, 331 Water children and, 53 displaced populations and, 314, 315, 315t filtration/purification, 55, 305 fluoridated drinking, 7 protection of, 10 safety threats, 149 supplies, contamination of case presentation for, 906 considerations for, 905 description of events during, 901–902, 902t–903t medical treatment of casualties from, 904–905 pitfalls of, 905–906 postincident actions after, 903–904, 905b preincident actions before, 902–903, 904t Waugh,W.L., 339 Waves, edge, 493 WC/ATWC. See West Coast/Alaska Tsunami Warning Center Weapons of mass destruction (WMDs), 21, 22, 80, 204, 284 CBRNE/, 363–364 Education Military, 324

952 INDEX

WEE. See Western equine encephalitis Weight for height index (WFH), 54, 506 Weil-Felix test, 630 West Coast/Alaska Tsunami Warning Center (WC/ATWC), 493 West Virginia, 274 Western equine encephalitis (WEE), 661 WFH. See Weight for height index WFP. See World Food Program White House Medical Unit (WHMU), 927 Whitedamp, 853 Whitman, Charles, 297 Whitmore’s disease. See Burkholderia pseudomallei WHMU. See White House Medical Unit WHO. See World Health Organization Wi-Fi networks, 291, 294 Wisconsin, 265, 320 WMA. See World Medical Association WMD-Civil Support Teams (WMD-CST), 396 WMDs. See Weapons of mass destruction Women, pregnant, 44, 877 Worker health/safety, 16–17 disaster response management and, 157–158 EMS personnel and, 161–162 firefighters and, 159–161 first responders and, 159 occupations and, 158–159 police and, 161 pre-event planning for, 157 recommendations for, 162 secondary responders and, 162 Working Group on Civilian Biodefense, 614, 618, 674 Workplaces, safe, 7 World Association for Disaster and Emergency Medicine (WADEM), 473 Health Disaster Management, 64 World Bank, 320, 889 World Commission on Environment and Development, 317 World Conference on Natural Disaster Reduction, 165, 232, 336 World Factbook, 329 World Food Program (WFP), 46 World Health Assembly, 369 World Health Organization (WHO), 5, 46, 105–106 Database on Child Growth and Malnutrition, 506

World Health Organization (WHO) (Continued ) Emergency Health Kits, 47 Flunet, 684 guidelines of, 240–242, 241b, 241t, 308 protocols, 56 reports, 426–427 roles of, 238–240, 255, 304–306 World Medical Association (WMA), 64, 68 World Trade Center 1993 bombing of, 377, 383, 759, 770 2001 bombing of, 3, 8, 18, 21, 31–32, 35, 71, 80, 205, 229, 243, 246, 382, 385, 770, 796, 864–867 World War I, 20–21, 124 World War II, 20–21, 27, 124, 400, 428, 813 World Wide Web, 130 Wyeth Laboratories, 147

X-rays, 518, 524

Yellow fever, 303, 674 Yersinia pestis (Y. pestis), 687, 882 attacks case presentation for, 616 considerations for, 615 description of events during, 613 medical treatment of casualties from, 614, 615t pitfalls of, 614 postincident actions after, 613–614 preincident actions before, 613 Yersinia pestis (Y.pestis), 3, 12, 17, 145, 148, 421, 425 Yokohama Strategy and Plan of Action for a Safer World: Guidelines for Natural Disaster Prevention, Preparedness and Mitigation, 165 Yousef, Ramzi Ahmed, 377 Yugoslavia, 43, 44, 334

Zaire, 52, 255, 671 Zombie agents, 923