Grabb and Smith's Plastic Surgery (GRABB'S PLASTIC SURGERY)

GRABB AND SMITH’S PLASTIC SURGERY S I X T H E D I T I O N Editor-in-Chief Charles H. Thorne, MD Associate Professor o...

Author: Thorne C.H. (Editor) | Bartlett S.P. (Editor) | Beasley R.W. (Editor)

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GRABB AND SMITH’S PLASTIC SURGERY S I X T H

E D I T I O N Editor-in-Chief

Charles H. Thorne, MD Associate Professor of Plastic Surgery NYU Medical Center New York, New York

Editors

Robert W. Beasley, MD Professor of Surgery, New York University, New York, New York Director of New York University Hand Surgery Services, Institute of Reconstructive Plastic Surgery and Bellevue Hospital Center, New York, New York Hand Surgery Consultant, Veteran’s Administration, New York, New York Consulting Surgeon, Hackensack University Hospital, Hackensack, New Jersey and Impartial Advisor to Chairman, New York State Workers’ Compensation Board

Sherrell J. Aston, MD Professor of Surgery (Plastic) New York University School of Medicine Chairman, Department of Plastic Surgery Manhattan Eye Ear and Throat Hospital New York, New York

Scott P. Bartlett, MD Professor of Surgery, University of Pennsylvania Mary Downs Endowed Chair in Pediatric Craniofacial Treatment and Research, Children’s Hospital of Philadelphia Philadelphia, Pennsylvania

Geoffrey C. Gurtner, MD, FACS Associate Professor of Surgery, Department of Surgery, Division of Plastic Surgery Stanford University School of Medicine Stanford, California

Scott L. Spear, MD, FACS Professor and Chief Division of Plastic Surgery Georgetown University Medical Center Washington, DC

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Copyright © 2007 by Lippincott Williams & Wilkins, a Wolters Kluwer business. Grabb and Smith's Plastic Surgery, Sixth Edition by Charles H. Thorne.

Acquisitions Editor: Brian Brown Developmental Editor: Cotton Coslett and Keith Donnellan, Dovetail Content Solutions Managing Editor: Julia Seto Project Manager: Alicia Jackson Senior Manufacturing Manager: Benjamin Rivera Associate Director of Marketing: Adam Glazer Design Coordinator and Cover Designer: Terry Mallon Production Service: Techbooks Printer: Edwards Brothers ©2007 by LIPPINCOTT WILLIAMS & WILKINS, a WOLTERS KLUWER BUSINESS 530 Walnut Street Philadelphia, PA 19106 USA LWW.com 5th edition ©1997 By Lippincott-Raven Publishers All rights reserved. This book is protected by copyright. No part of this book may be reproduced in any form by any means, including photocopying, or utilized by any information storage and retrieval system without written permission from the copyright owner, except for brief quotations embodied in critical articles and reviews. Materials appearing in this book prepared by individuals as part of their official duties as U.S. government employees are not covered by the above-mentioned copyright. Printed in the USA Library of Congress Cataloging-in-Publication Data Grabb and Smith’s plastic surgery.—6th ed. / editor-in-chief, Charles H. Thorne . . . [et al.]. p. ; cm. Includes bibliographical references and index. ISBN 978-0-7817-4698-4 ISBN 0-7817-4698-1 1. Surgery, Plastic. I. Thorne, Charles, 1952- II. Grabb, William C. III. Title: Plastic surgery. [DNLM: 1. Surgery, Plastic. 2. Reconstructive Surgical Procedures. WO 600 G7265 2007] RD118.G688 2007 617.9 5—dc22 2006033593 Care has been taken to confirm the accuracy of the information presented and to describe generally accepted practices. However, the authors, editors, and publisher are not responsible for errors or omissions or for any consequences from application of the information in this book and make no warranty, expressed or implied, with respect to the currency, completeness, or accuracy of the contents of the publication. Application of the information in a particular situation remains the professional responsibility of the practitioner. The authors, editors, and publisher have exerted every effort to ensure that drug selection and dosage set forth in this text are in accordance with current recommendations and practice at the time of publication. However, in view of ongoing research, changes in government regulations, and the constant flow of information relating to drug therapy and drug reactions, the reader is urged to check the package insert for each drug for any change in indications and dosage and for added warnings and precautions. This is particularly important when the recommended agent is a new or infrequently employed drug. Some drugs and medical devices presented in the publication have Food and Drug Administration (FDA) clearance for limited use in restricted research settings. It is the responsibility of the health care provider to ascertain the FDA status of each drug or device planned for use in their clinical practice. To purchase additional copies of this book, call our customer service department at (800) 638-3030 or fax orders to (301) 223-2320. International customers should call (301) 223-2300. Visit Lippincott Williams & Wilkins on the Internet: at LWW.com. Lippincott Williams & Wilkins customer service representatives are available from 8:30 am to 6 pm, EST. 10 9 8 7 6 5 4 3 2 1 Copyright © 2007 by Lippincott Williams & Wilkins, a Wolters Kluwer business. Grabb and Smith's Plastic Surgery, Sixth Edition by Charles H. Thorne.

CONTRIBUTING AUTHORS

Valerie J. Ablaza, MD, FACS

Bruce S. Bauer, MD, FACS, FAAP

Assistant Professor Department of Surgery Columbia University College of Physicians and Surgeons New York, New York

Professor of Surgery Department of Surgery Division of Plastic Surgery The Feinberg School of Medicine Northwestern University Chief Division of Plastic Surgery Children’s Memorial Hospital Chicago, Illinois

Al Aly, MD, FACS Attending Department of Plastic Surgery Iowa City Plastic Surgery Coralville, Iowa

P.G. Arnold, MD Professor of Plastic Surgery Department of Surgery, Division of Plastic Surgery Mayo Clinic Rochester, Minnesota

Christopher E. Attinger, MD Professor Department of Plastic Surgery Georgetown University Medical Director The Limb Center Georgetown University Hospital Washington, District of Columbia

John D. Bauer, MD Assistant Professor, Division of Plastic Surgery Department of Surgery UTMB at Galveston Galveston, Texas

Robert W. Beasley, MD Professor of Surgery, New York University Director of New York University Hand Surgery Services, Institute of Reconstructive Plastic Surgery and Bellevue Hospital Center Hand Surgery Consultant, Veteran’s Administration Impartial Advisor to Chairman, New York State Workers’ Compensation Board, New York, New York Consulting Surgeon, Hackensack University Hospital, Hackensack, New Jersey

Michael S. Beckenstein, MD, FACS Birmingham, Alabama

Alberto Aviles, MD Resident in Plastic Surgery Department of Plastic Surgery Medical College of Wisconsin Milwaukee, Wisconsin

Stephen B. Baker, MD, DDS, FACS Associate Professor Associate Program Director Department of Plastic Surgery Georgetown University Hospital Washington, District of Columbia Co-Director, Craniofacial Clinic Inova Fairfax Hospital for Children Falls Church, Virginia

Scott P. Bartlett, MD Professor of Surgery University of Pennsylvania Mary Downs Endowed Chair in Pediatric Craniofacial Treatment and Research Children’s Hospital of Philadelphia Philadelphia, Pennsylvania

Steven J. Bates, MD Chief Resident Division of Plastic Surgery Stanford University Medical Center Stanford, California

Sean Boutros, MD Attending Surgeon Houston Plastic and Craniofacial Surgery Hermann Hospital and Children’s Memorial Hermann Hospital Houston, Texas

James P. Bradley, MD Associate Professor, Sarnat Craniofacial Chair Division of Plastic Surgery UCLA David Geffen School of Medicine Chief Pediatric Plastic Surgery Division of Plastic Surgery Mattel Children’s Hospital Los Angeles, California

Lawrence E. Brecht, DDS Clinical Assistant Professor of Surgery Department of Surgery New York University School of Medicine Co-Director of Craniofacial Prosthetics Institute of Reconstructive Plastic Surgery New York University Medical Center Clinical Associate Professor of Prosthodontics Director of Maxillofacial Prosthetics Advanced Education Program in Prosthodontics New York University College of Dentistry New York, New York

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Contributing Authors

Arnold S. Breitbart, MD, FACS

Mihye Choi, MD

Assistant Professor of Clinical Surgery Adjunct Assistant Professor of Surgery Columbia University College of Physicians and Surgeons Weill Cornell University Medical College New York, New York

Assistant Professor Department of Surgery New York University New York, New York

Mark A. Codner, MD

Duc T. Bui, MD Department of Surgery Stony Brook University Medical Center Stony Brook, New York

Clinical Assistant Professor Department of Plastic and Reconstructive Surgery Emory University Atlanta, Georgia

Charles E. Butler, MD Associate Professor The University of Texas M.D. Anderson Cancer Center, Department of Plastic Surgery, Houston, Texas

Sydney R. Coleman, MD Assistant Clinical Professor Department of Plastic Surgery New York University School of Medicine New York, New York

Peter E. M. Butler, MB, BSc (Hons) Consultant Plastic Surgeon Royal Free Hospital University College London London, England

Grant W. Carlson, MD Professor Department of Surgery Emory University Chief of Surgical Services Crawford W. Long Hospital Atlanta, Georgia

Peter G. Cordeiro, MD Professor of Surgery Department of Surgery Weill Medical College of Cornell University Chief, Plastic & Reconstructive Surgery Service Department of Surgery Memorial Sloan-Kettering Cancer Center New York, New York

Alfred Culliford IV, MD Division of Plastic, Reconstructive and Hand Surgery Staten Island University Hospital Staten Island, New York

Benjamin Chang, MD, FACS Associate Professor of Clinical Surgery Division of Plastic Surgery University of Pennsylvania School of Medicine Attending Surgeon Division of Plastic Surgery Hospital of the University of Pennsylvania Philadelphia, Pennsylvania

Court Cutting, MD Professor of Surgery-Plastic Surgery Director, Cleft Lip and Palate Program Institute of Reconstructive Plastic Surgery NYU Medical Center New York, New York

Genevieve de Bese, MD

James Chang, MD Associate Professor Division of Plastic Surgery Stanford University Medical Center Attending Surgeon Lucile Packard Children’s Hospital at Stanford Stanford University Medical Center Palo Alto, California

Raymond R. Chang, MD Assistant Professor of Surgery Department of Surgery, Division of Plastic Surgery George Washington University Attending Department of Surgery, Division of Plastic Surgery George Washington University Hospital Washington, District of Columbia

James J. Chao, MD, FACS Associate Professor of Plastic Surgery Department of Surgery University of California, San Diego School of Medicine San Diego, California

General Manager and Director of Research American Hand Prostheses New York, New York

Mark DeLacure, MD Associate Professor of Otolaryngology and Surgery (Plastic Surgery) New York University Medical Center New York, New York

Joseph J. Disa, MD, FACS Associate Attending Surgeon Plastic and Reconstructive Surgery Service Memorial Sloan-Kettering Cancer Center New York, New York

Matthias B. Donelan, MD Associate Clinical Professor of Surgery Harvard Medical School Chief of Plastic Surgery Shriners Burns Hospital Boston, Massachusetts



Ivica Ducic, MD, PhD

Robert D. Galiano, MD

Associate Professor Chief–Peripheral Nerve Surgey Department of Plastic Surgery Georgetown University Hospital Washington, District of Columbia

Institute of Reconstructive Plastic Surgery New York University New York, New York

Roy G. Geronemus, MD, PC

Gregory A. Dumanian, MD, FACS Associate Professor of Surgery Department of Surgery, Division of Plastic Surgery Feinberg School of Medicine, Northwestern University Associate Professor of Surgery Department of Surgery, Division of Plastic Surgery Northwestern Memorial Hospital Chicago, Illinois

Laser and Skin Surgery Center of New York Clinical Professor Department of Dermatology New York Medical Center New York, New York

Giulio Gherardini, MD, PhD Rome, Italy

Mary K. Gingrass, MD, FACS

Charles J. Eaton, MD Hand Surgeon Department of Surgery Jupiter Medical Center Jupiter, Florida

Charles R. Effron, MD Rochelle Park, New Jersey

L. Franklyn Elliott II, MD Atlanta Plastic Surgery, P.C. Atlanta, Georgia

Gregory R. D. Evans, MD, FACS Professor of Surgery and Biomedical Engineering Chief Aesthetic Plastic Surgery University of California Irvine Professor of Surgery and Biomedical Engineering Chief Aesthetic Plastic Surgery UCI Medical Center Orange, California

Maryam Feili-Hariri, PhD Assistant Professor Surgery and Immunology University of Pittsburgh Pittsburgh, Pennsylvania

Assistant Clinical Professor Department of Plastic Surgery Vanderbilt University School of Medicine Chief of Plastic Surgery Department of Plastic Surgery Baptist Hospital Nashville, Tennessee

Cornelia N. Golimbu, MD Professor of Radiology Department of Radiology New York University Medical Center New York, New York

Arun K. Gosain, MD Professor Department of Surgery Case Western Reserve University University Hospital (Lakeside) Chief Section of Craniofacial and Pediatric Plastic Surgery Rainbow Babies and Childrens Hospital Cleveland, Ohio

Barry Grayson, DDS

Derek T. Ford, MD, FRCSC Private Practice Toronto, Ontario, Canada

M. Felix Freshwater, MD Miami, Florida

David W. Friedman, MD Assistant Professor Department of Surgery-Plastic New York University Fellowship Director Hand Surgery New York University Medical Center New York, New York

Associate Professor of Surgery (Orthodontics) Institute of Reconstructive Plastic Surgery New York University School of Medicine Tisch Hospital New York, New York

Arin K. Greene, MD, MMSc Craniofacial Fellow Department of Plastic Surgery Children’s Hospital Boston, Harvard Medical School Boston, Massachusettes

Geoffrey C. Gurtner, MD, FACS Associate Professor of Surgery Department of Surgery, Division of Plastic Surgery Stanford University School of Medicine Stanford, California

Jeffrey D. Friedman, MD

J. Joris Hage, MD, PhD

Assistant Professor Department of Plastic Surgery Baylor College of Medicine The Methodist Hospital Houston, Texas

Chief Department of Plastic and Reconstructive Surgery Netherlands Cancer Institute-Antoni van Leeuwenhoek Hospital Amsterdam, The Netherlands

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Elizabeth J. Hall-Findlay, MD, FRCSC

John N. Jensen, MD

Plastic Surgeon Mineral Springs Hospital Banff Alberta, Canada

Department of Plastic Surgery Medical College of Wisconsin Milwaukee, Wisconsin

Dennis C. Hammond, MD Center for Breast & Body Contouring Grand Rapids, Michigan

Michael Hausman, MD Assistant Professor Department of Orthopaedics Chief, Hand Service Mount Sinai Hospital New York, New York

Neil F. Jones, MD, FRCS Professor Division of Plastic & Reconstructive Surgery Department of Orthopedic Surgery University of California Los Angeles Chief of Hand Surgery UCLA Hand Center UCLA Medical Center Los Angeles, California

Robert J. Havlik, MD Professor Department of Surgery-Section of Plastic Surgery Indiana University School of Medicine Chief Section of Plastic Surgery Riley Hospital for Children Indianapolis, Indiana

Michael A. C. Kane, MD, BS

Alexes Hazen, MD

Nolan S. Karp, MD

Attending, Plastic Surgery Department of Plastic Surgery NYU Medical Center Chief Plastic Surgery Manhattan Veterans Administration Hospital New York, New York

David A. Hidalgo, MD New York, New York

Larry Hollier, Jr., MD Associate Professor/Residency Program Director Department of Plastic Surgery Baylor College of Medicine Texas Children’s Hospital Ben Taub General Hospital Houston, Texas

Richard A. Hopper, MD, MS Associate Professor Department of Surgery University of Washington Surgical Director The Craniofacial Center Seattle Children’s Hospital Seattle, Washington

Christopher J. Hussussian, MD Plastic Surgery Associates Waukesha, Wisconsin

Alamgir Isani, MD Clinical Assistant Professor Plastic Surgery New York University Medical Center New York, New York

Jeffrey E. Janis, MD Assistant Professor Chief of Plastic Surgery Parkland Health Hospital System Co-Director Plastic Surgery Residency Program University of Texas Southwestern Medical Center Dallas, Texas

Attending Surgeon Department of Plastic Surgery Manhattan Eye, Ear & Throat Hospital New York, New York

Associate Professor of Plastic Surgery NYU School of Medicine New York, New York

Armen K. Kasabian, MD Assistant Professor of Plastic Surgery Department of Plastic Surgery New York University Medical Center Chief, Section of Microsurgery Institute of Reconstructive Plastic Surgery New York, New York

Henry Kawamoto, Jr., MD, DDS Clinical Professor Department of Surgery, Division of Plastic Surgery UCLA Los Angeles, California

Patrick Kelley, MD Medical Director Craniofacial Center Children’s Hospital of Austin Austin, Texas

Amy Kells, MD, PhD Microsurgery Fellow Department of Plastic Surgery University of Mississippi Jackson, Mississippi

Karen H. Kim, MD Director of Research Laser and Skin Surgery Center of New York New York, New York

Arnold William Klein, MD Professor of Medicine and Dermatology Department of Medicine and Dermatology David Geffen School of Medicine at UCLA Beverly Hills, California



Matthew B. Klein, MD

Otway Louie, MD

Assistant Professor Department of Plastic Surgery University of Washington Associate Director University of Washington Burn Center Harborview Medical Center Seattle, Washington

House Staff Institute of Reconstructive and Plastic Surgery NYU Medical Center New York, New York

David W. Low, MD Associate Professor of Surgery Division of Plastic Surgery University of Pennsylvania School of Medicine Philadelphia, Pennsylvania

David M. Knize, MD Associate Clinical Professor of Plastic Surgery Department of Surgery University of Colorado Health Sciences Center Denver, Colorado Former Chief of Plastic Surgery Department of Surgery Swedish Medical Center Englewood, Colorado

Susan E. Mackinnon, MD Shoenberg Professor and Chief Division of Plastic and Reconstructive Surgery Washington University in St. Louis Barnes-Jewish Hospital St. Louis, Missouri

James Knoetgen, III, MD Consultant in Plastic Surgery Department of Surgery, Division of Plastic Surgery Mayo Clinic Rochester, Minnesota

John S. Mancoll, MD Fort Wayne, Indiana

Ralph T. Manktelow, MD, FRCS(c) Professor of Surgery University of Toronto Staff Surgeon Department of Surgery Toronto General Hospital Toronto, Ontario, Canada

Howard N. Langstein, MD Department of Plastic Surgery The University of Texas M. D. Anduson Cancer Center Houston, Texas

W. P. Andrew Lee, MD Professor of Surgery University of Pittsburgh Chief Division of Plastic Surgery University of Pittsburgh Medical Center Pittsburgh, Pennsylvania

Stephen J. Mathes, MD

Salvatore C. Lettieri, MD

Lawrence D. Bell Professor of Plastic Surgery Institute of Reconstructive Plastic Surgery NYU School of Medicine Director Institute of Reconstructive Plastic Surgery NYU Medical Center New York, New York

Institute of Reconstructive Plastic Surgery New York University Medical Center New York, New York

Joseph G. McCarthy, MD

Instructor Department of Plastic Surgery Mayo Graduate School Rochester, Minnesota Chief Department of Plastic Surgery Maricopa Medical Center Phoenix, Arizona

Babak J. Mehrara, MD Assistant Professor Department of Surgery Columbia University New York Hospital-Cornell MedicalCenter Assistant Attending Memorial Sloan-Kettering Cancer Center New York, New York

Jamie Levine, MD Assistant Professor Division of Plastic Surgery New York University Chief Plastic and Microsurgery Department of Surgery Bellevue Hospital New York, New York

Frederick J. Menick, MD

J. William Littler, MD Professor Emeritus of Clinical Surgery Columbia University Department of Surgery; and Retired Senior Attending Physician, Chief of Plastic and Reconstructive Surgery St. Luke’s-Roosevelt Hospital Center New York, New York

Associate Clinical Professor Division of Plastic Surgery University of Arizona Staff Surgeon Division of Plastic Surgery St. Joseph’s Hospital Tucson, Arizona

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Timothy A. Miller, MD

John A. Perrotti, MD

Professor and Chief Plastic Surgery University of California School of Medicine David Geffen School of Medicine at UCLA Department of Surgery UCLA Medical Center Los Angeles, California

Clinical Assistant Professor Department of Surgery New York Medical College Valhalla, New York Attending Surgeon Department of Plastic Surgery Manhattan Eye, Ear and Throat Surgery New York, New York

Blake A. Morrison, MD Private Practice North Texas Hand Surgery Dallas, Texas

Hannan Mullett, MD, FRCS (TR & ORTM) Consultant Orthopaedic Surgeon Department of Orthopaedic Surgery Beaumont Hospital Dublin, Ireland

John B. Mulliken, MD Professor of Surgery Harvard Medical School Director Craniofacial Centre Department of Plastic Surgery Children’s Hospital Boston, Massachusetts

Thomas A. Mustoe, MD Professor Department of Surgery, Division of Plastic Surgery Feinberg School of Medicine, Northwestern University Chief Department of Plastic Surgery Northwestern Memorial Hospital Chicago, Illinois

Terence M. Myckatyn, MD, FRCSC Assistant Professor Department of Plastic and Reconstructive Surgery Washington University School of Medicine St. Louis, Missouri

Randall Nacamuli, MD Resident Division of Plastic and Reconstructive Surgery Oregon Health Sciences University Portland, Oregon

James D. Namnoum, MD Atlanta Plastic Surgery, P.C. Atlanta, Georgia

Peter C. Neligan, MB, FRCSC, FACS Wharton Chair in Reconstructive Plastic Surgery Professor and Chair, Division of Plastic Surgery University of Toronto Toronto, Canada

Martin I. Newman, MD Active Staff Department of Plastic & Reconstructive Surgery Cleveland Clinic Florida Weston, Florida

John A. Persing, MD Professor and Chief Plastic Surgery, Professor of Neurosurgery Yale University School of Medicine Chief Plastic Surgery Yale-New Haven Hospital New Haven, Connecticut

Linda G. Phillips, MD Truman G. Blocker Distinguished Professor and Chief Division of Plastic Surgery UTMB Galveston Galveston, Texas

Michael L. Reed, MD Associate Clinical Professor Department of Dermatology New York University School of Medicine Attending Physician Department of Dermatology New York University Medical Center New York, New York

Rod J. Rohrich, MD, FACS Professor and Chairman Department of Plastic Surgery The University of Texas Southwestern Medical Center Chief of Plastic Surgery Department of Plastic Surgery University Hospital – Zale Lipshy Dallas, Texas

Harvey M. Rosen, MD, DMD Clinical Associate Professor Department of Surgery University of Pennsylvania Chief Division of Plastic Surgery Pennsylvania Hospital Philadelphia, Pennsylvania

George H. Rudkin, MD, FACS Clinical Associate Professor Department of Plastic Surgery UCLA Medical Center Chief, Plastic Surgery Department of Plastic Surgery VA West Los Angeles Los Angeles, California

Pierre B. Saadeh, MD Assistant Professor Attending Physician Department of Surgery, Plastic Surgery New York University School of Medicine New York, New York



Hrayr K. Shahinian, MD, FACS

Alisa C. Thorne, MD

Director Skull Base Institute Cedars-Sinai Medical Office Towers Los Angeles, California

Professor of Clinical Anesthesiology Weil Cornell School of Medicine Director of Ambulatory Anesthesia Memorial Sloan Kettering Cancer Center New York, New York

Sheel Sharma, MD Faculty Department of Plastic and Reconstructive Surgery Hackensock, New Jersey

Joseph H. Shin, MD Associate Professor of Surgery Director Yale Craniofacial Center Department of Plastic Surgery Yale University School of Medicine Attending Physician Yale New Haven Hospital New Haven, Connecticut

Sumner A. Slavin, MD Division of Plastic Surgery Beth Israel Deaconess Medical Center Harvard Medical School Brookline, Massachusetts

Hooman Soltanian, MD, FACS Attending Specialties of Plastic Surgery Hartford, Connecticut

Scott L. Spear, MD Chairman Department of Plastic Surgery Georgetown University Professor and Chairman Department of Plastic Surgery Georgetown University Hospital Washington, District of Columbia

Henry M. Spinelli, MD

Charles H. Thorne, MD Associate Professor Department of Plastic Surgery NYU School of Medicine New York, New York

John T. Tymchak, MD, FACS Clinical Assistant Professor Department of Surgery SUNY Health Science Center at Brooklyn Director, Division of Plastic Surgery and Hand Surgery Services Department of Surgery, Division of Plastic Surgery The Brookdale University Hospital and Medical Center Brooklyn, New York

Lok Huei Yap, MD Department of Plastic Surgery The University of Texas M.D. Anderson Cancer Center Houston, Texas

Michael J. Yaremchuk, MD Clinical Professor Department of Surgery Harvard Medical School Chief of Craniofacial Surgery Department of Plastic Surgery Massachusetts General Hospital Boston, Massachusetts

Paul Zidel, MD, MS, FACS

Clinical Professor of Surgery Department of Surgery Weill Medical College of Cornell University Attending Surgeon Department of Plastic Surgery New York Presbyterian Hospital – Weill Cornell New York, New York

Clinical Faculty Department of Surgery Nova Southeastern University Fort Lauderdale, Florida Attending Department of Surgery University Hospital Tamarac, Florida

G. Ian Taylor, AO

Ronald M. Zuker, MD, FRCSC, FACS

Professor Department of Anatomy and Cell Biology University of Melbourne Senior Consultant Department of Reconstructive Plastic Surgery Royal Melbourne Hospital Parkville, Victoria, Canada

Professor of Surgery Department of Surgery University of Toronto Staff Surgeon Division of Plastic Surgery The Hospital for Sick Children Toronto, Ontario, Canada

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PREFACE

Although I can vouch that the editors are humble, our task was not: to produce a comprehensive text covering all of plastic surgery in a single volume. Grabb and Smith’s Plastic Surgery is now the only single-volume text that attempts such a feat. In fact, the book was based on the belief that with proper editing, our single volume could contain all the essential information of any multiple-volume text. The second challenge was to make the book sufficiently new to justify calling it a “new” edition. Of the 93 chapters, over two thirds (64) are completely new, with new authors. The remaining 29 chapters were re-written, in many cases completely. The number of topics covered increased in all areas except Hand, with the largest expansion in the Breast and Cosmetic sections. We grouped ten chapters within a newly titled section, Congenital Anomalies and Pediatric Plastic Surgery. Every chapter is shorter than its counterpart in the previous edition, and references were limited to 15. Our authors are experts in their fields, and their skills in surgery are equaled by their writing skills. I am grateful that they accepted my editing,

some of which was quite deep in my attempts to keep chapters pithy. The downside of a single volume that is comprehensive enough for examination preparation is its weight! As our senior co-editor Dr. Beasley warned, “It should be light enough to take to bed with you.” In this regard, we may have failed, but we feel comfortable blaming the scope of the field rather than the competence of the editors. The book is intended for medical professionals and trainees at all levels: Practicing plastic surgeons, surgeons in related fields such as Ophthalmology, Otolaryngology, Oral Surgery, Orthopedics and General Surgery, surgery residents in all subspecialties, medical students, physicians assistants, nurses, and nurse practitioners. My thanks to the co-editors, authors, Lippincott Williams and & Wilkins, and Dovetail Content Solutions for their contributions to this worthy endeavor.

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Charles H. Thorne, MD

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CONTENTS

Contributing Authors vii Preface xv

PART I ■ PRINCIPLES, TECHNIQUES, AND BASIC SCIENCE

14

Mohs Micrographic Surgery 115 Karen H. Kim Roy G. Geronemus

15

Congenital Melanocytic Nevi 120 John N. Jensen Arun K. Gosain

1

Techniques and Principles in Plastic Surgery 03 Charles H. Thorne

2

Wound Healing: Normal and Abnormal 15 Geoffrey C. Gurtner

16

Malignant Melanoma 124 Christopher J. Hussussian

3

Wound Care 23 Robert D. Galiano Thomas A. Mustoe

17

Thermal, Chemical, and Electrical Injuries 132 Matthew B. Klein

4

The Blood Supply of the Skin 33 G. Ian Taylor

18

Principles of Burn Reconstruction 150 Matthias B. Donelan

5

Muscle Flaps and Their Blood Supply 42 Stephen J. Mathes Jamie Levine

19

Radiation and Radiation Injuries 162 James Knoetgen III Salvatore C. Lettieri P. G. Arnold

6

Transplant Biology and Applications to Plastic Surgery 52 W.P. Andrew Lee Maryam Feili-Hariri Peter E. M. Butler

20

Lasers in Plastic Surgery 169 David W. Low

7

Implant Materials 58 Arnold S. Breitbart Valerie J. Ablaza

8

Principles of Microsurgery 66 Lok Huei Yap Charles E. Butler

9

Microsurgical Repair of Peripheral Nerves and Nerve Grafts 73 Terence M. Myckatyn Susan E. Mackinnon

10

Tissue Expansion 84 Bruce S. Bauer

11

Local Anesthetics 91 Alisa C. Thorne

12

PART III ■ CONGENITAL ANOMALIES AND PEDIATRIC PLASTIC SURGERY Embryology of the Head and Neck 179 Arun K. Gosain Randall Nacamuli

22

Vascular Anomalies 191 John B. Mulliken

23

Cleft Lip and Palate 201 Richard A. Hopper Court Cutting Barry Grayson

24

Nonsyndromic Craniosynostosis and Deformational Plagiocephaly 226 Joseph H. Shin John A. Persing

25

Craniosynostosis Syndromes 237 Scott P. Bartlett

26

Craniofacial Microsomia 248 Joseph G. McCarthy

27

Orthognathic Surgery 256 Stephen B. Baker

Principles of Craniofacial Distraction 96 Joseph G. McCarthy

PART II ■ SKIN AND SOFT TISSUE 13

21

Dermatology for Plastic Surgeons 105 Alfred Culliford IV Alexes Hazen

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Contents

28

Craniofacial Clefts and Hypertelorbitism 268 James P. Bradley Henry Kawamoto, Jr.

29

Miscellaneous Craniofacial Conditions: Fibrous Dysplasia, Moebius Syndrome, Romberg’s Syndrome, Treacher Collins Syndrome, Dermoid Cyst, Neurofibromatosis 281 Robert J. Havlik

PART V ■ AESTHETIC SURGERY 44

Cutaneous Resurfacing: Chemical Peeling, Dermabrasion, and Laser Resurfacing 459 John A. Perrotti

45

Filler Materials 468 Arnold William Klein

46

Botulinum Toxin 475 Michael A.C. Kane

47

Structural Fat Grafting 480 Sydney R. Coleman

48

Blepharoplasty 486 Mark A. Codner Derek T. Ford

49

Facelift 498 Charles H. Thorne

50

Forehead Lift 509 David M. Knize

51

Skull Base Surgery 347 Hrayr K. Shahinian

Rhinoplasty 517 Jeffrey E. Janis Rod J. Rohrich

52

34

Craniofacial and Maxillofacial Prosthetics 350 Lawrence E. Brecht

Liposuction 533 Mary K. Gingrass

53

35

Reconstruction of the Scalp, Calvarium, and Forehead 358 Lok Huei Yap Howard N. Langstein

Abdominoplasty and Lower Truncal Circumferential Body Contouring 542 Al Aly

54

Facial Skeletal Augmentation With Implants 551 Michael J. Yaremchuk

55

Osseous Genioplasty 557 Harvey M. Rosen

56

Hair Transplantation 562 Michael L. Reed

30

Otoplasty and Ear Reconstruction 297 Charles H. Thorne

PART IV ■ HEAD AND NECK 31

Soft Tissue and Skeletal Injuries of the Face 315 Larry Hollier, Jr. Patrick Kelley

32

Head and Neck Cancer and Salivary Gland Tumors 333 Pierre B. Saadeh Mark D. DeLacure

33

36

Reconstruction of the Lips 367 Sean Boutros

37

Reconstruction of the Cheeks 375 Babak J. Mehrara

38

Nasal Reconstruction 389 Frederick J. Menick

39

Reconstruction of the Eyelids, Correction of Ptosis, and Canthoplasty 397 Martin I. Newman Henry M. Spinelli

57

Facial Paralysis Reconstruction 417 Ralph T. Manktelow Ronald M. Zuker Peter C. Neligan

Augmentation Mammoplasty and Its Complications 575 Sumner A. Slavin Arin K. Greene

58

Mastopexy and Mastopexy Augmentation 585 Nolan S. Karp

59

Breast Reduction: Inverted-T Technique 593 Scott L. Spear

60

Vertical Reduction Mammaplasty 604 Elizabeth J. Hall-Findlay

61

Gynecomastia 616 Nolan S. Karp

62

Breast Cancer for the Plastic Surgeon 621 Grant W. Carlson

63

Breast Reconstruction: Prosthetic Techniques 625 Joseph J. Disa

40

41

42

43

Mandible Reconstruction 428 Joseph J. Disa David A. Hidalgo Reconstruction of Defects of the Maxilla and Skull Base 438 Duc T. Bui Peter G. Cordeiro Reconstruction of the Oral Cavity, Pharynx, and Esophagus 447 Giulio Gherardini Gregory R.D. Evans

PART VI ■ BREAST


Contents

xix

64

Latissimus Dorsi Flap Breast Reconstruction 634 Dennis C. Hammond

79

Soft-Tissue Reconstruction of the Hand 771 John Tymchak

65

Breast Reconstruction: Tram Flap Techniques 641 James D. Namnoum

80

66

Breast Reconstruction—Free Flap Techniques 648 L. Franklyn Elliott

Fractures and Ligamentous Injuries of the Wrist 781 Hannan Mullett Michael Hausman

81

Fractures, Dislocations, and Ligamentous Injuries of the Hand 790 David W. Friedman Amy Kells Alberto Aviles

82

Tendon Healing and Flexor Tendon Surgery 803 Paul Zidel

83

Repair of the Extensor Tendon System 810 Steven J. Bates James Chang

84

Infections of the Upper Limb 817 James J. Chao Blake A. Morrison

85

Tenosynovitis 826 Hooman Soltanian

86

Compression Neuropathies in the Upper Limb and Electrophysioiogic Studies 830 Charles R. Effron Robert W. Beasley

87

Thumb Reconstruction 835 Charles J. Eaton

88

Tendon Transfers 847 Robert W. Beasley

89

Congenital Hand Abnormalities 856 Mihye Choi Sheel Sharma Otway Louie

90

Dupuytren’s Disease 864 M. Felix Freshwater

PART VIII ■ HAND

91

Replantation in the Upper Extremity 868 Neil F. Jones

76

Plastic Surgeons and the Development of Hand Surgery 737 J. William Littler

92

Upper Limb Arthritis 884 Alamgir Isani

77

Principles of Upper Limb Surgery 741 Benjamin Chang

93

Upper Limb Amputations and Prostheses 892 Robert W. Beasley Genevieve de Bese

78

Radiologic Imaging of the Hand and Wrist 746 Cornelia N. Golimbu

67

Nipple Reconstruction 657 Michael S. Beckenstein

PART VII ■ TRUNK AND LOWER EXTREMITY 68

Thoracic Reconstruction 665 Raymond R. Chang

69

Abdominal Wall Reconstruction 670 Gregory A. Dumanian

70

Lower-Extremity Reconstruction 676 Armen K. Kasabian Nolan S. Karp

71

Foot and Ankle Reconstruction 689 Christopher E. Attinger Ivica Ducic

72

Reconstruction of the Perineum 708 Jeffrey D. Friedman

73

Lymphedema 717 George H. Rudkin Timothy A. Miller

74

Pressure Sores 722 John D. Bauer John S. Mancoll Linda G. Phillips

75

Reconstruction of the Penis 730 J. Joris Hage

Index 901

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GRABB AND SMITH’S PLASTIC SURGERY S I X T H

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E D I T I O N



PART I ■ PRINCIPLES, TECHNIQUES, AND BASIC SCIENCE

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CHAPTER 1 ■ TECHNIQUES AND PRINCIPLES IN PLASTIC SURGERY CHARLES H. THORNE

Plastic surgery is a unique specialty that defies definition, has no organ system of its own, is based on principles rather than specific procedures, and, because of cosmetic surgery, is the darling of the media. What is plastic surgery? No complete definition exists. Joe McCarthy defines it as the “problem-solving specialty.” My wife, an anesthesiologist, calls plastic surgeons the “finishers” because they come in when “the other surgeons have done all they can do and the operation has to be finished.” An even more grandiose definition is the following from a plastic surgery resident: “Plastic surgery is surgery of the skin and its contents.” There is no way to define this specialty that has acquired “turf” through a combination of tradition and innovation. What is the common denominator between craniofacial surgery and hand surgery? Between pressure sore surgery and cosmetic surgery? Unlike other surgical specialties, plastic surgery is not organized around a specific organ system. Plastic surgery has only traditional areas of expertise and principles on which to rely for its existence and future. Because plastic surgery has loose boundaries and no specific anatomic region, it faces competition from regionally oriented specialties. Traditional areas of expertise can be lost as other specialties acquire the skills to perform the procedures developed by plastic surgeons. Consequently, plastic surgery has both freedom and vulnerability. It is this vulnerability that makes plastic surgery dependent on both the maintenance of superiority in the traditional areas of expertise and on continued innovation and acquisition of new techniques, new procedures, new problems to solve—that is, new turf. Plastic surgery is based more on principles than on the details of specific procedures. This allows the plastic surgeon to solve unusual problems, to operate from the top of the head to the tip of the toe, to apply known procedures to other body parts, and to be innovative. No specialty receives the attention from the lay press that plastic surgery receives. At the same time, no specialty is lesswell understood. Although the public equates plastic surgery with cosmetic surgery, the roots of plastic surgery lie in its reconstructive heritage. Cosmetic surgery, an important component of plastic surgery, is but one piece of the plastic surgical puzzle. Plastic surgery consists of reconstructive surgery and cosmetic surgery but the boundary between the two, like the boundary of plastic surgery itself, is difficult to draw. The more one studies the specialty, the more the distinction between cosmetic surgery and reconstructive surgery disappears. Even if one asks, as an insurance company does, about the functional importance of a particular procedure, the answer often hinges on the realization that the function of the face is to look like a face (i.e., function = appearance). A cleft lip is repaired so the child will look, and therefore hopefully function, like other children. A common procedure such as a breast reduction is enormously complex when one considers the issues of appear-

ance, self-image, sexuality, and womanhood, and defies categorization as simply cosmetic or necessarily reconstructive. This chapter outlines basic plastic surgery principles and techniques that deal with the skin. Cross-references to specific chapters providing additional information are provided. Subsequent chapters in the first section will discuss other concepts and tools that allow plastic surgeons to tackle more complex problems. Almost all wounds and all procedures involve the skin, even if it is only an incision, and therefore the cutaneous techniques described in this text are applicable to virtually every procedure performed by every specialty in surgery.

OBTAINING A FINE-LINE SCAR “Will there be a scar?” Even the most intelligent patients ask this preposterous question. When a full-thickness injury occurs to the skin or an incision is made, there is always a scar. The question should be, “Will I have a relatively inconspicuous fineline scar?” The final appearance of a scar is dependent on many factors, including the following: (a) Differences between individual patients that we do not yet understand and cannot predict; (b) the type of skin and location on the body; (c) the tension on the closure; (d) the direction of the wound; (e) other local and systemic conditions; and, lastly, (f) surgical technique. The same incision or wound in two different patients will produce scars that differ in quality and aesthetics. Oily or pigmented skin produces, as a general rule, more unsightly scars (Chapter 2 discusses hypertrophic scars and keloids). Thin, wrinkled, pale, dry, “WASPy” skin of patients of English or Scotch-Irish descent usually results in more inconspicuous scars. Rules are made to be broken, however, and an occasional patient will develop a scar that is not characteristic of his or her skin type. Certain anatomic areas routinely produce unfavorable scars that remain hypertrophic or wide. The shoulder and sternal area are such examples. Conversely, eyelid incisions almost always heal with a fine-line scar. Skin loses elasticity with age. Stretched-out skin, combined with changes in the subcutaneous tissue, produces wrinkling, which makes scars less obvious and less prone to widening in older individuals. Children, on the other hand, may heal faster but do not heal “better,” in that their scars tend to be red and wide when compared to scars of their grandparents. In addition, as body parts containing scars grow, the scars become proportionately larger. Beware the scar on the scalp of a small child! Just as the recoil of healthy, elastic skin in children may lead to widening of a scar, tension on a closure bodes poorly for the eventual appearance of the scar. The scar associated with a simple elliptical excision of a mole on the back will likely result

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4

Part I: Principles, Techniques, and Basic Science

FIGURE 1.1. Relaxed skin tension lines. (Reproduced with permission from Ruberg R. L. In: Smith DJ, ed. Plastic Surgery, A Core Curriculum. St. Louis: Mosby, 1994.)

in a much less appealing scar than an incisional wound. The body knows when it is missing tissue. The direction of a laceration or excision also determines the eventual appearance of the scar. The lines of tension in the skin were first noted by Dupuytren. Langer also described the normal tension lines, which became known as “Langer lines.” Borges referred to skin lines as “relaxed skin tension lines” (Fig. 1.1). Elective incisions or the excision of lesions are planned when possible so that the final scars will be parallel to the relaxed skin tension lines. Maximal contraction occurs when a scar crosses the lines of minimal tension at a right angle. Wrinkle lines are generally the same as the relaxed skin tension lines and lie perpendicular to the long axis of the underlying muscles. Other issues, which are not related to the scar itself but to perception, determine if a scar is noticeable. Incisions and scars can be “hidden” by placing them at the junction of aesthetic units (e.g., at the junction of the lip and cheek, along the nasolabial fold), where the eye expects a change in contour (Chapter 38). In contrast, an incision in the midcheek or midchin or tip of the nose will always be more conspicuous. The shape of the wound also affects ultimate appearance. The “trapdoor” scar results from a curvilinear incision or laceration that, after healing and contracture, appears as a depressed groove with bulging skin on the inside of the curve. Attempts at “defatting” the bulging area are never as satisfactory as either the patient or surgeon would like. Local conditions, such as crush injury of the skin adjacent to the wound, also affect the scar. So, too, will systemic conditions such as vascular disease or congenital conditions affecting elastin and/or wound healing. Nutritional status can affect wound healing, but usually only in the extreme of malnutrition or vitamin deficiency. Nutritional status is probably overemphasized as a factor in scar formation. Technique is also overemphasized (by self-serving plastic surgeons?) as a factor in determining whether a scar will be inconspicuous, but it is certainly of some importance. Minimizing damage to the skin edges with atraumatic technique, debridement of necrotic or foreign material, and a tension-free closure are the first steps in obtaining a fine-line scar. Ultimately,

however, scar formation is unpredictable even with meticulous technique. Two technical factors are of definite importance in increasing the likelihood of a “good” scar. First is the placement of sutures that will not leave permanent suture marks or the prompt removal of skin sutures so disfiguring “railroad tracks” do not occur. In other words, removing the sutures may be more important than placing them! Plastic surgeons have been known to mock other specialists for using heavy-gauge suture for skin closure, but the choice of sutures is irrelevant if the sutures are removed soon enough. Sutures on the face can usually be removed in 3 to 5 days and on the body in 7 days or less. Except for wounds over joints, sutures should rarely be left in for more than 1 week. A subcutaneous layer of closure and Steri-Strips are usually sufficient to prevent dehiscence. The second important technical factor that affects the appearance of scars is wound-edge eversion. In wounds where the skin is brought precisely together, there is a tendency for the scar to widen. In wounds where the edges are everted, or even hypereverted in an exaggerated fashion, this tendency is reduced, possibly by reducing the tension on the closure. In other words, the ideal wound closure may not be perfectly flat, but rather bulging with an obvious ridge, to allow for eventual spreading of that wound. Wound-edge eversion ALWAYS goes away. The surgeon need not ever worry that a hypereverted wound will remain that way; it will always flatten over time.

CLOSURE OF SKIN WOUNDS While the most common method of closing a wound is with sutures, there is nothing necessarily magic or superior about sutures. Staples, skin tapes, or wound adhesives are also useful in certain situations. Regardless of the method used, precise approximation of the skin edges without tension is essential to ensure primary healing with minimal scarring. Wounds that are deeper than skin are closed in layers. The key is to eliminate dead space, to provide a strong enough closure to prevent dehiscence while wound healing is occurring, and to precisely approximate the skin edges without tension. Not all layers necessarily require separate closure. A closure over the calf, however, is subject to motion, dependence, and stretching with walking, requiring a stronger closure than the scalp, which does not move, is less dependent, and not subject to tension in daily activities. Except for dermal sutures, which are placed with the knot buried to prevent it from emerging from the skin during the healing process, sutures should be placed with the knot superficial to the loop of the suture (not buried), so that the tissue layers can be everted (Fig. 1.2A). Buried dermal sutures provide strength so the external sutures can be removed early, but do not prevent the scar from spreading over time. There is no technique that reliably prevents a wound that has an inclination to widen from doing so.

Suturing Techniques Techniques for suturing are illustrated in Figure 1.2 and are listed below.

Simple Interrupted Suture The simple interrupted suture is the gold standard and the most commonly employed suture. The needle is introduced into the skin at an angle that allows it to pass into the deep dermis at a point further removed from the entry of the needle. This allows the width of suture at its base in the dermis to be wider


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Chapter 1: Techniques and Principles in Plastic Surgery

A

B

D

C

E

F

H

G

FIGURE 1.2. Types of skin closure. A: Simple interrupted. B: Vertical mattress. C: Horizontal mattress. D: Subcuticular continuous. E: Half-buried horizontal mattress. F: Continuous over-and-over. G: Staples. H: Skin tapes (skin adhesive performs a similar function).

than the epidermal entrance and exit points, giving the suture a triangular appearance when viewed in cross section and everting the skin edges. Care must be taken to ensure that the suture is placed at the same depth on each side of the incision or wound, otherwise the edges will overlap. Sutures are usually placed approximately 5 to 7 mm apart and 1 to 2 mm from the skin edge, although the location and size of the needle and caliber of the suture material make this somewhat variable.

Horizontal Mattress Suture Horizontal mattress sutures also provide approximation of the skin edges with eversion. They are particularly advantageous in thick glabrous skin (feet and hand). In the author’s opinion, horizontal mattress sutures are superior to their vertical counterparts.

Subcuticular Suture Vertical Mattress Suture Vertical mattress sutures may be used when eversion of the skin edges is desired and cannot be accomplished with simple sutures alone. Vertical mattress sutures tend to leave the most obvious and unsightly cross-hatching if not removed early.

Subcuticular (or intradermal) sutures can be interrupted or placed in a running fashion. In a running subcutaneous closure, the needle is passed horizontally through the superficial dermis parallel to the skin surface to provide close approximation of the skin edges. Care is taken to ensure that the sutures are placed at the same level. Such a technique obviates the need

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for external skin sutures and circumvents the possibility of suture marks in the skin. Absorbable or nonabsorbable suture can be used, with the latter to be removed at 1 to 2 weeks after suturing.

Half-Buried Horizontal Mattress Suture Half-buried horizontal mattress sutures are used when it is desirable to have the knots on one side of the suture line with no suture marks on the other side. For example, when insetting the areola in breast reduction, this method leaves the suture marks on the dark, pebbly areola instead of on the breast skin.

Continuous Over-and-Over Suture Continuous over-and-over sutures, otherwise known as running simple sutures can be placed rapidly but depend on the wound edges being more-or-less approximated beforehand. A continuous suture is not nearly as precise as interrupted sutures. Continuous sutures can also be placed in a locking fashion to provide hemostasis by compression of wound edges. They are especially useful in scalp closures.

Skin Staples Skin staples are particularly useful as a time saver for long incisions or to position a skin closure or flap temporarily before suturing. Grasping the wound edges with forceps to evert the tissue is helpful when placing the staples to prevent inverted skin edges. Staples must be removed early to prevent skin marks and are ideal for the hair-bearing scalp.

Skin Tapes Skin tapes can effectively approximate the wound edges, although buried sutures are often required in addition to skin tape to approximate deeper layers, relieve tension, and prevent inversion of the wound edges. Skin tapes can also be used after skin sutures are removed to provide added strength to the closure.

Skin Adhesives Skin adhesives have been developed, and may have a role in wound closure, especially in areas where there is no tension on the closure, or where strength of closure has been provided by a layer of buried dermal sutures. Adhesives, by themselves, however, do not evert the wound edges. Eversion must be provided by deeper sutures.

FIGURE 1.3. Elliptical excision. A: If the ellipse is too short, dog-ears (arrows) form at the ends of the closed wound. B: Correct method with length of ellipse at least three times the width.

Elliptical Excision Simple elliptical excision is the most commonly used technique (Fig. 1.3). Elliptical excision of inadequate length may yield “dog-ears,” which consist of excess skin and subcutaneous fat at the end of a closure. There are several ways to correct a dogear, some of which are shown in Figure 1.4. Dog-ears are the bane of plastic surgical existence and one must be facile with their elimination. Dog-ears do not disappear on their own.

Wedge Excision Lesions located at or adjacent to free margins can be excised by wedge excision. In some elderly patients, one third of the lower lip and one fourth of the upper lip can be excised with primary closure (Fig. 1.5)

Circular Excision

Methods of Excision Lesions of the skin can be excised with elliptical, wedge, circular, or serial excision.

When preservation of skin is desired (such as the tip of the nose) or the length of the scar must be kept to a minimum (children), circular excision might be desirable. Figure 1.6 shows some closure techniques. Figure 1.6 is included because these techniques

FIGURE 1.4. Three methods of removing a dog-ear caused by making the elliptical excision too short. A: Dog-ear excised, making the incision longer, or converted to a “Y”. B: One method of removing a dog-ear caused by designing an elliptical excision with one side longer than the other. Conversion to an “L” effectively lengthens the shorter side.



7

FIGURE 1.5. Wedge excisions of the ear, lower eyelid and lip.

may be of value, as well as for historical purposes. Circular defects can also be closed with a purse-string suture that causes significant bunching of the skin. This is allowed to mature for many months and may result in a shorter scar on, for example, the face of a child.

Serial Excision Serial excision is the excision of a lesion in more than one stage. Serial excision and tissue expansion (Chapter 10) are frequently employed for large lesions such as congenital nevi. The inherent viscoelastic properties of skin are used, allowing the skin to “stretch” over time. These techniques enable wound closure to be accomplished with a shorter scar than if the original lesion was elliptically excised in a single stage.

SKIN GRAFTING Skin grafts are a standard option for closing defects that cannot be closed primarily. A skin graft consists of epidermis and some or all of the dermis. By definition, a graft is something that is removed from the body, is completely devascularized, and is replaced in another location. Grafts of any kind require vascularization from the bed into which they are placed for survival. Any tissue which is not completely removed prior to placement is not a graft.

Skin Graft Types Skin grafts are classified as either split-thickness or fullthickness, depending on the amount of dermis included. Splitthickness skin grafts contain varying amounts of dermis, whereas a full-thickness skin graft contains the entire dermis (Fig. 1.7). All skin grafts contract immediately after removal from the donor site and again after revascularization in their final location. Primary contraction is the immediate recoil of freshly harvested grafts as a result of the elastin in the dermis. The more dermis the graft has, the more primary the contraction that will be experienced. Secondary contracture, the real nemesis, involves contraction of a healed graft and is probably a result of myofibroblast activity. A full-thickness skin graft contracts more on initial harvest (primary contraction) but less on healing (secondary contracture) than a split-thickness skin

FIGURE 1.6. Closure of wounds following circular excision. A: Skin graft. B: Sliding triangular subcutaneous pedicle flaps can be advanced to close the circular defect; the triangular defect is closed in a V-Y fashion. C: Transposition flaps based on a skin pedicle and rotated toward each other can also be used. Circular defects can also be closed by other local flaps (Figs. 1.10–1.15) or by pursestring suture.

graft. The thinner the split-thickness skin graft, the greater the secondary contracture. Granulating wounds left to heal secondarily, without any skin grafting, demonstrate the greatest degree of contracture and are most prone to hypertrophic scarring. The number of epithelial appendages transferred with a skin graft depends on the thickness of the dermis present. The ability of grafted skin to sweat depends on the number of glands transferred and the sympathetic reinnervation of these glands from the recipient site. Skin grafts are reinnervated by ingrowth of nerve fibers from the recipient bed and from the periphery. Full-thickness skin grafts have the greatest sensory return because of a greater availability of neurilemmal sheaths. Hair follicles are also transferred with a full-thickness

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FIGURE 1.7. Skin graft thickness.

skin graft. In general, full-thickness skin grafts demonstrate the hair growth of the donor site whereas split-thickness skin grafts, especially thin split-thickness skin grafts, are generally hairless.

skin grafts result in a “pebbled” appearance that, at times, is aesthetically unacceptable. In contrast, a sheet skin graft has the advantage of a continuous, uninterrupted surface, often leading to a superior aesthetic result, but has the disadvantages of not allowing serum and blood to drain through it and the need for a larger skin graft.

Requirements for Survival of a Skin Graft The success of skin grafting, or “take,” depends on the ability of the graft to receive nutrients and, subsequently, vascular ingrowth from the recipient bed. Skin graft revascularization or “take” occurs in three phases. The first phase involves a process of serum imbibition and lasts for 24 to 48 hours. Initially, a fibrin layer forms when the graft is placed on the recipient bed, binding the graft to the bed. Absorption of nutrients into the graft occurs by capillary action from the recipient bed. The second phase is an inosculatory phase in which recipient and donor end capillaries are aligned. In the third phase, the graft is revascularized through these “kissing” capillaries. Because the full-thickness skin graft is thicker, survival of the graft is more precarious, demanding a well-vascularized bed. To optimize take of a skin graft, the recipient site must be prepared. Skin grafts require a vascular bed and will seldom take in exposed bone, cartilage, or tendon devoid of their periosteum, perichondrium, or paratenon. There are exceptions, however, as skin grafts are frequently successful inside the orbit or on the temporal bone, despite removal of the periosteum. Close contact between the skin graft and its recipient bed is essential. Hematomas and seromas under the skin graft will compromise its survival, and immobilization of the graft is essential.

Skin Graft Adherence For the skin graft to take, it must adhere to the bed. There are two phases of graft adherence. The first begins with placement of the graft on the recipient bed, to which the graft adheres because of fibrin deposition. This lasts approximately 72 hours. The second phase involves ingrowth of fibrous tissue and vessels into the graft.

Meshed versus Sheet Skin Grafts Multiple mechanical incisions result in a meshed skin graft, allowing immediate expansion of the graft. A meshed skin graft covers a larger area per square centimeter of graft harvest and allows drainage through the numerous holes. Meshed

Skin Graft Donor Sites The donor site epidermis regenerates from the immigration of epidermal cells originating in the hair follicle shafts and adnexal structures left in the dermis. In contrast, the dermis never regenerates. Because split-thickness skin grafts remove only a portion of the dermis, the original donor site may be used again for a subsequent split-thickness skin graft harvest. Thus, the number of split-thickness skin grafts harvested from a donor site is directly dependent on the donor dermis thickness. Fullthickness skin graft donor sites must be closed primarily because there are no remaining epithelial structures to provide re-epithelialization. Skin grafts can be taken from anywhere on the body, although the color, texture, thickness of the dermis, vascularity, and donor site morbidity of body locations vary considerably. Skin grafts taken from above the clavicles provide a superior color match for defects of the face. The upper eyelid skin can also be used, as it provides a small amount of very thin skin. Full-thickness skin graft harvest sites are closed primarily and are therefore of smaller size. The scalp, abdominal wall, buttocks, and thigh are common donor sites for split-thickness skin grafts. Surgeons should avoid the mistake of harvesting split-thickness skin grafts from the most accessible locations such as the anterior thigh. Although donor sites heal by reepithelialization, there is always visible evidence that an area was used as a donor site. This can vary from keloids to simple hyper- or hypopigmentation. Less-conspicuous donor sites are the buttocks or scalp. Split-thickness skin grafts harvested from the scalp will have hair in them initially but no hair follicles and therefore will ultimately be hairless. The hair in the scalp donor site will return after re-epithelialization because the hair follicles were left undisturbed.

Postoperative Care of Skin Grafts and Donor Sites Causes of graft failure include collection of blood or serum beneath the graft (raising the graft from the bed and preventing revascularization), movement of the graft on the bed



9

Biologic Dressings

FIGURE 1.8. Tie-over bolster dressing for skin grafts.

interrupting revascularization (immobilization techniques include the use of bolster dressings as shown in Fig. 1.8), and infection. The risk of infection can be minimized by careful preparation of the recipient site and early inspection of grafts applied to contaminated beds. Wounds that contain more than 105 organisms per gram of tissue will not support a skin graft. In addition, an infection at the graft donor site can convert a partial-thickness dermal loss into a full-thickness skin loss. The donor site of a split-thickness skin graft heals by reepithelialization. A thin split-thickness harvest site (less than 10/1,000 of an inch) generally heals within 7 days. The donor site can be cared for in a number of ways. The site must be protected from mechanical trauma and desiccation. Xeroform, OpSite, or Adaptic can be used. Because moist, occluded wounds (donor sites) heal faster than dry wounds, the older method of placing Xeroform and drying it with a hairdryer is not optimal. An occlusive dressing, such as semipermeable polyurethane dressing (e.g., OpSite), will also significantly decrease pain at the site.

Skin grafts can also be used as temporary coverage of wounds as biologic dressings. This protects the recipient bed from desiccation and further trauma until definitive closure can occur. In large burns where there is insufficient skin to be harvested for coverage, skin substitutes can be used (Chapter 18). Biologic skin substitutes include human allografts (cadaver skin), amnion, or xenografts (such as pig skin). Allografts become vascularized (or “take”) but are rejected at approximately 10 days unless the recipient is immunosuppressed (e.g., has a large burn), in which case rejection takes longer. Conversely, xenografts are rejected before becoming vascularized. Synthetic skin substitutes such as silicone polymers and composite membranes can also be applied, and new skin substitutes are constantly being developed. Human epidermis can be cultured in vitro to yield sheets of cultured epithelium that will provide coverage for large wounds. The coverage is fragile as a result of the lack of a supporting dermis.

SKIN FLAPS Unlike a skin graft, a skin flap has its own blood supply. Flaps are usually required for covering recipient beds that have poor vascularity; covering vital structures; reconstructing the full thickness of the eyelids, lips, ears, nose, and cheeks; and padding body prominences. Flaps are also preferable when it may be necessary to operate through the wound at a later date to repair underlying structures. In addition, muscle flaps may provide a functional motor unit or a means of controlling infection in the recipient area. Muscle flaps and microvascular free flaps are discussed in Chapters 5 and 8. In an experimental study, Mathes et al. compared musculocutaneous flaps with “random” skin flaps to determine the bacterial clearance and oxygen tension of each (Fig. 1.9). Placement of 107 Staphylococcus aureus underneath random skin flaps in dogs resulted in 100% necrosis of the skin flaps within 48 hours; the musculocutaneous flaps, however, demonstrated long-term survival. The quantity of viable bacteria placed in wound cylinders under these flaps demonstrated an immediate reduction when placed deep to musculocutaneous flap. Oxygen

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FIGURE 1.9. “Old-fashioned” classification of skin flaps. A: Random pattern. B: Axial pattern.


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FIGURE 1.10. Rotation flap. The edge of the flap is four to five times the length of the base of the defect triangle. A back-cut or a Burow triangle can be used if the flap is under excessive tension. A: Pivot ¨ point and line of greatest tension. B: Backcut. C: Burow’s triangle.

tension was measured at the distal end of the random flap and compared to that underneath the muscle of the distal portion of musculocutaneous flap as well as in its subcutaneous area. It was found that the oxygen tension in the distal random flap was significantly less than in distal muscular and cutaneous portions of the musculocutaneous flap. This study has been used to justify transfer of muscle flaps in infected wounds. It may be that well-vascularized skin flaps would be equally efficacious as muscle flaps. Finally, a flap may be chosen because the aesthetic result will be superior. For example, a nasal defect from a skin cancer could be closed with a skin graft, leaving a visible patch. A local skin flap may require incisions in the adjacent nasal tissue, but may be aesthetically preferable in the long-term. There is no better tissue to replace nasal tissue than nasal tissue. Replace like with like. A skin flap consists of skin and subcutaneous tissue that are transferred from one part of the body to another with a vascular pedicle or attachment to the body being maintained for nourishment. Proper planning of a flap is essential to the success of the operation. All possible sites and orientations for the flap must be considered so that the most suitable option is selected. Planning the flap in reverse is an important principle. A pattern of the defect is transferred onto a piece of cloth toweling. The steps in the operative procedure are carried out in reverse order, using this pattern until the donor site is reached. The flap is designed slightly longer than needed, as some length will be lost in the rotation process and slight redundancy may avoid

FIGURE 1.11. Transposition flap. The secondary defect is often closed by a skin graft. A back-cut can be used if the flap is under excessive tension.

kinking of the flap blood supply. The process is repeated, being certain each time the base is held in a fixed position and not allowed to shift with the flap. Measure twice, cut once. It is easier to trim a flap that is slightly long than to add to one that is too small. Planning a transposition or rotation flap requires attention to ensure that the line of greatest tension from the pivot point to the most distal part of the flap is of sufficient length (Figs. 1.10, 1.11 and 1.12). Local skin flaps are of two types: flaps that rotate about a pivot point (rotation, transposition, and interpolation flaps) (Figs. 1.10 and 1.11) and advancement flaps (single-pedicle advancement, V-Y advancement, Y-V advancement, and bipedicle advancement flaps) (Figs. 1.17 and 1.18).

Flaps Rotating About a Pivot Point Rotation, transposition, and interpolation flaps have in common a pivot point and an arc through which the flap is rotated. The radius of this arc is the line of greatest tension of the flap. The realization that these flaps can be rotated only about the pivot point is important in preoperative planning. The rotation flap is a semicircular flap of skin and subcutaneous tissue that rotates about a pivot point into the defect to be closed (Fig. 1.10). The donor site can be closed by a skin graft or by direct suture of the wound.



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FIGURE 1.12. Importance of the pivot point. A skin flap rotated about a pivot point becomes shorter in effective length the farther it is rotated. Planning with a cloth pattern is helpful when designing such a flap.

A flap that is too tight along its radius can be released by making a short back-cut from the pivot point along the base of the flap. Because this back-cut decreases the blood supply to the flap, its use requires some degree of caution. With some flaps it is possible to back-cut only the tissue responsible for the tension, without reducing the blood supply to the flap. Examples of this selective cutting are found in the galea aponeurotica of the scalp and in areas over the trunk where the fascia within the thick subcutaneous layer can be divided. The necessity for a back-cut may be an indication of poor planning. A triangle of skin (Burow triangle) can be removed from the area adjacent to the pivot point of the flap to aid its advancement and rotation (Fig. 1.10c). This method is of only modest benefit in decreasing tension along the radius of the flap. The transposition flap is a rectangle or square of skin and subcutaneous tissue that also is rotated about a pivot point into an immediately adjacent defect (Fig. 1.11). This necessitates that the end of the flap adjacent to the defect be designated to extend beyond it (Figs. 1.12 and 1.13). As the flap is rotated, with the line of greatest tension as the radius of the rotation arc, the advancing tip of the flap will be sufficiently long. The flap donor site is closed by skin grafting, direct suture of the wound, or a secondary flap from the most lax skin at right

FIGURE 1.13. Transposition flap that can be used to close defects on the anterior cheek. A: Small defects can be closed by a single transposition cheek flap that follows the skin lines. B: Large defects can be closed by a double transposition flap that uses a flap of postauricular skin to close the secondary defect left by the cheek flap.

angles to the primary flap. An example of this latter technique is the ingenious bilobed flap (Fig. 1.14). The key to a successful bilobed flap is an area of loose skin to permit direct closure of the secondary flap defect. Pinching the skin between the examiner’s fingers helps find the loosest skin, for example, in the glabellar area and lateral to the eyelids.

FIGURE 1.14. Bilobed flap. After the lesion is excised, the primary flap (P) is transposed into the initial defect. The secondary flap (S) is then transposed into the defect left after the primary flap has been moved. The primary flap is slightly narrower than the defect caused by excision of the initial lesion, and the secondary flap is half the diameter of the primary flap. For the bilobed flap to be successful, the secondary flap must come from an area of loose skin so that the defect remaining after moving the secondary flap can be closed by approximation of the wound edges. Three possible choices for the secondary flap (S1, S2, S3) are depicted. The surgeon chooses the location of the secondary flap based on the skin laxity and the location of the eventual scar.

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FIGURE 1.15. Planning a rhomboid (Limberg) flap. The rhomboid defect must have 60- and 120-degree angles. The flap is planned in an area of loose skin so that direct closure of the wound edges is possible. The short diagonal BD (which is the same length as each side) is extended by its own length to point E. The line EF is drawn parallel to CD and is of the same length. After the flap margins have been incised, the flap is transposed into the rhomboid defect.

The Limberg flap is a type of transposition flap. This flap, like the bilobed flap and the Z-plasty (discussed below), depends on the looseness of adjacent skin, which can be located by pinching various areas of skin between thumb and forefinger. Fortunately, most patients who require local skin flaps are in the older age group and therefore have loose skin. A Limberg flap is designed for rhomboid defects with angles of 60 and 120 degrees, but most wounds can be made rhomboid, or imagined as rhomboid, so the principle is applicable to most facial wounds. The flap is designed with sides that are the same length as the short axis of the rhomboid defect (Figs. 1.15 and 1.16).

Advancement Flaps All advancement flaps are moved directly forward into a defect without any rotation or lateral movement. Modifications are the single-pedicle advancement, the V-Y advancement, and the bipedicle advancement flaps. Advancement flaps are also used in the movement of expanded skin (Chapter 10). The single-pedicle advancement flap is a rectangular or square flap of skin and subcutaneous tissue that is stretched forward. Advancement is accomplished by taking advantage of the elasticity of the skin (Fig. 1.17A) and by excising Burow triangles lateral to the flap (Fig. 1.17B). These triangular excisions help to equalize the length between the sides of the flap and adjacent wound margins. The V-Y advancement technique has numerous applications. It is not an advancement in the same sense as the forward movement of a skin flap just described. Rather, a V-shaped incision is made in the skin, after which the skin on each side of the V is advanced and the incision is closed as a Y (Fig. 1.18). This V-Y technique can be used to lengthen such structures as the nasal columella, eliminate minor notches of the lip, and, in certain instances, close the donor site of a skin flap.

Z-PLASTY Geometric Principle of the Z-Plasty

FIGURE 1.16. Four Limberg flaps are available for any rhomboid defect with 60- and 120-degree angles. The choice is made based on the location of the eventual scar, skin laxity, and blood supply of the flap.

The Z-plasty is an ingenious principle that has numerous applications in plastic surgery (Chapter 18). Z-plasties can be applied to revise and redirect existing scars or to provide additional length in the setting of scar contracture. The principle involves the transposition of two triangular flaps (Fig. 1.19). The limbs of the Z must be equal in length to the central limb, but can extend at varying angles (from 30 to 90 degrees) depending on the desired gain in length. The classic Z-plasty has an angle of 60 degrees (Table 1.1) and provides a 75% theoretical gain in length of the central limb by recruiting lateral tissue. Gain in length is in the direction of the central limb of the Z and depends on the angle used and the length of the central limb. Although the theoretical gain can be determined


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FIGURE 1.19. Classic 60-degree-angle Z-plasty. Inset shows the method of finding the 60-degree angle by first drawing a 90-degree angle, then dividing it in thirds by sighting. The limbs of the Z must be equal in length to the central member. A: Design. B: Transposition of flaps. C: Final result. Note central limb has changed direction by 90 degrees.

FIGURE 1.17. Single-pedicle advancement flaps. A: Advancement by taking advantage of the skin elasticity. B: Advancement by excising Burow triangles of skin laterally to equalize the length of the flap and the adjacent wound edge. C: Pantographic expansion. This method is frequently used after the skin expansion but is risky as the back cuts decrease the blood supply.

mathematically, the actual gain is based on the mechanical properties of the skin and is always less.

Planning and Uses of the Z-Plasty The resulting central limb, after flap transposition, will be perpendicular to the original central limb. In scar revision, the final central limb should lie in the direction of the skin lines and should be selected first. The Z-plasty is then designed. The Z-plasty principle can be used to increase the length of skin in a desired direction. For example, it is useful for release of scar contractures, especially in cases in which the scar crosses a flexion crease. Any number of Z-plasties can be designed in series, especially in cosmetically sensitive areas (such

FIGURE 1.18. V-Y advancement. It is the skin on each side of the V that is actually advanced.

as the face) to break up the appearance of a straight line or to release a contracture. Large Z-plasties, however, do not look good on the face and it is better to use many tiny Z-plasties. Congenital skin webs can also be corrected with Z-plasties. U-shaped or “trapdoor” scars may be improved by breaking up the contracting line. Circumferential scars are amenable to lengthening using Z-plasties, especially in constricting bands of the extremities. These deformities are best released one-half at a time because of concern over interruption of blood supply to the extremity. Borges described the W-plasty as another method of revising a scar. It is useful occasionally, but lacks the applicability and universality that Z-plasty has. This technique simply involves excising the scar in multiple small triangles that are so situated that they interdigitate (Fig. 1.20). Although the Wplasty changes the direction of the linear scar, it would only be by chance that one of the limbs of the W would lie in the same direction as the skin lines. Because a W-plasty does not lengthen a contracted scar line, it is best to use the Z-plasty for this purpose.

TA B L E 1 . 1 Z-PLASTY, ANGLES, AND THEORETICAL GAIN Angles of Z-plasty (degrees)

Theoretical gain in length (%)

30–30 45–45 60–60 75–75 90–90

25 50 75 100 120

medwedi.ru


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must be made very small to avoid worsening the appearance of the scar.

RECONSTRUCTIVE LADDER

FIGURE 1.20. The W-plasty can also be used to break up a long scar that does not lie in the direction of the skin lines.

Both the Z-plasty and the W-plasty have the additional attribute of breaking up a linear scar into an accordion-like scar that has some degree of elasticity to it. This change permits the skin to be more mobile in its contribution to facial expressions. To their detriment, both techniques more than double the length of the scar. If the W-plasty is employed, the triangles

The techniques described above are applicable to cutaneous defects. Plastic surgeons often are consulted regarding closing more complex defects. When analyzing a wound, whether cutaneous or more complex, the options for closure are evaluated beginning with the simplest and progressing up the “reconstructive ladder” to the more complex (Fig. 1.21). This progression from primary closure, to skin graft, to local flap, to regional flap, to microvascular free flap provides a framework that can be applied to any reconstructive situation. Application of the simplest option that meets the reconstructive requirements ensures a “lifeboat” should the procedure fail. In many situations, however, a higher “rung” on the ladder is intentionally chosen. For example, a local flap may be selected over a skin graft for a defect on the nose because it may provide a superior result, or a free flap may be chosen for a breast reconstruction when an attached, pedicled flap would suffice because the blood supply of the former is superior.

CONCLUSION FREE TISSUE TRANSFER

The application of fundamental principles in the practice of plastic surgery allows the surgeon to approach even the most complex problem in an organized, systematic fashion. This chapter presents fundamental principles that can be applied to any wound closure situation.

REGIONAL TISSUE TRANSFER

Suggested Readings LOCAL TISSUE TRANSFER

SKIN GRAFT

DIRECT TISSUE CLOSURE

ALLOW WOUND TO HEAL BY SECONDARY INTENTION FIGURE 1.21. Reconstructive ladder demonstrating the fundamental principle in planning closure of a defect from simple to more complex.

Birch J, Branemark PI. The vascularization of a free full thickness skin graft: a vital microscopic study. Scand Plast J Surg. 1969;3:1. Borges AF. Elective Incisions and Scar Revision. Boston: Little, Brown; 1973. Capla J, Ceradini D, Tepper O, et al. Skin graft vascularization involves precisely regulated regression and replacement of endothelial cells through both angiogenesis and vasculogenesis. Plast Reconstr Surg. 2005. In press. Converse JM, Rapaport FT. The vascularization of skin autografts and homografts: an experimental study in man. Ann Surg. 1956;143:306. Edgerton MT. The Art of Surgical Technique. Baltimore: Williams & Wilkins; 1988. Edgerton MT, Hansen FC. Matching facial color with split thickness skin grafts from adjacent areas. Plast Reconstr Surg. 1960;25:455. Furnas DW, Fischer GW. The Z-plasty: biomechanics and mathematics. Br J Plast Surg. 1971;24:144. Krizek TJ, Robson MC. Evolution of quantitative bacteriology in wound management. Am J Surg. 1975;130:579. Mathes S, Alpert B, Chang N. Use of the muscle flap in chronic osteomyelitis: experimental and clinical correlation. Plast Reconstr Surg. 1982;69:815. Robson MC, Krizek TJ, Heaggars JP. Biology of surgical infections. In: Ravitch MM, ed. Current Problems in Surgery. Chicago: 1973. Rudolph R. Inhibition of myofibroblasts by sham skin grafts. Plast Reconstr Surg. 1979;63:473. Tanner JC, Vandeput J, Olley JF. The mesh skin graft. Plast Reconstr Surg. 1964;34:287. Vogt PM, Andree C, et al. Dry, moist and wet skin wound repair. Ann Plast Surg. 1995;34:493.


CHAPTER 2 ■ WOUND HEALING: NORMAL AND ABNORMAL GEOFFREY C. GURTNER

THE RESPONSE TO INJURY What is wound healing? Definitions include the repair or reconstitution of a defect in an organ or tissue, commonly the skin. However, it is clear that the process of wounding activates systemic processes that alter physiology far beyond the confines of the defect itself. Inflammatory cascades are initiated that impact nearly every organ system and have potentially dire consequences for survival, as illustrated by multisystem organ failure. Furthermore, recent research implicating the participation of stem and progenitor cells in the wound-healing process requires a broader perspective than one that focuses solely on the defect itself (1,2). Wound healing is best understood as an organism’s global response to injury, regardless of whether the location is in skin, liver, or heart. Seen from this perspective, it is not an exaggeration to regard the response to injury as one of the most complex physiologic processes that occurs in life. The complexity of the process is easily demonstrated in cutaneous wound healing. During the progression from a traumatic injury to a stable scar, the intrinsic and extrinsic clotting systems are activated, acute and chronic inflammatory responses occur, neovascularization proceeds through angiogenesis and vasculogenesis, cells proliferate, divide, and undergo apoptosis, and extracellular matrix is deposited and remodeled. These (as well as other events) occur simultaneously, and also interact and influence each other at the level of gene transcription and protein translation in a dynamic and continuous fashion. On top of this, normally sterile tissues are encountering and interacting with bacteria and other elements of the external environment in a way that never occurs except following injury. It is not surprising that wound healing and the response to injury remain poorly understood by scientists and clinicians, except at a purely descriptive or empiric level. The number of commercially available products of unproven efficacy (see Chapter 3) is a testament to the lack of mechanistic understanding regarding this most common surgical problem. Most textbook chapters on wound healing are an encyclopedic catalogue of the phenomenology of wound healing. They list the multitude of cytokines and growth factors that are observed during wound healing, usually based on experimental data, or in in vitro systems that are prone to artifact. With the increasing sensitivity of new technologies such as quantitative polymerase chain reaction (Q-PCR), the list of cytokines, growth factors, chemokines, and the like that appear during wound healing continues to grow. How will we ever make sense of this mountain of data so that we can intervene and predict or alter the outcome of wound healing/response to injury? In this chapter, a theoretical framework is proposed for classifying wound healing. The broad biologic transitions that occur during cutaneous wound healing (i.e., inflammatory phase, proliferative

phase, remodeling phase) are described. An abbreviated list of major “factors” is provided but not discussed in detail as it remains unclear which of these factors are of primary or incidental importance in either functional or abnormal wound healing. Finally, there is a discussion of abnormal human healing within the proposed theoretical context. For a more detailed list of the myriad events occurring in wound healing, the reader is referred to a number of excellent recent reviews (3,4). However given the inherent lag in book publication and the rapid pace of the field, the reader should refer to Medline (www.ncbi.nlm.nih.gov/entrez/query.fcgi) and search for the latest reviews in the field of wound healing to obtain the most up-to-the-minute information.

SCAR FORMATION VERSUS TISSUE REGENERATION Wound healing is a broad and complex topic that covers a variety of responses to injury in a variety of different organ systems. However, some common features exist. Generally, wound healing represents the response of an organism to a physical disruption of a tissue/organ to re-establish homeostasis of that tissue/organ and to stabilize the entire organism’s physiology. There are essentially two processes by which this re-establishment of homeostasis occurs. The first is the substitution of a different cellular matrix as a patch to immediately re-establish both a physical and physiologic continuity to the injured organ. This is the process of scar formation. The second process is a recapitulation of the developmental processes that initially created the injured organ. By reactivating developmental pathways the architecture of the original organ is recreated. This is the process of regeneration (5). The dynamic balance between scarring and tissue regeneration is different in different tissues and organs (Fig. 2.1). For example, neural injury is characterized by little regeneration and much scarring, whereas hepatic and bone injury usually heals primarily through regeneration. It is important to note, however, that the liver can respond to injury with scarring as it does in response to repetitive insults with alcohol during hepatic cirrhosis. Moreover, the same injury in phylogenetically related species can result in very different responses. Thus, limb amputation in newts results in limb regeneration, whereas in humans, only scarring can occur. It is important to realize that the balance between scar and regeneration are likely subject to evolutionary pressures and may, in fact, be functional. Thus, a cutaneous injury in our prehistoric predecessors disrupted their homeostasis with respect to thermoregulation, blood loss, and, most importantly, prevention of invasive infection. In an era before antibiotics and sterility, invasive infection was clearly a threat to life. As such, a very rapid and dramatic recruitment of inflammatory


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16

Part I: Principles, Techniques and Basic Science

The Response to Injury TISSUE REGENERATION

SCAR FORMATION

corneal ulcer, a myocardial infarction, and a stage IV pressure sore have different functional implications for the organism, the dynamic balance of scarring and regeneration will be different in the attempt to re-establish homeostasis. The failure of either scar formation or regeneration may lead to similar appearing clinical problems that have a completely different underlying etiology. Hopefully, this type of analysis will lead to a more organized approach to the classification and treatment of injuries in a variety of different organ systems. Most importantly, it may suggest strategies for intervention to optimize the response to injury and prevent the undesirable sequelae of wound healing.

SEMANTICS OF WOUND HEALING FIGURE 2.1. The different ways organisms and organ systems respond to injuries. Scar formation refers to the patching of a defect with a different or modified tissue (i.e., scar). Tissue regeneration refers to the complete recreation of the original tissue architecture. Most processes involve both, but usually one predominates and may be the source of undesirable side effects. For cutaneous wounds, scar formation usually predominates (except in the unique situation of fetal wound healing) and is the source of many of the problems plastic surgeons address.

cells and a proliferative/contractile burst of activity to close the wound as quickly as possible was adaptive. The more leisurely pace of tissue regeneration was a luxury that could not be afforded. In the modern world, however, these adaptive responses often lead to the disfigurement and functional disability characteristic of burn scars. What was once functional has become unwanted, in part because of our ability to close wounds with sutures, circumventing the need for a vigorous contractile response following wound formation. In the same way that scar formation is not always bad, tissue regeneration is not always good. Peripheral nerve neuromas are dysfunctional and some attempts at regeneration of organ systems results in disabling conditions that threaten the entire organism. In these cases, scar formation is preferable. Indeed, the ablative measures used to treat these neuromas are attempts to prevent further regeneration. When analyzing an undesirable or dysfunctional response to injury in a tissue or organ system, it is useful to consider (a) what is the undesirable portion of the response to injury and (b) whether substitution of a new tissue (scar) or recreation of the pre-existing tissue (regeneration) is responsible for this undesirable effect. It is important to consider the possible adaptive role that the dysfunctional process might have. In the case of a neuroma, the case can be made that the occasional return of protective or functional sensibility following a partial nerve injury is more adaptive and has a survival advantage over the occurrence of complete anesthesia in a peripheral nerve territory. Similarly, with respect to fetal wound healing, in the sterile intrauterine environment, the predominance of regenerative pathways may be adaptive, whereas for the adult organism existing in a microbe-filled environment, it may not be. Such an analysis suggests strategies to correct the undesirable end result in a given tissue or organ. If the problem is overexuberant scar formation, then it is likely that measures to decrease scarring would be helpful. However, as this balance is a dynamic one, efforts at accelerating regeneration might also be effective. Perhaps even better still would be the simultaneous decrease in scar formation and increase in tissue regeneration. It is clear that the response to injury in different tissues involves different proportions of scar formation and tissue regeneration. By understanding the differences using the approach described above, we begin to understand why different organs and tissues respond to injuries in very different ways. Just as a

The nomenclature of both scientific and clinical wound healing research is imprecise and confusing. For example, what is the difference between a chronic wound and a nonhealing wound? For purposes of this chapter, several terms are defined. The vast majority of surgical wounds are incisional wounds that are reapproximated by sutures or adhesives and in the absence of complications will heal primarily or by primary intention. Generally such wounds heal with a scar and do not require special wound care or the involvement of a specialist in wound healing. This is in contrast to wounds that are not reapproximated (for any reason) and the subsequent defect is “filled in” with granulation tissue and then re-epithelialized. This is referred to as healing by secondary intention and generally results in a delay in the appearance of a healed or “closed” wound. Often these wounds require special dressings and treatments (discussed in detail in Chapter 3) and have a higher likelihood of progressing to a chronic wound. The discussion of normal wound healing that follows discusses healing by secondary intention, although the same phases occur in all wounds. An acute wound is a wound that has occurred within the past 3 to 4 weeks. If the wound persists beyond 4 to 6 weeks it is considered a chronic wound, a term that also includes wounds that have been present for months or years. Nonhealing wound or delayed healing wounds are terms used interchangeably to describe chronic wounds. In addition, chronic wounds are often referred to as a “granulating.” This refers to the appearance in the wound cavity of granulation tissue (see discussion of proliferative in Table 3.3) and is a sign that suggests that the wound is progressing, albeit slowly.

PHASES OF NORMAL WOUND HEALING The normal mammalian response to a break in cutaneous defect integrity occurs in three overlapping, but biologically distinct, phases (Fig. 2.2). Following the initial injury, there is an initial inflammatory phase the purpose of which is to remove devitalized tissue and prevent invasive infection. Next, there is a proliferative phase during which the balance between scar formation and tissue regenerations occurs. Usually, scar formation predominates, although in fetal wound healing an impressive amount of regeneration is possible. Finally, the longest and least understood phase of wound healing occurs, the remodeling phase, the purpose of which is to maximize the strength and structural integrity of the wound.

Inflammatory Phase The inflammatory phase (Fig. 2.3) of wound healing begins immediately following tissue injury. The functional priorities


Chapter 2: Wound Healing: Normal and Abnormal Inflammatory Phase

Proliferative Phase

17

Remodeling Phase

Fibroblasts

Endothelial Cells

Monocytes / Macrophages

Keratinocytes

Neutrophils

Platelets

0 Days

5 Days

10 Days

15 Days

during this phase are attainment of hemostasis, removal of dead and devitalized tissues, and prevention of colonization and invasive infection by microbial pathogens, principally bacteria. Initially, components of the injured tissue, including fibrillar collagen and tissue factor, act to activate the extrinsic clotting cascade and prevent ongoing hemorrhage. Disrupted blood vessels allow blood elements into the wound, and platelets clump and form an aggregate to plug the disrupted vessels. During this process, platelets degranulate, releasing growth factors such as platelet-derived growth factor (PDGF) and transforming growth factor-β (TGF-β). The end result of the intrinsic and extrinsic coagulation cascades is the conversion of fibrinogen to fibrin and subsequent polymerization into a gel. This provisional fibrin matrix provides the scaffolding for cell migration required during the later phases of wound healing. Removal of the provisional fibrin matrix will impair wound healing.

Inflammatory Phase

20 Days

25 Days

FIGURE 2.2. The three phases of wound healing (inflammatory, proliferative, remodeling), the timing of these phases in adult cutaneous wound healing, and the characteristic cells that are seen in the healing wound at these time points.

Almost immediately, inflammatory cells are recruited to the wound site. During the initial stages of wound healing, inflammatory cells are attracted by activation of the complement cascade (C5a), TGF-β released by degranulating platelets, and products of bacterial degradation such as lipopolysaccharide (LPS). For the first 2 days following wounding, there is neutrophilic infiltrate into the fibrin matrix filling the wound cavity. The primary role of these cells is to remove dead tissue by phagocytosis and to prevent infection by oxygen-dependent and -independent killing mechanisms. They also release a variety of proteases to degrade remaining extracellular matrix to prepare the wound for healing. It is important to realize that although neutrophils play a role in decreasing infection during cutaneous wound healing, their absence does not prevent the overall progress of wound healing (6). However, their prolonged persistence in the wound has been proposed to be a primary factor in the conversion of acute wounds into nonhealing chronic wounds.

Bacteria

Fibrin matrix Neutrophil

Necrotic tissue Platelets Fibroblast/matrix Blood vessel

FIGURE 2.3. The inflammatory phase of wound healing begins immediately following tissue injury and serves to obtain hemostasis, remove devitalized tissues, and prevent invasive infection by microbial pathogens.


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TA B L E 2 . 1 GROWTH FACTORS, CYTOKINES, AND OTHER BIOLOGICALLY ACTIVE MOLECULES IN WOUND HEALING Name

Abbreviation

Source

Description

Vascular endothelial growth factor

VEGF

Endothelial cells

Promotes angiogenesis

Fibroblast growth factor 2

FGF-2

Macrophages, mast cells, endothelial cells, T lymphocytes

Promotes angiogenesis. Stimulates endothelial cell migration and growth Promotes epithelialization via keratinocyte and fibroblast migration and proliferation

Platelet-derived growth factor

PDGF

Platelets, macrophages, endothelial cells

Enhances proteoglycan and collagen synthesis Recruits macrophages and fibroblasts

Keratinocyte growth factor

KGF

Fibroblasts

Controls keratinocyte growth and maturation Induces epithelial secretion of other growth factors

Epidermal growth factor

EGF

Platelets, macrophages

Stimulates collagenase secretion by fibroblasts to remodel matrix

Transforming growth factor-β

TGF-β

Platelets, macrophages, T and B cells, hepatocytes, thymocytes, placenta

Promotes angiogenesis Establishes chemoattractant gradients, induces adhesion molecule expression, and promotes proinflammatory molecules that stimulate leukocyte and fibroblast migration Induces extracellular matrix synthesis by inhibiting protease activity and up-regulating collagen and proteoglycan synthesis

Tumor necrosis factor-α

TNF-α

Macrophages, T and B cells, natural killer (NK) cells

Induces collagen synthesis in wounds Regulates polymorphonuclear (PMN) leukocyte margination and cytotoxicity

Granulocyte colonystimulating factor

G-CSF

Stromal cells, fibroblasts, endothelial cells, lymphocytes

Stimulates granulocyte proliferation, survival, maturation, and activation Induces granulopoiesis

Granulocyte-macrophage colony-stimulating factor

GM-CSF

Macrophages, stromal cells, fibroblasts, endothelial cells, lymphocytes

Stimulates granulocyte and macrophage proliferation, survival, maturation, and activation Induces granulopoiesis

Interferon-α

IFN-α

Macrophages, B and T cells, fibroblasts, epithelial cells

Activates macrophages; inhibits fibroblast proliferation

Interleukin-1

IL-1

Macrophages, keratinocytes, endothelial cells, lymphocytes, fibroblasts, osteoblasts

Proinflammatory peptide Induces chemotaxis of PMN leukocytes, fibroblasts, and keratinocytes Activates PMN leukocytes

Interleukin-4

IL-4

T cells, basophils, mast cells, bone marrow stromal cells

Activates fibroblast proliferation Induces collagen and proteoglycan synthesis

Interleukin-8

IL-8

Monocytes, neutrophils, fibroblasts, endothelial cells, keratinocytes, T cells

Activates PMN leukocytes and macrophages to begin chemotaxis Induces margination and maturation of keratinocytes

Endothelial nitric oxide synthase

eNOS

Endothelial cells, neurons

Synthesizes nitric oxide in endothelial cells with multiple downstream effects

Inducible nitric oxide synthase

iNOS

Neutrophils, endothelial cells

Synthesizes nitric oxide by macrophages and basal keratinocytes; multiple downstream effects

Monocyte/macrophages follow neutrophils into the wound and appear 48 to 72 hours after injury. They are recruited to healing wounds primarily by expression of monocyte chemoattractant protein 1 (MCP-1). Monocyte/macrophages are key regulatory cells for this and later stages of wound repair. Tissue macrophages originate from the circulation, where they are known as monocytes, and alter their phenotype following

egress into the tissue. By the third day after wounding they are the predominant cell type in the healing wound. Macrophages phagocytose debris and bacteria, but are especially critical for the orchestrated production of the growth factors necessary for production of the extracellular matrix by fibroblasts and the production of new blood vessels in the healing wound. Table 2.1 provides only a partial listing of chemokines,


Chapter 2: Wound Healing: Normal and Abnormal

Proliferative Phase

19

Keratinocyte proliferation and migration

Eschar

Macrophage Proliferating fibroblast Granulation tissue Capillary sprouts/ endothelial cell proliferation FIGURE 2.4. The proliferative phase of wound healing occurs from days 4 to 21 after wounding. During this phase, granulation tissue fills the wound and keratinocytes migrate to restore epithelial continuity.

cytokines, and growth factors present in the healing wound, as the list grows daily (7). The exact function for each of these factors is incompletely understood, and the literature is filled with contradictory data. However, it is clear that, unlike the neutrophil, the absence of monocyte/macrophages has severe consequences for healing wounds (8). The lymphocyte is the last cell to enter the wound and enters between 5 and 7 days after wounding. Its role in wound healing is not well defined, although it has been suggested that populations of stimulatory CD4 and inhibitory CD8 cells may usher in and out the subsequent proliferative phase of wound healing (9). Similarly, the mast cell appears during the later part of the inflammatory phase, but, again, its function remains unclear. Recently, it has become an area of intense research inquiry because of a correlation between mast cells and some forms of aberrant scarring. Given the consistent and precise appearance of different subsets of inflammatory cells into the wound, it is likely that soluble factors released in a stereotypic pattern underlie this phenomenon. The source of these factors, the upstream regulators for their production and the downstream consequences of their activity, is a complex topic and the subject of intense ongoing research. Again, Table 2.1 provides a partial list of growth factors thought to be important during wound healing. All are targets for the development of therapeutics to augment or block their action and either accelerate wound healing or decrease scar formation (10). However the biologic relevance of any one factor in isolation remains unclear.

Proliferative Phase The proliferative phase of wound healing is generally accepted as occurring from days 4 to 21 following injury. However, the phases of wound healing overlap. Certain facets of the proliferative phase, such as re-epithelialization, probably begin almost immediately following injury. Keratinocytes adjacent to the wound alter their phenotype in the hours following injury. Regression of the desmosomal connections between keratinocytes and to the underlying basement membrane frees the cells and allows them to migrate laterally. Concurrent with this is the formation of actin filaments in the cytoplasm of keratinocytes, which provides them with the locomotion to actively migrate

into the wound. Keratinocytes then move via interactions with extracellular matrix proteins (such as fibronectin, vitronectin, and type I collagen) via specific integrin mediators as they proceed between the desiccated eschar and the provisional fibrin matrix beneath (Fig. 2.4). The provisional fibrin matrix is gradually replaced by a new platform for migration: granulation tissue. Granulation tissue is composed of three cell types that play critical and independent roles in granulation tissue formation: fibroblasts, macrophages, and endothelial cells. These cells form extracellular matrix and new blood vessels, which histologically are the ingredients for granulation tissue. Granulation tissue begins to appear in human wounds by about day 4 postinjury. Fibroblasts are the workhorses during this time and produce the extracellular matrix that fills the healing scar and provides a platform for keratinocyte migration. Eventually this matrix will be the most visible component of cutaneous scars. Macrophages continue to produce growth factors such as PDGF and TGFβ 1 that induce fibroblasts to proliferate, migrate, and deposit extracellular matrix, as well as stimulating endothelial cells to form new vessels. Over time the provisional matrix of fibrin is replaced with type III collagen, which will, in turn, be replaced by type I collagen during the remodeling phase. Endothelial cells are a critical component of granulation tissue and form new blood vessels through angiogenesis and the newly described process of vasculogenesis, which involves the recruitment and assembly of bone marrow derived progenitor cells. Proangiogenic factors that are released by macrophages include vascular endothelial growth factor (VEGF), fibroblast growth factor (FGF)-2, angiopoiten-1, and thrombospondin, among others. The upstream activator of gene transcription of these growth factors may be hypoxia via HIF-1a protein stabilization. The relative importance of these different vascular growth factors and the precise timing of their arrival and disappearance is an area of active investigation. However, it is clear that the formation of new blood vessels and subsequent granulation tissue survival is important for wound healing during the proliferative phase of wound healing. Blocking this process with angiogenesis inhibitors impairs excisional wound healing and can be rescued with growth factors such as VEGF. One interesting element of the proliferative phase of wound healing is that at a certain point all of these processes need to be turned off and the formation of granulation tissue/extracellular


20


Remodeling Phase

Fibroblast Collagen remodeling

FIGURE 2.5. The remodeling phase of wound healing is the longest phase and lasts from 21 days to 1 year. Remodeling, although poorly understood, is characterized by the processes of wound.

matrix halted. It is clear that this is a regulated event because once collagen matrix has filled in the wound cavity, fibroblasts rapidly disappear and newly formed blood regress, resulting in a relatively acellular scar under normal conditions. So how do these processes turn off? It seems likely that these events are programmed and occur through the process of gradual selfdestruction called apoptosis. The signals that activate this program are unknown but must involve environmental factors as well as molecular signals. Because dysregulation of this process is believed to underlie the pathophysiology of fibrotic disorders such as hypertrophic scarring, understanding the signals for halting the proliferative phase is of obvious importance for developing new therapeutics for these disabling conditions.

Remodeling Phase The remodeling phase is the longest part of wound healing and in humans is believed to last from 21 days up to 1 year. Once the wound has been “filled in” with granulation tissue and after keratinocyte migration has re-epithelialized it, the process of wound remodeling occurs. Again, these processes overlap, and the remodeling phase likely begins with the programmed regression of blood vessels and granulation tissue described above. Despite the long duration of the remodeling phase and the obvious relevance to ultimate appearance, it is by far the leastunderstood phase of wound healing. In humans, remodeling is characterized by both the processes of wound contraction and collagen remodeling (Fig. 2.5). The process of wound contraction is produced by wound myofibroblasts, which are fibroblasts with intracellular actin microfilaments capable of force generation and matrix contraction. It remains unclear whether the myofibroblast is a separate cell from the fibroblast or whether all fibroblasts retain the capacity to “trans-differentiate” to myofibroblasts under the right environmental conditions. Myofibroblasts contact the wound through specific integrin interactions with the collagen matrix. Collagen remodeling is also characteristic of this phase. Type III collagen is initially laid down by fibroblasts during the proliferative phase, but over the next few months this will be replaced by type I collagen. This slow degradation of type III collagen is mediated through matrix metalloproteinases se-

creted by macrophages, fibroblasts, and endothelial cells. The breaking strength of the healing wound improves slowly during this process, reflecting the turnover in collagen subtypes and increased collagen crosslinking. At 3 weeks, the beginning of the remodeling phase, wounds only have approximately 20% of the strength of unwounded skin, and will eventually only possess 70% of the breaking strength of unwounded skin.

ABNORMAL RESPONSE TO INJURY AND ABNORMAL WOUND HEALING Just as it is overly simplistic to consider all the different responses to injury seen in different tissues as simply “wound healing,” it is na¨ıve to try to classify all the manifestations of abnormalities in this process as simply “abnormal wound healing.” To more accurately classify all the different types of abnormal wound healing, it is useful to consider the balance between attempts to replace tissue defects with new, substitute tissues (scar formation) against the recreation of the original tissue in situ (regeneration) as illustrated in Figure 2.1. It is also helpful to determine where within the normal phases of wound healing the problem occurs. The goal is to understand each abnormal process in terms of the dynamic balance and to propose therapeutic strategies to restore homeostasis. The process is not merely a semantic exercise but has potential therapeutic implications. Although a corneal ulcer, a peripheral neuroma, and stage IV pressure sores are all examples of abnormal healing, the treatment, as guided by an understanding of the mechanism underlying the abnormality, will vary. For the corneal ulcer, which represents a defect in epithelial regeneration, growth factor therapy to augment the potential for regeneration make senses. It makes less sense for a defect such as a peripheral neuroma. For the neuroma, treatments aimed at preventing nerve regeneration make more sense. In the following paragraphs, the various types of abnormal wound healing are classified using the dynamic balance between scar formation and regeneration. Such an analysis will elucidate and clarify new therapeutic opportunities targeting one component or the other, as illustrated in Figure 2.1.


Chapter 2: Wound Healing: Normal and Abnormal

Inadequate Regeneration Underlying an Abnormal Response to Injury The classic example of inadequate regeneration is found in central nervous system injuries. The response to injury in these cases is usually characterized by virtually no restoration or recovery of functional neural tissue. The absence of neural regeneration is compensated by a normal physiologic process of replacement with scar tissue, but in most cases this process does not appear excessive or overexuberant. Although attempts to decrease scar formation have been attempted, it is currently thought that these will be ineffective unless neural regeneration can also be achieved. Consequently, current efforts are focused on strategies to increase regeneration of central nervous system (CNS) components. Current modalities under investigation include the use of implanted neural stem/progenitor cells and the use of developmental morphogens to recapitulate the processes of neural development. Techniques to decrease neural scar formation might also be useful to provide a window of opportunity for regeneration to occur, but they are unlikely to be successful in and of themselves. Other examples of inadequate regeneration include bone nonunions and corneal ulcers.

Inadequate Scar Formation Underlying an Abnormal Response to Injury Many examples of impaired wound healing seen by plastic surgeons belong in this category. In most cases, these diseases result from a failure to replace a tissue defect with a substitute patch of scar (i.e., inadequate scar formation). In these conditions, stable scar tissue is sufficient to restore cutaneous integrity and eliminate the pathology. Regeneration of the skin, although perhaps ideal, is not required for an adequate functional outcome. Examples of these types of conditions include diabetic foot ulcers, sacral pressure sores, and venous stasis ulcers. In all these cases, restoration of cutaneous integrity is sufficient; thus, efforts must be made to understand and correct the defects in scar formation that are occurring in these disease states. Once the defect in scar formation is understood, therapy can be rationally designed. At times, it is useful to subdivide the scar formation defects further and examine whether the primary defect occurs in the inflammatory, proliferative, or remodeling phases of wound healing. For instance, in humans and experimental models, diabetic ulcers occur because of defects in the inflammatory and proliferative phases of wound healing. Accordingly, therapeutics are targeted toward these phases (10). In contrast, wounds occurring because of vitamin C depletion (i.e., scurvy) are a result of abnormal collagen crosslinking that occurs during the remodeling phase of wound healing. Treatment is best directed to this later phase. Although in both cases therapeutic efforts are focused on correcting defects in scar formation (as opposed to augmenting tissue regeneration), the targets will be different.

Excessive Regeneration Underlying an Abnormal Response to Injury These situations are relatively rare. In these cases, pathways of tissue regeneration lead to the recreation of the absent tissue but there are functional problems reintegrating the tissue into the systemic physiology. They often occur in peripheral nerve tissue, such as peripheral nerve regeneration leading to neuroma. Other examples include the hyperkeratosis that occurs

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in cutaneous psoriasis or adenomatous polyp formation in the colon. It is plausible that conditions we consider “precancerous” are the result of overexuberant attempts at tissue regeneration, leading to disordered and uncontrolled growth. In these situations, scar formation would be preferable to regeneration because of possible loss of growth control and transformation to overt cancer. In these disease states, therapeutic measures are targeted toward decreasing cellular proliferation and blocking or impeding the aberrant regenerative pathways. Irritant strategies to maximize scar formation may also play a role, as when alcohol is injected into a neuroma. The goal is to limit the ability of the tissue to activate pathways leading to regeneration. It is sobering to realize that although much current effort is focused on maximizing tissue regeneration, there are circumstances where this already occurs and has proven to be dysfunctional. It also illustrates the need for care and strict control of the technology of tissue generation using stem and progenitor cells.

Excessive Scar Formation Underlying an Abnormal Response to Injury When these conditions affect the skin, they are commonly treated by plastic surgeons, but they can occur elsewhere, as in pulmonary fibrosis or cirrhosis. “Excessive” cutaneous scar formation remains a poorly understood and ubiquitous disease for which there are few treatment options. Abnormal scarring is classified as either hypertrophic scarring or keloid formation. Both are manifestations of overexuberant scarring, although the upstream etiology is probably different. Keloids are less common, and have a genetic component that limits them to 8 mm) remain the most generally accepted criteria to indicate biopsy (Chapter 16).

PIGMENTED LESIONS Nevi Nevi are categorized as intradermal, junctional, or compound, depending on where the nevus cells are in the dermis, at the dermoepidermal junction or both, respectively. Junctional nevi appear smooth and flat and have irregular pigment. They can occur anywhere on the body and occur most commonly in early adulthood, although they can arise at any age. Junctional nevi generally transform to compound nevi in adulthood. Intradermal nevi are more commonly known as “moles.” They can appear anywhere on the body and are characteristically smooth, raised, flat, tan or pink, round or oval, and less than 6 mm in size.

Atypical Moles Atypical moles (formerly known as dysplastic nevi) are acquired lesions that are often mistaken for melanoma (Fig. 13.3). Histologically, they are formed from a cluster of melanocytes. The lesions vary in color from brown to black to pink, typically are smooth, may have irregular borders, and may be scaly. Lesions are usually between 5 and 10 mm. Atypical moles are most often sporadic, although they can be familial. Lesions tend to occur in sun-exposed areas. The risk of melanoma is higher in patients who have atypical moles, and the risk increases as the number of atypical moles increases. Most patients have a few atypical moles, although some patients may have more than 100 atypical lesions. These patients present a clinical challenge because atypical moles, by definition, are moles that have the appearance of melanomas. They require close follow-up with baseline total-body photography. It is impractical and infeasible to biopsy all lesions in such patients. Removal of lesions is reserved for those that exhibit changes, emphasizing the importance of close follow-up. When surgery is warranted, excisional biopsies should be performed, with histologic confirmation of clear margins. Other related pigmented lesions include blue nevus (Fig. 13.4), ephelis (Fig. 13.5), solar lentigo (Fig. 13.6), congenital nevi (Fig. 13.7), and nevus of Ota. Although there is a recognized malignant potential for a congenital nevus to transform to malignant melanoma, the true incidence varies widely in the literature (Chapter 16). Malignant degeneration of a blue nevus is rare and close observation is necessary. The nevus of Ota is totally benign, occurs in the distribution of the first and second branches of the trigeminal nerve, and management can use the Q-switched ruby, neodymium:yttrium-aluminumgarnet (Nd:YAG), or alexandrite lasers (Chapter 20). The other lesions are benign and may be excised (with a minimal area of surrounding tissue) for cosmetic purposes.

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Part II: Skin and Soft Tissue

FIGURE 13.1. Cross-section view of skin.

There are many different categorizations of benign, premalignant, and malignant skin tumors. A particularly useful categorization is to classify tumors according to their primary origin. Thus the tumors that originate from the epidermis are categorized together.

EPIDERMAL LESIONS Seborrheic Keratosis Seborrheic keratoses (SKs), also known as verruca senilis or pigmented papilloma, are extremely common and arise from the basal layer of the epidermis. They are composed of welldifferentiated basal cells, and contain cystic “inclusions” of keratinous material called “horn cysts.” Typically lesions exhibit hyperkeratosis, acanthosis, and papillomatosis. The growth and depth of pigmentation vary directly with exposure to sunlight. Microscopically, a benign epithelial proliferative process is seen. If left untreated, they will gradually enlarge and increase in thickness; there is no spontaneous involution. SKs are most commonly seen on the head, neck, and trunk after the fifth decade of life. They are often distinctly marked and have a waxy, stuck-on appearance. The surface is soft, verrucoid, often pedunculated and oily to the touch. They can vary in color from light tan to yellow, dark brown, and black. They range in size from 1 mm to 5 cm. No treatment is necessary but these lesions

FIGURE 13.2. Melanoma of the lower extremity.

are unsightly and patients frequently request removal for cosmetic purposes. Cutaneous malignancies (including small cell carcinoma [SCC], basal cell carcinoma [BCC], and melanoma) can develop within seborrheic keratoses. For typical SKs, shave techniques tend to be efficient and effective. Dermabrasion and cryotherapy can also be used. For larger lesions and pigmented lesions where the diagnosis is unclear, excisional biopsy may be performed.

Verruca Vulgaris The common wart is an infection caused by the human papilloma virus; it is not a true neoplasm. It can be solitary or occur in clusters. Verruca most often occurs on the upper extremity, occasionally on the face, and is most common in children and young adults. The lesion has a characteristic scaly and rough appearance with variegations and a cap of friable keratotic material. A lesion can persist for months to years, although most often is self-limited and resolves spontaneously. Histology shows hyperkeratosis and parakeratosis. Lesions arise from

FIGURE 13.3. Atypical mole.


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FIGURE 13.4. Blue nevus.

FIGURE 13.6. Solar lentigo.

the stratum granulosum of the epidermis. Various treatments are possible, including cryotherapy and chemical ablation, but multiple treatments may be necessary. Excision is reserved for a lesion that is painful or resists other treatment options.

ment. An estimated 5% to 20% of patients with these lesions will develop SCC. Treatment involves monitoring closely and removal. Patients with multiple lesions and lesions with significant erythema should be biopsied. Multiple treatment modalities are effective in the treatment of AKs, including cryosurgery, typically with liquid nitrogen, electrodesiccation and curettage, topical treatments, and laser and surgical excision. Many topical treatments are effective, including 5-fluorouracil (5-FU) cream, imiquimod 5% (Aldara), chemical peels using trichloroacetic acid (TCA) or phenol, and combination gel treatments using diclofenac and hyaluronic acid. Aldara is popular for the treatment of AKs and viral infections. It can be administered three times a week for 8 to 12 weeks and works by stimulating an immune response. 5-FU can be used in 5% (Efudex), 1% (Fluoroplex), and 0.5% (Carac) concentrations. Some patients experience sensitivity with 5-FU, resulting in significant erythema, scaling, and crusting; however, lower concentrations seem to be well tolerated by most patients. Laser resurfacing with a carbon dioxide laser or the YAG laser directed at the lesion can result in removing the epidermis, which can be effective in small areas, particularly on the lips. Loss of pigment is a sometimes unwelcome side effect

Actinic Keratosis Otherwise known as solar keratoses, actinic keratoses (AKs) occur on sun-exposed skin (Fig. 13.8). An aggressive form of AK called actinic cheilitis occurs on the lips. Fair-skinned individuals with blue or green eyes are at highest risk, and patients with immune compromise are also at risk. AKs represent the most common premalignant skin lesion. Despite the similarity of the name, AKs are totally distinct from seborrheic keratoses. Lesions are most often multiple and small (2 cm in diameter have higher rates of recurrence. Mohs surgery is the treatment of choice for these tumors. Recurrent tumors often have ill-defined margins given the presence of fibrosis from previous interventions. Tumors previously treated with other modalities, including radiation therapy, electrodesiccation and curettage, surgical excision, and cryotherapy, may have subclinical extension when they recur (4). Recurrence rates of previously treated tumors is 18% with excision, 10% with radiation therapy, 40% with electrodesiccation and curettage, and 12% with cryotherapy. Mohs surgery yields the most favorable recurrence rate of 3.4% to 7.9%, establishing it as the treatment of choice for recurrent skin tumors (5). For lesions in cosmetically or functionally important areas such as the nose, eyes, and lips, Mohs surgery is an excellent treatment choice because of the tissue-sparing advantage. The genitalia, digits, and the nipple area are locations with very little tissue laxity. Given the need for tissue preservation, Mohs surgery is the optimal treatment. Cutaneous tumors occurring in immunosuppressed patients should also be treated with Mohs surgery, as these tumors


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TA B L E 1 4 . 1

TA B L E 1 4 . 3

KEY FEATURES OF MOHS MICROGRAPHIC SURGERY Curettage Beveled incision Specimen orientation Color coding and mapping Specimen flattening Horizontal frozen section Histologic review by Mohs surgeon Immediate repair

can behave aggressively. Two other groups that deserve special mention are patients with a genetic predisposition for developing multiple skin cancers, such as patients with basal cell nevus syndrome and patients with xeroderma pigmentosa. Mohs surgery is ideal because of its tissue-sparing capability and superb cure rates. Table 14.3 is a complete list of tumors treatable by Mohs surgery.

BASAL CELL CARCINOMA AND SQUAMOUS CELL CARCINOMA Basal cell carcinoma (BCC) is the most commonly diagnosed skin cancer, representing 75% of all cutaneous malignancies. This is followed by squamous cell carcinoma (SCC), which represents 20% of all cutaneous malignancies. Mohs micrographic surgery is the treatment of choice for basal and squamous cell carcinomas that display aggressive histologic features and unfavorable location. Morpheaform, infiltrative, sclerosing, and basosquamous BCCs typically have ill-defined clinical margins and deep-tissue invasion, and tend to have higher rates of recurrence with treatment methods other than Mohs surgery. Large tumors, measuring >2 cm in diameter, also tend to behave more aggressively and have higher recurrence rates, and are better treated with Mohs surgery. Tumors located on the ear, periauricular region, nose, temporal region, periocular region, melolabial sulcus, and upper lip

TA B L E 1 4 . 2 INDICATIONS FOR MOHS MICROGRAPHIC SURGERY Location Areas prone to recurrence: midface, ear, lip, nose, temple On or near a critical structure: eyes, lips, digits, genitalia Recurrent tumors: basal cell carcinoma and squamous cell carcinoma Large tumors (>2 cm) Ill-defined tumor margins Aggressive histology Basal cell carcinoma—morpheaform, infiltrative, basosquamous, perineural Squamous cell carcinoma—poorly differentiated, invasive, perineural Special hosts Immunosuppressed patients Basal cell nevus syndrome patients Xeroderma pigmentosa patients

TUMORS TREATED BY MOHS SURGERY Basal cell carcinoma Squamous cell carcinoma Keratoacanthoma Verrucous carcinoma Erythroplasia of Queyrat Bowen disease Extramammary Paget disease Melanoma in situ Dermatofibrosarcoma protuberans Atypical fibroxanthoma Microcystic adnexal carcinoma Sebaceous carcinoma Cutaneous leiomyosarcoma Malignant granular cell tumor Merkel cell carcinoma Eccrine/apocrine adenocarcinoma Angiosarcoma Trichilemmal carcinoma

(the H-zone) have higher recurrence rates and are cosmetically sensitive areas with a limited amount of surrounding tissue. Given these circumstances, such tumors are best treated with Mohs surgery. The nose is the most common site for BCC and is the site with the highest recurrence rate. In contrast to other treatment modalities, Mohs surgery has the highest cure rate (97% to 99%) for BCCs on the nose and is the optimal treatment method. Periauricular tumors are also best treated with Mohs surgery because of the high recurrence rate given the proclivity for cartilaginous spread or extension into the external auditory canal. Unlike BCCs, which can recur but tend not to metastasize, squamous cell carcinomas have metastatic potential and therefore pose a more threatening problem. This emphasizes the need to use the optimal treatment modality with excellent cure rate. Complete removal of SCC is critical, because recurrent tumors are very difficult to treat and are associated with a 25% to 45% rate of metastasis. Mohs surgery has the highest cure rate (98%) in the treatment of SCCs (6). SCCs on the scalp often extend widely beyond clinically obvious borders. Tissue inelasticity of the scalp can make subsequent repair challenging. Mohs surgery minimizes the defect size while maximizing cure rate. Mohs surgery is also an excellent option for SCCs involving the digits without bony involvement. Especially helpful in the periungual region, Mohs surgery can avoid the need for disfiguring, functionally compromising surgery or amputation. SCCs exhibiting perineural involvement or malignancies arising from previous radiation, burn, or scar should be treated with Mohs surgery because of the infiltrative nature of the tumor and high risk of recurrence.

OTHER TUMORS TREATED BY MOHS MICROGRAPHIC SURGERY Dermatofibrosarcoma protuberans is a fibrous tumor that tends to extend widely beyond clinical borders. Prior to the availability of Mohs surgery, treatment was fraught with high rates of recurrence. Mohs surgery has had tremendous success in the treatment of dermatofibrosarcoma protuberans, with a recurrence rate of only 1.6% seen in Mohs surgerytreated tumors, compared to a 20% recurrence rate with wide


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excision (7). Other fibrous tumors that have been successfully treated with Mohs surgery are atypical fibroxanthomas and their deeper counterpart, malignant fibrous histiocytoma. Variants of SCCs that are suitable for Mohs surgery include verrucous carcinoma, Bowen disease, and erythroplasia of Queyrat. Other tumors successfully treated with Mohs micrographic surgery are sebaceous carcinoma, which commonly occurs on the eyelid and has high rates of local recurrence and metastasis, and extramammary Paget disease, which often has subclinical extension. Mohs surgery has also been used for the treatment of lesscommon cutaneous malignancies, including leiomyosarcoma, angiosarcoma, and liposarcoma. Microcystic adnexal carcinoma, or sclerosing sweat duct carcinoma, occurs on the upper lip or cheek and chin area, and tends to behave aggressively, invading deeply. It is also treated with Mohs surgery.

MELANOMA The role of Mohs micrographic surgery in the treatment of melanoma is controversial and has been the subject of extensive discussion. The difficulty in identifying single atypical melanocytes in frozen section because of freeze artifact has prevented this technique from being used widely in invasive melanoma. However, some Mohs surgeons have applied the procedure to melanoma in situ and invasive melanoma (8). Immunohistochemical stains to label melanocytes have been used as an adjunct to improve the diagnostic accuracy of Mohs surgery with melanomas, especially in equivocal sections. Unfortunately, currently available stains have low sensitivity and prolong procedure time, without much discernible improvement over standard wide excision.

FIGURE 14.2. Curettage to delineate clinical borders.

Mohs surgery is performed in an outpatient setting under local anesthesia. All tumors are first biopsied for diagnostic confirmation. Depending on the lesion, additional studies may be obtained, including computed tomographic (CT) scans, magnetic resonance imaging (MRI), and radiographs, to evaluate for tumor invasion into bone or regional lymph node involvement. If the lesion is located in an area where a significant motor or sensory nerve may need to be sacrificed, this is discussed with

the patient prior to surgery. Regional lymph node examination is performed as well. When the patient presents for surgery, the tumor is identified and marked with a skin marker (Fig. 14.1). Mohs micrographic surgery is performed using standard surgical preparation of the skin with sterile instruments and drapes. The area is infiltrated with local anesthesia (usually lidocaine with epinephrine). The tumor is debulked and lateral margins are delineated with a sharp curette (Fig. 14.2). The tumor is cut via a tangential incision around the circumference of the lesion, with the scalpel held at a 45-degree angle to the skin (as opposed to the customary 90-degree angle) (Fig. 14.3). Approximately 2 mm of clinically normal skin is removed in the periphery. The deep margin is cut in a horizontal fashion, parallel to the surface of the skin. Prior to tissue removal, a thin cut is made on the specimen and the surrounding skin, for location identification in the event that additional tissue needs to be taken from a particular area. The tissue is removed and divided into smaller pieces. Skin edges are painted with different colors corresponding to specific sites on the tumor map. Painting the edges also assures the histotechnician that the complete margin is being properly sectioned, as the color dye remains present during the processing and is readily identifiable on the glass slide. Peripheral and deep skin edges are flattened such that specimen edges

FIGURE 14.1. Preoperative view of recurrent basal cell carcinoma on the nose.

FIGURE 14.3. Beveled incision during Mohs surgery (first stage).

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FIGURE 14.6. Additional tissue excision (second stage).

FIGURE 14.4. Excision of skin tumor placed on labeled paper towel, adjacent to tumor map.

are lying completely flat. This step is critical because it ensures complete margin assessment. The surgical specimen is put on a cryostat object disk and fixed in optimal cutting temperature (OCT) embedding compound. A heat extractor can be applied to facilitate fixation. The tissue is flipped and pressure is applied to flatten the tissue such that the three-dimensional tissue becomes two-

FIGURE 14.5. Areas of residual tumor marked on tumor map after microscopic examination.

dimensional. The tissue is cut into 6- to 10-μm–thick sections in the cryostat. The sections are placed on a glass slide and stained with either hematoxylin and eosin or toluidine blue. The Mohs surgeon reviews the histologic sections. If any tumor is identified on the slide, it is marked on the tumor map and that area is removed in the same manner (Figs. 14.4 and 14.5). Each time the surgeon repeats the process, it is an additional “stage” (Figs. 14.6 and 14.7). Once the tumor has been completely extirpated, reconstruction options are explored (Fig. 14.8). Patients are informed that the procedure in its entirety may take anywhere from 1 to 4 hours, based on the size and depth of the tumor. The majority of time is attributed to tissue processing time. Tissue processing typically takes 20 to 40 minutes, depending on the size of the tissue and the skill of the laboratory technician. The central tenet of Mohs micrographic surgery is that the Mohs surgeon handles the tissue personally, starting with the initial incision through the transfer of the tissue to the histotechnician. This quality assurance minimizes mistakes in labeling and orientation and ensures optimal results. The laboratory for tissue processing is essential for Mohs surgery. It must be located on the premises to allow the Mohs surgeon and histotechnician to work together closely.

FIGURE 14.7. Another map is drawn based on excised tissue.


Chapter 14: Mohs Micrographic Surgery

FIGURE 14.8. Final defect after margins are clear of tumor (after four stages).

A critical feature of Mohs surgery is the horizontal sections of the frozen tissue that is examined. This differs from perpendicular vertical sections that are obtained in standard surgical pathology laboratories. In routine paraffin-embedded slides, vertical sections are cut like slices of a bread loaf and representative slices from various sections throughout the specimen are examined to look for margin clearance. In Mohs surgery, horizontal sections enable microscopic examination of the entire deep and peripheral margins of the specimen in one continuous layer. So, theoretically, there is no skip area and the tissue margins are viewed in total.

CONCLUSION Mohs micrographic surgeons are usually trained in approved 1- or 2-year fellowships under the auspices of the American College of Mohs Micrographic Surgery and Cutaneous Oncology. Fellows receive training in surgical technique, preparation and reading of horizontal frozen sections, and repair of postsurgical wounds. In the majority of cases, the Mohs surgeon repairs the defect immediately. When the defect is extensive or in specialized anatomic regions, the Mohs surgeon coordinates reconstruction with another surgical specialty, such as plastic surgery or oculoplastic surgery. Mohs micrographic surgery has the highest cure rate among the various therapeutic modalities available for skin cancer treatment. The recurrence rate is 2% or less for primary skin

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cancers treated with Mohs surgery. Conservative removal of tissue can be performed without compromising the excellent cure rate (9). Management of complex skin cancers that might otherwise have required general anesthesia, the use of operating rooms, and potential hospitalization are obviated with Mohs surgery. Given the ambulatory nature of the procedure and the low incidence of complications, Mohs surgery is a cost-effective technique when used appropriately (10, 11). Cost analysis comparing Mohs surgery with traditional surgical excision of facial and auricular nonmelanoma skin cancers demonstrates Mohs micrographic surgery to be cost comparable with traditional wide excision (12). Mohs surgery is also less expensive than traditional surgery performed in the office or in ambulatory surgery centers with frozen section margin control (13). It is an enormous convenience for patients as well, because they can be assured when they leave the office postprocedure, they are tumor free and are able to resume their lifestyle immediately. The unique features of Mohs micrographic surgery make it the treatment of choice for most cutaneous malignancies.

References 1. Snow SN, Madjar DD. Mohs surgery in the management of cutaneous malignancies. Clin Dermatol. 2001;19:339–347. 2. Tromovitch TA, Stegman SJ. Microscopically controlled excision of skin tumors. Arch Dermatol. 1974;110:213–232. 3. Russell BA, Amonette RA, Swanson NA. Mohs micrographic surgery. In: Freedberg IM, Eisen AZ, Wolff KM, eds. Fitzpatrick’s Dermatology in General Medicine. Vol. 2 5th ed. New York, McGraw-Hill; 1999. 4. Rowe DE, Carroll RJ, Day CL. Mohs surgery is the treatment of choice for recurrent (previously treated) basal cell carcinoma. J Dermatol Surg Oncol. 1989;15:424–431. 5. Mohs FE. Chemosurgery and Microscopically Controlled Surgery for Skin Cancer. Springfield, IL: Charles C Thomas; 1978. 6. Vuyk HD, Lohuis PJFM. Mohs micrographic surgery for facial skin cancer. Clin Otolaryngol. 2001;26:265–273. 7. Gloster HM, Harris KR, Roenigk RK. A comparison between Mohs micrographic surgery and wide excision for the treatment of dermatofibrosarcoma protuberans. J Am Acad Dermatol. 1996;35:82–87. 8. Beinart TN, Trotter MJ, Arlette JP. Treatment of cutaneous melanoma of the face by Mohs micrographic surgery. J Cutan Med Surg. 2003;7:25–30. 9. Swanson NA, Grekin RC, Baker SR. Mohs surgery: techniques, indications and applications in head and neck surgery. Head Neck Surg. 1983;6:683– 692. 10. Cook JL, Perone JB. A prospective evaluation of the incidence of complications associated with Mohs micrographic surgery. Arch Dermatol. 2003;139:143–152. 11. Lang PG. The role of Mohs micrographic surgery in the management of skin cancer and a perspective on the management of the surgical defect. Clin Plast Surg. 2004;31:5–31. 12. Bialy TL, Whalen J, Veledar E, et al. Mohs micrographic surgery vs. traditional surgical excision: a cost comparison analysis.2004;140:736–742. 13. Cook J, Zitelli J. Mohs micrographic surgery: a cost analysis. J Am Acad Dermatol. 1998;39(5 Pt 1):698–703.


CHAPTER 15 ■ CONGENITAL MELANOCYTIC NEVI JOHN N. JENSEN AND ARUN K. GOSAIN

DEFINITION Nevus cells are distinguished from melanocytes by their lack of dendrites. Congenital nevi are theorized to represent a disruption of the normal growth, development, and migration of melanoblasts. Congenital melanocytic nevus (CMN) contains nevus cells and is present at birth or, in some cases, may appear within the first year of life. In the latter case, it is believed that the lesions are present at birth but do not become pigmented until the postnatal period. The lesions are thought to form between weeks 5 and 24 of gestation. Most are thought to be sporadic, but familial association is occasionally observed. Color ranges from light to dark brown, and may appear blue in more darkly pigmented individuals. Lesions are usually round or oval with well-defined borders, and vary considerably in size, pattern, and anatomic location. Although some may lesions have no raised qualities, most cause some degree of skin surface distortion. Small nevi are those 20 cm in greatest dimension in adulthood. Because growth of these lesions is usually commensurate with overall growth, this corresponds roughly to a 9-cm scalp or a 6-cm trunk lesion in an infant (1). A more precise classification of giant CMN relates the lesion’s size as compared to body surface area, with those occupying 2% or more body surface area considered to be giant. However, because it is more difficult to determine the size of a lesion relative to body surface area, the majority of authors report nevus size in terms of the greatest diameter of the lesion.

EPIDEMIOLOGY Approximately 1% of the general population is thought to have CMN, most of which are of the small variety. The incidence of large (>10 cm) CMN is estimated at 1 in 20,000 livebirths (2). The very large “bathing trunk” examples are rarer still, occurring in approximately 1 in 500,000 live births.

HISTOLOGIC CHARACTERISTICS Histologic features of large and small congenital melanocytic nevi include nests of nevomelanocytes at the epidermal–dermal junction or within the epidermis. In a large CMN, the morphology of nevus cells can vary and is usually more complex. The finding of nevocellular nests in the middle to deep reticular dermis is more characteristic of a congenital nevus than of the acquired variety, but no single feature is unique to either. Nevus cells present in structures deeper than the skin (e.g., bone,

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cranium, muscle) rarely occur except in very large congenital melanocytic nevi.

CLINICAL CHARACTERISTICS The most common anatomic location for a large CMN is the trunk, followed in frequency by the legs, arms, and head and neck (3). Giant nevi often cross multiple anatomic zones, resulting in a more descriptive terminology to denote their pattern. Specific anatomic patterns of these lesions are observed; most notable are the “bathing trunks” and “glove-stocking” distributions. They often may appear with multiple smaller satellite lesions dispersed over the trunk, extremities, or head and neck. Often, the natural course of these lesions is to become less (or sometimes more) pigmented, and to develop hypertrichosis and a variegated texture, including nodularity. Figure 15.1 shows an infant who presented with a giant CMN in the bathing suit distribution. The differential diagnosis for CMN includes other congenital pigmented lesions, such as epidermal nevus, nevus sebaceous, café-au-lait spot, and Mongolian spot. Features that should prompt biopsy, if not complete early excision, include those suggestive of dysplasia or melanoma, such as ulceration, uneven pigmentation, a change in shape, and nodularity.

MALIGNANT TRANSFORMATION The risk for malignant transformation of a CMN to melanoma was appreciated in the 19th century. Less than 0.5% of melanomas appear in preadolescent children, but 33% of those are thought to arise from CMN. There is some controversy regarding the risk of melanoma transformation. Previous attempts at quantification of the incidence of malignant transformation have been criticized, and newer studies question the existence of significant risk. Most experts believe that melanoma may arise directly from CMN (3–6). Some studies reported only extracutaneous melanoma in patients with CMN. No studies convincingly show that excision of large CMN effectively reduces the rate of malignant transformation to melanoma. This raises the question of the efficacy of prophylactic excision of CMN (7). Even those studies that cannot demonstrate a direct link between CMN and melanoma do recognize the possibility that melanoma originated in a lesion that was incompletely excised or in which the primary tumor was not clinically discovered. In the Swedish prospective trial in which no malignant transformation was proven, the incidence of CMN was reported as 0.2% (8). However, the rate of excision, especially of large (i.e., high-risk) lesions, was 40%, which might have affected the melanoma incidence. The slight variation in risk for melanoma between trials can be explained by several


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A

B

C FIGURE 15.1. A, B: A 2-week-old female presented with a giant congenital melanocytic nevus in a bathing trunk distribution. Note that multiple satellite nevi are often associated with these lesions. There was a small area of ulceration within a portion of the nevus over the buttock. Clinical suspicion for congenital melanoma is an indication for early incisional biopsy prior to initiating more extensive reconstructive procedures. C: Risk factors in this patient were high for neurocutaneous melanosis: the presence of a large CMN overlying the posterior midline and multiple satellite nevi. A screening magnetic resonance imaging scan demonstrated a focus of neurocutaneous melanosis in the left occipital lobe (arrow) which was asymptomatic.

factors, including imprecise definition of “large” CMN, variable excision of primary lesions, and unclear histologic analysis of specimens (3). What is significant is the consistency with regard to risk between separate studies performed in different geographic areas by different groups (1,3–6). When considering malignant transformation, it is essential to distinguish between small and large congenital melanocytic nevi. The lifetime risk for melanoma arising in small congenital melanocytic nevi is between 0% and 5%; the risk in large congenital melanocytic nevi is estimated to be between 5% and 10% (9). In larger congenital melanocytic nevi, melanoma usually develops deep to the dermal–epidermal junction or occurs extracutaneously (e.g., the central nervous system [CNS] or

retroperitoneum), is more difficult to detect, and usually (70%) occurs in the first decade of life. This has obvious clinical implications; removal of large and giant congenital melanocytic nevi must be undertaken much earlier and the excision must be more aggressive than for small lesions. When melanoma is reported, it tends to occur in the trunk (3) and head and neck; it has never been reported in satellite lesions. Clinically, malignant transformation may manifest as increasingly dark pigmentation, accelerated growth, a change in shape, the appearance of nodularity, pain, ulceration with or without bleeding, or pruritus. Unfortunately, many of these features are also common to the benign course of CMN. Transformation may occur later in life, and underscores the


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importance of long-term follow-up, even after surgical intervention. In addition to melanoma, patients with large congenital melanocytic nevi are at increased risk to suffer from neurocutaneous melanocytosis, in which collections of melanocytes are present in the leptomeninges. Malignant transformation can also occur in neurocutaneous melanosis and result in primary central nervous system (CNS) melanoma. Even without malignant transformation, neurocutaneous melanosis can carry significant morbidity and mortality, often from seizures, hydrocephalus, and other signs of CNS irritation. Neurocutaneous melanosis may also present asymptomatically, as illustrated by the patient in Figure 15.1 whose presentation included a large CMN in the posterior midline with multiple satellite lesions (Fig. 15.1C). Magnetic resonance imaging (MRI) screening of the CNS early in life is recommended for those patients who are at high risk for malignant transformation, particularly when the presentation includes a large nevus in the posterior midline and/or multiple satellite nevi. The incidence of rhabdomyosarcoma is also increased in patients with large congenital melanocytic nevi. In summary, all pigmented lesions have the potential to give rise to melanoma, and congenital melanocytic nevi are believed by most physicians to have a measurable risk for malignant transformation. The risk is thought to be related to the size of the lesion, but melanoma is also documented to have arisen from small congenital melanocytic nevi. Moreover, the larger the lesion, the more likely it is accompanied by greater depth into the dermis and subcutaneous tissue. Although malignant transformation to melanoma is rare, it is the essential concern in the management of these lesions.

MANAGEMENT Many different treatment regimens have been advocated for CMN, including partial and complete excision, dermabrasion, chemical peel, and laser ablation. The fundamental guiding principle is related to achieving a balance between treatment goals; namely, elimination (or at least reduction) of the risk for malignant transformation, preservation of function, and improved cosmesis. Central to these considerations, in turn, is an understanding of the psychological impact caused both by the original appearance of the lesion and any functional or cosmetic impairment from therapeutic intervention. Dermabrasion, chemical peels, and lasers have been reported as treatment for CMN (10). Cosmetic improvement usually is demonstrated in these reports, but none of these modalities is effective in the complete removal of nevus cells. In fact, at least one report suggests the possibility of a link between the kind of energy emitted by lasers and an increased metastatic potential in vitro (9). An additional criticism of these techniques is that lightening the nevus while selectively leaving unaffected nevus cells in the deeper layer of the dermis and subcutaneous tissue makes it more difficult to monitor the patient for clinical signs of malignant transformation of the remaining nevus cells. To address the malignant potential, only complete excision of the nevus can be recommended as a solution. However, in some cases the nevus cells extend deeply into the subcutaneous tissue and the underlying muscle. Although it is not always possible to clear the peripheral surgical margins in all giant congenital melanocytic nevi, an effort should be made to clear the deep margin of nevus. If the deep margin of resection remains positive, it is impossible to monitor the behavior of residual nevus on a clinical basis following reconstruction. In more complex cases, anatomic structures that cannot be effectively reconstructed, like the perineum, may be involved and contribute to the difficulty. Moreover, even though some studies

report melanoma as arising from congenital melanocytic nevi, other studies demonstrate only extracutaneous melanoma. Surgical excision in these cases does not appear to lower the risk; in fact, no study to date has objectively demonstrated that prophylactic excision lowers the risk for melanoma in these patients. Conversely, an overall decline in melanoma risk from large congenital melanocytic nevi has been reported and may be partly a consequence of a greater acceptance of surgical excision of these lesions as newer techniques have been developed. Several surgical algorithms have been reported (11,12). The mainstays of surgical management of CMN remain one-stage excision with primary closure, serial excision, tissue expansion, and excision with skin grafting. A combination of these techniques is often employed. Newer synthetic skin substitutes are being employed with success. Serial excision is preferable in most cases when complete excision can be accomplished in two stages or less. In cases of extensive nevi formation and limited normal donor skin for grafting, an option is to expand the donor skin prior to harvest. A sensible approach is to consider the lesion or lesions within an anatomic context. In the scalp and face, multimodality treatment is often indicated. For example, tissue expansion is the first choice in hair-bearing scalp. Full-thickness skin grafts, however, are preferred for structures like the ear and eyelids, where serial excision would cause a deformity. Tissue expansion is associated with more morbidity and a higher failure rate in the extremities. For larger lesions distal to the knee or elbow, skin grafting is preferred in lesions not amenable to serial excision. Finally, clinical surveillance remains an important treatment option, especially for lesions that are amenable to serial observation, are minimally disfiguring, or are such that ablative surgery would cause significant anatomic or functional disruption. Given the low risk for malignant transformation in CMN, it is difficult to justify potentially mutilating procedures for its excision. This is weighed against the risk of malignant transformation, and those patients who are probably at greatest risk (because they have large, thick, deeply textured lesions) are also the least likely to show signs that could allow early diagnosis of melanoma. Because sun exposure is thought to increase the risk for malignant transformation, strict sun avoidance should be advised as a prophylactic measure in these patients. In summary, congenital pigmented nevi can be thought of as falling into two groups: large CMN and all others. Large CMN represent the greater risk for malignant transformation; require earlier, more aggressive intervention; and represent the most complex reconstructive challenges. A number of surgical techniques may be indicated and employed to reduce the risk for malignant transformation and to minimize functional and cosmetic deformity, while considering the psychological impact of intervention versus nonintervention. Should intervention be chosen, we recommend that the modality chosen not mask the clinician’s ability to monitor any residual nevus for signs of malignant transformation. Until data contradict these principles, we recommend caution when treating CMN with laser, chemical peel, or dermabrasion. If surgical resection of CMN is chosen, particular effort should be made to achieve a clear, deep margin of resection so subsequent surgical reconstruction will not mask residual nevi.

References 1. Marghoob AA, Schoenbach SP, Kopf AW, et al. Large congenital melanocytic nevi and the risk for the development of melanoma: a prospective study. Arch Dermatol. 1996;132:170–175. 2. Castilla EE, da Graca Dutra M, Orioli-Parreiras IM. Epidemiology of


Chapter 15: Congenital Melanocytic Nevi

3. 4. 5. 6. 7.

congenital pigmented nevi: incidence rates and relative frequencies. Br J Dermatol. 1981;104:307–315. Egan CL Oliveria SA, Elenitsas R, et al. Cutaneous melanoma risk and phenotypic changes in large congenital nevi: a follow-up study of 46 patients. J Am Acad Dermatol. 1998;39:923–932. Quaba AA, Wallace AF. The incidence of malignant melanoma (0 to 15 years of age) arising in “large” congenital nevocellular nevi. Plast Reconstr Surg. 1986;78(2):174–179. Ruiz-Maldonado R, Tamayo L, Laterza AM, et al. Giant pigmented nevi: clinical, histopathologic, and therapeutic considerations. J Pediatr. 1992;120:906–911. Swerdlow AJ, English JSC, Qiao Z. The risk of melanoma in patients with congenital nevi: a cohort study. J Am Acad Dermatol. 1995;32:595–599. Watt AJ, Kotsis SV, Chung KC. Risk of melanoma arising in large

8. 9. 10. 11. 12.

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congenital melanocytic nevi: a systematic review. Plast Reconstr Surg. 2004;113(7):1968–1974. ¨ B. Congenital nevocytic nevi: follow-up of a Swedish birth Berg P, Lindelof register sample regarding etiologic factors, discomfort, and removal rate. Pediatr Dermatol. 2002;19(4):293–297. Burd A. Laser treatment of congenital melanocytic nevi [letter]. Plast Reconstr Surg. 2004;113(7):2232–2233. Marghoob AA. Congenital melanocytic nevi: evaluation and management. Dermatol Clin. 2002;20:607–616. Gur E, Zucker RM. Complex facial nevi: a surgical algorithm. Plast Reconstr Surg. 2000;106(1):25–35. Gosain AK, Santoro TD, Larson DL, et al. Giant congenital nevi: a 20-year experience and an algorithm for their management. Plast Reconstr Surg. 2001;108(3):622–631.


CHAPTER 16 ■ MALIGNANT MELANOMA CHRISTOPHER J. HUSSUSSIAN

Melanoma results from malignant transformation of the melanocyte, the pigment-producing cell of the body. As such, it can occur anywhere melanocytes are present, including skin, eye, and the mucous membranes of the upper digestive tract, sinuses, anus, and vagina. By far, the most common tissue in which melanomas arise is the skin. The incidence of cutaneous melanoma in the United States has increased steadily over the last 50 years and is now 15 per 100,000. It represents approximately 4% of all cancers and in 2005, it is estimated that 59,580 new cases of melanoma will be diagnosed, with 7,770 deaths (1). The incidence varies widely: In Australia it is 45 per 100,000, whereas in China it is 6 mm, and Evolution. This schema is probably more useful for public awareness, as benign lesions often fulfill one or more of these criteria. Additionally, approximately 5% of melanomas are amelanotic (nonpigmented), and in the earliest stages of development, most melanomas are 20%) there is systemic response to injury that leads to capillary leakage throughout the body. In 1979, Arturson demonstrated that increased capillary permeability occurs both locally and systemically in burns greater than 25% (1), and Demling demonstrated that half of the fluid administered following 50% TBSA burns ends up in uninjured tissue (2). Therefore, burn resuscitation must not only account for the loss of fluid at the site of injury, but to the leak of fluid throughout the body. These losses are even greater if an inhalation injury is present because there will be increased fluid leak into the lungs as well as an increased release of systemic inflammatory mediators. Capillary leak usually persists through the first 8 to 12 hours following injury. The use of formal fluid resuscitation is reserved for patients with burns involving more than 15% to 20% TBSA. Awake and alert patients with burns less than 20% TBSA should be allowed to resuscitate themselves orally as best as possible. A number of approaches using a number of different solutions have been proposed for intravenous fluid resuscitation.

Crystalloid The Parkland formula, as described by Baxter, is still the most commonly used method for estimation of fluid requirements (Table 17.4). The formula (4 cc × weight in kilograms ×%TBSA) provides an estimate of fluid required for 24 hours. The fluid administered should be lactated Ringer (LR) solution. LR is relatively hypotonic and contains sodium, potassium, calcium chloride, and lactate. Sodium chloride is not used because of the risk of inducing a hyperchloremic acidosis. Half the calculated fluid resuscitation should be administered over the first 8 hours, and the second half administered over the next 16 hours. Children who weigh less than 15 kg should also receive a maintenance IV rate with dextrose-containing solution because young children do not have adequate glycogen stores.

TA B L E 1 7 . 4 THE PARKLAND FORMULA FOR FLUID RESUSCITATION Formula: 4 cc/kg/%TBSA = total fluid to be administered in the first 24 hours 50% of fluid should be given in the first 8 hours 50% of fluid should be given in the next 16 hours Fluid should be lactated Ringer solution Sample calculation: 70-kg person with a 50% TBSA burn 4 × 70 × 50 = 14 L of fluid 7 L in the first 8 hours (875 cc/hr) 7L in the next 16 hours (437 cc/hr) The formula is only a guideline. Fluid administration should be titrated to urine output of 30 cc/hr for adults and 1 cc/kg/hr for children. Pediatric patients weighing less than 15 kg should also receive maintenance fluid based on their weight.

It is important to remember that the formula provides merely an estimate of fluid requirements. Fluid should be titrated to achieve a urine output of 30 cc/hr in adults and 1 cc/kg/per hour in children. A Foley catheter should be used to accurately track urine output. If urine output is inadequate, the fluid rate should be increased; conversely if the urine output is greater than 30 cc/hr, the fluid rate should be decreased. Fluid boluses should only be used to treat hypotension, and should not be used to improve urine output. Patients with deeper, fullthickness burns and patients with inhalation injury tend to require higher volumes of resuscitation.

Colloid Protein solutions have long been used in burn resuscitation and have been the subject of debate for decades. The use of colloid has the advantage of increasing intravascular oncotic pressure, which could minimize capillary leak and potentially draw fluid back intravascularly from the interstitial space. The Brooke and Evans formulas, developed during the 1950s and 1960s, both included the use of colloid in the first hours of resuscitation. However, the use of colloid in the early postburn period can lead to the leakage of colloid into the interstitial space, which can aggravate tissue edema. Consequently, colloid is typically not used until 12 to 24 hours following burn injury, when the capillary leak has started to seal. Several different colloid formulations have been used. Albumin is the most oncotically active solution and does not carry a risk of disease transmission. Fresh-frozen plasma has also been used, but because this is a blood product, there is a risk, albeit small, of disease transmission. Dextran is a nonprotein colloid that has also been used in burn resuscitation. Dextran is available in both a low- and a high-molecular-weight form. Low-molecular-weight dextran (dextran 40) is more commonly used. Because dextran increases urine output with its osmotic effect, urine output may not be an accurate indicator of volume status. Additionally, dextran has been reported cause fatal allergic reactions in some patients.

Hypertonic Saline Hypertonic saline solutions have been used for many years for burn resuscitation. Advocates of hypertonic saline argue that hypertonic solutions increase serum osmolarity and minimize the shift of water into the interstitium. This should theoretically maintain intravascular volume and minimize edema. However, this theory is not well substantiated in the literature. Several


Chapter 17: Thermal, Chemical, and Electrical Injuries

studies show similar resuscitation volumes and edema formation with either hypertonic or nonhypertonic solutions (3). The principal risk of hypertonic solutions is the development of hypernatremia. Regardless of the type of resuscitation fluid used, urine output is the best indicator of resuscitation. Tachycardia is often present as a result of the body’s systemic inflammatory response, pain, or agitation, and, therefore, should not be used as a barometer of volume status. The use of pulmonary artery catheter parameters to guide fluid resuscitation leads to overresuscitation. Serial lactates and hematocrits serve as secondary indicators of resuscitation so decisions regarding fluid administration and titration should be dictated by urine output. Poor urine output is likely the result of hypovolemia, and is therefore appropriately treated with increased fluid administration not diuretics or pressors. The risks of underresuscitation—hypovolemia and worsening organ dysfunction—are well understood. More recently, the risks of overresuscitation are becoming clear. The need for intubation and prolonged ventilation, worse extremity edema that can extend the zone of burn injury, and the potential for extremity and abdominal compartment syndrome can all result from excessive fluid resuscitation. Although there are several formulas to guide fluid resuscitation during the first 24 hours following burn injury, it is important to remember that patients may continue to have large fluid requirements for several days following injury. At the conclusion of the first 24 hours, fluids should not be discontinued; rather, continue to titrate fluids for a goal urine output of 30 cc/hr. Patients with large burns will have large volumes of insensible loses that require replacement with intravenous fluids.

Decision not to Resuscitate Advances in burn care and fluid resuscitation, particularly the practice of early burn wound excision, have significantly increased survival following burn injury. However, there may be some cases of such extensive burn injury that the decision needs to be made whether or not efforts at resuscitation may be futile. This is a difficult decision. The decision is based on several factors, including an accurate assessment of the patient’s injury, location of burns, depth of burns, presence of inhalation injury, the patient’s age and comorbidities, and the typical mortality level based on these factors. Several formulas have been described for estimating mortality, but none is perfect. Baux suggested that adding age and TBSA gives an estimate of mortality. Zawacki’s description of the Z score is another formula that estimates mortality. The score is based on several factors, including extent of burn injury, extent of full-thickness burn injury, presence of inhalation, and age. Part of the difficulty in determining survivability is that each burn is quite different. In addition, each patient is quite different. This is particularly true in older patients (≥65 years), because there is great heterogeneity in patients of the same age. Prior to making a decision regarding resuscitation, frank discussion with the patient’s family, if possible, should occur. Members of the burn team—particularly the nurses caring for the patient—should be included in the discussion and comfortable with the sometimes very difficult decision not to resuscitate. Patients who are awake and alert who are not candidates for resuscitation should also be involved in the process. These patients should be informed of the decision not to resuscitate and given the opportunity to talk with family members. Often patients with extensive full-thickness burns can be extubated and be awake and alert enough to have an opportunity to say goodbye to family members.

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INHALATION INJURY The inhalation of the products of combustion can lead to devastating pulmonary injury. Direct thermal injury to the lungs occurs rarely and usually only in the case of steam burns. Inhalation injury caused by products of combustion significantly increases burn mortality for a given percent skin burn. Carbon monoxide inhalation is particularly devastating because carbon monoxide will bind to hemoglobin and interfere with the delivery of oxygen. Diagnosis of inhalation injury is best made by consideration of the circumstances surrounding the burn injury and findings on physical examination. Typically, patients who are trapped inside a burning room or house are at increased risk of inhalation injury because of prolonged exposure to smoke and products of production. Conversely, flash burns that occur outdoors will rarely result in inhalation injury. On physical examination, the presence of carbonaceous sputum, raw oral and nasal mucosa, and soot on the vocal cords (on laryngoscopy) all signify inhalation injury. In addition, patients may have a cough, hoarse voice, and difficulty breathing. The presence of singed nasal and facial hair may be suggestive of inhalation injury but, alone, is not diagnostic. Evaluation of inhalation injury should include an arterial blood gas and carboxyhemoglobin level. Although an elevated carboxyhemoglobin is consistent with inhalation injury, patients who smoke cigarettes will have an elevated baseline carboxyhemoglobin, sometimes as high as 10. In addition, the carboxyhemoglobin level should be interpreted in light of the time since injury and the level of oxygen support the patient has received since the injury. The half-life of carboxyhemoglobin on 100% oxygen is 40 minutes, so a patient with a carboxyhemoglobin level of ten 40 minutes following injury may have had an initial level of 20. Chest radiographs are of little usefulness in the evaluation of inhalation injury. Radionuclide studies have been used to diagnose inhalation injury but they might not add much more reliable diagnostic information beyond good clinical evaluation. Bronchoscopy can demonstrate mucosal inflammation in the upper airways, subglottic edema, and carbonaceous particles, and therefore can be useful in making the diagnosis of inhalation injury. However, the diagnosis can usually be made without the need for bronchoscopy. Management of inhalation injury is usually supportive. Patients with signs and symptoms of inhalation injury may require intubation. In general, it is better to secure a patient’s airway early in the postburn period, particularly if the patient will require large volumes of fluid resuscitation. In addition, if a patient is admitted with a suspected inhalation injury and has a worsening respiratory status, intubation should be promptly performed. Aggressive pulmonary toilet, bronchodilators, and clearing of secretions are all essential components of patient management. Steroids are not beneficial in the treatment of inhalation injury and the use of prophylactic antibiotics should be avoided. Radiographs may be useful following admission to evaluate possible pneumonia. Repeat bronchoscopy can be useful in obtaining sputum samples for culture and for assistance in suctioning sloughed mucosa that the patient is unable to clear. Patents who sustain inhalation injury are at increased risk for respiratory failure and subsequent infection. Patients who develop signs of adult respiratory distress syndrome (ARDS) should be placed on low (protective) tidal volumes on the ventilator in order to protect the pulmonary parenchyma from additional damage. Typically, these lower tidal volumes result in hypercapnia, which should be permitted in order to protect the lungs. The usefulness of hyperbaric oxygen for patients with elevated carboxyhemoglobin levels has long been debated. The

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potential benefit of hyperbaric oxygen is the rapid reduction of carbon monoxide levels with the potential to minimize potential neurologic sequelae of carbon monoxide poisoning. Hyperbaric oxygen can reduce the half-life of carbon oxide from 40 minutes on 100% FiO2 (fraction of inspired oxygen) to 20 minutes. However, hyperbaric oxygen is not without risk. Hyperbaric oxygen can cause pneumothorax and perforation of the tympanic membranes. If the patient must be transported to another medical center for hyperbaric oxygen, it may be possible to effectively treat an elevated carboxyhemoglobin with 100% oxygen in the time it takes to transport the patient to the hyperbaric chamber. One must also carefully weigh the risks of placing a critically ill patient in a chamber where patient access might be limited. Any patient who is hemodynamically unstable, requiring aggressive resuscitation, and hypothermic should probably not be transported for hyperbaric oxygen.

PATIENT MANAGEMENT Nutrition Nutritional support is a cornerstone of burn patient management. Hypermetabolism and hypercatabolism both occur following burn injury. This increased metabolic rate begins immediately following injury and persists until complete wound coverage is achieved, which may take months. In addition, the nutritional requirements to heal burn wounds, skin grafts, and donor sites all increase the nutritional needs of the burn patient. Feeds, whether oral or enteral, should be initiated as soon following admission as possible. Most patients with burns of under 20% TBSA can obtain enough calories on their own. However, patients with larger burns and patients who will be intubated for several days should have an enteral feeding tube placed on admission. Ileus following burn injury commonly occurs, and it may take days for the return of gastrointestinal function. However, ileus can be prevented by starting feeds in the immediate postinjury period. The burn team’s dietician should be consulted to assist in determining nutritional needs, to provide monitoring of caloric intake, and to make appropriate adjustments to the patient’s nutrition plan. Because of the high levels of narcotics patients receive, routine use of stool softeners should also begin on admission to prevent constipation and feed intolerance. Parenteral nutrition is associated with higher rates of infection, attributable, in part, to the prolonged need for central venous access. Parenteral nutrition should only be used in cases when the patient has a prolonged paralytic ileus, pancreatitis, bowel obstruction, or other contraindication to enteral feeding. Enteral feeds can be continued when the intubated patient is taken to the operating room unless the patient needs to be placed in the prone position. If the patient is not intubated and requires intubation for surgery, feeds should be discontinued 6 hours prior to surgery and restarted as soon as possible following the completion of surgery and extubation. There are several equations for the estimation of caloric requirements. The two most commonly used formulas for calculating caloric requirements are the Curreri formula and the Harris-Benedict formula. The Curreri formula differs for children and adults as follows: Adult: 25 kcal × weight (kg) + 40 kcal × %TBSA Children: 60 kcal × weight (kg) + 35 kcal × %TBSA The Harris-Benedict formula provides an estimate of basal energy expenditure (BEE): Men: 66.5 + 13.8 × weight (kg) + 5 × height (cm) − 6.76 × age (years)

Women: 65.5 + 9.6 × weight (kg) + 1.85 × height (cm) − 4.68 × age (years)4 The calculated BEE is multiplied by an injury factor (typically 2.1 for patients with large burns) to provide an estimate of caloric requirements. Because the Curreri formula generally overestimates caloric requirements, particularly in the elderly, and the Harris-Benedict formula underestimates caloric requirements, an average of the two is often used. Indirect calorimetry using a metabolic chart can be used for patients on a ventilator. However, the calorimetric formula is less reliable at FiO2 levels above 50%. The metabolic chart will provide an estimate of energy expenditure by measuring oxygen consumption and carbon dioxide production. In addition, a respiratory quotient can be calculated from these data that will provide information about whether the patient is being over- or underfed (4). Protein requirements should also be calculated. Burn patients catabolize significant amounts of skeletal muscle and require protein replacement to maintain muscle mass and function and to provide building blocks for wound healing. Patients with normal renal function should receive 2 g of protein per kilogram per day. Supplemental vitamins and minerals should also be provided to optimize wound healing. Vitamins A and C, as well as zinc, have known benefits in wound healing, and the use of vitamin E, selenium, and iron supplements have also been described. Regular nutrition monitoring, particularly for intensive care unit patients, should be performed weekly with C-reactive protein, albumin, prealbumin, and vitamin C levels, as well as a 24-hour total urea nitrogen. Calorie counts should be used to monitor the patient’s oral intake and to help determine when enteral feeds can be safely weaned and ultimately discontinued. Patient blood glucose levels should be closely monitored, particularly if the patient is in the intensive care unit. Enteral feeding, along with the body’s systemic inflammatory response, can increase blood glucose levels. The benefits of tight glucose control in a critically ill patient is well documented. Slidingscale insulin coverage should be initiated for all burn patients in the intensive care unit and there should be a low threshold for initiating an insulin drip, because this allows for tighter blood sugar control.

Gastrointestinal Prophylaxis Stress ulcers (Curling ulcers) were once a common complication following severe burn injury. The development of prophylactic agents, including histamine receptor blockers, sucralfate, and protein pump inhibitors have minimized the incidence of stress ulcers. Perhaps the best protection against stress ulcers is feeding the patient. Feeding the stomach early in the hospital course minimizes post-traumatic gastric atony, provides continuous coating of the stomach, and is easier to place at the bedside than a duodenal tube. Stress ulcer prophylaxis is only necessary in those patients who are not taking oral diet or enteral feeds or in patients with previous history of peptic ulcer disease.

DEEP VENOUS THROMBOSIS Patients who sustain burn injuries often have multiple risk factors for deep venous thrombosis. Injuries to an extremity as well as the occasional need for prolonged bedrest (particularly in the intubated patient) and indwelling catheters increase the risk of venous thrombosis. Consequently, deep venous thrombosis prophylaxis is required in burn patients who are hospitalized and unable to regularly ambulate. The use of



sequential compression devices and antiembolism stockings may not be practical for use in patients with lower-extremity burns. These patients should receive subcutaneous heparin. Patients who develop sudden extremity swelling or acute hypoxia should be evaluated for deep venous thrombosis and pulmonary embolism. Duplex ultrasound imaging of both the upper and lower extremities is performed if the patient has burns to the upper extremities or subclavian intravenous lines. It is also important to be aware that pediatric patients can sustain deep venous thrombosis and pulmonary embolus. Therefore, deep venous thrombosis prophylaxis should be considered in the pediatric patient who is on prolonged bedrest.

Infection Infection remains a significant risk following burn injury. Prolonged intensive care unit stay, prolonged periods of intubation and mechanical ventilation, and potential colonization of burn eschar contribute to the risk of infection. In addition, indwelling vascular and bladder catheters provide another source of invasive infection. Burn patients are also functionally immunocompromised for a number of reasons. First, the skin, which serves as the principal barrier between an individual and the environment, is lost. Similarly, the mucosal barrier of the respiratory tract may also be injured. In addition, the cellular and humoral portions of the immune response are compromised following burn injury. Decreased production of antibodies, impaired chemotaxis, and phagocytosis all increase the risk of infection and decrease the body’s ability to fight infection (5). For many decades, patients who survived the first week following injury frequently succumbed to burn wound sepsis. Colonization of devitalized eschar would lead to bacterial invasion and, ultimately, to burn wound sepsis. The best treatment for burn wound sepsis is prevention. The practice of early burn wound excision has significantly decreased the incidence of burn wound sepsis and improved survival. However, infection remains a reality in the management of the burn patient. The diagnosis and management of infection in the burn patient can be challenging. Fevers and leukocytosis can result from the systemic inflammatory response to burn injury and not necessarily infection. Thrombocytosis is also frequently observed in stable burn patients. Nearly all patients with greater than 15% TBSA burns are febrile within the first 72 hours following burn injury. Therefore, routine culture of these patients in this early time period is unnecessary. However, following the initial 72 to 96 hours, periodic cultures are important in making a diagnosis of infection. Temperature spikes warrant culturing of urine, sputum, blood, and central lines. In addition, any change in the patient’s status including hypotension, altered mental status, intolerance of tube feeds, hyperand hypoglycemia should raise the suspicion of infection. Management of infections in burn patients must be culturedriven. Presumptive broad-spectrum antimicrobial coverage is fraught with potential complications, including breeding resistant organisms and increasing the risk of fungal infections. Selection of antibiotics should be based on culture results. In the case of suspected pneumonia, bronchoscopic samples may be helpful in differentiating pneumonia from airway colonization. Although the most common sites of infection include the blood, urine, and lungs, patients with a prolonged intensive care unit course can also develop sinus infections, pancreatitis, cholecystitis, meningitis, and endocarditis. Thus, persistent fevers and signs of infection may require a more thorough evaluation beyond routine culture.

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Pain Control Pain management is an important factor in caring for the burn patient. Burn patients typically have two types of pain: background and procedural. Background pain is present on a daily basis with little variation. Procedural pain occurs during daily wound care and therapy. The best approach to pain management is to keep it simple. Polypharmacy can easily occur on a patient who is hospitalized for a long time and will make weaning the patient from the medications very difficult. Narcotics are the most commonly used analgesics. Nonsteroidal medications are typically not used in patients who are going to undergo surgery because of the increased risk of bleeding. However, they may be useful following discharge and for the pain and muscle soreness associated with increasing range of motion and increasing activity level. Background pain is best treated with longer-acting agents. Methadone can be used for patients who are going to have a long hospital course. Methadone has a half-life of 6 hours and can reduce the need for high doses of other agents. However, patients on methadone require a taper prior to discontinuation of the medication. Oxycodone or morphine can then be used for breakthrough pain. It is probably best to use only one of the two agents. If the patient is tolerating an oral diet, using an oral agent is probably better. For procedural pain, shorter-acting agents are probably best because wound care is usually a short-duration activity. If the patient requires something stronger than oral analgesics, fentanyl is the agent of choice for procedural pain. Many patients may also benefit from low-dose benzodiazepines because wound care can be anxiety provoking for many patients. Again, the use of short-acting benzodiazepines is favorable. Intubated patients are usually treated with morphine and Ativan—longer-acting agents—for background pain and sedation. Procedural pain is usually managed with fentanyl.

SURGICAL MANAGEMENT Early burn excision and skin grafting is the standard of care for full-thickness burn wounds. The concept of early excision was popularized in the early 1970s by Janezovic (6). Traditionally, burn eschar was left on the wound, and the proteolytic enzymes produced by neutrophils and bacteria led to the separation and sloughing of the eschar. The underlying granulating wound was then skin grafted. It has become clear, however, that in cases of extensive burn injury, this delay in management results in more extensive bacterial colonization, and an increased likelihood of burn-wound sepsis, multiple organ failure, and, ultimately, death. The benefits of early burn excision are clear and are well documented (7). Early excision and grafting results in increased survival, decreased infection rates, and decreased length of hospital stay. In addition, early removal of burn eschar also appears to decrease the risk of hypertrophic scarring. If feasible, early staged excision should begin on post-burn day 3 for major burns that are clearly full thickness. Operations can be spaced 2 to 3 days apart until all eschar is removed and the burn wound covered. The interval days are to allow for stabilization and resuscitation of the patient. Debrided wounds can be temporarily covered with biologic dressings or cadaveric allograft until autogenous donor sites are available.

Techniques of Excision The two techniques of burn-wound excision are tangential excision and fascial excision. Tangential excision is the sequential

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FIGURE 17.7. Tangential excision. Tangential excision is performed using a Watson (shown) or Goulian knife. Tissue is serially excised until viable, bleeding tissue, which can accept a graft, is reached.

removal of layers of eschar and necrotic tissue until a layer of viable, bleeding tissue, which can support a skin graft, is reached. Tangential excision is carried out using a Watson or Goulian (Weck) knife (Fig. 17.7). The Watson knife has a dial to set the depth of excision and Goulian knives have guards of varying opening size to allow adjustment of excision depth. These settings and guards are only guides, and ultimate depth of excision is determined by the surgeon. There are two principal disadvantages of tangential excision. First, when excising a large surface area there can be substantial blood loss; second, it may be difficult to accurately assess the viability of the excised wound bed. This particularly can be a problem when excision is carried down to fat. Fascial excision involves excision of the burned tissue and subcutaneous tissue down to the layer of the muscle fascia. Fascial excision can be carried out using electrocautery, which makes for a more hemostatic excision (Fig. 17.8). In addition, by carrying out excision through a well-defined anatomic plane, it is easier to control bleeding by identifying and ligating

FIGURE 17.9. The VersaJet water dissector. This relatively new technology can be very useful for the excision of eyelid (shown), ear, and web space burns.

larger vessels. However, in performing fascial excision, it is possible to excise viable subcutaneous tissue. Fascial excision also can result in an unsightly contour deformity and lymphedema of the excised extremities. A newer device for burn excision is the water jet-powered VersaJet (Smith and Nephew, Largo, Florida). This device provides a relatively facile and precise tool for the excision of eschar and is particularly useful for excision of concave surfaces of the hand and feet, as well as for excision of the eyelids, ear, and nose (Fig. 17.9). Regardless of which technique is used, extremity excisions should be performed under tourniquet control to minimize blood loss. In addition, suspension of upper and lower extremity from overhead hooks can facilitate excision and graft placement, particularly on the posterior aspect of the lower extremities. The risks of blood loss and probable need for transfusion should be clearly communicated to the anesthesia team prior to the start of excision. In addition, the operating room should be warmed and bear huggers should be used when possible to minimize hypothermia. Adequate hemostasis is critical to minimizing hematoma formation and, ultimately, graft loss. Telfa pads (Kendall, Mansfield, MA) soaked in an epinephrine solution (1:10,000) are a mainstay of hemostasis, and are combined with topical pressure and cauterization when necessary. More recently, the use of tissue sealants such as Tisseel Fibrin Sealant (Baxter, Deerfield, IL) has gained popularity in assisting with hemostasis and with graft fixation.

Technical Aspects of Skin Grafting

FIGURE 17.8. Full-thickness chest burn. This elderly patient had fullthickness burns to the chest, which were excised using a fascial excision. The edges of the wound were sutured to the pectoral fascia to minimize the step-off or ledge at the perimeter of the excision.

The process of engraftment is essentially that of revascularization of the graft. Initially the graft has no vascular connection with the recipient bed and survives through the process of diffusion of nutrients from the wound bed, a process known as plasma imbibition. Typically, the process of revascularization begins 48 hours after graft placement. The process of revascularization occurs by a combination of neovascularization (ingrowth of host vessels into the graft) and inosculation, the direct biologic anastomosis of cut ends of recipient vessels in the graft bed with those of the graft itself. Concomitant with revascularization of the graft is the organization phase, which



describes the process by which the graft integrates with the wound bed (see Chapter 1). Skin grafts are typically classified according to their thickness as either split (partial) thickness or full thickness, depending on whether they include the full thickness of dermis or just a portion of it. Split-thickness grafts are further classified into thin, intermediate, and thick, depending on the amount of dermis. The thinner a skin graft is, the more contraction that occurs at the recipient site following transplantation. Thicker grafts contract less at the recipient site, but leave a greater dermal deficit at the donor site, which will therefore take longer to heal and have an increased risk of hypertrophic scarring. Skin grafts can also be meshed or unmeshed (sheet grafts). From an aesthetic viewpoint, sheet grafts are always superior to meshed grafts. It is best to perform sheet grafting over the face, hands, and forearms because these are exposed areas. In larger burns there is inadequate skin available to perform sheet grafting over all burned areas and the skin grafts need to be meshed. Skin grafts can be meshed 1:1, 2:1, 3:1, 4:1, and even 6:1. However, for practical and cosmetic purposes, mesh of 2:1 is the most commonly used. Meshing of skin grafts allows for the egress of fluid from the wound bed, which minimizes seroma and hematoma formation and therefore decreases the risk of graft loss. In addition, meshing a graft allows for expansion, which provides greater wound coverage. Skin grafts can be affixed to the wound bed using a variety of techniques. Staples are the most commonly used and are probably the most expeditious way to secure grafts when a large area of the body is being covered. Suturing of grafts is particularly useful in children because absorbable sutures need not be removed. My burn center has had a great deal of success using Hypafix (Smith and Nephew, London, England), particularly for fixation of sheet grafts. Hypafix is an elastic adhesive dressing can be easily applied using Mastisol as an adhesive. The Hypafix remains in place and can only be removed by using Medisol. Fibrin glue and other tissue sealants have also been used to affix skin grafts to the wound bed. There are numerous options for skin-graft dressings. Typically, the decision is guided by the type of graft—meshed or unmeshed—and the location of the graft. A number of dressings can be used for meshed skin grafts. Wet dressings, consisting of antimicrobial solution (Sulfamylon) provide a moist environment to accelerate epithelialization of the interstices. Greasy gauze and Acticoat (Smith and Nephew, London, England) have also been used as dressings over meshed grafts. Acticoat is a relatively new antimicrobial dressing that consists of a polyethylene mesh impregnated with elemental silver. Silver provides antimicrobial activity by disrupting bacterial cellular respiration. Both greasy gauze and Acticoat are capable of providing a moist environment that accelerates closure of graft interstices. Bolsters of cotton or greasy gauze are needed when grafts are placed over areas of convexity or concavity. Sheet grafts can be left open to the air to allow for monitoring or can be dressed with a nonadherent gauze. Typically, dressings over sheet grafts are removed on the day following skin grafting to allow for evacuation of seroma or hematoma that can occur. Facial skin grafts should similarly be covered with a nonadherent or greasy gauze, and we will commonly use a Jobst skin featureless face mask garment (Bielsdorf-Jobst, Rutherford College, NC) to minimize graft shearing. The Vacuum Assisted Closure (V.A.C.) device (Kinetic Concepts, San Antonio, TX) is another option for skin graft coverage. The V.A.C. device is a negative pressure device that is able to prevent graft sheering and is particularly useful over areas of convexity or concavity. The V.A.C. device can be left in place over a skin graft for 5 days, and then can be easily removed at the bedside. Alternatively, an Unna boot dressing

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can be applied over grafts of the arm and leg. The Unna boot dressing provides vascular support and prevents graft shearing while allowing early mobilization.

Donor Site Selection and Care Selection of donor sites is often dependent on the availability of unburned skin. For children, the buttock and scalp provide the most inconspicuous donor sites. Plasmalyte can be infused subcutaneously to facilitate graft harvest in these areas. When larger amounts of skin are needed, the thighs and back can be used. The ideal donor-site dressing minimizes pain and infection, accelerates epithelialization, and is cost-effective. There are a number of donor-site dressings available, which may suggest that no perfect dressing exists. Greasy gauze and Acticoat are two commonly used donor-site dressings. They are applied at the time of surgery and left in place until epithelialization is complete, at which time, they can be easily removed. Alternatively, OpSite, a transparent polyvinyl adherent dressing, can be used. Although OpSite allows for observation of the underlying healing wound, the accumulation of fluid beneath the dressing can lead to leakage, which is both uncomfortable and disturbing to the patient. In addition, OpSite is not well suited for use over joint or convex surfaces. For children with buttock skin donor sites, Silvadene in the diaper works particularly well. The Silvadene can be replaced with each diaper change.

Management of Specific Areas Face Plastic surgeons who do not routinely care for burn patients may be called on to manage both acute and reconstructive facial burns. Few areas of burn care can be more challenging than the management of facial burns. The aesthetic and functional outcomes are critical to the daily life of the patient and are intimately related to feelings of self-esteem. Management of facial burns begins at the time of admission. Many patients with facial burns sustain inhalation injuries and are intubated. The endotracheal tube should be secured in such a way as to minimize pressure necrosis of the lip. Patients who are going to be intubated for a long period of time may benefit from the wiring of the endotracheal tube to the teeth or to a segment of an arch bar that can be wired to the upper teeth. This provides a reliable and sturdy method for tube fixation and will minimize pressure on the lip. This will also allow for facile and secure positioning of the tube in the operating room (Fig. 17.10). Similarly, if a feeding tube is placed, care must be taken to minimize alar or columellar pressure necrosis. All patients with periorbital burns should undergo an intraocular exam with a Wood lamp. If this exam is positive, an ophthalmologic consult is required. In addition, if the patient has a lagophthalmos it is important to keep the eyes well moisturized with ophthalmic ointment to prevent exposure keratitis. Tarsorrhaphy is rarely necessary in the early burn period. The practice of excising facial burns has long been debated in the literature. The traditional method of facial burn management was to perform daily wound care until the face either healed or the underlying eschar lifted, leaving a granulating wound bed that could accept a skin graft. It is now clear that better outcomes are achieved if nonhealing areas are excised and then subsequently skin grafted. As in other parts of the body, it is generally easy to determine the healing capacity of shallow burns and deep burns. The burns of indeterminate depth pose a greater challenge.

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postoperative day so any blebs or fluid collections that might impair graft take can be drained.

Neck Excision and grafting of the neck can also be challenging. The key to management of the neck is to make every effort to minimize wound and graft contraction. Whenever possible, it is best to cover the neck with sheet grafts. The grafts should be placed with the neck in maximal hyperextension. For the first several days following graft placement, the neck should be immobilized in a splint. Once the grafts have taken, the patient should be started on aggressive range-of-motion exercises. Aggressive range-of-motion exercises are critical for patients who heal without grafting and for patients who undergo grafting. These exercises should continue for the several months it takes for the grafts to mature.

Hands

FIGURE 17.10. Securing of the endotracheal tube. The endotracheal tube can be secured to a segment of an arch bar and then suspended from the ceiling using a rope. This provides both stable fixation of the tube and complete access to the face for excision.

Over the past 25 years it has been our practice at the University of Washington to excise facial burns. Our protocol and results can be found in a recent publication (8). Patients who are admitted with facial burns undergo debridement of loose blisters and debris and then daily wound care. It is our practice to assess patients with facial burns at day 10, at which time it is usually clear which burns will heal within 3 weeks and which will not. Patients with burns that are thought unlikely to heal within 3 weeks are scheduled for excision and grafting. It is important to note that patients with full-thickness burns with clearly no healing potential should be operated on in the 7 to 10 days if the patient is stable and there are no other more urgent areas of excision. Facial excision is typically carried out using Goulian knives. Traction sutures are frequently used on the upper and lower eyelids to aid in excision. More recently, the availability of the VersaJet water dissector has helped in excising areas with difficult contour, such as the eyelids and ears. Small areas of exposed cartilage of the ear should be excised and the skin closed primarily over the defect. Sheet autograft should always be used for coverage of the face. The appearance of meshed grafts to the face is cosmetically unacceptable. The scalp is an excellent source of autograft, given the color match with the face. However, in the case of full-facial burns, scalp skin is usually inadequate and a different donor site is needed so there is uniformity in the coloring of the skin grafts. A face mask (such as a Jobst featureless face mask) should be placed in the operating room to help immobilize the skin grafts. Skin grafts should be inspected on the first

Hand burns occur from a variety of mechanisms. In the pediatric population, hand burns frequently occur as a result of contact with a fireplace or wood stove, or from grabbing a hot object. The palm has excellent healing capacity and these pediatric palm burns rarely require grafting. However, it is critical to emphasize to the patient’s parents the importance of range-of-motion exercises. Stretching should be performed on a routine basis—either during diaper changes or feeding times, to minimize contractures of the palm and digits. In the case of deeper palm burns, nocturnal extension splints may be necessary. It is also important to emphasize to parents to let the child use his or her hands as soon following injury as possible and that bulky dressings that inhibit mobility should be minimized. Similarly, adult hand burns often heal without the need for skin grafting. Patients should be encouraged to begin rangeof-motion exercises as soon following burn injury as possible. Range-of-motion exercises reduce extremity edema and optimize the return of function once the skin wounds have healed. Static splinting is not recommended, unless the patient is intubated and unable to participate in therapy. If splinting is necessary, the wrist should be placed in mild extension, the metacarpophalangeal joints in 70 degrees to 90 degrees of flexion, and the interphalangeal joints in extension. Even in those instances, however, therapists should regularly range the extremities. If it is clear that a burn wound will not heal within 3 weeks, the best treatment is excision and grafting. With few exceptions, burns of the hand should be grafted with sheet grafts. Hand excision, particularly of the web spaces and digits, can be challenging. Great care should be taken to not expose tendons. In addition, excision should occur under tourniquet control. If a burn is so deep that adequate excision would surely expose tendons, then flap coverage should be considered. Following excision and grafting of the hand, splint immobilization should occur for at least 5 days afterwards. The wrist should be positioned in slight extension, the metacarpophalangeal joints should be placed in flexion, the interphalangeal joints in extension, and the thumb in abduction. Graft take should be assessed at postoperative day 5 and the decision for initiation of range-of-motion exercises should be made. Once graft healing is complete, compression gloves, which will minimize hand edema and possibly scar hypertrophy, should be worn.

Perineum Scald burns remain the most common burns of the perineum, and they typically result from the spilling of hot beverages that are held between the legs while driving. These scald burns tend to heal within 1 to 2 weeks, and wound care and pain control



are the mainstays of treatment. Full-thickness burns can occur as part of a larger flame burn, and the healing potential of these injuries can be more varied. It is not necessary to place a Foley catheter on all patients who sustain perineal burns. In fact, all patients should be given the option to void spontaneously; a catheter should be placed only if they have difficulty voiding. An external genital burn is unlikely to lead to urethral (internal) stenosis. Deep burns to the penis and scrotum should be given ample time to heal. In fact, the scrotum is rarely grafted because it can usually heal by contraction and not leave a noticeable scar. Patients who sustain full-thickness, charred burns of the genitals and who cannot have a Foley catheter placed, should be evaluated by urologists for placement of a suprapubic tube.

Lower Extremities Of all the burns treated in the outpatient setting, patients with feet and leg burns tend to have the most difficulty. Edema can delay wound healing and increase patient discomfort. The key to treating lower-extremity burn wounds is to encourage the patient to ambulate, with the appropriate support of an Ace bandage or Tubigrip (ConvaTec, Princeton, NJ). Ambulating minimizes the pooling of blood in the distal aspect of the extremity and thereby decreases edema. In addition, the sooner the patient is able to ambulate, the sooner the patient will be able to resume a normal level of activities once the wounds heal. While not ambulating, leg elevation can help to minimize edema. If leg or foot burns require excision and grafting, the postoperative physical therapy plan should be considered. Small burns of the leg and foot can be grafted and dressed with greasy gauze and then covered with an Unna boot dressing. The Unna boot dressing provides support and immobilization of the graft and allows for early mobilization. This is an excellent dressing for both adults and children. Patients with insensate feet are poor candidates for Unna boot dressings. Patients who require grafting both above and below the knee should be fitted with knee immobilizers postoperatively to maintain knee extension.

Outpatient Burn Management Most burn patients will have some aspect of their care in the outpatient burn clinic. Again, a multidisciplinary approach in this setting is crucial to the success of outpatient burn-wound management. Experienced nurses, physical and occupational therapists, and psychologists all play an important role in patient management, even in the outpatient setting. Issues of range of motion, optimization of function, and the psychosocial aspects of reintegration into society all must be dealt with in the outpatient clinic. Prior to discharging a patient from the hospital to the clinic, a well-thought-out discharge plan should be established in conjunction with the clinic staff. Some patients receive all of their care as an outpatient. Patients evaluated for the first time in the clinic need to have their wounds cleansed and debrided, after which a decision can be made regarding appropriate wound management. Patient education should focus on the wound-healing process, the risks of abnormal pigmentation, the risks of hypertrophic scarring, and the importance of range of motion. Burned extremities should not be immobilized. Patients should be encouraged to range injured extremities and to walk without the use of crutches and wheelchairs as soon as possible. Patients with burns to the plantar surface of their feet should similarly be encouraged to ambulate. Issues related to returning to work also need to be addressed. Patients should be given a reasonable estimate of a return-towork date so both the patient and the employer can prepare appropriately. When returning a patient to work, modified or

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part-time work may be required in order to allow the patient to regain the strength and endurance required to do their job. Several other issues are particularly relevant to outpatient care. Newly healed burn wounds and donor sites are highly susceptible to blistering and to breakdown. The new epithelium lacks the connections to the underlying wound bed that prevent shearing. It can take as long a year for these critical basement membrane structures to be reconstituted. Blisters should be decompressed with a sterile pin, the epithelial layer can be left in place, and the area covered with a plastic bandage. Patients should be instructed to soak the plastic bandage prior to removal to protect against the adhesive causing further injury. Protection from the sun is another important component of caring for the healed burn. Whether a wound has been skin grafted or healed by re-epithelialization, protection from the sun is critical. Newly healed wounds remain highly sensitive to the sun. In addition, sun exposure can increase the risk of hyperpigmentation of both grafted and nongrafted burn wounds. Patients should be encouraged to use sunscreen with a sun protection factor (SPF) of at least 15 as well as wear hats and protective clothing when outdoors. It is important to reinforce that sun-protective measures should be taken even on cloudy days. Patients also frequently complain of pruritus of newly healed wounds. Moisturizer use is essential because newly grafted or healed wounds lack the glands that usually keep skin moist. Dry and scaly wounds are often itchy and feel tight, which can restrict range of motion. Frequent moisturizer application minimizes these symptoms. No special moisturizer is needed and patients often need to try several types to see which works best. We discourage the use of perfumeor alcohol-containing moisturizers because these can irritate newly healed wounds. Even with liberal use of moisturizers, pruritus remains a problem for many patients. The use of systemic antihistamines may be helpful in these cases. The development of inclusion cysts is another problem commonly encountered in the clinic. Inclusion cysts can occur when skin grafts are placed over an excised wound bed that still contains a layer of dermis containing adnexal structures. Secretions from adnexal structures can accumulate beneath the graft to form inclusion cysts, which should be treated by unroofing the cyst with a sterile needle.

Chemical Injuries Traditionally, chemical injuries are classified as either acid burns or alkali (base) burns. The severity of chemical injuries depends on the composition of the agent, concentration of the agent, and duration of contact with the agent. In general, alkaline burns cause more severe injury than acid burns because alkaline agents cause a liquefaction necrosis that allows the alkali to penetrate deeper, extending the area of injury. Chemical injuries are also classified according to their mechanism of tissue destruction: reduction, oxidation, corrosive agents, protoplasmic poisons, vesicants, and desiccants. The first step in managing a chemical injury is removal of the inciting agent. Clothes, including shoes, that have been contaminated should be removed. Areas of affected skin should be copiously irrigated with water. Adequate irrigation can be verified by checking the skin pH. Burns from chemical powders are the one exception to the rule of water irrigation because the water can activate the chemical. The powder should first be dusted off, and then irrigation can take place. Neutralization of the inciting agent should never be attempted because this will produce an exothermic reaction that will superimpose a thermal injury on top of the chemical injury. Occasionally, the burned individual may not know specifically with which agent they were working and therefore it may be

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necessary to contact a plant manger or the manufacturer of the suspected inciting agent. If ocular injury has occurred, the eyes should also be copiously irrigated. Eye wash stations should be located in most workplaces where chemicals are used. It is important that the eye be forced open to allow for adequate irrigation. An ophthalmologist should be consulted to assist in the management of these patients. Certain chemical agents have specific treatments. Hydrofluoric acid requires specific mention. Hydrofluoric acid is commonly used in the glass and silicon chip industries, as well as in a number of industrial cleaning solutions. Hydrofluoric acid readily penetrates the skin and continues to injure tissue until it comes into a calcium source, likely bone. Given the ability of the fluoride ion to chelate calcium, patients with even small hydrofluoric acid burns are at risk for the development of hypocalcemia, which can be severe enough to have cardiac effects. In fact, hydrofluoric acid burns in excess of 10% can be fatal. The use of calcium is the most effective treatment agent. Calcium gluconate gel can be applied topically if the patient is treated rapidly enough; that is, before the hydrofluoric acid has penetrated the skin. Although direct injection of calcium gluconate into the burned area has long been advocated, this may not effectively neutralize the hydrofluoric acid and may cause skin necrosis. If copious irrigation and topical treatment with calcium has been ineffective, the patient should be treated with an intra-arterial infusion of calcium gluconate. Diminished pain is the hallmark of effective treatment. Patients with extensive hydrofluoric acid burns, and certainly patients with intra-arterial infusions, require close monitoring and should have frequent serum calcium checks. Ingestion of chemically toxic agents can occur by children or by adults as part of a suicide gesture or attempt. Again, the principle of lavage to dilute the inciting agent is practiced. These injuries are typically managed by, or in conjunction with, gastroenterologists, pulmonary specialists, or general surgeons. Laryngoscopy and endoscopy should be performed to help define the extent of injury. Enteral feeding beyond the zone of injury is often necessary.

Electrical Injuries Electrical injuries are potentially devastating events that result in damage to the skin as well as other tissues, including nerve, tendons, and bone. Electrical burns can take several forms, including injury from the electrical current itself, flash burns, flame burns, contact burns, or a combination thereof. Traditionally, electrical injuries have been divided into low voltage (less than 1,000 volts) and high voltage (greater than 1,000 volts). The considerations and management issues between the two are often different. Following electrical injury the ATLS protocol is followed, and the patient’s airway, breathing, and circulation are assessed. Once stabilized, the circumstances surrounding the injury, the voltage of the injuring current, the presence/absence of loss of consciousness and the existence of other associated injuries (e.g., fall from a cherry picker basket) are ascertained. Most importantly, it is determined if a cardiac or respiratory arrest occurred. Evaluation in the emergency room includes a thorough physical examination, during which the percent TBSA is calculated (if there was a flame burn) and the neurovascular status of injured extremities is determined. In addition, all patients who sustain electrical injuries should have an electrocardiogram (ECG) in the emergency room. Patients with a low-voltage injury who had no loss of consciousness and who have no dysrhythmia can be discharged home. The notable exception is a child who has an oral burn

FIGURE 17.11. Electrical burn. This patient sustained a high-voltage electrical injury and presented with a contracted wrist and tight forearm compartment. He was taken emergently to the operating room for forearm fasciotomy and carpal tunnel release.

from biting an electrical cord. These patients require admission and monitoring for labial artery bleeding. Management of patients with high-voltage injuries is dictated by the extent of injury, the presence of cutaneous burns, and the presence of myoglobinuria. There is no formula for fluid management of electrical burn patients per se. If there are extensive cutaneous burns, then the Parkland formula (Table 17.4) is applied and fluid administration is titrated to achieve a urine output of 30 mL/hr. If myoglobinuria is present, intravenous fluids should be titrated to a goal urine output of 100 mL/hr until the urine clears. Serial urine myoglobin checks are usually unnecessary, because treatment is initiated based on the presence of tea-colored urine and should be continued until the urine clears. If myoglobinuria persists despite fluid resuscitation, mannitol can be administered. Alkalinization of urine has also been advocated following electrical injury in order to prevent precipitation of myoglobin in the kidney tubules. Patients who sustain high-voltage injuries are placed on a cardiac monitor for the first 24 hours following admission. This has been the traditional practice regardless of whether or not a dysrhythmia is present at the time of admission. There is no data substantiating routine monitoring of high-voltage injuries, and this is a practice that may change over time. Early surgical management of electrical injuries should focus on the need for fasciotomy or compartment release. Peripheral neurovascular exams should be performed to monitor for signs of compartment syndrome. Some patients will present with a contracted upper limb and tight forearm compartments, and these patients should undergo immediate fasciotomy and carpal tunnel release (Fig. 17.11). Otherwise, progressive sensory and motor loss, as well as increased compartment pressures, should be indicators of the need for fasciotomy. Many surgeons believe that all patients should undergo immediate surgery for nerve decompression and debridement of necrotic tissue. On the one hand, carpal tunnel release and fasciotomy are relatively facile operations to perform and, if the patient derives even a small amount of benefit, the procedures may be worthwhile. On the other hand, the risks of the procedures, particularly if not necessary, can be significant. Exposure of the median nerve and forearm musculature increases the risk of tissue desiccation and necrosis. It is often difficult to determine preoperatively who will benefit from the decompression procedures. Decreased sensation



and motor function may represent a neurapraxia from direct current injury to the nerve. Mann et al. explored the issue of routine immediate decompression of high-voltage injuries (10). They concluded that a select group of patients require immediate decompression of the arm or hand or both to prevent additive injury from pressure. Clinical indications for this group of patients include progressive motor and sensory exam, severe pain, loss of arterial Doppler signal, and inadequate resuscitatation because of suspected ongoing myonecrosis. Patients with a fixed neurologic deficit typically do not benefit from decompression. The ideal timing for tissue debridement has similarly been controversial. The ideal time to determine the presence of myonecrosis is typically 3 to 5 days following injury. Therefore, early debridement might not be sufficient because irreversibly injured tissue may not have demarcated. At 3 to 5 days, all unhealthy tissue can be debrided and definitive wound closure can be achieved. In cases of extensive limb injury, free tissue transfer might be necessary to provide wound coverage or to preserve limb length for optimal prosthesis fitting. In these cases, definitive wound closure can be performed at a second operation following wound debridement to allow for appropriate planning and patient counseling. There are several long-term sequelae of electrical burns of which the patient and physician should be aware. Neurologic deficits, including peripheral and central nervous system disorders, can develop weeks to months following electrical injury. Consequently, all patients who sustain high-voltage electrical injuries should undergo a thorough neurologic evaluation at the time of admission and prior to hospital discharge. Cataracts can also occur following electrical injury. The exact mechanism is unknown, but all patients should undergo a baseline ophthalmologic examination following high-voltage electrical injury. A number of complications can also arise in the injured extremity, including heterotopic ossification, neuromas, phantom limb pain, and stump breakdown if the patient has undergone amputation.

Cold Injury Exposure to extremes of cold (and wet) conditions can lead to cellular injury and death. Cell death and tissue necrosis occur from the formation of ice crystals within the cells and extracellular space, as well as from microvascular thrombosis. Cellular injury from ice crystal formation occurs during the period of cold exposure, whereas microvascular thrombosis is thought to occur during reperfusion when the affected limb is rewarmed. Similar to burn injury, frostbite injury is classified according to the depth of injury. Mild frostbite, also known as frost nip, is similar to a superficial burn injury, with tissue erythema, pain, and edema. Second-degree frostbite is marked by blistering and partial-thickness skin injury. Third-degree frostbite occurs when there is full-thickness necrosis of the skin, and fourth-degree frostbite occurs when there is full-thickness skin necrosis as well as necrosis of the underlying muscle and/or bone. Again, it is important to note that determination of the full depth of tissue injury is not possible until several weeks following injury. The first step in management of frostbite is removal of all wet clothes, gloves, socks, and shoes. Patients should then be wrapped in warm blankets. Frostbite can also be associated with hypothermia. In these cases, care must be taken to rewarm the entire body. In cases of extreme hypothermia (less than 32◦ C) warming can be achieved with use of warm intravenous fluids, bladder irrigation with warm solutions, placement of peritoneal catheters and chest tubes through which warm fluids can be administered, and even, if available, cardiopulmonary bypass. Frostbitten extremities should be rapidly rewarmed in

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water that is 104◦ F (40◦ C). Typically, rewarming can be completed in 20 to 30 minutes. Adjunctive use of anti-inflammatory medications and anticoagulants has also been described. Patience is required in determining which areas require debridement. There is an old adage that states “frostbite in January, amputate in July (11).” While this might be hyperbole, the concept of allowing tissue to fully demarcate is essential because it is difficult to determine which tissue may survive in the immediate postinjury period. Early debridement and amputation are necessary if soft-tissue infection occurs during the waiting period.

Skin Replacement Early excision and skin grafting has become the standard of care for surgical management of the burn wound. However, in cases of extensive burn wounds the surface area burned may exceed the available donor sites. In these cases, burn wounds are excised and covered with biologic dressings until complete coverage with autografts can occur. These cases of extensive burn injury have demonstrated the need for a replacement for human skin. Efforts over the past two decades have focused on the development of a temporary and, ideally, permanent replacement to native human skin. The relatively simple biology of the epidermis and the ability to culture and expand keratinocytes in the laboratory into a stratified layer of cells has allowed for the development of pure epidermal replacement. However, epidermal replacement alone ignores the fundamental importance of the dermis in providing the skin with its integrity and durability. The retarded formation of basement membrane structures using cultured epidermal autografts (CEAs) alone results in high rates of culture loss and high rates of infection. Although early reports in the literature documented successful coverage of more than 90% TBSA burns with cultures alone, today CEAs are rarely used alone. Dermal replacement provides a more formidable challenge. The complex acellular dermal structure and the inability of dermis to regenerate have prevented the facile development of cultured dermis. A number of products have been developed over the past two decades that can serve as a dermal replacement in combination with a thin split-thickness autograft. One of the pioneering attempts at dermal replacement was Integra (Integra Life Sciences, Plainsboro, NJ), initially developed by Burke and Yannas in the late 1970s. Integra is available today as a bilayer construct. The bottom layer consists of bovine collagen and chrondroitin-6-sulfate and the outer layer is a silastic membrane that serves as a temporary epidermal replacement. Integra is placed on a newly excised wound bed and fixed into place. The silastic layer remains in place until the dermal component vascularizes, which is typically 2 to 3 weeks. The patient is then taken back to the operating room, the silastic is removed, and a thin (0.006-in.) autograft is placed on top. The Integra neodermis serves as a scaffold for the ingrowth of tissue from the patient’s wound bed (Fig. 17.12). Integra has been used in the management of extensive burns, as well as for pediatric burns, with a great deal of success. In addition, there are several recent reports of Integra used in grafting of the face, small areas of exposed bone and tendon, as well as in secondary reconstruction. Integra can be placed on a freshly excised wound bed. It must be emphasized, however, that for Integra to vascularize completely, it must be applied to a viable, noninfected wound bed. In addition, meticulous surgical technique and appropriate postoperative care are critical for a successful outcome. Another product marketed for dermal replacement is AlloDerm (LifeCell, Woodlands, TX), which is an acellular dermal matrix produced from human cadaveric skin. The cadaveric

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A

B

C

FIGURE 17.12. The use of Integra for burn wound coverage. A: Fullthickness burn wound prior to excision. B: Fascial excision of burn wound leaving a viable, well-vascularized wound bed. C: Application of Integra with silastic left in place.

skin is first stored in normal saline for 15 hours to remove the epidermal component. The cadaveric dermis is then incubated in sodium dodecyl sulfate to extract any remaining cellular components. The decellularized substrate is freeze dried and reconstituted by soaking it in crystalloid solution before use. AlloDerm can be used for immediate wound coverage in combination with a thin split-thickness autograft. Data from multicenter trials indicate that AlloDerm works best with thin (0.006 to 0.008-in.) autografts: The thicker the autograft, the lower the take rates (12). AlloDerm has also been used for abdominal wall reconstruction and for soft-tissue augmentation in the face. A product known as TransCyte (Smith and Nephew, London, England)—formerly Dermagraft-TC—is approved by the U.S. Food and Drug Administration (FDA) as a temporary (as opposed to permanent) cover for full-thickness wounds after excision. TransCyte is produced by seeding neonatal fibroblasts isolated from foreskin onto Biobrane, a synthetic dressing consisting of silastic attached to a nylon mesh, which is coated with porcine peptides prepared from type I collagen. The silastic layer of Biobrane serves as a temporary impermeable barrier, whereas the fibroblast-impregnated nylon mesh serves as a dermal component. TransCyte is placed on an excised wound bed; when clinically indicated, it is removed and replaced with split-thickness autograft. TransCyte is statistically equivalent to cryopreserved human allograft skin with respect to adherence to the wound bed, fluid accumulation, and ease of removal. It has also been used as a dressing for partial-thickness wounds, including donor sites. Dermagraft (Smith and Nephew, London, England), in contrast, is employed as a permanent dermal replacement. Dermagraft consists of human neonatal fibroblasts seeded onto an absorbable polyglactin mesh scaffold, which is intended to mimic the native dermal architecture. It is approved by the FDA for treatment of venous stasis ulcers, but it was developed for coverage of excised burn wounds in conjunction with a split-thickness autograft. Although a permanent off-the-shelf skin replacement has yet to be developed, the available products have already significantly influenced the management of burn wounds. In addition, the shortcomings of each product has improved our understanding of skin biology and physiology, and confirmed the importance of both the epidermis and the dermis in the structure and function of skin.

LATE EFFECTS OF BURN INJURY Hypertrophic Scarring Hypertrophic scarring is one of the most distressing outcomes of burn injury. Hypertrophic scars can be both unsightly as well as painful and pruritic. Hypertrophic scarring can occur in grafted wounds and unexcised wounds that take longer than 2 to 3 weeks to heal (Chapter 18). Patients with pigmented skin tend to be at a higher risk for the development of hypertrophic scarring. The biologic and molecular basis of hypertrophic scarring is not well understood, limiting our ability to prevent hypertrophic scarring. However, several strategies exist to prevent or minimize hypertrophic scarring. Pressure garments are commonly used over areas that have been grafted or have taken longer than 3 weeks to heal. No study has clearly demonstrated that garments prevent hypertrophic scarring, but the elastic support of the garments can help symptoms of throbbing and pruritus. Silicone has similarly been advocated for the treatment and prevention of hypertrophic scarring. There are several theories as to how and why silicone works, but there is no well-accepted explanation. Steroid injection has also been used to minimize the symptoms associated with hypertrophic scarring.

Marjolin’s Ulcer Marjolin’s ulcer is one of the most dreaded long-term complications of a burn wound. Marjolin’s ulcer is the malignant degeneration of a chronic wound or a wound that took months or years to heal. The tumor can occur decades following injury. Typically, these tumors are aggressive and occur in areas that were not skin grafted. The presence of an ulceration in a previously healed burn wound should raise the suspicion of malignancy and warrants biopsy and appropriate evaluation.

Heterotopic Ossification Heterotopic ossification results from the deposition of calcium in the soft tissue around joints. These calcium deposits block normal joint functioning. Heterotopic ossification most



commonly affects the elbow and shoulder joints and occurs 1 to 3 months following injury. Patients who develop heterotopic ossification have increased pain and decreased range of motion of the affected joint. Radiographs demonstrate calcium in the soft tissue. Although several medical treatments have been described, few have proven effective. Surgical management involves direct excision of the heterotopic bone and is usually best carried out once complete wound coverage has been achieved.

Rehabilitation Patients who sustain major burn injuries and require a prolonged hospital course often require a period of inpatient rehabilitation following discharge from the hospital. In reality, rehabilitation begins in the early postburn period. Careful attention to appropriate splinting, range-of-motion exercises, and even aspects of surgical management all impact long-term rehabilitation potential. Many burn centers have their own rehabilitation units, which facilitate a smooth transition from acute care to rehabilitation. Clearly, a structured rehabilitation plan is necessary, incorporating physical and occupational therapy needs, nutritional needs, as well as psychosocial issues, which will be crucial to reintegration into society. Many patients will have ongoing wound care requirements and still be on narcotics, from which they will need to be weaned during the rehabilitation stay. Patients who live far from the burn center may prefer to be at a rehabilitation facility closer to home. Careful planning is required to ensure that patient needs in all aspects of rehabilitation can be met before selecting a facility. Many therapists and rehabilitation physicians have little experience in the specialized needs of the burn patient, particularly in issues related to wound care and scar management.

FUTURE HORIZONS The management of burn injuries has evolved over the past several decades. Burn resuscitation fluids, topical antimicrobial agents, and early burn wound excision have all significantly increased survival following burn injury. However, there is still room for improvement in several areas of burn care. With the increased specialization of critical care medicine, many aspects of acute burn care are evolving. The use of plasmapheresis in patients who are failing resuscitation is being used at several centers. There are also reports of the benefits of high-frequency oscillatory ventilators for patients with severe inhalation injury and ARDS. In addition, the potential protective effects of high doses of vitamins C and E following major burn injury are also being investigated. Advances in burn wound management are also on the horizon. There has been a proliferation of silver-impregnated dressings that purportedly provide enhanced antimicrobial protection. The skin replacement technologies introduced over the past two decades have positively impacted burn care, yet much additional research will be needed in order to achieve an off-

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the-shelf skin replacement. Virtual reality is being used to minimize pain during wound care and to increase patient compliance with range-of-motion exercises.

CONCLUSION Despite all the advances in burn care over the past century and the exciting prospects on the horizon, the core of burn care remains the burn team. As each aspect of burn care becomes increasingly complex, with increasingly specialized fields of knowledge, the importance of a team of experts becomes even more critical to successful care. Plastic surgeons must always be an integral member of that team.

References 1. Arturson G. microvascular permeability to macromolecules in thermal injury. Acta Physiol Scand Suppl. 1979;463:111. 2. Demling RH, Mazess RB, Witt TM, et al. The study of burn wound edema using dichromatic absorptiometry. J Trauma. 1978;18:124. 3. Gunn ML, Hansbrough JF, Davis JW, et al. Prospective randomized trial of hypertonic sodium lactate versus lactated Ringer’s solution for burn shock resuscitation. J Trauma. 1989;29:1261. 4. Saffle J, Hildreth M. Metabolic support of the burn patient. In: Herndon D, ed. Total Burn Care, 2nd ed. New York: WB Saunders, 2002;271. 5. Barlow Y. T lymphocytes and immunosuppression in the burned patient: a review. J Burn Care Rehabil. 1990;20:487. 6. Janzekovic Z. A new concept in the early excision and immediate grafting of burns. J Trauma. 1970;10:1103. 7. Heimbach D. Early burn excision and grafting. Surg Clin North Am. 1987;67:93. 8. Sutcliffe J, Duin N. A History of Medicine. New York: Barnes and Noble Books, 1992. 9. Cole JK, Engrav LH, Heimbach DM, et al. Early excision and grafting of face and neck burns in patients over 20 years. Plast Reconstr Surg. 2002;109:1266. 10. Mann R, Gibran N, Engrav L, et al. Is immediate decompression of high voltage electrical injuries to the upper extremity always necessary? J Trauma. 1996;40:584. 11. Erikson U, Ponten B. The possible value of arteriography supplemented by a vasodilator agent in the early assessment of tissue viability in frostbite. Injury. 1974;6:150. 12. Lattari B, Jones LM, Varcelotti JR, et al. The use of a permanent dermal allograft in full thickness burns of the hand and foot: a report of three cases. J Burn Care Rehabil. 1997;18:147.

Suggested Readings Luce EA. Burn care and management. Clin Plast Surg. 2000;27:1. Fraulin FO, Illmayer SJ, Tredget EE. Assessment of cosmetic and functional results of conservative versus surgical management of facial burns. J Burn Care Rehabil. 1996;17:19. Heimbach DM, Engrav LH. Surgical Management of the Burn Wound. New York: Raven Press, 1984. Herndon D. Total Burn Care. New York: W.B. Saunders, 2002. Hunt JL, Purdue GF, Spicer T, et al. Face burn reconstruction—does early excision and autografting improve aesthetic appearance? Burns Incl Therm Inj. 1987;13:39. Jonsson CE, Dalsgaard CJ. Early excision and skin grafting of selected burns of the face and neck. Plast Reconstr Surg. 1988;88:83. Practice guidelines for burn care. J Burn Care Rehabil. 2001. Van den Berghe G, Wouters P, Weekers F, et al. Intensive insulin therapy in critically ill patients. N Engl J Med. 2001;345:1359.

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CHAPTER 18 ■ PRINCIPLES OF BURN RECONSTRUCTION MATTHIAS B. DONELAN

Reconstructive surgery following burn injury involves almost all aspects of plastic surgery. The patient population includes children and adults. All areas of the body can be involved. Deep structures can be injured either acutely or secondarily. Satisfactory outcomes require correction of both functional and aesthetic deformities. Yet, at the same time, the reconstruction of burn deformities requires a unique perspective and an emphasis on certain fundamentals and techniques that make it a specialized area of reconstructive surgery. The surgeon must thoroughly understand the processes of wound healing and contraction. The effect of time on the maturation of scars is of pivotal importance and requires patience and judgment on the part of the surgeon and patient. Correct timing of surgery is essential. Multiple operations are the rule and frequently take place over a period of many years. Donor sites are frequently compromised. Successful surgical outcomes require a well-functioning support system, including nurses, therapists, psychosocial practitioners, and, hopefully, a supportive family. All of these factors affect the outcome of surgery. Burn injuries obviously vary greatly in severity and extent. Yet virtually all postburn deformities have similar components that must be addressed for reconstructive surgery to be successful. This chapter provides a strategic approach to burn reconstruction based on surgical principles particularly relevant to this field that will help in the analysis, management, and surgical treatment of this large and challenging group of patients.

GENERAL CONCEPTS Over the past 50 years, primary excision and grafting of deep second-degree and full-thickness burns has become the standard of care in the United States and in most developed countries (1,2). Early excision and grafting has decreased the mortality and morbidity of acute burn injuries (3). The duration of acute hospitalization has been greatly reduced. Early excision and grafting has also decreased the frequency and severity of contractures and hypertrophic scarring; occasionally, however, one still encounters patients who were treated “expectantly” with late grafting and disastrous results (Fig. 18.1). All burns of the second or third degree result in open wounds. Open wounds heal by contraction and epithelialization. Contraction may be decreased by early excision and grafting, but it is always present to some degree. Contraction leads to tension, and tension is one of the principal causes of hypertrophic scarring and unfavorable scarring in general. Understanding the role of tension in the evolution of postburn deformities is essential for their successful treatment. Burn reconstruction is fundamentally about the release of contractures and the correction of contour abnormalities. It should not be focused on the excision of burn scars. Scar excision is an oxymoron. A scar can only be traded for another scar of a different variety. When the fundamental problem is that

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of inadequate skin and soft tissue, further excision of “scars” can easily add to the clinical problem. Well-healed burn scars, if given enough time to mature, are often an excellent example of nature’s camouflage. The subtle and gradual transition from unburned skin to scar helps the deformity to blend into its surroundings. A burn scar that is conspicuous at 1 year because of hypertrophy, contracture, and erythema, can become inconspicuous with further maturation. Healed second-degree burn deformities under tension with resulting hypertrophy are unsightly. With time and relief of tension they will greatly improve. Premature early excision of such scars with primary closure frequently results in a wide iatrogenic scar, which then becomes a more obvious permanent deformity. Lacking camouflage, the surgical scar can be more noticeable than the burn scar and increased tension from the excision can create contour deformities. Excision and primary closure of burn scars should be limited and reserved for small scars in conspicuous locations that will allow a favorably oriented closure. Although counterintuitive, it is helpful to learn to love burn scars. After all, without scarring, healing cannot occur, so scars are our friends. For successful burn reconstruction, one must learn to appreciate them and understand their behavior. Scars under tension are angry and respond with erythema, hypertrophy, pruritus, pain, and tenderness. Relaxed scars are happy scars. They respond by flattening, softening, and becoming pale and asymptomatic. Directing reconstructive surgery towards relieving tension is practical, achievable, and can result in great improvement. Ill-advised attempts to excise scars can be simplistic and are potentially harmful. Burn reconstruction must always strive to make the patient clearly better, not just different from normal in a different way. Contracture releases can be carried out with local tissue rearrangement such as Z-plasties or transposition flaps or they can be carried out by releases and skin grafting of the resulting defects. Releases can be performed by either incising scars or excising scars. Release by incision takes advantage of the healing that has already occurred and because of the relief of tension, it will usually improve the appearance and quality of the tissue that is retained. Mature scars and grafts are a known commodity and will not contract significantly after release. New grafts are less predictable. Incisional releases also obviously create a smaller defect and, therefore, conserve donor sites. When the contracted tissue is of unacceptable quality, or too irregular, excision of scars should be done to give the best result (Fig. 18.2). In most cases, however, it is better to work with the grafts and scars that are already present than to excise them. Grafts can either be split-thickness skin grafts or full-thickness skin grafts. Releases can also be carried out and the resulting defects closed with distant flaps transferred with either traditional or microsurgical techniques. The choice of the appropriate intervention and the timing of reconstructive surgery are the essential ingredients that result in either successful or unsuccessful burn reconstruction.


Chapter 18: Principles of Burn Reconstruction

FIGURE 18.1. Late grafting. A 4-year-old boy from Central America treated with months of dressings and late grafting, resulting in severe contractures.

TIMING OF RECONSTRUCTIVE SURGERY Patients with postburn deformities typically present to the plastic surgeon in one of three ways. The ideal circumstance is when the plastic surgeon is involved in the patient’s care from the time of the acute injury. The involvement may either be as the treating physician or as a consultant and occasional participant in the patient’s acute care. It is a truism that the reconstruction of burn deformities begins with the acute care. Plastic surgical consultation can help prevent secondary deformities by initiating appropriate acute surgical intervention. It can also enhance outcomes by helping in aesthetic decisions such as skin graft donor-site conservation. The second group of patients are those who only recently received their acute burn care at another facility and then come to the plastic surgeon for another opinion. The third group of patients are those who sustained their acute burn injury in the past and now present with mature scars and grafts and established burn deformities. The timing of burn reconstruction falls into three distinct phases: acute, intermediate, and late. As a general rule, burn reconstruction is best delayed until all wounds are closed, inflammation has subsided, and scars and grafts are mature and soft. Acute reconstructive intervention is required during the early months following burn injury when urgent procedures are necessary to facilitate patient care, to close complex wounds such as open joints, or to prevent acute contractures from causing irreversible secondary damage. Examples of indications for acute surgical intervention are eyelid contractures with exposure keratitis, cervical contractures causing airway issues, and

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“fourth-degree burns,” such as in electrical injuries, where acute flap coverage is required. The intermediate phase of burn reconstruction is best described as scar manipulation designed to favorably influence the healing process. After a patient’s wounds have closed, physical and occupational therapy must continue to correct or prevent contractures, as well as enhance scar maturation with the use of pressure garments, silicone gels, and massage. The efficacy of such treatments has been demonstrated over many years (4,5). Enthusiastic support of these ancillary measures by the plastic surgeon and the entire burn team can be very helpful in maximizing patient compliance. The length of time required to reach the end point of burn scar maturation is considerably longer than is generally appreciated. Scars that are thick, raised, and erythematous at 1 year or longer, will improve dramatically if given significantly more time, often several years. When tension is present, scars never heal well. Judicious surgical intervention to relieve tension during this period can positively influence scar maturation. A longitudinal scar across the antecubital space subjected to constant tension and relaxation will remain contracted and hypertrophic despite pressure, silicone, massage, and splinting, and may result in ulceration or “spontaneous release.” Relieving tension by either carrying out Z-plasties within the scarred tissue or performing a release and graft can help the entire scar to improve after the tension has been eliminated. Hypertrophic scars are common in healed second-degree burns under tension. When the tension is relieved, the subsequent improvement in appearance and elasticity is often remarkable. Steroids are effective in diminishing and softening hypertrophic scars. They must be used carefully because of potential problems with atrophy of the scar and the underlying subcutaneous tissue. Topical steroids are helpful. Steroid injections are powerful. Their use should be limited to situations where time, pressure, silicone therapy, and massage are ineffective and surgery is not an option, for example, isolated hypertrophy without tension such as on the face or shoulders. A solution of triamcinolone (10 mg/mL mixed half and half with 1% Xylocaine with epinephrine) administered by intralesional injection with a glass tuberculin (TB) syringe, never more frequently than once a month, is efficacious in decreasing hypertrophy and preventing undesirable side effects. Intermediate-phase scar manipulation is of particular benefit in the management of facial burn deformities. This is an area where treatment is evolving and there is considerable potential for improvement using multiple modalities. Computergenerated clear face masks with silicone lining are expensive but efficacious and well tolerated by patients. Relief of tension on facial scars by eliminating extrinsic contractures from the neck, as well as from the inconspicuous periphery of the face by release and grafting or Z-plasties, can be exceedingly beneficial to the healing of facial burns. The pulsed dye laser is effective in decreasing facial erythema when used in this intermediate phase and seems to result in more favorable long-term scar maturation. Z-plasties within the hypertrophic scar to decrease tension and more favorably align scars can achieve dramatic results over time (Fig. 18.3). Late-phase reconstructive surgery includes all postburn deformities that are essentially stable and consist of mature scars and grafts. It is not uncommon in this group of patients for hypertrophic scars to present with areas of open ulceration. This is almost always caused by chronic tension. The resulting ischemia in the scar causes unstable epidermal coverage. Operations directed at relief of the tension will usually cure the chronic open wounds. The transition from acute burn injury to the late phase of reconstructive surgery can be prolonged and is unique for each patient. The experience, judgment, and expertise of the plastic surgeon are extremely important during this period. It is


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FIGURE 18.2. Excisional release. A: A 15-year-old girl with bilateral lower-pole breast contractures. B: Excisional release of the lower half of the breasts with split-thickness skin grafting allowed the compressed breast tissue to expand and assume its normal shape. C: Breast augmentation and nipple areola complex reconstruction achieved a satisfactory aesthetic outcome.

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FIGURE 18.3. Multimodal scar manipulation. A: An 8-year-old boy 6 months following flame burn injury with diffuse facial hypertrophic scarring and contractures. B: Ten years later following pressure, massage, steroid injections, and multiple Z-plasties within the scar tissue, the hypertrophy has resolved. The depth of the burn is indicated by the absence of beard growth.



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intermediate phase following an acute burn or at the time of consultation with a new patient who has established postburn deformities. Planning the reconstructive sequence is helpful to the patient, the family, and the surgeon. Because the patient’s priorities may be different from the surgeon’s, education, careful consultation, and mutual agreement are of extreme importance. Operations to improve essential function are the initial priority, but appearance, particularly of the face and hands, should always be a consideration. All reconstructive procedures should try to improve both the function and appearance of the operated area as much as possible. The planning process gives the patients perspective and helps them develop a positive attitude as they look forward to significant improvement in the future. Enthusiasm and optimism on the part of the surgeon and the entire reconstructive team is essential. Including the patient’s family in these discussions is important. A strong support system is necessary for what is often a long and arduous process.

Fundamentals Several basic concepts and techniques are worth reviewing in the context of burn reconstruction.

Contractures

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FIGURE 18.4. Iatrogenic deformity. A: A 13-year-old girl with hypertrophic, contracted, medial popliteal scar 1 year following burn injury. B: Tissue expander in place prior to scar excision and flap rotation. C and D: Postoperative result of scar excision shows a conspicuous surgical scar, and abnormal leg contour with compression of the calf. The flap fills and deforms the medial popliteal concavity.

common after the acute phase of a burn injury is over for the patient and the patient’s family to desire expeditious reconstructive surgery. Patients would like their scars to be “removed” and they want to “get on with their lives.” Most of the time, this is not in the patient’s best interest. As mentioned before, the amount of time that is required for burn scars to reach their final state of maturation is not generally appreciated. If the prolonged process of scar maturation is allowed to occur, particularly when aided by appropriate help from the surgeon and therapists, hypertrophic, contracted, and conspicuous scars that are problematic at 1 year or longer can improve greatly with more time. Because of the gradual and subtle transition from unburned skin to burn scar, mature scars are usually less conspicuous than would be the surgical scars resulting from excision and primary closure. Education of the patient and the patient’s family is essential in order to help guide them to the best possible outcome. The desire for “excision” can lead to iatrogenic deformities such as shown in Figure 18.4. This unfortunate result could have been completely avoided with more time and Z-plasties performed within the maturing hypertrophic scar tissue.

Reconstructive Plan A prospective plan for reconstructive surgery should be worked out either with the patient and the patient’s family during the

Burns cause tissue loss, wounds heal with contraction, and contractures result. Contractures can be either intrinsic or extrinsic. Intrinsic contractures result from injury or loss of tissue in the affected area, causing subsequent distortion and deformity of the part. Extrinsic contractures occur when tissue loss at a distance from an affected area creates tension that distorts the structure. Eyelid ectropion, for example, can result from either intrinsic or extrinsic contractures. Although this concept is obvious and well known, the frequency with which it is ignored in burn reconstruction is astounding. Contracture deformities must be carefully evaluated and an accurate diagnosis made. Corrective measures can then be directed at the cause. There is very rarely any indication for release and graft or Z-plasty in unburned skin because of a deformity resulting from an extrinsic contracture.

Tension For scars to mature as well as possible, tension must be eliminated. Tension deforms normal body contours, and the resulting abnormal shape draws attention to the injured area. Relief of tension and restoration of normal contour by either release and grafting or Z-plasties is perhaps the most basic fundamental of all burn reconstruction. The amount of tension in the skin following a burn injury is often not obvious, particularly to inexperienced surgeons. When releases are carried out and defects are created, the amount of tissue required to close the open defects can be surprising.

Donor Sites Donor site availability is often problematic in burn reconstruction. Severe burns are usually extensive, and successful reconstruction requires careful allocation of donor-site material. Split-thickness grafts from the buttocks, thighs, and postaxial trunk are best used for contracture releases of the trunk and extremities. Full-thickness skin grafts from the retroauricular area, cervicopectoral area, and the upper inner arms, are best reserved for head and neck reconstruction. The lower abdomen and groin are excellent donor sites for full-thickness grafts, usually allowing primary closure of the donor site. Full-thickness skin grafts from these areas tend to have a yellowish hue in


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A FIGURE 18.5. Failure to limit release to superficial tissue. A: Incisional release in the antecubital space violated the subcutaneous fat creating a severe contour deformity. B: With elbow flexion, the depression and skin prolapse is a conspicuous iatrogenic deformity.

fair-skinned patients, which is a disadvantage for facial reconstruction.

Release and Grafting Nothing could be simpler than the concept of a surgical release and graft. Attention to detail is important, however, to obtain the best result. Burn contractures are usually limited to the superficial scars or grafts and a thin layer of fibrous connective tissue just beneath the skin surface. The underlying structures, such as subcutaneous fat, breast gland, and orbicularis muscle, are merely compressed and displaced. Releasing incisions or excisions should be limited whenever possible to the superficial scarred tissues alone. When this is done, normal contour is restored as the deep tissues unfurl, expand, and return to their normal shape (Fig. 18.2). Failure to limit the release to the superficial scar causes iatrogenic contour deformities that are

often impossible to correct (Fig. 18.5). Releases should always try to overcorrect the contracture deformity and grafts should be sutured in with a bolster dressing. Placing fishtail darts at the ends of the releasing incisions adds additional skin and helps to prevent recurrent contracture by creating W-plasties at the ends of the graft. Postoperative management of grafts with pressure and conformers is essential to minimize graft contracture and wrinkling. The raised edges of the grafts that result from overcorrection and the tie-over dressing will virtually always flatten. If not, they can easily be excised or revised.

Z-plasty The Z-plasty operation is an essential and powerful tool in the surgeon’s armamentarium for burn reconstruction. For more than 150 years, the Z-plasty has been used for its ability to lengthen linear scars by recruiting relatively lax adjacent

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FIGURE 18.6. Z-plasty. Transposing the flaps of a Z-plasty lengthens the central limb and also narrows the involved scar by the medial transposition of the flaps. The flap tips should be incised perpendicular to the central limb for a short distance to supply more tissue and enhance the blood supply. Following transposition, the more irregular borders help to camouflage the scar.


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lateral tissue. The Z-plasty, however, is much more than a simple geometrical exercise in lengthening a linear scar. When executed properly, it causes a profound beneficial effect on the physiology of scar tissue (6). Burn scar contractures are frequently diffuse, and excision is neither practical nor desirable. When a Z-plasty is performed properly, recruiting lateral tissue, two goals are accomplished. The central limb is lengthened, decreasing longitudinal tension on the scar, and the width of the scarred area is decreased by the medial transposition of the lateral flaps (Fig. 18.6). The narrowing of scars by Z-plasty revision can be very effective. A 60-degree Z-plasty lengthens a scar by 75% while narrowing it by approximately 30%. The Z-plasty also adds to scar camouflage by making the borders more irregular. For a Z-plasty to lengthen a burn scar and restore elasticity, the lateral limbs must extend beyond the margins of the scar. After a successful Z-plasty, the hypertrophic scar resolves, becomes more elastic, and it also has been narrowed by the procedure. The physiology of this phenomenon is related to the immediate and ongoing remodeling of collagen that occurs in hypertrophic scars following the relief of tension (7). Hypertrophic scar remodeling also takes place

when tension is relieved by release and graft, but the use of the Z-plasty is simple, elegant, and powerful. As John Stage Davis said, “It is difficult to realize how much permanent relaxation can be secured by the use of scar infiltrated tissue in this type of incision until one is familiar with the procedure and its possibilities. In addition, the improvements in the appearance of scars following Z-plasty revision is often dramatic” (6). When the Z-plasty flaps are incised, the tips should be cut perpendicular to the central limb for a short distance as shown in Figure 18.6. This adds additional tissue to the flap tips and improves blood supply. Wherever burn scar crosses a concave surface, there is a tendency for the scar to contract, hypertrophy, and “bowstring.” Z-plasty can alleviate this frequently occurring problem. The Z-plasty can also be used at the same time to enhance contour by appropriately designing the flaps. A Z-plasty release should be designed so that, following the transposition of flaps, the tight transverse limb of the Z-plasty is located where a normal concavity would occur. For example, the Z-plasties shown in Figure 18.7 both release contractures and are used to emphasize jawline definition. The axilla, antecubital space,

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FIGURE 18.7. Z-plasty to increase jawline definition. A: Hypertrophic contracted neck scars create an extrinsic contracture deforming the lower eyelid, oral commissure, and the jawline. B: Z-plasty design incorporates the scarred tissues in the flaps. C: Four years following Zplasties the facial deformities are corrected and the scar is flat, soft, and asymptomatic.


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FIGURE 18.8. Correction of cervical contracture using regional flap. A: Recurrent anterior cervical contracture in a 17-year-old boy following split-thickness skin grafting. B and C: Transposition flap from the unburned right cervicopectoral area restores normal function and appearance.

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and popliteal space are frequent sites of hypertrophic scar contracture with bowstringing and are often suitable for treatment with Z-plasty. The medial popliteal scar in Figure 18.4 could easily have been corrected with one or two Z-plasties within the scar, releasing the contracture, improving the appearance to the scar, and restoring the normal concave contour. Linear hypertrophic scar contractures are seen less frequently across extensor surfaces. The two exceptions are the wrist and anterior ankle because of their ability to dorsiflex.

Grafts Skin grafts are pivotal in burn reconstruction. A few generalizations about their characteristics may be helpful. Split-thickness skin grafts contract more than full-thickness skin grafts, have more propensity to wrinkle, and always remain shiny with

a “glossy finish” look. Thick split-thickness skin grafts contract less and provide a more durable skin coverage, but do not possess elastic properties. Meshed split-thickness grafts are rarely indicated in burn reconstruction surgery. The meshed pattern is permanently retained and has an unattractive “reptilian” appearance. Hyperpigmentation of grafts is a frequent problem in dark-skinned patients, particularly those of African descent. Full-thickness skin grafts are reliable workhorses in facial burn reconstruction. The use of full-thickness skin grafts in other areas of burn reconstruction should be carefully considered on an individual basis. Full-thickness grafts are elastic, contract less, have a “matte finish” like normal skin, and create a durable, resilient, skin surface. Full-thickness grafts, however, require a well-vascularized bed, primary closure or grafting of the donor site, and are best reserved for reconstruction of the



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C FIGURE 18.9. Multiple Z-plasties for axillary contracture. A: Extensive posterior axillary contracture with hypertrophic scarring. B and C: Multiple Z-plasties and local flaps in series easily release the contracture. D: Eight years later complete release has been maintained, the scars are flat and soft, and the contours are normal.

head and neck or the hand. Composite grafts from the ear are useful for complex facial burn reconstruction, but should only be used when there is adequate blood supply in the recipient bed.

Flaps Flaps, with or without tissue expansion, are useful for burn reconstruction. They are mandatory for complex defects such as open joints or exposed vessels, or to provide tissue coverage that allows for later complex reconstruction, such as tendon or nerve grafting in the hand. Large flaps involve a

considerable tradeoff because of their donor-site morbidity. Their elasticity and minimal contracture, as well as excellent color and texture match, make them an excellent option when available for the correction of cervical contractures (Fig. 18.8). Flaps are frequently recommended in the literature for axillary contractures. The normal axilla is concave and lined with exquisitely thin skin. This allows the arm to rest comfortably at the side. Transposition of flaps into the axilla can effectively release contractures, but can also create terrible contour deformities. When potential flap tissue is available, either posterior or anterior to the axilla, multiple Z-plasties in series can usually release axillary contractures and preserve or restore


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A FIGURE 18.10. Tissue expansion. A: A 7-year-old girl with extensive alopecia involving the vertex, parietal, and occipital areas of the scalp. B: Ten years later following two tissue expansions, alopecia has been eliminated and a normal temporal hairline and sideburn restored.

normal contour (Fig. 18.9). When diffuse axillary scarring is present, release and graft is the best option, even though it requires postoperative splinting and often more than one intervention.

Tissue Expansion Tissue expanders have transformed the treatment of postburn alopecia. Bald areas of 50% of the scalp or more can be successfully reconstructed, frequently requiring more than one expansion. Although there is conflicting data in the literature regarding complications, in general the scalp is a privileged site for tissue expansion (8,9). The scalp is an ideal site for tissue expansion because of its blood supply, convex shape, and the unyielding skull against which to expand (Fig. 18.10). The use of tissue expansion in other areas of burn reconstruction is more problematic. Because the underlying theme of almost all burn deformities is tension and tissue deficiency, stretching adjacent tissue in order to carry out scar excision can result in increased tension and iatrogenic contour abnormalities (Fig. 18.4). The complication rate of tissue expansion in burn patients is high, particularly in the extremities, reaching 25% to 50% in some reports (10). After alopecia, the most common use of tissue expansion is probably in the reconstruction of facial burn deformities. Care must be taken when advancing or transposing expanded flaps from the cervicopectoral area to the face. It is easy to create extrinsic contractures with a downward vector resulting in a “sad” facial appearance that is distressing to patients. Contour deformities can also be created in the neck with loss of jawline definition.

Evaluation and Treatment Successful burn reconstruction requires perspective, patience, a thorough understanding of the problem and judicious application of the fundamentals of burn reconstruction. As noted previously, burn reconstruction is primarily about the release of contractures and the correction of contour abnormalities. When contractures have a predominantly linear component and there is a relative excess of vascular, elastic tissue lateral to the contracture, the Z-plasty is simple, reliable, and has the least morbidity. Z-plasty minimizes the need for most postoperative therapy, including pressure garments, and the benefit of the procedure is prolonged. The relaxed scar tissue will continue to soften, flatten, and loosen for many months to years after the operation is performed. Z-plasties can be used on the narrower, linear, components of diffuse areas of hypertrophic scarring to separate islands of scar and restore elasticity. Contour abnormalities can be corrected at the same time. The relief of tension leads to improved maturation. Following the benefit of initial scar revision, repeat surgery can be carried out 1 or 2 years later. Typically, this secondary surgery is directed toward scars that previously were not conspicuous or symptomatic but have become so after the treated scars flattened, softened, and become less noticeable. It is often remarkable how much improvement in appearance, contour, and softness can be accomplished by such Z-plasties. Patients are almost always pleased with the outcome and frequently ask for subsequent similar procedures, a true indication of successful surgery (Fig. 18.11).



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B

A

FIGURE 18.11. Effect of Z-plasties on hypertrophic scars. A: Diffuse hypertrophic scarring of the anterior chest and abdomen in an 8-year-old boy with deformity of the normal contours. B: Broad areas of scar were separated with multiple Z-plasties on two separate occasions as noted in the text. C: Ten years later, after two Z-plasty procedures, the scars are flat, soft, and elastic. The normal chest and abdominal contours have been restored.

C

When contracted scars or grafts are diffuse and Z-plasty or other local flap rearrangement is not possible, then release and split-thickness skin grafting is usually the best option to correct contractures. Care must be taken to preserve and restore normal tissue contours when releases are carried out to prevent unsightly iatrogenic contour abnormalities. Flaps are excellent for cervical contractures when available (Fig. 18.8). Otherwise, release and split-thickness skin grafting is usually the best option for the neck, although this requires meticulous postoperative management and often more than one release and graft (11). Microvascular free tissue transfer has been advocated for anterior neck contractures but its use has been limited because of complexity and morbidity. Tissue expansion is the ideal treatment for postburn alopecia. Even when the area of alopecia is relatively small, scalp expansion should be considered. Excision and direct closure of

scalp alopecia usually results in a straight-line scar under tension that tends to widen and become conspicuous over time. Tissue expansion allows the closure to be carried out without tension, incorporating interdigitating local flaps and Z-plasties that obscure the scar and prevent widening. Whenever possible, the use of a single large expander is desirable, even if that requires expansion of some areas of alopecia. The larger the expander, the less separation of hair follicles occurs. When expansion is accomplished with a single large expander placed through a single small incision, manipulation of the scalp at the time of alopecia excision is facilitated because incisional scars are less likely to complicate the design of the best possible flaps for closure. Facial burn reconstruction is complicated and can seem to be overwhelming in severe cases. The importance of time and allowing for maximal scar maturation to occur, along with the use of ancillary techniques such as pressure, silicone gel,


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B

A FIGURE 18.12. Type I patient. A: A 24-year-old woman following extensive acid burns to the face. B: Nasal reconstruction was performed with turn down flaps and split-thickness skin grafting. Four facial scar revisions with Z-plasties and local flaps were carried out over a 3-year period.

A

B FIGURE 18.13. Type II patient. A: A 30-year-old male fireman following a severe facial burn with facial burn stigmata. B: Eight years later following extensive reconstructive surgery with full-thickness grafts, composite grafts, and multiple scar revisions.



TA B L E 1 8 . 1

TA B L E 1 8 . 2

FACIAL BURN CATEGORIES Type

Description

I

Essentially normal faces with focal or diffuse burn scarring with or without contractures Panfacial burn deformities with some or all of the stigmata of facial burns (see Table 18.2)

II

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steroids, judicious surgical intervention, and the use of the laser for erythema cannot be overemphasized. It can be helpful to think of patients with facial burn deformities as falling into two fundamentally different categories as described in Table 18.1. Type I deformities consist of essentially normal faces that have focal tissue loss or diffuse burn scarring with or without associated contractures. Type II deformities make up a much smaller number of patients who have “panfacial” burn deformities consisting of what can be referred to as facial burn stigmata. Table 18.2 lists the stigmata of facial burns, which include lower eyelid ectropion, shortening of the nose with ala flaring, a short retruded upper lip, lower lip eversion, inferior displacement of the lower lip, flattening of facial features, and loss of jawline definition. The surgical goals when treating type I deformities should be different from those appropriate for treating type II deformities. Type I patients have essentially normal faces and surgical intervention should not adversely affect overall facial appearance. The surgeon must not fall into the trap of compromising normal features and contours to “excise scars.” Iatrogenic deformities create an abnormal look and can easily become grotesque. A normal-looking face with scars is more attractive than an even slightly grotesque face with fewer scars. Surgery should only be performed when it is reasonably certain it will make the patient definitely better, not just deformed in a different way. Scar revision with Z-plasties and local flaps is usually the best option for type I patients (Fig. 18.12). Full-thickness skin grafts from the most appropriate available donor sites are excellent for focal contractures. All human appearance is a mosaic to some degree and mosaic faces with normal movement and expression look much better in real life than they do in images. The pulsed dye laser is helpful in decreasing erythema. Type II patients present a completely different clinical situation. The surgical goals for these patients should be the restoration of normal facial proportion and the return to normal of the position and shape of facial features. When normal facial proportion has been restored and facial features have been returned to their normal location and shape without tension, it is remarkable how much improvement in appearance can be accomplished in even severe facial burns (Fig. 18.13). Cosmetics are effective in covering or minimizing abnormalities of color and texture in all body areas, but their application requires skill and commitment, and their use is usually limited to the face. Many female patients become exceedingly adept at cosmetic camouflage. Male patients are less likely to take advantage of this opportunity to minimize their deformity.

STIGMATA OF FACIAL BURNS Lower eyelid ectropion Short nose with ala flaring Short retruded upper lip Lower lip eversion Lower lip inferior displacement Flat facial features Loss of jawline definition

CONCLUSION Advances in the care of acutely burned patients have created a challenge and an opportunity. More patients survive today with extensive areas of healed burn scar and graft. But this increased challenge provides great opportunity for plastic surgery. Although much gloom and doom tends to surround the acute care and reconstruction of burn patients, nothing could be further from the truth. Other than the burn scars and contractures, these patients are usually completely healthy, and successful reconstructive surgery can often restore them to a happy and productive life. Large series have shown excellent long-term outcomes in even extensively injured patients when compared with normal controls (12). Patience, persistence, and determination are essential to accomplish successful reconstruction. The skillful application of basic surgical techniques to the reconstruction of postburn deformities can be gratifying to patients and surgeons alike. The ultimate principle of burn reconstruction is learning to understand, appreciate, and favorably influence the processes of wound healing and scar maturation.

References 1. Cope O, Langohr JL, Moore FD, et al. Expeditious care of full thickness burn wounds by surgical excision and grafting. Ann Surg. 1947;125:1. 2. Janzekovic A. A new concept in early excision and immediate grafting of burns. J Trauma. 1970;10:1103. 3. Burke J, Bondoc CC, Quinby WC. Primary burn excision and immediate grafting: a method for shortening illness. J Trauma. 1974;14:389. 4. Larson D, Abston S, Evans DB, et al. Techniques for decreasing scar formation and contractures in the burn patient. J Trauma. 1971;11:807. 5. Ahn S, Monafo WW, Mustoe TA. Topical silicone gel: a new treatment for hypertrophic scars. Surgery. 1989;106:781. 6. Davis J. The relaxation of scar contractures by means of the Z-, or reversed Z-type incision: stressing the use of scar infiltrated tissues. Ann Surg. 1931;94:871. 7. Longacre J, Berry HK, Basom CR, et al. The effects of Z-plasty on hypertrophic scars. Scand Plast Reconstr Surg. 1976;10:113. 8. Neale H, High RM, Billmore DA, et al. Complications of controlled tissue expansion in the pediatric burn patient. Plast Reconstr Surg. 1988;82(5): 840. 9. Pisarski G, Mertens D, Warden GD, et al. Tissue expander complications in the pediatric burn patient. Plast Reconstr Surg. 1998;102:1008. 10. Friedman R, Ingram AE, Rohrich RJ, et al. Risk factors for complications in pediatric tissue expansion. Plast Reconstr Surg. 1996;98:1242. 11. Cronin T. The use of a molded splint to prevent contracture after split-skin grafting on the neck. Plast Reconstr Surg. 1961;27:7. 12. Sheridan R, Hinson MI, Liang MH, et al. Long-term outcome of children surviving massive burns. JAMA. 2000;283:69.


CHAPTER 19 ■ RADIATION AND RADIATION INJURIES JAMES KNOETGEN, III, SALVATORE C. LETTIERI, AND P. G. ARNOLD

Roentgen’s 1895 discovery of x-rays was closely followed by the introduction of radiation therapy for the treatment of a variety of cancers and other disease processes. Although radiation therapy provides both diagnostic and therapeutic benefits, the resulting changes to exposed tissues can pose woundhealing problems and reconstructive dilemmas to the plastic surgeon. This chapter explains the basics of radiation therapy and discusses the radiation wound issues that are most commonly faced by the plastic surgeon, providing specific emphasis on the unique problems posed by various anatomic locations. Radiation refers to the high-energy particles (α-particles, β-particles, neutrons) and electromagnetic waves (x-rays, γ rays) that are emitted by radioactive substances (uranium, radon, etc). α-Particles are large, positively charged, helium nuclei. Radium and radioactive isotopes can be consumed orally or intravenously to emit α-particles into surrounding tissues. βParticles are small, negatively charged electrons and are used in electron-beam therapy (e.g., treatment of mycosis fungoides), and can penetrate up to 1 cm of tissue. γ -Rays are uncharged photons produced by the natural decay of radioactive materials (radium, cobalt 60, etc.) and can penetrate into deep tissues. Roentgen rays (x-rays) are similar to γ -rays, except they are artificially emitted from tungsten when bombarded with electrons. Radiation doses are measured in a variety of units, and these units measure the energy absorbed from a radiation source per unit mass of tissue. The units include the roentgen (R), the gray (Gy), the rad, and the sievert (Sv). The sievert is equal to the gray except that it is adjusted to take into account the biologic effects of different types of radiation. In current nomenclature, the Gy has replaced the rad, so that 1 Gy = 100 rad, or 1 rad = 100 centigray (cGy). The two main forms of radiation exposure are irradiation and contamination. Irradiation refers to radiation waves that pass directly through the human body, whereas contamination is contact with and retention of radioactive material. Contamination is usually the result of an industrial accident. The plastic surgeon is most concerned with irradiation as opposed to contamination as current regulations have made industrial accidents and exposures very rare. Irradiation is a local therapy applied to a specific body site containing a tumor or disease process, or to draining lymph node beds thought to contain or potentially contain microscopic or gross disease. Large tumors may be treated preoperatively with radiation therapy (induction therapy) to decrease the tumor burden prior to surgery. Adjuvant radiation therapy is performed in addition to the surgical extirpation with the goal of treating the tumor’s resection bed and regional lymph nodes in patients with specific clinical scenarios, such as large tumors, recurrent tumors, extracapsular lymph node involvement, and positive resection margins. The potential advantage of radiation therapy over surgery is local treatment of disease

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with preservation of surrounding uninvolved structures. Disadvantages include the length of treatment, the need for access to appropriate facilities and equipment, and the potential additive and chronic effects of radiation therapy.

DELIVERY OF RADIATION THERAPY Radiation therapy is delivered via external or internal routes. The delivery technique most commonly used is external beam radiotherapy, which originates from a source external to the patient, a linear accelerator (LINAC). A variety of radiation beams can be delivered in this manner, such as low-energy radiation beams from a cobalt source in a cobalt machine. Other atomic particles, such as neutrons, are also delivered via this mechanism. This technique allows daily fractionated delivery of radiation over a several-week course. External-beam therapy can be delivered as an independent treatment preoperatively, intraoperatively, or postoperatively. Delivery of radiation from within the patient’s body is termed brachytherapy. Radioactive sources are inserted into the patient for temporary or permanent irradiation. This technique allows for continual treatment of the tumor with radiation over a course that usually lasts several days. Its advantages include decreased treatment time and greater ability to spare uninvolved local tissues. Brachytherapy may also be indicated in patients who have been previously irradiated and are therefore no longer candidates for external beam therapy because they have already received the maximum recommended dose for the specific anatomic area.

RADIATION DAMAGE Regardless of delivery technique, radiation therapy works by damaging the targeted cells through complicated intracellular processes that continue to be studied to this day. The interaction of radiation with water molecules within the cell creates free radicals that cause direct cellular damage. A range of biochemical lesions occur within DNA following exposure to radiation, and can result in two different modes of cell death: mitotic (clonogenic) cell death, and apoptosis. The biochemical lesion most often associated with cell death is a double-stranded break of nuclear DNA (1). Irradiated tissues suffer both early and late effects. Early effects occur during the first few weeks following therapy and are usually self limited. They result from damage to rapidly proliferating tissues, such as mucosa and skin. Erythema and skin hyperpigmentation are the most common problems and these are treated expectantly with moisturizers and local wound care. Dry desquamation occurs after low to moderate doses of


Chapter 19: Radiation and Radiation Injuries

radiation, whereas higher doses result in moist desquamation. At the tissue level, stasis and occlusion of small vessels occurs, with a consequent decrease in wound tensile strength. Fibroblast proliferation is inhibited, and may result in permanent damage to fibroblasts. This creates irreversible injury to the skin, which may be progressive. Although the plastic surgeon is often not required to treat early radiation injuries, chronic injuries frequently require the plastic surgeon’s attention. Late, or chronic, radiation effects can manifest anytime after therapy, from weeks to years to decades after treatment. Although acute effects are uncomfortable and bothersome to the patient, they are generally self-limited and resolve with minimal treatment and local wound care. Chronic effects, however, can be progressive, disabling, cumulative, permanent, and even life-threatening. Late injuries include, but are not limited to, tissue fibrosis, telangiectasias, delayed wound healing, lymphedema (as the result of cutaneous lymphatic obstruction), ulceration, infection, alopecia, malignant transformation, mammary hypoplasia, xerostomia, osteoradionecrosis, and endarteritis. Long-term effects of radiation therapy also include constrictive microangiopathic changes to small and medium sized vessels (2), which is very important when performing reconstructions with pedicled and free flaps.

GENERAL PRINCIPLES OF TREATING IRRADIATED WOUNDS In most circumstances, a radiated wound will not heal as well as a nonirradiated wound. Consequently, plastic surgeons are often consulted for the wound closure of these patients (Fig. 19.1). The plastic surgeon is generally called on to care for two different populations of irradiated patients. The first population is those who have not yet received irradiation but who will receive radiation therapy intraoperatively or postoperatively. This is often seen in the immediate breast-reconstruction patient who is undergoing mastectomy and potential postoperative radiation therapy and in the sarcoma patient under-

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going extirpation with intraoperative radiation therapy. Also, bronchial stumps can be reinforced when a completion pneumonectomy is anticipated, usually with intrathoracic transposition of a serratus muscle flap (3). The second population includes patients who have already received radiation therapy and now have a recurrent or new tumor, or a radiation wound with exposure of vital or significant structures such as bone, vital organs, or neurovascular bundles. This patient requires tumor extirpation or wound debridement followed by reconstruction. The patient’s treatment varies depending on which of these categories the patient falls into, the depth of the injury and tissues involved, and which specific anatomic area is affected. Intraoperative radiation therapy is occasionally used in the treatment of sarcomas, pelvic tumors, and other malignancies. Plastic surgeons are often consulted for the closure of these wounds. In this situation, the reconstructive ladder is applicable, and if enough well-vascularized soft tissue is present, a primary layered closure can be attempted. Many of these wounds will heal well even though they have received intraoperative radiation therapy. However, if bone, prosthetic material, or neurovascular bundles are exposed, coverage with a well-vascularized flap is indicated to protect these structures. Likewise, if the wound lacks adequate soft-tissue coverage, a vascularized flap should be used to create a stable reconstruction. When confronted with a wound that has late radiation changes, the plastic surgeon’s first step is to rule out the presence of a recurrent or new tumor (possibly radiation induced). Diagnosis is often assisted by standard radiographs, computerized tomography (CT), and magnetic resonance imaging (MRI) scans, and confirmed with a tissue biopsy. If tumor is present, a full work-up and evaluation by the appropriate extirpative surgeon is required. After tumor extirpation is complete, reconstructive efforts of the resulting defect are then initiated. If tumor is not present, the most critical first step in management of irradiated wounds is complete resection and debridement of all nonviable irradiated tissues and foreign bodies (sternal wires, previous sutures, etc.) (4). Primary closure or skin grafting of the irradiated wound may fail because of the poor

FIGURE 19.1. A to F: A sample of radiation wounds. (Photos courtesy of Dr. P.G. Arnold, Mayo Clinic, Rochester, MN.)


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vascularity and fibrosis of the wound bed. Likewise, muscle flaps transposed into a poorly vascularized irradiated wound bed may not heal well. So it is imperative that the plastic surgeon first establish a clean wound with well-vascularized edges before proceeding with reconstruction. This is often accomplished in multiple debridements rather than a single operative endeavor, as the extent of radiation injury often exceeds what grossly appears to be the boundary of damaged tissue. The main cause of recurrent infections, sinus tracts, and wound healing problems is retention of nonviable materials such as foreign bodies, bone, or cartilage secondary to inadequate debridement. If at the time of wound closure the nonirradiated tissue, such as omentum, is larger than the initial defect created by the debridement, then more of the radiated tissue can be removed, thus improving the chance of a well-healed wound. The “extra” omentum may also be placed beneath the remaining radiated skin thus reconstructing the missing or fibrotic subcutaneous tissue that was lost secondary to the radiation. This brings in additional blood supply to this skin, increases its “mobility,” and vastly improves mobility of surrounding tissue to correct the situation where, for example, the skin was previously very thin and tightly adherent to the chest wall. Patients always appreciate this change toward normal. If the radiated tissue does not survive, the viable well-vascularized tissue (omentum) deep to it can be skin grafted. When incising severely irradiated tissue, a defect much larger than anticipated is often created. This is because the irradiated tissue is often tight and creates a constricted skin envelope. When incised, the wound edges will often retract

and create a larger defect than expected (Fig. 19.2B). This is an important concept to understand when planning the reconstruction, as one may need more nonirradiated tissue for reconstruction than originally estimated. Once debridement is complete, stable wound closure is obtained. Thorough preoperative planning and a systematic approach to reconstruction of irradiated defects are needed. Reconstruction usually includes transposition of a well-vascularized nonirradiated soft-tissue flap into the wound bed. Reconstruction of these defects is often challenging and associated with relatively high complication rates. When planning the reconstruction, the plastic surgeon must choose which soft-tissue flap will best obtain a healed wound and maximize preservation of function. It is generally accepted that when performing a reconstruction, irradiated muscles should be avoided if possible, as this may result in partial or complete muscle necrosis (5). The transfer of a muscle whose pedicle has been irradiated may also be associated with a higher complication rate (6). If a well-vascularized muscle flap or the greater omentum is not available, a free tissue transfer may be required. Another basic tenet of reconstructing irradiated wounds is that the first-line choice is either a muscle flap or the greater omentum. Although reconstruction of irradiated wounds with fascial or fasciocutaneous flaps has been reported, it is generally accepted that muscle flaps and the greater omentum have a better blood supply and, therefore, have a better chance of healing without complications. The remainder of this chapter addresses the pertinent issues of irradiated wound treatment by anatomic area.

A

B

C

D FIGURE 19.2. A to D: A patient with a radiation wound of the chest wall, reconstructed with a pedicled greater omentum flap. (Photo courtesy of Dr. P.G. Arnold, Mayo Clinic, Rochester, MN.)



Skin Nonmelanoma skin malignancies can be treated with approximately a 90% cure rate with irradiation (see Chapter 13). Compared with extirpation, the radiation therapy option requires both prolonged therapy and access to radiation therapy facilities. Long-term complications, such as fibrosis, ulceration, ectropion, osteitis, and chondritis, make this treatment option less desirable. Consequently, it is generally reserved for patients who are not surgical candidates. Low-dose radiation therapy can also be used postoperatively in the treatment of keloids and hypertrophic scars. This technique takes advantage of fibroblast inhibition caused by ionizing radiation. Radiation therapy is part of a multimodal approach to keloid treatment in some institutions.

Extremities Soft-tissue sarcomas of the extremities can be aggressive tumors involving multiple structures and tissue planes. Surgical extirpation is often combined with intraoperative or postoperative radiation therapy, either external-beam or brachytherapy. Consequently, treatment of these patients requires a multidisciplinary approach, often involving surgical oncologists, vascular surgeons, orthopedic surgeons, radiation oncologists, plastic surgeons, and others. The goal is to obtain locoregional tumor control while simultaneously attempting limb salvage and maximal preservation of limb function. Patients may have received irradiation before extirpation, which is important in the planning of the radiation therapy (i.e., the patient may require brachytherapy as opposed to external-beam therapy or a modification of the external-beam dose). The sequence is especially important to the plastic surgeon and the planning of wound closure and reconstruction. Wide local tumor resections of the extremity often result in large soft-tissue defects, as well as osseous defects. Osseous defects require orthopedic reconstruction with prosthetic materials, total arthroplasties, or bone grafts. All bone, tendons, prosthetic materials, and neurovascular bundles must be covered with well-vascularized viable tissue in order to obtain stable soft-tissue reconstruction and a healed wound. The addition of radiation therapy to the tumor bed, including all previous irradiation, must be considered when planning reconstruction. The goal of soft-tissue reconstruction is to obtain stable coverage of all vital structures. Although the “reconstructive ladder” generally proceeds from primary wound closure through skin grafting, local flaps, regional flaps, and free microvascular flaps, occasionally, in complicated circumstances, such as patients who have received radiation therapy, the “reconstructive elevator” must be employed to ensure wound healing. In other words, it may be prudent to bypass one or more of the standard rungs of the reconstructive ladder to arrive at a more stable construct. For example, a defect in the medial thigh created by resection of a liposarcoma and irradiation that would normally be treated with primary closure may benefit from coverage with a pedicled musculocutaneous flap, especially if the femoral vessels are exposed. A soft-tissue defect over the knee may not be amenable to coverage with a gastrocnemius muscle flap if this muscle was within the field of previous irradiation and is fibrotic, and thus may be better treated with a free muscle flap. Obliteration of a soft-tissue defect is not the only goal when reconstructing these wounds. Preserving and maintaining maximal function also is important. When critical muscles or large muscle masses are resected and/or irradiated, it is often advantageous to perform a neurotized muscle reconstruction. This can often give patients at least partial function of a joint or

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limb. The development and refinement in the use of pedicled and free muscle, bone, and fasciocutaneous flaps has increased the plastic surgeon’s ability to obtain stable wound closures in these complex clinical situations of the extremity that previously required amputation.

Breast The breast is undoubtedly the anatomic structure most frequently cared for by the plastic surgeon that has the potential to be irradiated. Breast reconstructions using autologous or prosthetic materials are commonly performed by plastic surgeons. These reconstructions can be made more complicated if the treatment plan includes radiation therapy. The plastic surgeon generally encounters two breast patient populations: (a) the patient who has already received radiation therapy to the breast(s) for the treatment of a previous malignancy and is now in need of further extirpation and/or reconstruction, and (b) the patient who is undergoing mastectomy and may need to receive postoperative radiation therapy, usually because of tumor size or nodal involvement. The first clinical scenario requires the plastic surgeon to perform a breast reconstruction in an irradiated field. The surgeon must first evaluate the breasts and assess the degree of radiation damage. The patient should be examined for erythema, hyperpigmentation, and the degree of fibrosis of the breast and surrounding tissues and skin. A basic tenet of reconstructing the irradiated breast is that delivery of well-vascularized tissue via autogenous reconstruction will yield a better result than prosthetic implants alone. Reconstruction with tissue expansion and implants has been demonstrated to yield a higher rate of wound-healing problems and implant exposure, as well as a higher incidence of Baker III and IV capsular contracture (7,8). Reconstruction with autogenous tissue, usually via pedicled or free transverse rectus abdominis musculocutaneous (TRAM) flaps or a latissimus dorsi muscle flap with an expander/implant (see Chapter 65), will often yield a superior result. If autologous breast reconstruction is not an option, some surgeons advocate immediate insertion of a breast tissue expander/implant at the time of mastectomy with completion of expansion prior to irradiation (9), although this is a controversial opinion and not widely accepted. An alternative technique employs placement of a tissue expander before radiation therapy to create and maintain a soft-tissue envelope for a later reconstruction that includes autologous tissue, with or without an implant. A critical issue that requires consideration when performing autologous breast reconstruction is the quality of irradiated vessels within pedicled flaps (internal mammary vessels in TRAM flaps and the thoracodorsal vessels in latissimus dorsi muscle flaps), and the quality of irradiated recipient vessels in autologous reconstruction with free flaps (TRAM, deep inferior epigastric perforator [DIEP], superior gluteal artery perforator [S-GAP], etc.). When the pedicle is exposed to radiation preoperatively, pedicled TRAM flaps have a higher incidence of both skin and flap necrosis (6), and an increased incidence of pedicled TRAM flap failure (10). When performing a pedicled TRAM flap with irradiated vessels, decreased complications in this group may be achieved with a flap delay, a bipedicled TRAM flap, or by turbocharging the flap (although turbocharging pedicled flaps is a controversial subject). The alternative is a free tissue reconstruction using a flap that has not been irradiated. When performing a free tissue transfer for breast reconstruction, the surgeon must inspect the quality of the irradiated recipient vessels. Significant scarring and fibrosis surrounding the vessels and radiation damage to the lumen of the recipient vessels can increase the chance of a failed free tissue transfer. Radiation therapy can result in constrictive microangiopathic changes to small- and


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medium-size vessels, as well as inhibition of fibroblast function, which can increase the risk of anastomotic failure (2). Occasionally, at the time of mastectomy, the need for postoperative irradiation is uncertain. In this setting, the plastic surgeon must decide whether to perform immediate reconstruction or delay reconstruction until after the potential radiation therapy is completed. Most plastic surgeons agree that superior outcomes are achieved with a delayed autologous reconstruction, rather than with an immediate reconstruction and postoperative radiation of the flap (11,12). Consequently, it is prudent to delay reconstruction until the final decision about postoperative irradiation is made.

Head and Neck Because head and neck malignancies are frequently aggressive with high recurrence rates, treatment requires both surgical extirpation and radiation therapy. Surgical extirpation often results in large defects with exposure of vital structures that require complicated soft-tissue and/or osseous reconstruction. Reconstruction of these defects is often quite challenging, and is made more difficult if the irradiated tissues are fibrotic and if the vessels are damaged. Osteoradionecrosis of the mandible and maxilla is a complication occasionally seen after radiation therapy that requires resection/debridement of affected tissue followed by osseous reconstruction. Although these defects were traditionally reconstructed with local and regional flaps, free tissue transfer is now the standard reconstruction technique. Historically, the pectoralis major muscle flap has been used for soft-tissue coverage of neck defects. However, this flap is limited by its bulkiness, the difficult arc of rotation, and its limited extension into the oral region. Free tissue transfer allows well-vascularized, nonradiated tissues from a distant site to be used for reconstruction of the radiated defect. Because of the vital structures located in the head and neck region, it is imperative to obtain a stable closure with viable flaps. Success is measured not only by the cure or control of the tumor, but also by wound healing and preservation of function. Full-thickness defects of the head and neck region require reconstruction of several layers, including the intraoral lining, osseous reconstruction of the mandible or maxilla, and soft-tissue/skin coverage. Partial-thickness defects may only require intraoral lining or soft-tissue coverage. Usually, local flaps are not readily usable, except, perhaps, for a temporalis muscle flap to obliterate the maxillary sinus or the palate region. Free tissue transfer is usually preferred, especially in irradiated defects. The types of free tissue transfers often used include a thin fasciocutaneous flap (radial forearm flap), or intermediate-thickness flap (scapula or parascapular flap), or variable-thickness flap (anterolateral thigh flap). Muscle flaps (rectus abdominus or latissimus dorsi) can also be used. The omentum is excellent as a “carrier” for bone and skin grafts but offers no structural strength. Generally, vessels in the neck are readily available and of adequate caliber. However, even if the vessel caliber is adequate, irradiated vessels may be more difficult to dissect and use for microanastomosis because of local fibrosis and radiation injury to the vessels. Local fibrosis makes the dissection difficult, as the soft-tissue planes that are ordinarily present may be unidentifiable. Consequently, thoughtful preoperative planning with a “plan A” and at least one “plan B” is necessary before undertaking the surgery. If the radiated vessels are deemed unsatisfactory for microvascular anastomosis, the surgeon should be prepared to find vessels in other areas of the neck, such as the contralateral side or the supraclavicular region. This is performed with vein grafts, so it is important to warn patients preoperatively about the potential need for

surgery to other parts of their body. Although vein grafting generally increases microanastomotic failure rates, vein grafting into an area that is easily dissected with a technically easier anastomosis is better than a difficult anastomosis to poor vessels without a vein graft. Quite often, vein grafts are necessary for coverage of irradiated scalp defects. Many surgeons prefer to use the larger arteries and veins in the neck in lieu of smaller vessels near the scalp, such as the superficial temporal artery. Although several authors have been successful with the superficial temporal artery, it is generally accepted that the neck vessels are easier to work with and have less chance of causing anastomotic problems. The timing of reconstruction in reference to the delivery of radiation also needs to be taken into consideration. Induction radiation therapy, used to downstage (shrink) tumors preoperatively, tends to create more bleeding and inflammation in the affected area. Although the irradiated vessels may be adequate for use, the dissection may be tenuous because of the inflammation. Chronic radiation injury, however, tends to have more fibrosis in the affected area, as well as thickening of the tissue planes and absence of standard anatomic landmarks, which makes dissection slow and difficult. Patients who will be having postoperative irradiation do not have these problems and will have unoperated tissues and virgin surgical planes. In fact, after the neck dissection is performed, the vessels are exposed and often prepared for use. It is often prudent to recommend to the extirpative surgeon that an adequate length be left on the vessels that are ligated and resected during the dissection, so as to have a cuff for anastomosis, rather than ligating the branch flush with the larger vessel from which it arises. Osseous reconstructions of the head and neck offer additional reconstructive challenges. Mandible resections are usually reconstructed with the fibula free tissue transfer to deliver well-vascularized nonirradiated tissue to the irradiated wound bed. Generally, a complex full-thickness defect with defects of the bone and intraoral lining are best served by a vascularized bone flap. In the absence of any viable alternatives for vascularized bone graft, a free tissue transfer with a nonvascularized bone graft could then be used. This is not an ideal option considering the adjunctive radiation that is often administered postoperatively. Although some authors report successes with bone grafting or a cancellous “tray,” these reconstructions need to be performed within a well-vascularized bed and thus are not often indicated in irradiated wounds. An uncommon, yet potentially lethal, complication of radiation therapy to the head and neck is an infection that leads to wound dehiscence and exposure of the vessels. This can result in vessel rupture or anastomotic leak, which can be lethal given the large size of these blood vessels. In the absence of irradiation to the neck, incorporation of the vessels and softtissue flap into the surrounding wound bed usually occurs and establishes stable coverage of the vessels, making this complication rare in the nonirradiated patient. Previous irradiation, however, impairs the progress of soft-tissue incorporation and therefore increases the risk of exposure.

Chest Radiation therapy to the chest wall is used in the treatment of lymphomas, large chest wall or pulmonary tumors, and for recurrent malignancies after previous resections. Postradiation complications in this patient population include radiation ulcers, infected wounds, persistent or recurrent tumors, and cardiac and pulmonary disorders. As the thoracic cavity houses a variety of vital organs, radiation damage to the chest wall can create a potentially lethal clinical scenario requiring immediate



attention from the cardiothoracic surgeon as well as the plastic surgeon. These patients are often quite ill, requiring prolonged stays in the intensive care unit and a multidisciplinary team approach. The first step in evaluating a patient with one of these problems is to rule out the presence of new or recurrent tumor. This work-up includes standard imaging studies such as chest radiograph, CT, or MRI, and possibly bronchoscopy. After the extent of tumor involvement is determined, it must be completely resected with negative pathologic margins before reconstructive options are considered. If tumor is not present, then the radiation ulcer or infected wound must be thoroughly debrided, and all fibrotic radiated tissue and foreign bodies must be resected. Many chronic sinus tracts in the chest wall can be traced to a sternal wire, retained suture, or persistent infected cartilage. Debridements are often performed in multiple serial procedures, as it is often difficult to judge the extent of remaining nonviable tissue after only one procedure. As occurs in other anatomic areas, the extent of radiation injury often exceeds what initially appear to be the boundaries of damaged tissue. After resection and debridement is complete, the wound must be evaluated to determine if it is a partial- or full-thickness defect. Because the chest wall is a relatively thin structure, most chest wall defects following thorough debridement are full thickness and will require chest wall reconstruction prior to soft-tissue coverage. Chest wall reconstruction is performed by either the thoracic surgeon or plastic surgeon experienced in chest wall reconstructions. Prosthetic material, such as GoreTex (W.F. Gore, Phoenix, AZ) sheeting or Prolene (Ethicon, Sommerville, NJ) mesh, is employed for this reconstruction, if the wound permits. The goal is to obtain an airtight seal at the time of closure so as to maintain appropriate intrathoracic negative pressure for respiration. The prosthetic material is then covered with a viable soft-tissue flap, usually a musculocutaneous flap or a muscle flap with a skin graft. Flaps frequently used for chest wall reconstruction include one or both of the pectoralis major muscles, latissimus dorsi muscles ( ± the serratus anterior muscle), and rectus abdominis muscles, as well as the greater omentum (4). Advantages of the pedicled greater omental flap are its large surface area and excellent vascularity. Complete debridement of irradiated chest wounds often results in large irregular defects, and the omentum tends to cover these defects nicely as it can be molded into irregular defects quite easily (Fig. 19.2). Many radiated wounds result in partial-thickness chest wall defects when there is no recurrent tumor present. There may be a full-thickness resection, but even then the lung may be adherent to the pleura secondary to the previous radiation and/or inflammation. In either case, the omentum with a skin graft is adequate, and underlying foreign bodies in the form of meshes can be avoided in contaminated wounds, thus taking advantage of this postradiation fibrosis. The omentum is procured through an upper midline laparotomy incision, mobilized, and usually based on the usually dominant right gastroepiploic vessels (85% to 95% of cases). Skin grafting is generally performed in a delayed fashion after a few days of dressing changes and one is sure that all of the transposed omentum is well vascularized. This gives the plastic surgeon time to observe the omental flap; debride any nonviable portions, and re-advance or redistribute the pliable omentum as necessary. Disadvantages of the omentum are similarly the lack of structural strength. It is simply a vascularized “carrier” for skin in this case. There is also the addition of an upper midline laparotomy and violation of a second body cavity, but its large size, malleability, vascularity, and acceptable donor defect make it an attractive option. The omentum can also be used for lower back closures by tunneling it through the retroperitoneum and paraspinous muscles.

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There are very special situations in patients with problematic radiated wounds of the chest that may involve disruption of the aerodigestive tract or the heart with the great vessels. These have been dealt with on some occasions with intrathoracic muscle flaps (3). Because of the abundance of local pedicled muscles and the greater omentum, free tissue transfer is often not needed for a standard chest wall reconstruction. However, the radiated patient may not have adequate local muscles because of multiple surgeries and debridements and radiation damage to the muscles and vessels. Transposition of irradiated muscles can result in partial or total necrosis (5). If the greater omentum is not available, a free tissue transfer may be required in these extreme situations (13). As in the treatment of all radiation wounds, the key to obtaining a well-healed chest wall reconstruction relies on adequate initial debridement of all nonviable irradiated tissues. Only then should attempts at chest wall and soft-tissue reconstruction be attempted.

Perineum Gynecologic malignancies occasionally require extensive perineal resections and/or pelvic exenterations. These tumors will often be treated with radiation therapy as well and the resulting perineal wound is usually not amenable to primary closure. Similar perineal defects are created after abdominoperineal resections for anal, recurrent, or low rectal tumors. When combined with radiation therapy, these wounds often heal poorly. The addition of a well-vascularized soft-tissue flap is therefore warranted. Reconstructive options include a pedicled rectus abdominis musculocutaneous flap, which is often the flap of choice. If not available, other options include the use of thigh muscles (rectus femoris, gracilis) and fasciocutaneous flaps (anterolateral thigh flap). The greater omentum has been used for decades to treat the chronic vesicovaginal fistula and to fill the severely irradiated pelvis with well vascularized tissue (14,15). It can also be employed to support a primary closure or, if no other options are available, it can be used alone with a skin graft (although the omentum is sometimes resected by the extirpative surgeon in cases of gynecologic malignancies). The aforementioned muscle flaps can also be used to reconstruct the vagina, in addition to filling the dependent pelvic defect. In the male, a musculocutaneous flap can serve the purpose of obtaining a healed perineal wound and filling the most dependent portion of the pelvic defect to promote wound healing, prevent evisceration, and attempt to prevent adhesions deep in the pelvis.

CONCLUSION Although radiation therapy has many benefits, late changes following irradiation have been well described and offer the plastic surgeon many reconstructive challenges. Each anatomic location offers unique problems to the plastic surgeon. But the basic tenets of treating irradiated wounds are the same, regardless of anatomic location, and they are as follows: 1. Establish a diagnosis (rule out malignancy, determine the extent of tissue damage, etc.) 2. If tumor is present, perform the appropriate work-up and treatment. 3. Thoroughly debride the radiated wound of all nonviable tissue and foreign bodies and plan to transfer as much tissue as possible to permit resection of even more of the periphery in questionable wounds.


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4. After adequate debridement has been obtained, usually in stages, reconstruct osseous defects with vascularized bone and soft-tissue defects with well-vascularized, nonirradiated soft tissue. All neurovascular bundles, bone, tendon, prosthetic material, etc., must be covered with well-vascularized soft tissue. 5. In the case of pedicled flaps, it is better to base a flap on a nonirradiated pedicle; in the case of free tissue transfer, it is best to use nonirradiated recipient vessels. 6. Reconstruction of these defects is challenging and fraught with high complication rates, so always have a “plan B” in mind and anticipate complications.

References 1. Ross GM. Induction of cell death by radiotherapy. Endocr Relat Cancer. 1999;6:41. 2. Fajardo LF, Berthrong M. Vascular lesions following radiation. Pathol Ann. 1988;23:297. 3. Arnold PG, Pairolero PC. Intrathoracic muscle flaps. An account of their use in the management of 100 consecutive patients. Ann Surg. 1990;211(6):656. 4. Arnold PG, Pairolero PC. Chest wall reconstruction: an account of 500 consecutive patients. Plast Reconstr Surg. 1996;98:5. 5. Arnold PG, Lovich SF, Pairolero PC. Muscle flaps in irradiated wounds: an account of 100 consecutive cases. Plast Reconstr Surg. 1994;93:324.

6. Jones G, Nahai F. Management of complex wounds. Curr Probl Surg. 1998;35:194. 7. Evans RD, Schusterman MA, Kroll SS, et al. Reconstruction and the radiated breast: is there a role for implants? Plast Reconstr Surg. 1995;96(5): 1111. 8. Forman DC, Chiu J, Restifo RJ, et al. Breast reconstruction in previously irradiated patients using tissue expanders and implants: a potentially unfavorable result. Ann Plast Surg. 1998;40:360. 9. McCarthy CM, Pusic AL, Disa J, et al. Unilateral postoperative chest wall radiotherapy in bilateral tissue expander/implant reconstruction patients: a prospective outcomes analysis. Plast Reconstr Surg. 2005;116(6):1642. 10. Hartrampf CR Jr, Bennett GK. Autogenous tissue reconstruction in the mastectomy patient: a critical review of 300 patients. Ann Surg. 1987;205:508. 11. Tran NV, Evans GR, Kroll SS, et al. Postoperative adjuvant irradiation: effects on transverse rectus abdominis muscle flap breast reconstruction. Plast Reconstr Surg. 2000;106:313. 12. Spear SL, Ducic I, Low M, et al. The effect of radiation on pedicled TRAM flap breast reconstruction: outcomes and implications. Plast Reconstr Surg. 2005;115(1):84. 13. Cordeiro PG, Santamaria E, Hidalgo D. The role of microsurgery in reconstruction of oncologic chest wall defects. Plast Reconstr Surg. 2001;108(7):1924. 14. Turner-Warwick RT, Wynne EJ, Handley-Ashken M. The use of the omental pedicle graft in the repair and reconstruction of the urinary tract. Br J Surg. 1967;54(10):849. 15. Turner-Warwick RT, Chapple C. The value and principles of omentoplasty and omental inter-position. In: Turner Warwick RT, Chapple C, eds. Functional Reconstruction of the Urinary Tract and Gynaeco-Urology: An Exposition of Functional Principles and Surgical Procedures. Oxford, UK: Blackwell; 2001:155.


CHAPTER 20 ■ LASERS IN PLASTIC SURGERY DAVID W. LOW

The public is fascinated by high technology, and laser therapy has been, and continues to be, at least partially misrepresented as “state-of-the-art” treatment for a variety of conditions, most of them cosmetic in nature. Often described as painless, and exaggerated as producing perfect results, lasers have been misused as a marketing tool to lure patients away from conventional low-tech techniques that can often produce equivalent results at significantly lower cost. On the other hand, some conditions, such as port-wine stains, are best treated by laser, and the standard of care demands familiarity with this treatment modality. The modern plastic surgeon faces the dilemma of trying to sort out which lasers are best for which conditions, which manufacturers’ claims are realistic or incredible, and, ultimately, which lasers are the safest investment in a rapidly changing world of high-tech solutions to a variety of reconstructive and cosmetic problems. This chapter is a basic introduction to laser technology, laser tissue interactions, and examples of what conditions are appropriate for laser treatment with currently available laser technology. Laser safety, discussed at the end of the chapter, is an important consideration for both the patient and the treating physician.

A laser tube has a mirror at each end and contains a solid, liquid, or gas medium whose electrons are in a resting state. As energy is added to the system, the majority of the electrons become excited (population inversion) and begin releasing photons. Only those photons that hit the mirrors directly are reflected back into the lasing medium, creating an increasing number of photons that travel back and forth between the mirrors, parallel to the tube. Because the photons are in phase, the intensity of the light increases in the tube. This phenomenon has been described as light amplification by the stimulated emission of radiation, or the more familiar term LASER. To allow light to escape from the tube, one mirror is only partially reflecting. The emitted light is coherent; that is, it is in phase, parallel, and in most cases monochromatic. In contrast, incandescent light is noncoherent, meaning it has many wavelengths and is not parallel. Light energy can be visible or invisible depending on its wavelength. The spectrum of electromagnetic radiation ranges from long radio waves (wavelength >10 cm) to extremely short γ rays (40 mm). In the growing child, excessive distance may be considered anything greater than 25 mm. Orbital dystopia may be either vertical or horizontal. The midline number 14 cleft may have horizontal or transverse dystopia with the bony orbits displaced laterally (orbital hypertelorism) or medially (hypotelorism), whereas, the lateral number 10 through 13 clefts may have a component of vertical dystopia or asymmetric orbital hypertelorism with the orbits on different horizontal planes. Correction of hypertelorbitism may be achieved with a facial bipartition or orbital box osteotomy. A facial bipartition involves coronal and gingivobuccal sulcus incisions, a craniotomy for exposure, orbital and midface osteotomies, central wedge ostectomy (between the orbits), rotation of the orbits to an intradacyron distance less than 17 mm and rigid fixa-

tion. Medial canthi bolsters and correction of excessive glabellar soft tissue is necessary. In addition to narrowing the orbital distance, a facial bipartition procedure will also widen a constricted palatal arch. Alternatively, an orbital box osteotomy can be used to narrow orbital distance or correct vertical dystopia, with no effect on the palate or upper dental arch.

Number 30 Cleft The median cleft of the lower jaw was first described by Couronne. These median clefts of the lower lip and mandible are caudal extensions of the number 14 cranial cleft and number 0 facial cleft.

Soft-Tissue Involvement Soft-tissue involvement (Fig. 28.18) of this midline cleft may be as mild as a notch in the lower lip. However, often the entire lower lip and chin may be involved. The anterior tongue may be bifid and attached to the split mandible by a dense fibrous band. Ankyloglossia and total absence of the tongue have been reported with midline mandibular clefts.

Skeletal Involvement Skeletal involvement is typically a cleft between the central incisors extending into the mandibular symphysis. This anomaly is thought to be caused by failure of fusion of the first branchial arch. However, associated neck anomalies are believed to be caused by failure of fusion of other lower branchial arches. For instance, the hyoid bone many times is absent and the thyroid cartilages may fail to completely form. The anterior neck strap muscles are often atrophic and replaced by dense fibrous bands that may restrict chin flexion.


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the intervening tissue is excised. For the oral commissure (as in cleft number 7), the lateral element is closed in a straight line. The medial aspect is closed with a Z-plasty so that the vertical limb is along the nasolabial fold. For the lower lip (as in cleft number 30), V-excision and layered closure is performed. For the mandibular reconstruction (as in cleft combinations 6, 7, and 8 in both craniofacial microsomia and Treacher Collins syndrome), costochondral grafts may be used for severe deformities and distraction osteogenesis may be used for moderate deformities in mid-childhood (6 to 8 years of age). Mild maxillary deformities should be corrected as an adult with a Le Fort I osteotomy with or without a concomitant mandibular procedure. Surgical correction of the periorbital region is necessary in many craniofacial clefts. For the eye, urgent intervention is necessary if the eye is exposed and at risk for corneal ulceration. However, early reconstructive procedures for globe protection must be balanced to allow enough eye opening to prevent deprivation amblyopia. For the eyelid, “lid-switch” transposition flaps are used for skin/muscle deficiencies. Accurate repositioning of the medial canthus may be performed with transnasal wiring. Lateral canthopexies are sometimes needed to achieve symmetry. Palatal grafts may be used for lower lid conjunctival lining. Correction of number 8 (lateral eye) clefts are performed with Z-plasty flaps. For the lacrimal apparatus, disruption of the canalicular system may be corrected with silastic stents or formal dacryocystorhinostomy. For the orbit, bone grafts are used to correct dystopia or restore continuity. As mentioned above, orbital dystopia is corrected with a facial bipartition, orbital box osteotomy, or subcranial Le Fort III. FIGURE 28.18. Number 30 cleft. Patient with a lower lip midline cleft and notching of his mandibular midline alveolar ridge.

TREATMENT OF CRANIOFACIAL CLEFTS Standardized treatment plans are not possible because of the variety of craniofacial clefts and levels of severity. However, guiding principles are helpful in determining the proper timing and stages for corrective surgery. If the malformation is severe, or if there are functional problems, like ocular exposure, surgery is performed early. If the malformation is mild, surgery should be delayed. During infancy (3 to 12 months of age), cranial defects and soft-tissue clefts are corrected. Midface reconstruction and bone grafting are performed in older children (6 to 9 years of age). Orthognathic procedures are delayed until skeletal maturity (14 years of age or older). Surgical techniques used for correction of craniofacial clefts depend on the anatomic regions involved. The original descriptions for correction of soft-tissue craniofacial clefts involved the use of Z-plasty flaps. Presently, flaps are designed to respect aesthetic units by leaving scars along aesthetic lines. For the nose (as in cleft numbers 0 thru 3), the cleft is excised, nasal cartilages are repaired with the use of cartilage grafts or composite grafts, and local rotation flaps are used for alar retraction. Secondary nasal reconstruction may be performed with cantilevered cranial bone grafts. For the upper lip (as in cleft numbers 0 thru 5), correction of cleft defects involves aligning the vermilion and restoring the muscular continuity, as in common cleft lip repair. If the cleft is lateral to the philtral column,

Conclusion Craniofacial clefts are highly variable and range from a mild, barely noticeable form fruste (microform), to disfiguring, complete defects of the skeletal and soft tissue. Tessier’s description of craniofacial clefts based on bony and soft tissue landmarks provides a classification that has been validated by the neurometric theory of neuroembryology.

Suggested Readings Carstens M, Development of the facial midline. J Craniofac Surg. 2002;13:129– 187. Converse JM, Horowitz LS, Coccaro PJ, et al. The corrective treatment of the skeleton asymmetry in hemifacial microsomia. Plast Reconstr Surg. 1973;52: 221. Converse JM, Ransohoff J, Mathews ES, et al Ocular hypertelorism and pseudohypertelorism. Advances in surgical treatment. Plast Reconstr Surg. 1970;45:1. David DJ, Moore MH, Cooter RD. Tessier clefts revisited with a third dimension. Cleft Palate J. 1989;26:163. Gorlin RJ, Jue KL, Jacobsen U, et al. Oculoauriculovertebral syndrome. Pediatr J. 1963;63:991. Kawamoto HK Jr. The kaleidoscopic world of rare craniofacial clefts: order out of chaos (Tessier classification). Clin Plast Surg. 1976;3:529. Kawamoto HK Jr. Rare craniofacial clefts. In: McCarthy JG, ed. Plastic Surgery. Philadelphia: WB Saunders; 1990:2922–2973. Longaker MT, Lipshutz GS, Kawamoto HK Jr. Reconstruction of Tessier no. 4 clefts revisited. Plast Reconstr Surg. 1997;99:1501. Obwegeser HL. Correction of skeletal anomalies of otomandibular dysostosis. J Maxillofac Surg. 1974;2:73. Tessier P. Anatomical classification of facial, cranio-facial and latero-facial clefts. J Maxillofac Surg. 1976;4:69.


CHAPTER 29 ■ MISCELLANEOUS CRANIOFACIAL CONDITIONS Fibrous dysplasia, moebius syndrome, romberg’s syndrome, treacher collins syndrome, dermoid cyst, neurofibromatosis ROBERT J. HAVLIK

This chapter includes a diverse spectrum of disorders that do not “fit” together with other conditions in plastic surgery, or for that matter, with other conditions in medicine. As such, they represent the “outliers.” With the exception of neurofibromatosis, they are distinctly uncommon.

FIBROUS DYSPLASIA Fibrous dysplasia is a benign disorder of bone that affects both the axial and the craniomaxillofacial skeleton. Fibrous dysplasia is not “classically” a congenital disorder, as it is not usually evident at birth, but becomes clinically evident during late childhood or adolescence. It occurs sporadically, and genetic transmission has not been documented. Fibrous dysplasia has been traditionally divided into three main categories: monostotic (or monocystic) fibrous dysplasia, polyostotic fibrous dysplasia, and the McCune-Albright syndrome. The majority of patients (∼70% to 80%) present with a single area of bony involvement (monostotic or monocystic fibrous dysplasia), whereas the balance of patients present with multiple sites of bone involvement (polyostotic fibrous dysplasia). Of the patients with polyostotic fibrous dysplasia (20% to 30%), approximately 3% present with a triad of polyostotic fibrous dysplasia, precocious puberty, and skin pigmentation known as the McCune-Albright syndrome. This skin pigmentation presents as “café-au-lait” spots present with a highly irregular border, described as being similar to the coastline of Maine. In addition to this classic triad, McCune-Albright syndrome is also associated with several different endocrine disorders, all caused by autonomous hormonal overproduction, such as pituitary adenomas secreting growth hormone, hyperthyroid goiters, and adrenal hyperplasia. The craniomaxillofacial structures are involved in approximately 25% of cases with monostotic fibrous dysplasia and up to 50% of cases with polyostotic involvement. The most common presentation in the craniofacial skeleton is that of a painless, enlarging mass of bone. The maxilla is the bone most often involved, followed in frequency by the frontal bone, but all bones of the craniomaxillofacial skeleton may show involvement. The clinical manifestations of fibrous dysplasia include expansive growth leading to aesthetic and functional compromise. Maxillary lesions can lead to dental malocclusions, tilting of the occlusal plane, or significant facial deformity and asym-

metry. In lesions with orbital involvement, visual disturbance, ocular proptosis, and orbital dystopia can occur. In lesions with sphenoid involvement, blindness may occur as a result of impingement on the optic nerve. The difficulty in the diagnosis of fibrous dysplasia varies with the extent of presentation of the disease. The polyostotic and McCune-Albright forms of fibrous dysplasia are relatively easily diagnosed based upon clinical and radiologic investigation, whereas establishing the diagnosis of the monostotic form is more difficult because of the number of other important lesions that are included in the differential diagnosis. In the axial skeleton, the lesions frequently appear as well-circumscribed radiolucent lesions with a thin sclerotic periphery. In contrast, the lesions of the craniofacial skeleton are more poorly defined and more radiopaque. Bone biopsy in many areas of the axial skeleton in fibrous dysplasia is generally avoided, especially where the risk of pathologic fracture is high. However, in the mandible, where monostotic involvement is most frequent in the craniomaxillofacial skeleton and therefore there is the greatest difficulty differentiating this from other solitary bony lesions, bone biopsy has not been reported to cause a pathologic fracture in fibrous dysplasia. Malignant degeneration of fibrous dysplasia has been reported to occur in 0.5% of cases with monostotic involvement, and in up to 4% of cases with McCune-Albright syndrome. Notably, the most frequent site for sarcomatous degeneration is the craniofacial skeleton.

Pathogenesis The basis of this disorder is centered on a structural and functional change in the cellular transduction mechanism involving G-proteins. The G-protein is a membrane-bound intracellular signaling mechanism that carries the message of extracellular hormone into the cell. The G-proteins themselves have an intrinsic activity that causes hydrolysis of guanosine triphosphate (GTP) to guanosine diphosphate (GDP). In fibrous dysplasia, the G-protein has a decreased ability to hydrolyze GTP, resulting in the G-protein remaining in an activated state, leading to continued stimulation of cyclic adenosine monophosphate (cAMP) and multiple other effects. Significantly, many of the adrenal, pituitary, thyroid, and gonadal cells of patients with McCune-Albright syndrome show the same mutations,

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thereby leading to increased “ON” activity, and constitutively increased hormone production. The somatic mutation theory implies that fibrous dysplasia arises from the development of cellular mosaicism. It has been postulated that the timing at which this mutation occurs may determine the clinical extent of the disease. In other words, a mutation that occurs late in embryologic development will lead to a decreased number of cells with the mutation and to the development of monostotic bone involvement. In contrast, a mutation that occurs in early embryologic development would lead to a larger number of afflicted cells and multicentric involvement (polyostotic fibrous dysplasia). If the mutation occurs early enough in development, it may lead to the involvement of additional tissues (endocrine disorders, McCune-Albright syndrome, etc.). As noted above, there are no documented cases of genetic transmission of fibrous dysplasia, and it may be that a germline mutation, or a mutation that occurs early enough in embryologic development, is a lethal mutation.

Treatment Treatment of fibrous dysplasia in the craniofacial skeleton is determined by the functional or aesthetic problems created by the disease process. The mere existence of fibrous dysplasia does not mandate treatment. In bones of the axial skeleton, the expansile process, coupled with cortical resorption, can lead to decreased structural strength and pathologic fracture. This is seldom the case in the craniomaxillofacial skeleton, and indications for treatment are more frequently related to aesthetic imbalance, facial disfigurement, distortion of the functional occlusion, orbital dystopia, ocular proptosis, and impingement on neural foramina. Impingement on the optic nerve has led to visual disturbance and blindness. Older publications suggest that fibrous dysplasia will “burn out” in the postpubertal adolescent state. Unfortunately, there is no data to support this contention. Surgical treatment is designed to counter the effects of mass expansion and the consequent deformity that occurs in the facial skeleton. In most cases, surgery of the craniofacial skeleton consists of either a contour reduction of the afflicted area, or resection and replacement of the afflicted bone. Contour reduction is a more limited operation; however, it is accompanied by a higher likelihood of recurrence. Resection and replacement overrides cure. A decision is made regarding the rate of tumor growth, or the “aggressiveness” of this benign process. Resection is followed by reconstruction with either alloplastic materials or bone autograft. In the cranial vault, the frontal bone is the most frequently involved bone, followed by the sphenoid bone. The case illustrated in Figure 29.1 used both resection and contour reduction techniques for treating areas of hyperostotic fibrous dysplasia in the right fronto-orbital region and the right parietal region. The resection and cranial bone autograft reconstruction was performed in the right orbit and frontal bone, where the potential problems with recurrent tumor and repeat resection would be more problematic. The parietal bone was completely removed, and contour reduction was performed down to the level of cortical plate. When fibrous dysplasia involves the skull base, the surgeon must assess the risk of continued expansion versus the risk of resection and the potential outcomes of the planned treatment. Fibrous dysplasia of the orbit raises several special considerations. First, the mass effect of bone growth can lead to dystopia and visual disturbances. The potential problems of recurrence in this area, particularly with the potentially more difficult surgery in the recurrent field from scarring, swing the balance toward resection of the afflicted bone and replacement.

Second, specific to the orbit is the concern that growth of fibrous dysplasia can lead to optic nerve compression, subsequently leading to visual change and blindness. Visual loss has been cited as the most common neurologic complication of fibrous dysplasia involving the skull. Although optic nerve decompression in patients with fibrous dysplasia of the sphenoid surrounding the optic canal and with documented visual changes is widely accepted, “prophylactic” decompression of the optic nerve is generally not recommended. Furthermore, decompression after visual decrement or visual loss may not restore the visual deficit (1). The risks involved with surgical decompression of the nerve include a lack of improvement in vision, which occurs in 5% to 33% of cases, and blindness resulting from the surgery (1,2). Fibrous dysplasia involving the maxilla leads to overgrowth, aesthetic irregularities, tilting of the occlusal plane, and other occlusal irregularities. Successful surgical treatment relies on two key outcomes: an acceptable aesthetic result and an acceptable and functional occlusal result. If the dentition is to be maintained, surgical correction can be obtained by either contour reduction or resection of the maxilla in the plane above the Le Fort I level, coupled with reconstruction of the orbital floor and free tissue transfer for obliteration of the defect. The alternative treatment is formal maxillectomy and reconstruction with free tissue transfer. Treatment planning involves maintaining the existing dentition or a suitable alternative—either reconstructive or prosthodontic. Fibrous dysplasia of the mandible presents as a mass lesion with cortical expansion. Because the presentation with mandibular disease is frequently monostotic, bone biopsy may be indicated to establish or confirm the diagnosis. As noted previously, biopsy of the mandible can be safely accomplished in fibrous dysplasia without a significant risk of fracture. Depending on the severity of the involvement, either contour reduction or resection can be performed. In lesions involving the ramus in which the temporomandibular joint (TMJ) is spared, every effort should be made to plan the resection and reconstruction using the existing joint. In larger lesions, resection of the tumor with free fibula reconstruction is a reasonable approach (see Chapter 41). Until recently, surgical treatment was the only option for the treatment of fibrous dysplasia. Recently, several small series have been published using medical therapy with pamidronate, an aminobisphosphonate. This treatment has resulted in an increase in bone mineral density and radiologic signs of healing with the thickening of cortical bone in some cases. In many cases, there has also been a significant decrease in pain with pamidronate therapy. Radiation therapy is contraindicated because of an increased propensity for malignant transformation.

MOEBIUS SYNDROME Moebius syndrome is a rare disorder characterized by paralysis of the cranial nerves. Classically, Moebius syndrome is defined by paralysis of the sixth and seventh cranial nerves resulting in a masklike facies, incapable of animation, and an inability to laterally deviate the eyes (abducens palsy) (3). Facial expression forms a fundamental and important component of human communication and socialization, and the inability to show a facial response to verbal and nonverbal communication is a devastating deficiency (see Chapter 40). In the United Kingdom, there were approximately 90 cases of Moebius syndrome in a population of 50 million people, yielding a prevalence of 1 in 550,000 (4). By extrapolation, approximately 500 cases would be expected in the United States. In some publications, Moebius syndrome is defined more broadly, including


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Chapter 29: Miscellaneous Craniofacial Conditions

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D FIGURE 29.1. Fibrous dysplasia involving the right orbit, right frontal bone, and right parietal bone. A: Pre-operative lateral view. B: Preoperative “worm’s eye” view. C: Preoperative axial computed tomography (CT) image. D: Intraoperative view showing increased density of fibrous dysplasia involving right frontal and right parietal bones. E: Planned split-graft donor site using metallic template fabricated in F (illustration by Min Li, MD). F: Intraoperative view following completed resection of tumor and reconstruction of orbital roof and supraorbital bar using split cranial bone grafts from left parietal bone and contour reduction of right parietal bone. G: Completed reconstruction using contour reduction of right parietal bone. H: Three-year postoperative “bird’s-eye” three-dimensional CT scan showing symmetry of reconstruction and no evidence of recurrence. I: Three-year postoperative frontal view. J: Three-year postoperative “worm’s-eye” view.

patients with additional facial nerve palsies. Involvement of nearly all of the facial nerves has been documented, but the third, ninth, tenth, and twelfth nerves are most commonly involved (3). In addition to the characteristic facies associated with the sixth and seventh nerve palsies, ptosis, nystagmus, or strabismus may be present, and epicanthal folds are frequent (Fig. 29.2). The nose typically has a high, broad bridge, and this increased breadth extends to the nasal tip. The mouth opening is typically small. In addition, there can be hypoplasia of the tongue, either unilaterally or bilaterally. There frequently is poor palatal mobility, poor suck, inefficient swallowing, and drooling. The mandible tends to be hypoplastic. These factors can contribute to difficulty feeding during the first year of life, frequently leading to poor growth. A coarse voice and speech impairment can be present, although hearing is usually normal. As the child grows, the ability to open the mouth and feed

tends to improve. The facial paralysis and masklike facies tend to bias early estimates of psychomotor activity. Only 10% to 15% of children are mentally retarded (3).

Etiology and Pathogenesis The etiology of this disorder has not been elucidated. It occurs sporadically and, in cases of “classic Moebius syndrome” involving only sixth and seventh cranial nerves, genetic transmission is rare. For Moebius syndrome, four separate and distinct, although not mutually exclusive, pathogenetic mechanisms have been advanced: (a) aplasia/hypoplasia of the cranial nerve nuclei; (b) destruction of the cranial nerve nuclei; (c) peripheral nerve abnormalities; and (d) primary myopathy.

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drooling and an improved ability to drink. The surgery also has a definite benefit on speech.

ROMBERG DISEASE (PROGRESSIVE HEMIFACIAL ATROPHY) Progressive hemifacial atrophy (PHA) is widely known by the eponym of Romberg disease. In an era of molecular and genetic analysis, PHA remains as perhaps the most enigmatic of the craniofacial disorders. The etiology of this disorder remains unknown.

Clinical Findings

FIGURE 29.2. Moebius syndrome with typical mask-like facies and downslanted oral commissures. (Photo courtesy of Ron Zuker, MD.)

Operative findings and postmortem examinations have supported each of these four mechanisms (3,5).

Treatment Treatment has progressed more rapidly than our understanding of this rare disorder, and focuses on one of the most socially devastating problems of this disorder—the inability to show a facial response. Facial reanimation surgery is effective in restoring function in many different etiologies of facial nerve deficits, and this treatment has been extended to Moebius syndrome. Zuker et al. have reported excellent results with microvascular free tissue transfer of the gracilis muscle to the face, and this procedure represents the state of the art (5). Although they initially used the hypoglossal or accessory nerve, they have refined their technique to use the branch of the trigeminal nerve to the masseter muscle as the motor nerve of choice (see Chapter 40). This motor nerve has the advantage of being largely spared in Moebius syndrome, and the function can reliably be assessed preoperatively. The nerve is located in proximity to the transfer, in the region of the sigmoid notch of the mandible. Furthermore, the innate function of this motor nerve is relatively synergistic with the desired posttransplant function of facial animation. The surgery is accomplished in two separate stages, one stage for each side of the face. Zuker et al. report a series of 10 patients who had an average movement of their oral commissures following bilateral microvascular transfers of 1.37 cm, allowing for meaningful and deliberate facial animation (5). In addition, the children showed improvement with

PHA may involve any or all of the facial tissues, typically involving skin and subcutaneous tissue, but also potentially muscle, cartilage, and bone. Pensler et al. (6) have reviewed the clinical course in 41 patients and report that the initial presentation involved the distribution of V1 (first division of trigeminal nerve) in 35% of cases, the distribution of V2 in 45% of cases, and the distribution of V3 in the remaining 20% of cases. Either side of the face is equally likely to be involved, and involvement is unilateral in 95% of cases. The initial presentation typically involves the skin and may be quite subtle, sometimes including pigment changes in which there may be either a brownish or bluish discoloration, or even hypopigmentation. Alternatively, the disorder may first present as a limited area of atrophy of the subcutaneous fat. A striking archetypal presentation often includes a nearly vertical linear depression of the forehead extending into the eyebrow and frontal hairline, known as the coup de sabre, or “cut of the saber” (Fig. 29.3). This “clinical sign” was thought to be pathognomonic for Romberg disease, but can also been noted in linear scleroderma, a subtype of localized scleroderma, leading to a potential overlap of these diagnoses. PHA is not a congenital disorder, with the typical onset being in the first or second decade of life. The hallmark of the disorder is a slowly progressive course, with an “active phase” of disease characterized by involution, or “wasting away” of the skin, subcutaneous tissue, and muscle. This “active phase” lasts from 2 to 10 years. The subcutaneous tissue is the most severely involved, followed by substantial involvement of the skin and muscle. The facial musculature undergoes thinning, but usually maintains sufficient power to animate the face. The muscle involvement commonly includes atrophy of the tongue and palatal tissues. Patients with an early age of onset (during facial growth), are much more likely to have significant skeletal involvement. Pensler et al. (6) report that 65% of their patients had osseous involvement, and they found a strong correlation between the age at onset and the degree of bone hypoplasia. However, in their review, they noted no correlation between the other findings of severity of soft-tissue atrophy, the duration of the disease, the initial site of skin changes, and the eventual location or magnitude of the skeletal involvement. In cases where the disease occurs during the first decade of life, there can be profound skeletal hypoplasia of the afflicted side of the face. This stands in distinct contrast to those cases that present initially in the second decade of life. In these cases, there is typically limited impact on the facial skeleton, with the gross morphologic changes being confined to skin and subcutaneous tissue. The patient in Figure 29.3 had disease onset at 10 years of age. There is clinical involvement of the skin, eyebrow, and periocular tissues. There is clearly hypoplasia or atrophy of the right nasal sidewall and cartilaginous atrophy of the nasal ala. Her dental development and occlusal relations show no signs of involvement. In view of this strong correlation

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D FIGURE 29.3. Progressive hemifacial atrophy in a 14-year-old adolescent with onset at age 10 years. A: Frontal view illustrates large area of alopecia of scalp, mild soft-tissue depression, loss of medial eyebrow, and vertical deficiency of right alar rim consistent with a mild coup de sabre-type deformity. The nose not only shows vertical deficiency, but also thinning and collapse. Radiographic evaluation revealed no evidence of skeletal irregularity. B: Intraoperative view showing dermal fat graft in position for grafting soft-tissue deficiency of forehead. An ear cartilage conchal bowl composite graft was used to reconstruct the alar deficiency. C: Initial postoperative result of ala reconstruction. Unfortunately, she developed a late Pseudomonas infection, and although she has a significantly improved patency of her internal and external nasal valves, the vertical correction has diminished as seen below. D: Postoperative result. The dermal fat graft initially led to significant overcorrection of the deficiency, but now yields a favorable result.

of the severity of this disorder with the age of onset, it is unclear whether the facial skeleton actually undergoes atrophy. More likely the bone fails to develop fully in the field of overlying atrophy of skin and subcutaneous tissue. The skeletal “atrophy” in PHA is more accurately termed hypoplasia.

In early onset cases, the skeletal involvement often involves the mandible and midface, with concomitant implications for the occlusal relationships and facial appearance. There can be hypoplasia of the mandible, including significant vertical undergrowth of the ramus and a deficiency in posterior facial



height. The mandible may also show significant sagittal undergrowth. The maxilla may also manifest both vertical and sagittal undergrowth in the sagittal plane. Because the involvement is unilateral, profound tilting of the occlusal plane develops. When PHA involves the V1 distribution of the nerve, the periocular tissues are typically involved as well. In these cases, enophthalmos is a frequent finding. Pensler et al., based on radiographic orbital measurements, suggest that the enophthalmos is not caused by a skeletal change in the orbital volume, but that it is related to atrophy of the periorbital soft tissues (6). PHA can be associated with many other findings, including areas of skin and subcutaneous atrophy elsewhere on the body distinct from the face. The disorder is associated with nervous system dysfunction, including Horner syndrome, trigeminal neuralgia, and unilateral mydriasis. Central nervous system involvement has been reported in smaller series by several authors, ranging from magnetic resonance imaging (MRI) changes to seizure disorders. However, the relative paucity and inconsistency of data at this point preclude any definitive correlation between these reports.

Etiology The etiology of PHA is unknown. PHA does not show any genetic predilection, is found in all races, and there is no evidence of a hereditary basis. It does occur more frequently in females in most series. Patients will frequently remember an “initiating event” in PHA, and the onset of the disorder is often linked to an episode of trauma or infection. However, it is unclear whether this is simply an event that calls attention to a subtle area of initial clinical involvement, or whether there are true pathogenetic associations. Traditionally, three theories have been advocated for the etiology of Romberg disease: the infection hypothesis, the trigeminal-peripheral neuritis hypothesis, and the sympathetic hypothesis. The infectious hypothesis was historically linked to an irritation of nerves. In the current era of a new understanding of infectious agents (viruses, prions, mad cow disease, chronic wasting disease of deer, etc.), the infectious hypothesis may be remain a tenable etiology until a definitive understanding of this disorder is truly established. The trigeminal-peripheral neuritis hypothesis suggests a neuritis involving the trigeminal nerve, and is supported by episodes of pain in the involved areas prior to the onset of tissue involution. The sympathetic hypothesis is based on an association of Horner syndrome, pilomotor reflex changes, unilateral mydriasis, vasomotor disorders, unilateral migraine, and perspiration disorders. Based on current evidence, no definitive etiology has been established. The insightful work of Pensler et al. has provided some enhanced understanding. First, in their clinical review, as previously noted, they found no evidence of sensory, sympathetic, parasympathetic, or sudomotor dysfunction. Muscles of mastication and facial expression were found to be fully functional. Biopsies revealed epidermal atrophy and a variable perivascular mononuclear cell infiltrate, with morphologic characteristics of lymphocytes and monocytes, that were grouped around dermal neurovascular bundles. Many of the venules were noted to have striking degenerative alteration in the lining epithelium with reduplication of the basal lamina. Significantly, they also noted that elastic fibers were present and morphologically intact (in contrast to linear scleroderma). They interpret these findings as lymphocytic neurovasculitis, and they advance this theory as a pathogenetic mechanism. Understanding the pathogenesis of this disease is complicated further by the apparent overlap between the disorder of linear scleroderma and PHA. It is very likely that many of the cases that have historically been termed Romberg disease may

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include cases of linear scleroderma, as differentiating the two clinically is difficult, if not impossible. Linear scleroderma may also show monocytic infiltrates. The only finding that has been reported as useful to differentiate these two disorders is the absence of elastic fibers in the scleroderma group, and their preservation in the PHA group (4).

Treatment Many surgeons will defer treatment until the disease “burns out,” or reaches a stable plateau phase. For milder asymmetry and atrophy of the skin and subcutaneous tissue, injection of collagen and hyaluronic acid derivatives or fat injection may provide some short-term benefit. For small areas of asymmetry, dermal grafts, fat grafts, or dermal-fascial-fat grafts are considered. These can be tailored to smaller defects and provide an acceptable improvement with a limited operative approach and limited operative time and risk (Fig. 29.3). However, because of the variability in graft survival, overcorrection is necessary. In addition, there is typically a postoperative period that is characterized by induration. Overall, the experience in the literature with nonvascularized transfer of fat tissue, particularly with larger transfers, has been inconsistent. Microvascular free tissue transfer is the gold standard in reconstruction of patients with Romberg disease. Upton et al. (7) reported microvascular transfer of scapular and parascapular flaps in 30 patients, five of whom were patients with Romberg disease. They used long fat-fascial extensions with these transfers to fill isolated areas. They noted no postoperative atrophy in the 30 flaps, but they did note that in patients who gained weight, the flap volume increased. In addition, there were isolated areas, such as the upper lip, that tended to be undercorrected. They also noted no evidence that free tissue transfer altered the natural history of the disease process in PHA. In children with the early onset of the disorder, there is often distortion of the orbit and the zygomaticomaxillary complex, leading to vertical orbital dystopia. Depending on the severity, this can be corrected either through corrective osteotomies and vertical repositioning of the orbit, or through bone grafting of the orbital floor. Involvement of the V2 and V3 distributions of the trigeminal nerve can lead to severe maxillary and mandibular asymmetries, with distortion of both the facial midline and occlusal plane. Bimaxillary surgery is necessary to correct of the occlusal plane.

TREACHER COLLINS SYNDROME Treacher Collins syndrome, or mandibulofacial dysostosis, is a craniofacial disorder that has an incidence of between 1 in 25,000 births and 1 in 50,000 births and is characterized by a range of clinical presentations. The full clinical presentation is characterized by hypoplasia/aplasia of the body and arch of the zygoma, a significantly increased facial convexity, mandibular hypoplasia, a retrusive chin with increased vertical height, and external and middle-ear anomalies. A key distinguishing feature of this entity is that it is bilateral and symmetrical. The periorbital soft tissues show an antimongoloid slant of the palpebral fissures. The lower eyelid is hypoplastic with a coloboma located at the junction of the medial two-thirds and lateral third of the lower lid. The deficiency involves both the skin of the eyelid, and the cartilage of the tarsal plate eyelid also lacks eyelashes typically over the medial third. These findings, along with the hypoplastic zygoma, lead to a striking clinical appearance (Fig. 29.4). The nose is broadened in the midnasal dorsum, and can have a slightly elongated appearance. The midface is

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FIGURE 29.4. Treacher Collins syndrome. A: Characteristic facies with orbital findings, including vertically deficient lower lid, lower eyelid coloboma, downslanting palpebral fissures (antimongoloid slant), and hypoplastic malar eminences. B: Five-year-old male with result of lid-switch procedure with conjunctival grafting and canthopexy performed at age 3 years. C: Approximately 1-year result after dermal fat grafting shows improved contour in the malar eminence in 7-year-old.

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hypoplastic, particularly at the level of the zygomatic body and arch, but also in the maxillae. The mandible is characteristically hypoplastic, with a chin that has the unusual combination of increased vertical height and deficiency in sagittal projection. An anterior open bite is often present. This combination exacerbates the overall clinical appearance of a facial profile that is much too convex. Cephalometric analysis has revealed that this facial convexity is attributable to the mandibular hypoplasia and position, as the relationship between this midface and the anterior cranial base is essentially within the normal range (SNA angle). In addition, the occlusal plane tends to be quite steep, with a clockwise rotation of the mandibular plane (hypoplastic posteriorly with decreased posterior facial height). There are characteristically significant deformities of both the external and middle ear present, with a low-lying hairline with

tongue-shaped caudal extensions of hair-bearing scalp in the preauricular areas.

Pathogenesis Treacher Collins is an autosomal dominant disorder, with a markedly variable penetrance. While up to 60% of cases are thought to arise de novo, the variability in penetrance occurs at both the interfamilial and the intrafamilial level. All known cases of Treacher Collins result from mutations in the TCOF 1 gene. The TCOF 1 gene has been mapped to the 5q31.3– 5q33.3 gene locus. Identification of family specific mutations and tracing these specific mutations through family pedigrees shows that the actual number of cases arising de novo may be



less, and the familial transmission rate may actually be higher, as family members previously thought to be unaffected in fact may show the genetic mutation.

Treatment Patients with Treacher Collins syndrome often require a lifesaving tracheostomy at birth. The cranial vault may show a mild deficiency in bitemporal diameter, but this is never of the magnitude to merit surgical intervention. The orbital changes, however, are striking and pathognomonic for this disorder. The orbital changes are consistent with the hypoplasia of the zygoma that characterizes the disorder. Treatment goals include correction of both the lower eyelid deficiency and the zygomatic deficiency. No perfect procedure exists for the lower eyelids. The cutaneous deficiency can then be addressed through a lid-switch operation. The lid-switch operation, with a laterally based banner flap consisting of skin and orbicularis oculi muscle, has the advantage of providing vascularized tissue with an excellent skin color match (Fig. 29.4). The lid switch also has a salutary benefit of vertical repositioning of the lateral canthus contributing to the correction of the antimongoloid slant of the palpebral fissure. This flap, however, may become edematous and remain “prominent” for an indefinite period of time. It is of critical importance that the cutaneous reconstructions be coupled with adequate conjunctival release with a widely offset incision and appropriate conjunctival reconstruction. Several different techniques have been described for reconstruction of the hypoplastic zygoma, including split-thickness and full-thickness cranial bone grafts, vascularized calvarial grafts based on a temporalis muscle pedicle, and rib grafts. The cranial bone grafts are typically cut as one-piece T-shaped grafts that serve to reconstruct both the body of the zygoma, the zygomatic arch, and the inferior orbital rim. Technical problems include the paucity of soft tissue in the malar eminence that is available for coverage of the skeletal reconstruction, a soft-tissue problem exacerbated by the net volume expansion required with the reconstruction. Bone grafts in this area of craniofacial skeleton eventually undergo resorption. This may be partially a result of the overlying soft-tissue “matrix” in this disorder, and partially attributable to the inherent tendency of bone grafts to undergo resorption with revascularization. The deficiency of soft-tissue coverage may also influence the problems with graft revascularization. A component of the controversy regarding reconstruction of the zygoma includes consideration of the timing of reconstruction of the zygoma and the age of the patient. Posnick et al. (8) have reported favorable results with reconstruction of the zygoma using full-thickness bicortical grafts for reconstruction of the zygoma at an age of 5 to 7 years. An alternative in the younger child about to start school is the use of dermal fat grafts to help correct the soft-tissue deficiency and effectively camouflage the skeletal deficiency (Fig. 29.4). Siebert has employed bilateral soft-tissue free flaps to camouflage the skeletal deficiency with results that rival or exceed any skeletal reconstruction (9). The nasal deformity in Treacher Collins includes a broad midnasal dorsal hump, further accentuated by the retrusive chin. The nasal dorsum is correctable through conventional rhinoplasty approaches and procedures, with the usual caveats regarding avoiding airway obstruction. Approximately one-third of Treacher Collins patients have a cleft of the palate. Strict attention is directed to ventilatory status before considering repair of the cleft palate, to avoid ventilatory obstruction. In many cases, this requires correction of the hypoplastic mandible or tracheostomy prior to attempts at closure of the palatal cleft.

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Ears The ears are characteristically involved in Treacher Collins syndrome, and this includes the auricle, the external auditory canal, and the middle ear. Both left and right sides are afflicted, and the deficiencies tend to be symmetrical. Middle-ear malformations are common, and include aplasia, hypoplasia, and/or ankylosis of the ossicles. Most patients (96%) have a moderate or greater degree of hearing loss. This is critical to recognize and treat appropriately as adequate hearing is essential for speech development and speech production. External hearing assistance through hearing aids is often necessary (see Chapter 30). The external ear deformities pose unique problems. First, the low hairline and “tongue” of hair-bearing scalp that descends in the preauricular area often precludes reconstruction with native mastoid skin and requires the alternative use of a temporoparietal fascial flap with skin graft. Second, the external auricle reconstruction must be coordinated with the mandibular reconstruction and the reconstruction of the zygoma. If there is inadequate non–hair-bearing mastoid skin for ear reconstruction, as is often the case, incisions in proximity to the ear must be carefully planned to preserve the superficial temporal artery. If there is favorable mastoid skin for reconstruction, no incisions should be planned prior to placement of the cartilage framework, as these violate the blood supply and can contribute to skin breakdown above the tension of a cartilage framework reconstruction. Because the mandibular reconstruction must take into consideration obstructive airway concerns and the timing of palatal closure, careful planning and coordination of each step in the child’s reconstruction is necessary.

Mandible The mandibular deformity in Treacher Collins syndrome is extremely variable and can include the entire spectrum of mandibular hypoplasia. There is typically an exaggerated antegonial notch, clockwise rotation to an anterior open bite deformity, and the appearance of excess facial convexity. There is a decreased posterior facial height and an increased height of the lower anterior face, partly as a result of the increased vertical height of the chin. The mandibular body is also foreshortened in sagittal dimension. The Kaban-Mulliken modification of the Pruzansky classification of the mandibular deformity in hemifacial microsomia is directly applicable and widely used to characterize the deficiency in Treacher Collins syndrome (Fig. 29.5) (10). In general, patients with types I and IIA deformities have normal TMJ function that should be preserved. Mandibular deficiency in most of these patients can be corrected during adolescence using conventional orthognathic procedures including sagittal split osteotomy of the mandibular ramus and Le Fort I osteotomy of the midface to correct the angle of the occlusal plane and to close any anterior open bite. In addition, an osseous genioplasty designed to decrease the vertical height of the chin and improve the sagittal projection of the chin is routinely added. In patients with type IIA mandibles with a significant loss of posterior facial height, and in patients with type IIB mandibles, reconstruction can often best be obtained using the technique of mandibular distraction osteogenesis. The technique uses a mandibular osteotomy, followed by application of an external framework, and slow lengthening of the bone segments. It has the advantages of predictably lengthening bone with a minimal degree of relapse, unlike conventional bone grafting techniques. In type III mandibles, there is only a cortical shell of a mandible behind the dentition. This anatomy often precludes distraction osteogenesis. These children often require a tracheostomy in the perinatal period for mandibular hypoplasia. These children require reconstruction of the mandibular

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FIGURE 29.5. Kaban-Mulliken classification. This classification of hemifacial microsomia that can be extended to classify and discuss the mandible of Treacher Collins patients. Hypoplasia of the mandible is broken into four groups: Type I—normal architecture but smaller dimensional size of mandible and TMJ; type IIA—moderate hypoplasia of mandible with hypoplasia of ramus and condyle but some TMJ development adequately positioned for symmetrical opening of the joint; type IIB—moderate to severe hypoplasia of ramus, condyle, and TMJ joint that is malpositioned inferiorly, medially, and anteriorly and is “operationally equivalent” to a type III child; type III—total absence of mandibular ramus behind dentition making it unsuitable for bone distraction. (Illustration by Min Li, MD.)

ramus using a costochondral graft designed and positioned to abut against the skull base, because there is hypoplasia of the glenoid fossa. The costochondral rib grafts are harvested and positioned through Risdon (neck) incisions. Incisions in the preauricular are frequently necessary to assist in reconstruction of the zygomatic arch and glenoid fossa. This creates a posterior “stop” for the costochondral graft and facilitates mandible function. This surgery can be performed at 6 to 10 years of age, as the costochondral grafts are of adequate caliber to perform the surgery at that age. Significantly, these steps should be postponed until after ear reconstruction is completed, for the reasons of skin tension and vascularity previously noted. Ultimately, these children will require secondary double-jaw surgery to correct the malpositioned midface, correct the occlusal plane angle, and correct the facial height discrepancies discussed above. A Le Fort I osteotomy and a sagittal split osteotomy of the rib graft can be used, but obvious care must be taken in the rib graft osteotomy.

CONGENITAL DERMOID TUMORS Congenital dermoid inclusion cysts of the face are common entities most commonly located in the upper lateral orbit and the upper lateral orbital rim, although they also can be found in the forehead and nasal areas (11). These lesions are benign, and embryologically these cysts represent displacement or retention of dermal and epidermal cells into embryonic lines of development. These benign tumors are more common in females than males (11). Surgical removal is the only effective treatment, and complete resection is necessary for successful management.

Clinical Findings Congenital dermoid inclusion cysts can be subdivided into two groups, those involving the orbital/periorbital area (including


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D FIGURE 29.6. Dermoid sinus/cysts. A: Infected dorsal nasal dermoid sinus after local attempt at excision; this lesion extended intracranially. B: Patent foramen cecum in anterior skull base that transmitted dermoid sinus intracranially. C: Bifid crista galli on coronal CT scan. D: Intraoperative photograph of intracranial extension of nasal dermoid sinus cyst after “keystone” portion of supraorbital bar was removed.

the midline lower forehead) and those involving the nasal area. The lesions typically present at birth as firm, but not hard, nodular lesions involving the upper lateral orbital rim or the central forehead above the nose that slowly increase in size. They range in size from a few millimeters to a few centimeters, but most are between 1 and 2 cm in diameter. In lesions in the orbital and lower forehead areas, the presence of an external ostium or punctum is uncommon, whereas in the nasal dermoid lesions the presence of a punctum occurs frequently. In a recent large series of patients, 80% of the lesions in this series were located in either the upper lateral orbit or the upper lateral orbital rim (11); 10% of the lesions involved the upper medial orbit. The nasal lesions account for approximately 5% to 10% of all dermoid lesions, and have a distinct clinical presentation and a distinct etiology. Nasal dermoid cyst/sinuses are typically located in the midline and they can have multiple presentations, including nasal pits, hair growth within a punctum,

intermittent drainage of sebaceous material, chronic draining sinus tracts, abscess, and soft-tissue infections, including cellulitis. They can also present as recurrent lesions after failed incision and drainage procedures (Fig. 29.6A).

Etiology and Pathogenesis The etiology of orbital and periorbital congenital dermoid inclusion cysts is thought to be related to migrating tissue being “trapped” below the surface along lines of embryologic fusion as embryologic development progresses. Dermoid inclusion cysts are distinguished from simple epidermoid inclusion cysts by the presence of dermis and skin adnexa in the wall of the lesion. Because the cysts have skin adnexa present, the cysts or sinuses can contain cellular debris, sebum, and hair. The lesions subsequently enlarge over time.

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The etiology of nasal dermoid inclusion cysts and sinuses is distinct from that of orbital or periorbital dermoids. Although three separate theories have been advocated to account for these nasal dermoid sinus/cysts, the one that has been most often acknowledged is the “nasocranial deep trilaminar” theory. During normal embryogenesis the nasal and frontal bones develop by intramembranous ossification, but remain separated by a small fontanelle called the fonticulus nasofrontalis. A prenasal space between the nasal bones and cartilaginous nasal capsule extends from the skull base to the nasal tip. Dura extends through the fonticulus nasofrontalis, into the prenasal space, and comes into contact with skin. Normally, the dura and skin separate as the nasal process of the frontal bone grows. The dura recedes and the fonticulus nasofrontalis and foramen cecum fuse, forming the cribriform plates. Nasal dermoid cysts and sinuses are formed when the dura remains fused to the overlying skin, instead of separating. As the dura recedes intracranially, it pulls ectodermal tissue with it, most frequently along the tract through the foramen cecum. A sinus tract is formed when the misplaced dermal and epidermal lined tract maintains a connection with the skin, whereas a cyst is formed when ectoderm is trapped without egress to the skin, trapping the sloughed contents below the surface.

Treatment Complete surgical removal of these benign lesions is the only successful therapeutic strategy. For the 90% of these lesions that are located in the orbital or forehead areas, no preoperative diagnostic evaluation is warranted. The lesions can be approached through a supratarsal fold upper-eyelid incision. Dissection is carried through the orbicularis muscle and directly down onto the cyst wall. The dissection then meticulously proceeds on the cyst wall around the lesion. The lesions are frequently below the periosteum, so incision of this slightly tougher layer must occur as part of the complete excision of the cyst. For the 10% of these lesions that are true nasal dermoids, the critical issue in management is to establish whether or not there is intracranial extension of the cyst/sinus. The midline location is a harbinger of the potentially more complicated problem. If the lesion extends intracranially, a formal craniotomy is often necessary. Preoperative imaging with fine-cut computed tomography (CT) scan through the anterior cranial base is essential and can differentiate whether there is a patent foramen cecum and a bifid crista galli present, two signs of intracranial extension (Fig. 29.6B and C). Although the presence of a bifid crista galli and an open cecum does not confirm intracranial extension, it is agreed that a normal size and appearance of the crista galli and foramen cecum rules out intracranial extension. If the CT findings are positive, an MRI may provide additional insight. If the MRI is positive with an obvious intracranial extension, then surgical planning should include neurosurgical involvement and a formal craniotomy. If a coronal incision and formal craniotomy are required, then the majority of the dissection and retrieval should be accomplished from the coronal approach. This can be facilitated by outfracture of the “keystone” portion of the supraorbital bar (12) (Fig. 29.6D). If the MRI findings are equivocal or absent but the CT findings are positive, a frequent clinical scenario, then planning should still include the possible need for a craniotomy and neurosurgical consultation and evaluation. In this case, the nasal lesion can be approached by an incision around the lesion and dissection cephalad, or through an open rhinoplasty approach with a small incision around the base of the nasal punctum. The dissection proceeds cephalad, meticulously dissecting the stalk of the lesion dorsal to the cartilage but deep to the nasal bones. If the stalk can be completely removed, there

is no need for the craniotomy. Otherwise, the craniotomy is required to ensure complete removal (Fig. 29.6D). Recurrence rates have been reported to be as high as 12%, and incomplete removal can be associated with complications such as infection and osteomyelitis.

NEUROFIBROMATOSIS Neurofibromatosis is common, with an estimated 100,000 cases in the United States alone. The disorder can involve both the central and peripheral nervous systems. The clinical hallmark of the disorder is the development of multiple cutaneous and subcutaneous nodular tumors. The disease has protean manifestations, a variable age of onset, a variable presentation, variability in clinical findings, and a variable but progressive course. Over the past 20 years, our understanding of neurofibromatosis has advanced significantly. Critical to this advance was a National Institutes of Health Consensus Statement in 1987 that established the diagnostic criteria for “peripheral neurofibromatosis,” now known as neurofibromatosis-1, and “central neurofibromatosis,” now known as neurofibromatosis-2 (Table 29.1). Although refinements of these criteria have been proposed, the establishment of the criteria in 1987 effectively focused thought about neurofibromatosis throughout the world. Surgical resection remains the mainstay of treatment for enlarging or symptomatic tumors. TA B L E 2 9 . 1 CLINICAL DIAGNOSTIC CRITERIA FOR NEUROFIBROMATOSIS 1987 National Institutes of Health Consensus Conference Neurofibromatosis-1 Diagnostic criteria are met in an individual if two or more of the following are found: • Café-au-lait spots (six or more larger than 5 mm in greatest dimension in prepubertal individuals and larger than 15 mm in postpubertal individuals) • Two or more neurofibromas of any type or one plexiform neurofibroma • Freckling in the axillary or inguinal region • Optic glioma • Two or more Lisch nodules (hamartomas of the iris) • A distinctive osseous lesion such as sphenoid wing dysplasia or thinning of long bone cortex with or without pseudoarthrosis • A first-degree relative (parent, sibling, or offspring) with neurofibromatosis-1 by the above criteria Neurofibromatosis-2 Diagnostic criteria are met in an individual who has: • Bilateral eighth nerve masses seen with appropriate

imaging techniques • A first-degree relative with neurofibromatosis-2 and

either: 1. Unilateral eighth nerve mass, or 2. Two or more of the following • Neurofibroma • Meningioma • Glioma • Schwannoma • Juvenile posterior subcapsular lenticular opacity


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Clinical Presentation Plastic surgeons and craniofacial surgeons are primarily concerned with the manifestations of neurofibromatosis-1 (NF1). The clinical presentation of is most commonly heralded by the appearance of café-au-lait spots. These lesions are cutaneous hyperpigmented areas, typically 20 to 30 mm in diameter, with greater than six lesions found in 90% to 99% of all cases (11). These lesions can be difficult to differentiate from congenital nevi, but this can be accomplished by a punch biopsy. Most children present with café-au-lait spots as the earliest and as the only manifestation of NF-1, but more than 80% will develop additional signs of the disorder. Axillary freckling generally appears before age 5 years and is seen in approximately 80% of all cases of NF-1 (13,14). Lisch nodules are pigmented, dome-shaped nodules seen on the surface of the iris that are best seen by ocular exam with slitlamp microscopy. They usually have an onset by 10 years of age and are present in nearly all NF-1 cases by 20 years of age. The NF-1 gene is a tumor-suppressor gene that regulates cell proliferation, and intracranial tumors are frequent occurrences in these NF-1 patients. Optic pathway gliomas are the most common central nervous system tumors, occurring in ap-

proximately 15% of cases, and are histologically identified as low-grade pilocytic astrocytomas (13,14). NF-1 patients also have an increased incidence of brainstem gliomas, as well as an apparent increase in the occurrence of benign and malignant astrocytomas, ependymomas, meningiomas, medulloblastomas, and malignant schwannomas. Skeletal abnormalities associated with NF-1 include sphenoid wing aplasia, macrocephaly, scoliosis, and thinning of long bone cortex, causing anterior tibial bowing. The sphenoid wing aplasia is present in 5% to 7% of NF-1 cases and is characterized by unilateral agenesis of the greater wing of the sphenoid (Fig. 29.7A and B). This agenesis creates a large communication between the middle temporal fossa and the orbit, and can lead to ocular proptosis, pulsatile exophthalmos, and exposure problems for the eye. It can also be associated with neurofibromas within the cone of periocular tissues. Neurofibromas, the hallmark of the NF-1 disease, are nerve sheath tumors that arise anywhere along a nerve sheath from the dorsal root ganglion to the terminal nerve branches (13,14). They are composed of Schwann cells, fibroblasts, mast cells, and perineural cells. Neurofibromas occur in five main types: localized cutaneous neurofibromas, diffuse cutaneous neurofibromas, localized intraneural neurofibromas, massive soft-tissue neurofibroma, and plexiform neurofibromas.

B A

D

C FIGURE 29.7. Neurofibromatosis. A: Three-dimensional CT scan demonstrating large defect in sphenoid wing. B: Coronal CT scan of orbit revealing expanded orbit, vertical dystopia, and intraorbital neurofibromas. C: Postoperative three-dimensional CT scan showing decrease in size of aperture between orbit and middle fossa. This aperture allows passage of the ophthalmic nerve and contents of the superior orbital fissure. D: Postoperative CT scan showing titanium and bone graft composite reconstruction of posterior sphenoid wing. E: Massive plexiform neurofibromatosis of right face showing significant overgrowth with extensive distortion evident on frontal view. F: Postoperative result following staged resection and suspension of soft tissue from zygomatic arch using sutures and fascia lata suspension. The recurrent laxity is evident.

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E

F FIGURE 29.7. (Continued )

Plexiform neurofibromas are virtually unique to NF-1 and are composed of nerve sheath cells that proliferate along the length of a nerve. Plexiform neurofibromas are frequently associated with hypertrophy of the soft tissue and hyperpigmentation or hypertrichosis of the overlying skin. Their growth can cause destruction or compression of local tissue, causing significant morbidity. Plexiform lesions occur in 16% to 40% of patients with NF-1, and are found on the trunk in 43% to 44%, the extremities in 15% to 38%, and the head and neck in 18% to 42% of patients (15). Craniofacial plexiform neurofibromas most frequently involve the second and third divisions of the fifth cranial nerve and each occur in approximately 5% of patients with NF-1. In contrast to the other types of neurofibromas, these plexiform neurofibromas are believed to be congenital in origin, and usually become clinically evident by 2 years of age. Their growth is unpredictable, but occurs frequently during early infancy and times of hormonal change such as preadolescence/adolescence and pregnancy. Craniofacial neurofibromas cause significant facial disfigurement. Malignant degeneration of peripheral nerve sheath tumors is more frequent than may be appreciated by conventional wisdom, occurring in up to 13% of patients with NF-1 (16). Malignant peripheral nerve sheath tumors, which were formerly known as neurosarcomas or malignant schwannomas, arise from Schwann cells. More than 50% of patients with malignant nerve sheath tumors have NF-1. Only the plexiform neurofibromas have a high propensity for malignant degeneration. Medium and large nerves, such as those involving the thigh, the buttock, the brachial plexus, and the paraspinal nerves, are most frequently involved. Pain is the most reliable indicator of malignant degeneration. Prompt medical attention is warranted and surgical biopsy is indicated. Once diagnosed, management consists of an aggressive attempt at total surgical resection. Metastases are common. Malignant soft-tissue neo-

plasms occur approximately 34 times more frequently than in a control group, and accounted for 9.4% of the deaths of patients with NF-1 (11). Despite treatment, the 5-year survival rate of malignant peripheral nerve sheath tumors is estimated to be between 16% and 52%.

Etiology and Pathogenesis Plastic surgeons and craniofacial surgeons are primarily concerned with the manifestations of NF-1, which is more than 10 times more common than neurofibromatosis-2 (NF-2). The gene for NF-1 has been localized to band 11.2 of the long arm of chromosome 17, clearly distinct from that for NF-2, which has been localized to the middle of the long arm of human chromosome 22. NF-1 is transmitted as an autosomal dominant disorder with variable penetrance and expressivity. Families must be counseled that there is a 50% chance of an affected individual having an affected child.

Treatment The craniofacial problems associated with NF-1 typically are of two types: the orbitopalpebral neurofibromas associated with sphenoid wing dysplasia (cranio-orbital neurofibromatosis) and the plexiform neurofibromas involving the soft tissue of the face, largely in the distribution of the trigeminal nerve. These two types may exist together in the same patient, but most frequently occur separately. Several core issues must be addressed in treatment planning. First, the surgery is treating the deformity only. The underlying process of neurofibromatosis remains, and the recurrence of the neurofibromas is common. Second, both the timing of surgery and the extent of surgery must be carefully considered. Third, neurofibromas of



the face and cranio-orbital region tend to bleed significantly during surgery, the bleeding is difficult to control with electrocautery, and blood loss can be substantial. Jackson reported the option of packing the facial wound open with compression, and returning in 48 hours to complete the operation (17). Appropriate patient monitoring and intravenous access must be a component of preoperative planning, and consideration should be given to hypotensive anesthesia (17,18). Fourth, the resected tumor is prone to recurrence. The soft tissue of the face in neurofibromatosis, including the skin, ligaments, tendons, and subcutaneous tissues, appears to have a decreased tensile strength, and there is a strong tendency toward stretch and “relaxation,” with recurrence of the original deformity. Finally, the surgical management of this disorder must balance aesthetic outcome with the preservation of function. While these considerations are acknowledged, surgery is the most powerful tool for helping these patients, and these patients are often extremely grateful and appreciative of surgical intervention, even though the aesthetic result may be less than the surgical team had desired. Surgical approaches vary from limited surgery at intervals to massive “one-stage” surgical resections of the involved tissues. It is likely that the optimal approach lies somewhere between these two ends of the spectrum, and should be decided by the surgeon based on the degree of the deformity and in consultation with the patient and family.

Management of Cranio-Orbital Disorders The orbital-palpebral neurofibromas associated with sphenoid wing dysplasia form a discrete subtype of neurofibromatosis, frequently described as cranio-orbital neurofibromatosis (17–19). The principal findings in this disorder are pulsatile exophthalmos, an enlarged bony orbit, orbital neurofibroma, dysplasia or aplasia of the sphenoid wing with the presence of a herniation of the temporal lobe into the orbit, and a bulging temporal fossa. In addition to the exophthalmos, there is also frequently vertical dystopia of the globe. Overall, cranioorbital-temporal neurofibromatosis has been found to exist in from 1% to 10% of patients with NF-1. Although several etiologies have been advocated for the sphenoid dysplasia, including a direct effect of the orbital neurofibroma on the bone versus a congenital mesodermal maldevelopment with defective ossification of the sphenoid bone, the etiology of the sphenoid defect has not been clearly demonstrated. The management of the orbital structures is one of the most complex issues in neurofibromatosis. In most cases, when vision exists in the afflicted eye, although potentially compromised, the eye is preserved. In patients with functional vision, Jackson approaches mild cases with little change in orbital volume through the upper eyelid, whereas in cases with significant bony enlargement, he recommends use of a coronal flap, and a C-shaped osteotomy through the lateral orbital wall, zygoma, and horizontally through the maxilla below the inferior orbital nerve. The neurofibroma is resected through either approach, although he notes that it may be inadvisable to remove the tumor completely in the plexiform variety where there is significant involvement of the neuromuscular structures, as this may cause a disturbance of eye movement and resultant diplopia. The sphenoid wing is reconstructed with a bone graft, using either split-rib grafts or cranial bone graft. The greatly stretched levator aponeurosis is repaired directly to the tarsal plate, but Jackson cautions against excess shortening of the levator aponeurosis and also against excess skin resection. In patients with a loss of vision, an orbital exenteration is performed. The temporal lobe is reduced into the middle cranial fossa, and the entire defect in the sphenoid wing is reconstructed using a bone graft. The eyelid skin is invaginated

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into the orbit and used as skin cover. Once healing is complete, the orbital defect is fitted with prosthesis. An alternative way to approach these ocular problems is through the use of a coronal incision and a frontal craniotomy. The incision placement can be selected to allow for a forehead lift and direct excision of skin in those cases with involvement of the forehead and eyebrow and resultant ptosis of the eyebrow. The supraorbital bar and orbital roof are removed, allowing both direct exposure of the entire orbit and the opportunity to reposition the supraorbital bar in cases of dystopia or orbital volume change. The coronal approach allows for excellent visualization and separation of the dura from the periorbital structures. It also allows favorable visualization as dissection proceeds medially and the ophthalmic nerve and vessels are approached. The cranial bone graft is cut precisely and placed to allow for separation of the middle cranial fossa from the orbital contents, minimizing the area of defect that must remain to allow passage of the ophthalmic nerve and contents that usually pass through the superior orbital fissure (Fig. 29.7B and C). Many surgeons have commented about the tendency for these grafts to absorb over time, and the use of a “composite” graft of cranial bone and titanium mesh is often useful to tolerate the pulsations of the brain and provide osseous healing and stability (Fig. 29.7D). As difficult as the skeletal reconstruction may be, the softtissue structures are problematic as they appear to have a decreased tensile strength, tending to stretch and “relax” and recreate the original deformity. The management of the medial and lateral canthal structures is performed using standard techniques, but it should be noted that these tissues are subject to relaxation and, therefore, relapse (18). Similarly, this same problem can occur with the ptosis correction, which frequently must be repeated. One must avoid the temptation to overcorrection of the ptosis, as a foreshortened eyelid with ocular exposure is a disastrous complication. It is much better to repeat the surgery and repair the levator aponeurosis again. As is true of many aspects of management of neurofibromatosis, improvement can be significant, but correction is both difficult to achieve and harder to maintain.

Management of Plexiform Neurofibromas of the Face Plexiform neurofibromas involving the face typically involve either the temporal fossa, or originate from one or more divisions of the trigeminal nerve. Grabb et al. have said that neurofibromas “are woven into the normal fabric of the face and usually defy all but partial treatment.” The plexiform neurofibromas that originate from one or more divisions of the trigeminal nerve cause significant distortion of the facial soft tissue and skeletal framework. The characteristic overgrowth of the soft tissue leads to distortion of the eyebrow, thickening of the eyelids, ptosis, visual obstruction, dysconjugate gaze, glaucoma, ectropion, and can lead to visual loss. Epiphora is frequently present. The cheek is usually grossly involved and ptotic. There can be hypertrophy of the nose and distortion of the nasal soft and cartilaginous tissue (Fig. 29.7E and F). There can be significant dental involvement and distortion of the maxillary and mandibular occlusal plane. Plexiform infiltration of the mandibular division of the trigeminal nerve can lead to compromise of buccal, oropharyngeal, and retropharyngeal tissue causing speech apraxia and oropharyngeal dysfunction. These patients can have such profound disfigurement that they suffer from profound psychosocial problems related to the facial deformity, and they can be desperate for any improvement in appearance.

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Surgical management of neurofibromatosis of the temporal fossa needs to include a careful assessment of risks and expected outcomes. These are benign tumors that seldom cause major problems in this location. Certainly, the simple presence of a neurofibroma in this location, as elsewhere, does not warrant surgery. Many times there is a simple, subtle enlargement of the soft tissue of the temporal fossa. If pain and considerable enlargement supervene, then surgery can be considered. Occasionally, these lesions will cause deformity of the mandible and maxilla by a mass effect. The temporalis muscle can be densely infiltrated by the neurofibromas. The caveat of blood loss during these procedures in NF-1 patients must be acknowledged and planned for in these corrective skeletal procedures. Following resection, the most obvious problem is frequently a soft-tissue deficiency. Reconstruction can be performed using microvascular free tissue transfer, dermal-fascial-fat grafts, or onlay of the skull using bone substitutes. The exact method for reconstruction depends on the severity of the soft-tissue deficit, with free tissue transfer typically being reserved for larger deficiencies. Soft-tissue plexiform neurofibromas of the forehead can be approached through a coronal or “hairline” frontal incision. These approaches allow excellent exposure, and can be used to lift the redundant skin vertically as needed, thereby allowing correction of eyebrow ptosis. Separate incisions may be necessary to address orbital changes. Surgery to correct the hypertrophy of the cheek, nose, and lips should follow skeletal correction, if this is planned. Similar to the principles for reconstruction of congenital defects, the skeletal framework correction should be performed first. In general, this consists of reduction of osseous structures with leveling of the occlusal plane through modifications of standard orthognathic approaches and techniques. The correction of the soft tissue of the cheek, nose, and lip can then be undertaken. The redundancy of the cheek skin can be approached through a facelift incision/approach or a Weber-Ferguson approach. If the facelift incision is used, every attempt should be made to preserve the function of the facial nerve. Although many of the facial muscles may have limited function as a result of involvement by a neurofibroma, the nerve should be preserved wherever possible. Direct full-thickness excision of redundant tissue is necessary. The skin incisions usually heal very favorably and do not tend to be either prominent or noticeable after surgery. The tendency toward relapse should be counteracted by using permanent sutures to anchor the tissue to the bony skeleton at the zygomatic arch and wherever possible. In severe cases of redundancy, it may be worthwhile considering the use of tensor fascia lata slings to suspend the soft-tissue structures and minimize the tendency toward relapse of the position of the soft tissue. In cases with significant redundancy of the soft tissue, facial animation may not occur to any appreciable extent, and static suspension of the soft tissues is appropriate and yields a

significant clinical improvement. The redundancy of the tissue of the lip and nose should be addressed through direct excision. Both vertical and horizontal excisions may be necessary to obtain the desired position of these structures, and considerable improvement can reliably be obtained. Surgery for plexiform neurofibromas of the face must consider the initial deformity, the blood loss, the aesthetics of the expected result, and the likely durability of that result, given the laxity of the soft tissues and the tendency toward recurrence of the deformity. Surgery can provide tremendous improvement both aesthetically and functionally. Although we can seldom provide complete correction, amelioration is a desirable and significant goal.

References 1. Chen Y-R, Breidahl AMS, Chang C-N. Optic nerve decompression in fibrous dysplasia: indications, efficacy, and safety. Plastic Reconstr Surg. 1997; 99(1):22. 2. Sassin JF, Rosenberg RN. Neurologic complications of fibrous dysplasia of the skull. Arch Neurol. 1968;18:363. 3. Gorlin RJ, Cohen MM, Levin LS. Syndromes of the head and neck. 3rd ed. Oxford, England: Oxford University Press; 1990:642. 4. Harrison DH. Facial reanimation in children with Mobius syndrome after segmental gracilis muscle transplantation (discussion). Plastic Reconstr Surg. 2000;106:9. 5. Zuker RM, Goldberg CS, Manktelow RT. Facial animation in children with Mobius syndrome after segmental gracilis muscle transplant. Plastic Reconstr Surg. 2000;106:1. 6. Pensler JM, Murphy GF, Mulliken JB. Clinical and ultrastructural studies of Romberg’s hemifacial atrophy. Plastic Reconstr Surg. 1990;85:6669. 7. Upton J, Albin RE, Mulliken JB, et al. The use of scapular and parascapular flaps for cheek reconstruction. Plastic Reconstr Surg. 1992;90:959. 8. Posnick JC, Goldstein JA, Waitzman A. Surgical correction of the Treacher Collins malar deficiency: quantitative CT scan analysis of long term results. Plastic Reconstr Surg. 1993;92:12. 9. Siebert JW. Unpublished findings. 10. Kaban LB, Moses MH, Mulliken JB. Surgical corrections of hemifacial microsomia in the growing child. Plastic Reconstr Surg. 1980;82:9. 11. Barlett SP, Lin KY, Grossman R, et al. The surgical management of orbitofacial dermoids in the pediatric patient. Plastic Reconstr Surg. 1993;91: 1208. 12. van Aalst JA, Luerssen TG, Whitehead WE, et al. “Keystone” approach for intracranial nasofrontal dermoid sinuses. Plastic Reconstr Surg. 2005;116:13. 13. Friedman JM. Neurofibromatosis 1: clinical manifestations and diagnostic criteria. J Child Neurol. 2002;17:548. 14. Young H, Hyman S, North K. Neurofibromatosis 1: clinical review and exceptions to the rules. J Child Neurol. 2002;17:613. 15. Rosser T, Packer RJ. Neurofibromas in children with neurofibromatosis 1. J Child Neurol. 2002;17:585. 16. Rasmussen S, Yang Q, Friedman J. Mortality in neurofibromatosis 1: an analysis using U.S. death certificates. Am J Med Genet. 2001;68:1110. 17. Jackson IT. Neurofibromatosis of the skull base. Clin Plast Surg. 1995; 22(3):513. 18. Poole MD. Experiences in the surgical treatment of cranio-orbital neurofibromatosis. Br J Plast Surg. 1989;72:155. 19. Jackson IT, Laws ER, Martin RD. The surgical management of neurofibromatosis. Plastic Reconstr Surg. 1983;71:751.


CHAPTER 30 ■ OTOPLASTY AND EAR RECONSTRUCTION CHARLES H. THORNE

PROMINENT EARS The term prominent ears, for the purposes of this chapter, refers to ears that, regardless of size, “stick out” enough to appear abnormal. When referring to the front surface of the ear, the terms front, lateral surface, and anterior surface are used interchangeably. Similarly, when referring to the back of the auricle, the terms back, medial surface, and posterior surface are used synonymously. The normal external ear is separated by less than 2 cm from, and forms an angle of less than 25 degrees with, the side of the head. Beyond these approximate normal limits, the ear appears prominent when viewed from either the front or the back.

Anatomic Causes of Prominent Ears To correct prominent ears, the anatomic abnormality must be determined (Fig. 30.1). The three most common causes of prominent ears may be present alone or in combination: 1. Underdeveloped antihelical fold. As a result of inadequate folding of the antihelix, the scapha and helical rim protrude. This anatomic abnormality causes prominence of the upper third and, in many cases, the middle third of the ear. 2. Prominent concha. The concha may be excessively deep, the concha/mastoid angle may be excessive, or there may be a combination of these two factors. This anatomic abnormality causes prominence of the middle third of the auricle. 3. Protruding earlobe. The protruding earlobe causes prominence of the lower third of the ear. Although most prominent ears are otherwise normal in shape, some prominent ears have additional deformities. The conditions enumerated below are examples of abnormally shaped ears that may also be prominent. The term macrotia refers to excessively large ears that, in addition to being large, may be “prominent.” Constricted ears (Fig. 30.2) are abnormally small but tend to appear “prominent” because the circumference of the helical rim is inadequate, causing the auricle to cup forward. The Stahl’s ear deformity (Fig. 30.3) consists of a third crus, in addition to the crura of the triangular fossa, which traverses the scapha. This may give the ear a “Mr. Spock” pointed appearance in addition to being prominent. Cryptotia (Fig. 30.4) describes the auricle in which the upper pole of the helix is buried beneath the temporal skin. Question mark ears earn their name because deficiency of the supralobular region gives the ear the shape of a question mark.

Goals of Otoplasty The goal of otoplasty is to set back the ears in such a way that the contours appear soft and natural, the setback is harmonious and there is no evidence of surgical intervention. When examined from the various angles, the corrected auricle should have the following characteristics: 1. Front view. When viewed from the front the helical rim should be visible, not set back so far that it is hidden behind the antihelical fold. 2. Rear view. When viewed from behind, the helical rim should be straight, not bent like a “C” or a “hockey stick.” If the helical rim is straight, the setback will be harmonious; that is, the upper, middle, and lower thirds of the ear will be setback in correct proportion to each other. If, for example, the middle third is set back too much relative to the upper and lower thirds, the helical rim will form a “C” when viewed from behind, creating the so-called telephone deformity. Similarly, if the earlobe is insufficiently set back, the rear view will reveal a hockey stick appearance to the helical rim contour. 3. Lateral view. The contours should be soft and natural, not sharp and “human-made.”

Timing of Otoplasty There is no absolute rule about when otoplasty should be performed. In young children with extremely prominent ears, a reasonable age is approximately 4 years. In cases of macrotia associated with prominence, the author has performed the procedure as early as age 2 years, thinking that any restriction of growth is an advantage. Regardless of the exact age, the procedure requires general anesthesia. In other cases, usually more minor, the parents may choose to wait until the child can participate in the decision. This may allow the procedure to be performed under local anesthesia, although it is a rare child that can tolerate local anesthesia before age 10 years, and many not until they are adults.

Operative Procedure Numerous methods have been described for correcting the anatomic abnormalities described above. The techniques that have stood the test of time are the simplest, most reliable, and least likely to cause complications or an “operated” look. The techniques described below are used alone or in combination depending on the anatomic deformity and the choice of the surgeon.


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FIGURE 30.1. Comparison of normal and prominent ear anatomy. A: Normal ear. B: Components of the prominent ear. (Reproduced with permission of Charles H. Thorne, MD. Copyright Charles H. Thorne, MD.)

Antihelical Fold Manipulation ■

Suturing of cartilage. Mattress sutures are placed from the scapha and/or triangular fossa to the concha, as described by Mustarde, and are tied with sufficient tension to increase the definition of the antihelical fold, thereby setting back the helical rim and scapha (Fig. 30.5).

■

■

Stenstrom technique of anterior abrasion. The anterior surface of the antihelical fold cartilage is abraded, causing the cartilage to bend away from the abraded side (principle of Gibson) toward the side of intact perichondrium (Fig. 30.6). Full-thickness incisions. A single full-thickness incision along the desired curvature of the antihelix permits folding with slight force, creating an antihelical fold (Luckett procedure). Because the fold is sharp and unnatural

A

B FIGURE 30.2. Constricted ear. A: Mildly constricted ear. Otoplasty requires increasing the circumference of the helical rim by advancing the crus of the helix into the helical rim (see Fig. 30.7). B: Severely constricted ear. This degree of constriction can only be repaired by discarding some of the cartilage and performing an ear reconstruction as in microtia. (Courtesy of David Furnas, MD.)


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Chapter 30: Otoplasty and Ear Reconstruction

Conchal Alteration ■

■

■

Suturing. The angle between the concha and the mastoid skull can be decreased by placing sutures between the concha and the mastoid fascia as described by Furnas (Fig. 30.5). Conchal excision. From either an anterior or posterior approach, a full-thickness crescent of cartilage is removed from the posterior wall of the concha (taking care not to violate or deform the antihelical fold), thereby reducing the conchal height. The conchal defect is meticulously closed with sutures to avoid a visible ridge within the concha. The excision is designed so that the eventual closure will lie at the junction of the floor and posterior wall of the concha where it is least conspicuous and causes the least distortion of the normal auricular contours (Fig. 30.5). A combination of Furnas suture and Conchal excision techniques (Fig. 30.5).

Correction of Earlobe Prominence

FIGURE 30.3. Stahl’s ear. Note the third crus that traverses the scapha. (Courtesy of David Furnas, MD.)

appearing, this single-incision technique was modified. In the Converse/Wood-Smith technique, a pair of incisions is made, parallel to the desired antihelical fold, and tubing sutures are placed to create a more defined fold.

Earlobe prominence is not corrected by the above maneuvers. In fact, these maneuvers may increase the prominence of the earlobe, making earlobe repositioning the most difficult and neglected part of the procedure. An auricle that has been repositioned in its upper two thirds but still has a prominent lobule will appear just as abnormal and disharmonious as the original deformity. It has been said that suturing the tail of the helical cartilage to the concha will correct earlobe prominence. Unfortunately the tail of the helix does not extend into the lobule and setting it back does not reliably set back the earlobe. Other authors have described techniques involving skin excision and sutures between the fibrofatty tissue of the lobule and the tissues of the neck. The best technique in the author’s experience is the technique described by Gosain, or a variation

A

B FIGURE 30.4. Cryptotia. A: Patient in whom a relatively normal helical rim is buried in the temporal soft tissues. The upper portion of the auricle can be exposed by outward traction on the ear. B: Outward traction (in a different patient) causes the upper portion of the ear to emerge from its hiding place. (Courtesy of David Furnas, MD.)


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FIGURE 30.5. Otoplasty technique. The combination of a Mustarde scapha-conchal suture, conchal resection with primary closure, and a Furnas conchal-mastoid suture. Note that the conchal closure is at the junction of the floor and posterior wall of the concha. A: Sutures placed. B: Sutures tightened to create the desired contour. C: Same sutures as seen through the retroauricular incision. (Reproduced with permission of Charles H. Thorne, MD. Copyright Charles H. Thorne, MD.)

thereof, in which skin is excised on the medial surface of the earlobe. When this defect is closed with sutures, a bite of the undersurface of the concha is taken, which pulls the earlobe toward the head.

Alteration of the Position of the Upper Auricular Pole Depending on the degree of prominence preoperatively of the upper third of the ear, the antihelical fold creation may be inadequate to correct the position of the helical rim, near the root

of the helix. An additional mattress suture between the helical rim and the temporal fascia may be required.

Choice of Otoplasty Technique The final operative plan for an otoplasty is a combination of surgical maneuvers based in part on the anatomic diagnosis of the deformity, and in part on the surgeon’s personal preferences. The author’s preferred technique involves Mustarde sutures to recreate the antihelix and setback the upper and middle thirds of the ear. The abrasion techniques are unreliable, uncontrollable, and unnecessary and may result in sharp edges or an overdone appearance. In the conchal region, the author frequently uses both a conchal resection and Furnas conchal mastoid sutures as shown in Figure 30.5. The combination allows the resection to be small (1–2 mm), minimizing iatrogenic deformity. When conchal excision is used alone, a deformity of the posterior wall of the concha may result. When Furnas sutures are used alone the correction may be inadequate, the patient may have pain, the external auditory canal can be narrowed, and the depth of the retroauricular sulcus is decreased. As mentioned above, earlobe repositioning is the most difficult part of the procedure. The Webster technique of repositioning the helical tail has not been effective in the author’s hands for correction of earlobe prominence. Rather, the Webster technique appears to reposition the ear just above the earlobe, exaggerating the earlobe prominence.

Other Deformities

FIGURE 30.6. Stenstrom technique. The antihelical fold is scored. The cartilage bends away from the scoring, moving the helical rim closer to the head and increasing the prominence of the antihelix.

Macrotia. To reduce the size of the ears, the incision is made on the lateral surface of the ear, just inside the helical rim. The scapha is reduced and a segment of helical rim is excised and closed primarily to avoid redundancy. Constricted ear. In mild cases, the crus of the helix is advanced out of the concha and into the helical rim and standard otoplasty techniques are used in addition (Fig. 30.7). In severe cases, the cartilage is discarded and a complete auricular reconstruction performed as in microtia. Stahl ear. Various techniques have been described to excise the extra crus. None is perfect. Cryptotia. The superior aspect of the auricular cartilage is pulled out from under the scalp (Fig. 30.4), an incision is made



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FIGURE 30.7. Antia-Buch helical advancement. A: An incision is designed inside the helical rim and around the crus of the helix. B: The incision is made through the skin and the cartilage, but not through the posterior skin. The helical rim is advanced to allow closure and a dog-ear of skin (dotted line) is removed on the back of the ear. C: Closure showing the crus of the helix advanced into the helical rim. (Reproduced with permission of Charles H. Thorne, MD. Copyright Charles H. Thorne, MD.)

around the now-visible helical rim, and the medial surface of the freed cartilage is resurfaced with a graft or flap. In some cases, the buried cartilage is quite normal, and in other cases, it is markedly abnormal. Question mark ear. The deficiency is variable and is usually treated with a cartilage graft and a V-Y advancement flap from the retroauricular skin. Often there is excess in the upper third of the ear requiring reduction. In severe cases, the entire ear is reconstructed as in microtia.

Postoperative Care A bulky, noncompressive dressing is placed for a few days. Excessive pressure from the dressing will cause pain, increase swelling, and may lead to abrasion or even necrosis of auricular skin. When the dressing is removed, the patient wears a loose headband at night for 6 weeks. Again, the headband should only be tight enough that it does not fall off. The purpose is to prevent the corrected ear from being pulled forward when the patient rolls over in bed. A tight headband can erode the lateral surface of the ear, creating an open wound.

Nonoperative Technique in Infants During the early weeks of infancy, the auricular cartilage has unusual plasticity, attributed to circulating maternal estrogens. During this privileged period, prominent ears and related deformities can be corrected permanently by molding the ears into the correct shape with tape and soft dental compound. The splints and tape are replaced regularly and the skin is checked compulsively for erosion. The process is continued for several months or until there is no further improvement in auricular contour. This ability to mold cartilage is currently being exploited in presurgical molding of the cleft nasal deformity (Chapter 23). It is not clear how long cartilage retains this “moldability” and therefore it is not clear when infants are too old to have this technique attempted.

Complications Hematoma. Hematomas are one of the few early complications of otoplasty. Excessive pain or bleeding necessitates immediate removal of the dressing to rule out and, if necessary, evacuate a hematoma.

Infection. Cellulitis is rare after otoplasty but is treated aggressively with intravenous antibiotics in an attempt to avoid chondritis. The latter may require debridement and leave the ear permanently disfigured. Suture complications. By far the most common complication of otoplasty in the author’s experience is related to suture extrusion in the retroauricular sulcus. Such sutures are easily removed but may be associated with unattractive and/or painful granulomas. The use of absorbable sutures might eliminate this complication but the author has not had the courage to abandon permanent sutures. Monofilament sutures are more likely to protrude but are less likely to create granulomas. Braided sutures are the opposite: Less likely to protrude but more likely to be associated with granulomas. Overcorrection/unnatural contours. The most common significant complication of otoplasty is overcorrection. Attention to the principles outlined above will minimize overcorrection and the creation of unnatural contours. My personal thoughts about otoplasty are as follows: 1. Incisions. The incision is best placed in the retroauricular sulcus, not up on the back of the ear. The latter is more convenient for the surgeon and more expeditious, but may leave a scar that is visible when the patient is viewed from behind. Specific indications (macrotia, constricted ear, or ears with inadequate helical rim) call for an incision on the front (lateral surface) of the ear, where it is ideally made just inside the helical rim. 2. Skin excision. Skin excision is unnecessary, does not contribute to the correction, and may lead to hypertrophic or undesirable scars. The only exception is the earlobe where it may be necessary. When performing the latter, care is taken to remove only enough skin, adjacent to the retrolobular sulcus, to allow repositioning and to leave a full, free earlobe for ear piercing and an aesthetically normal earlobe. 3. Techniques. The simplest techniques are best. Techniques that involve abrasion or full-thickness incisions and/or tubing to create the antihelical fold are unnecessary and should be avoided. 4. Choice of sutures. The author has returned to monofilament permanent sutures because of occasional granulomas associated with braided sutures such as Mersilene. A long-lasting monofilament suture such as polydioxanone suture (PDS) may be the best choice, but the author has no experience with this suture and therefore cannot credibly recommend it.


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5. Degree of correction. Overcorrection of the ears is the most common problem. Contours should be soft, round, and natural rather than sharp and surgical in appearance.

PARTIAL ACQUIRED DEFECTS Most auricular deformities are acquired, partial defects for which there is a good solution. The more superior on the ear the defect is located, the more choices there are for reconstruction. Reconstruction of the lobule is the most difficult and is aesthetically the most important. Although some defects can be closed by soft tissue alone, cartilage is frequently needed for support. For smaller defects, a conchal cartilage graft may suffice. However, for larger defects the rules of Firmin are extremely helpful: Defects that consist of 25% or more of the helical rim or involve more than two planes (i.e., involve antihelix as well as helix and scapha) will require rib cartilage for support. Conchal cartilage will not provide sufficient support in these cases.

Specific Regional Defects External Auditory Canal Stenosis is best treated by a full-thickness graft applied over an acrylic mold, provided a reasonable recipient vascular bed can be prepared. Occasionally, multiple Z-plasties are used to relieve webbing of the orifice, or a local flap is used to line the canal and break up the contracture. An acrylic stent is then used for several months to counteract the inexorable tendency toward contracture.

Helical Rim Acquired losses of the helical rim vary from small defects to major portions of the helix. The former, which usually result from tumor excisions or minor traumatic injuries, are best closed by advancing the helix in both directions, as described by Antia and Buch (Fig. 30.7). The success of this excellent technique depends first on freeing the entire helix from the scapha via an

incision in the helical sulcus that extends through the cartilage but not through the posterior skin. The posterior auricular skin is undermined, dissecting just superficial to the perichondrium until the entire helix is hanging as a chondrocutaneous flap on the posterior skin. Extra length can be gained by a V-Y advancement of the crus helix, as described in the correction of the constricted ear, and defects up to 2 cm can often be closed with moderate tension. The surgeon can “cheat” by removing some of the scaphal cartilage, which will take tension off the reapproximated helical rim. Although originally described for upper-third auricular defects, this technique is also effective for middle-third defects, as well as for defects at the junction of the middle and lower thirds. If the helical rim alone is missing, as may occur in burn injuries, a thin tube of retroauricular skin can be applied to the residual scapha with acceptable results (Fig 30.8). This is one example where cartilage may not be necessary. The disadvantage of this technique is that it requires three stages to “waltz” the tube into place: (a) formation of the tube in the sulcus, (b) transfer and insetting of one end of the tube, and (c) transfer and insetting of the other end of the tube.

Upper-third Defects Techniques available for upper-third defects in increasing order of size and complexity are as follows (Fig. 30.9): 1. Local skin flaps (Fig. 30.9A, B) 2. Helical advancement (Fig. 30.9C, D). 3. Contralateral conchal cartilage graft covered with a retroauricular flap (Fig. 30.9E, F). 4. Chondrocutaneous composite flap. (Fig. 30.9G, H). 5. Rib cartilage graft covered with retroauricular skin or temporoparietal flap/skin graft (see Fig. 30.11).

Middle-third Defects Techniques available for middle-third defects are as follows: 1. Primary closure with excision of accessory triangles (Fig. 30.10).

A,B

C,D FIGURE 30.8. Helical reconstruction with a thin caliber tube flap. A: Burn deformity of the helix. B: Construction of the tube flap in the retroauricular sulcus. C: Transfer of one end of the tube. D: Final result. (Courtesy of Burt Brent, MD.)



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E,F

G,H FIGURE 30.9. Four techniques for repairing upper-third auricular defects. A and B: Preauricular flap. The flap is transposed to repair a minor rim defect. C and D: Antia-Buch helical advancement. E and F: The combination of a retroauricular flap and conchal cartilage graft. G and H: Chondrocutaneous conchal flap to reconstruct the helical rim. Of the upper-third techniques, the only one not shown is a rib cartilage graft, which is shown in Figure 30.11. (Courtesy of Burt Brent, MD.)

2. Helical advancement. 3. Conchal cartilage graft and retroauricular flap. 4. Rib cartilage graft and retroauricular flap and/or temporoparietal flap (Fig. 30.11). Cartilage grafts can be inserted via the Converse tunnel procedure in which the skin is not detached at the junction of the

A

B

FIGURE 30.10. Wedge resection and primary closure with excision of accessory triangles. A: Wedge excision performed and accessory triangles designed. B: Closure of the defect. The accessory triangles help prevent the auricle from cupping forward. (Reproduced with permission of Charles H. Thorne, MD. Copyright Charles H. Thorne, MD.)

residual ear and the retroauricular skin. The problem is that precise placement of the graft with exact coaptation to remaining cartilage is difficult using this approach, and a detached retroauricular flap (Fig. 30.11) is often necessary. Middle-third auricular tumors are excised and closed by either a wedge resection with accessory triangles (Fig. 30.10) or a helical advancement, as previously described.

A

B

FIGURE 30.11. Reconstruction of a partial defect using rib cartilage framework and retroauricular flap. The technique is a workhorse for partial defects. A: The incision is designed. B: The cartilage has been placed and the flap closed over it. (Reproduced with permission of Charles H. Thorne, MD. Copyright Charles H. Thorne, MD.)


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Lower-third Auricular Defects Various techniques have been described to reconstruct earlobe defects using soft-tissue flaps. These techniques are not as effective as those that employ cartilaginous support. Like the alar rim, the normal earlobe does not contain cartilage. A reconstructed earlobe, however, maintains its shape better if cartilage is included, analogous to the nonanatomic alar rim grafts to the nose. The author prefers to use thin, flat cartilage obtained from the nasal septum. The cartilage is placed beneath the cheek/retroauricular skin in the first stage. In the second stage, an incision is made around the cartilage graft and the flap is advanced beneath the earlobe as in a facelift (Fig. 30.12).

MICROTIA Microtia literally means small ear. The simplicity of the term belies the vast complexity of this entity, both in terms of the variable clinical presentation and the difficulty of surgical reconstruction.

History Gillies is credited with the first use of rib cartilage for construction of an auricular framework in 1920. The importance of his contribution was temporarily obfuscated by several reports using allogeneic cartilage. The allogeneic cartilage, whether from a living donor such as the patient’s parent or preserved cadaver cartilage, always underwent gradual resorption. The modern era of auricular reconstruction began with Tanzer who reintroduced the technique of autogenous costal cartilage grafts as a method of auricular reconstruction.

Tanzer’s results inspired Brent who modified, improved, and standardized a four-stage technique of auricular reconstruction. Nagata developed a more complex technique that condensed microtia repair to two stages. The Nagata technique, requires more cartilage and the construction of a higher profile, more detailed framework than the Brent technique. Firmin analyzed those characteristics of a “Brent ear” that fall short of a normal ear and reported a large series using her modification of the Nagata technique. Although the technique of autogenous auricular reconstruction was evolving, silastic was also used, instead of rib cartilage, as the auricular framework. This material, as well as other artificial materials, led to a high incidence of extrusion. More recently, the use of porous polyethylene frameworks has been explored and has become the standard treatment offered by some surgeons. The largest series was reported by Reinisch. Early attempts were associated with a 42% incidence of framework extrusion leading to modifications of the original technique and coverage of the framework using a temporoparietal fascial flap. According to Reinisch, this drastically reduced the complication rate and is the technique of choice in his opinion. Finally, an auricular prosthesis is another option. The introduction of titanium osseointegrated fixtures by Branemark has made prosthetic reconstruction of the auricle a more stable and user-friendly alternative. The role of prosthetic reconstruction in microtia will also be discussed below.

Anatomy and Surgical Challenge The ear is composed of a delicate and complex-shaped cartilage framework covered on its visible surface with thin, tightly adherent, hairless skin. A reconstructed auricular framework

B

A FIGURE 30.12. Earlobe reconstruction using nasal septal cartilage. A: Original defect secondary to discoid lupus erythematosus. B: Final result after two-stage reconstruction using thin cartilage from the nasal septum. (Courtesy of Charles H. Thorne, MD.)



must be more rigid than the cartilage framework of a normal ear. When the auricular framework is placed beneath the skin in the temporal region, a combination of the tight skin envelope and the progressive scar contracture will gradually obliterate the fine details if the framework is built to mimic the delicate framework of the normal ear. As such, any reconstructed ear that maintains its projection and definition in the long-term will be more bulky and will lack the flexibility of the normal ear. Consequently, even the best result using current techniques for auricular reconstruction is imperfect. The deficiencies of current techniques make it even more important that the reconstructed auricle be the correct size, be located in the proper position such that one earlobe is not higher than the other, and be properly angulated relative to the other facial structures.

Embryology The middle and external ears are derived from the first (mandibular) and second (hyoid) branchial arches. Most patients with microtia have atresia (absence) of the external auditory canal and tympanic membrane with variable deformities of the middle ear ossicles. Rarely a patient will present with microtia and a patent, stenotic canal. Least common but most difficult to repair are patients with an auricular vestige that is markedly abnormal in position. Because the meatus can only be moved a limited distance, the surgeon must consider complete excision of the canal. The inner ear is derived from totally separate embryologic tissues from the middle/external ear and is, therefore, almost always normal in patients with microtia. In other words, the hearing loss in microtia/atresia patients is conductive in nature.

Incidence/Genetics The incidence of microtia varies widely among ethnic groups. Textbooks cling to the figure of 1 in every 6,000 births. The incidence is higher in patients of Asian ethnicity. In addition, microtia is almost twice as common among males as females and almost twice as common on the right side compared to the left. Bilateral microtia occurs in somewhere between 10% and 20% of patients with microtia. Most cases of microtia occur in an isolated fashion. Only rarely does microtia appear to run in families. One exception is Treacher Collins syndrome, which frequently presents with bilateral microtia and is inherited in an autosomal dominant fashion.

Microtia in Hemifacial Microsomia Older publications suggest that isolated microtia and hemifacial microsomia are distinct entities. In fact, microtia is part of the spectrum of hemifacial microsomia deformities, all of which owe their origin to maldevelopment in the first and second branchial arches. At one end of the spectrum is the patient with microtia who appears to have an otherwise symmetrical face. At the other end of the spectrum is a patient who manifests underdevelopment of all tissues on one side of the face including microtia, aural atresia, underdevelopment of the mandible, underdevelopment of the soft tissues of the cheek, and underdevelopment of the facial nerve. Microtia and hemifacial microsomia should not be considered as separate entities (Chapter 26).

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Canaloplasty and Middle Ear Reconstruction Patients with unilateral microtia/atresia usually have normal hearing in the contralateral ear. This should be verified by an otologist as early as possible after birth. The main goal then becomes protection of the better hearing ear throughout development. It is important that otitis media in the ear with normal hearing be treated completely and that a hearing test be repeated after completion of treatment. Residual middle ear fluid in the only normal ear may result in hearing impairment and consequently interference with speech development. Patients with unilateral microtia do well from an otologic point of view. These patients have some difficulty localizing sounds but, in many cases, require no amplification device and no special treatment in the classroom. There is, however, a movement in the otologic community to be more aggressive with bone conduction aids that result in binaural hearing. Patients with bilateral microtia/atresia are in an entirely different situation. These patients are functionally deaf with complete conductive hearing loss bilaterally. These patients are fitted with a bone-conduction hearing aid as early as possible in life and benefit from a bone-anchored hearing aid retained with a titanium abutment when they get older. Approximately one-half of the patients with microtia/aural atresia have middle ear anatomy that can be reconstructed surgically. In bilateral cases, this is extremely important and may eliminate the need for a hearing aid or at least decrease total dependence on such a device. The issue in the unilateral case is not as clear because, as stated above, these patients function reasonably well. Most otologists around the world do not recommend canaloplasty in patients with unilateral microtia. The surgical results are prone to stenosis of the external auditory canal meatus as well as scar contracture of the reconstructed tympanic membrane. The hearing in the reconstructed ear tends to worsen with time. This nonsurgical recommendation, however, is not universal and good results have been reported by Jahrsdorfer in unilateral cases. The timing of the auricular reconstruction relative to the canaloplasty is important. The auricular reconstruction is best performed before the canaloplasty. Auricular reconstruction is possible after canal surgery but the result is compromised by the scarring in the region.

Classification The microtia deformity itself is enormously variable. At one end of the spectrum is an auricle that is slightly small but otherwise normal in appearance. At the other end of the spectrum is the patient with complete anotia. Various classifications have been proposed to deal with this vast variability in clinical presentation. The Nagata classification is useful because it correlates with the surgical approach. ■

■

■

■ ■

Lobule type. These patients have an ear remnant and malpositioned lobule but have no concha, acoustic meatus, or tragus. Concha type. These patients present with an ear remnant, malpositioned earlobe, concha (with or without acoustic meatus), tragus, and antitragus with an incisura intertragica. Small concha type. These patients present with an ear remnant, malpositioned lobule, and a small indentation instead of a concha. Anotia. These patients present with no, or only a minute, ear remnant. Atypical microtia. These patients present with deformities that do not fit into any of the above categories.


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Surgical Reconstruction The following are the three options for reconstruction of microtia: 1. Autogenous reconstruction. 2. Composite autogenous/alloplastic reconstruction using an alloplastic ear framework. 3. Prosthetic reconstruction.

Autogenous Reconstruction The two main techniques described for autogenous reconstruction of the auricle using a rib cartilage framework are the Brent technique and the Nagata technique. The Brent technique involves four stages: 1. Creation and placement of a rib cartilage auricular framework (Figs. 30.13 and 30.14). 2. Rotation of the malpositioned ear lobule into the correct position (Fig. 30.15). 3. Elevation of the reconstructed auricle and creation of a retroauricular sulcus (Fig. 30.16). 4. Deepening of the concha and creation of the tragus (Fig. 30.17). The Nagata technique is performed in two stages: 1. Creation of an auricular framework including the tragus and rotation of the lobule into the correct position (in other words, combining stages 1, 2, and 4 from the Brent technique) (Figs. 30.18 and 30.19). 2. Elevation of the reconstructed ear and creation of the retroauricular sulcus (Fig. 30.20). Technical Details of the Two Techniques. The patient is examined standing and the location of the earlobe on the normal side is transferred to the affected side. This is the single most important marking because symmetrical earlobes is one of the primary goals of the procedure. The normal ear is traced on clear x-ray film and sterilized. Using this tracing, additional templates are made. A template of the desired framework is

made, approximately 3 to 4 mm shorter and narrower than the eventual ear. If the Nagata technique is performed, additional templates are constructed of the antihelix/triangular fossa piece and the tragus/antitragus piece. The exact location and orientation of the desired auricle are drawn on the patient. Decisions are made about the location of the incisions. In the Brent technique, an incision is designed that can be used again at the time of lobule rotation and at the time of tragus construction. If the Nagata technique is used, the incision is designed as shown in Figure 30.19, to allow rotation of the lobule. The incision is made and the cartilage remnant is removed, carefully preserving the skin and avoiding buttonholes if possible. The pocket is dissected beyond the outline of the eventual auricle. In the Nagata technique, a pedicle is maintained to the dissected flap to improve blood supply. Attention is turned to the chest. Although a transverse incision will heal more favorably than an oblique incision, the latter provides better exposure. The rectus abdominis muscle is divided. In the Brent technique, two pieces of cartilages are harvested. In the Nagata technique, five pieces are required. In addition to the synchondrosis of two cartilages and a free rib for the helical rim, the Nagata technique requires removal of a piece for the antihelix/triangular fossa, a piece for the tragus/antitragus, and a piece to be banked in the chest for the second stage. This piece is wedged into the sulcus at the second stage to provide projection of the auricle. Nagata harvests the cartilages in a subperichondrial plane, leaving the perichondrium in the chest when the cartilages are removed. The author tends to take the cartilages with the perichondrium and has not noticed a significant difference in the chest wall deformity. If a pneumothorax is created, a catheter is placed into the pleural cavity. After the incision is closed the catheter is withdrawn while the anesthesiologist applies positive pressure ventilation. An additional catheter is left in the wound for the administration of Marcaine postoperatively. Details are applied to the base using gouges. In the Nagata technique, the antihelix/triangular fossa piece is attached. The helical rim is attached in a similar fashion in both techniques. The difference is that Nagata recommends waiting until

FIGURE 30.13. Fabrication of ear framework from rib cartilage. Brent technique, stage 1. A: The base block is obtained from the synchondrosis of two rib cartilages. The helical rim is obtained from a “floating” rib cartilage. B: Carving the details into the base using a gouge. C: Thinning of the rib cartilage to produce the helical rim. D: Attaching the rim to the base block using nylon sutures. E: Completed framework.


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A,B

C FIGURE 30.14. Insertion of the ear framework. Brent technique, stage 1. A: Preoperative markings indicating the desired location of the framework (solid line) and the extent of the dissection necessary (dotted line). B: Insertion of cartilage framework. C: Appearance after the first stage. A suction catheter is using to suck the skin into the interstices of the framework. (Courtesy of Burt Brent, MD.)

the child is 10 years old, which yields cartilages that are long enough to reconstruct the crus of the helix. Finally, the tragus/antitragus piece is attached in the Nagata technique. Nagata uses wire sutures. The author has used nylon sutures, rather than wire, for both the Brent and Nagata techniques, with adequate fixation and a low incidence of suture extrusion. The framework is inserted into the pocket along with two suction drains. Once the closure has been accomplished and the dressing has been applied, the drains are attached to Vacutainer tubes. The tubes are changed every half hour for 2 hours, then every hour for 2 hours and then every 4 hours overnight. The dressing is removed on the second postoperative day and the patient is discharged. Complications. Complications of the Brent technique are rare in experienced hands. Complications of the Nagata technique, at least in the author’s hands, are relatively common. The most common complication is exposure of the cartilage framework. Management requires experience, but these wounds usually heal without surgical intervention unless they are large. Exposed areas of more than 1 cm in greatest dimension require urgent coverage with a temporoparietal flap and skin graft. In fact, if there is the slightest question about whether an exposed area will heal, then flap coverage is indicated. One never re-

grets performing flap coverage of an exposed area of cartilage framework, but one may certainly regret not performing such a procedure. Elevation of framework. In the third stage of the Brent technique and the second stage of the Nagata technique, the previously placed framework is elevated and the retroauricular sulcus is resurfaced. Nagata adds a piece of rib cartilage covered with a temporoparietal flap. The cartilage is banked under the skin at the time of the first stage and is wedged into the sulcus to provide projection to the reconstructed auricle in the second stage. The fascial flap covers the graft and provides a bed for skin grafting. (Fig. 30.20) In both techniques the scalp is advanced into the depth of the sulcus and the medial surface of the elevated framework is resurfaced with a skin graft. Both Nagata and Brent recommend a split thickness graft for this stage. The grafts contract significantly, however, in some cases obliterating the reconstructed sulcus. For this reason the author prefers a full thickness graft from the groin. The disadvantage is a visible scar but the full thickness graft resists contracture and is more likely to result in maintenance of the reconstructed sulcus.

Composite Autogenous/Alloplastic Reconstruction In these patients, an auricular framework composed of porous polyethylene (Medpor) is used instead of costal cartilage. Reinisch originally reported a 42% incidence of implant exposure. He modified the technique, adding temporoparietal flap coverage of the framework, and reports a vastly decreased complication rate.

Prosthetic Reconstruction

A

B

FIGURE 30.15. Rotation of lobule. Brent technique, stage 2. The earlobe is rotated from its vertical malposition into the correct position at the caudal aspect of the framework. A: Design of lobe rotation is made such that the same incision can be used in stage 4, tragus construction. B: After rotation of the lobule. (Reproduced with permission of Charles H. Thorne, MD. Copyright Charles H. Thorne, MD.)

Prior to the introduction of implant retention of prostheses, prosthetic reconstruction depended on adhesive retention and was impractical. Branemark osseointegrated titanium implants have made prosthetic reconstruction somewhat more practical but this technique remains, in the author’s opinion, a second choice to autogenous reconstruction (see Chapter 34). Children are poor candidates for prostheses, often refusing to wear them regardless of the retention mechanism. Children also tire of the maintenance required of the abutments and the surrounding soft tissue. If adequate hygiene is not maintained, the skin/abutment interface becomes inflamed and use of the prosthesis must be discontinued awaiting resolution of the inflammation. Additionally, the daily removal and replacement of the prosthesis serves as a constant reminder of the deformity. In contrast, children with an autogenous reconstruction


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A

B

FIGURE 30.16. Elevation of framework and skin graft to sulcus. Brent technique, stage 3. A: Incision is designed behind the ear. B: The retroauricular scalp is advanced into the sulcus so that the eventual graft will not be visible. C: Full-thickness graft to the exposed medial surface of the auricle. (Reproduced with permission of Charles H. Thorne, MD. Copyright Charles H. Thorne, MD.)

C

incorporate the new ear into their sense of self. Finally, prostheses lack the warmth and texture of autogenous reconstructions and, despite the superior details, are not more “lifelike.” It is important to note that prostheses require replacement every several years for the life of the patient and, therefore, prosthetic reconstruction is more expensive in the long-term than autogenous reconstruction. To this author’s thinking, the only absolute indication for prosthetic reconstruction in a child with microtia is failed autogenous reconstruction with inadequate soft tissue for either a second autogenous reconstruction or a Medpor reconstruction. In such a patient, a prosthesis may represent the only salvage procedure available. Relative indications for the use of prosthetic reconstruction include a very low hairline where a temporoparietal flap would be required to allow autogenous reconstruction or extreme hypoplasia of the tissues with a concavity where the auricle will eventually be located.

Personal Thoughts on Surgical Reconstruction The author has extensive experience with both the Brent and the Nagata techniques of auricular reconstruction and it is on

A

the basis of that experience that the following comparative statements are made. The Nagata procedure was designed to address the perceived weaknesses of the Tanzer/Brent technique, particularly the region of the concha, crus of the helix, tragus, and incisura intertragica. As such, the best possible Nagata-type result may have superior details to the best possible Brent-type result. The problem is that the “best possible results” do not occur most of the time. The Nagata procedure, at least in the hands of this author, is definitely associated with a higher complication rate. The framework is much higher profile, much more complex in its details, and contains many more sutures. As such, the chance of cutaneous necrosis with framework exposure is significantly greater using the Nagata technique. On the other hand, these areas of exposure are generally small and heal without further surgical intervention and do not necessarily compromise the result. The individual surgeon must decide, factoring in his/her experience, whether the possibility of a superior result is worth the increased risk of the Nagata procedure. In his own practice, this author currently uses the Nagata/Firmin technique in most patients. In patients with extremely tight skin, or the presence

B

C

FIGURE 30.17. Construction of tragus. Brent technique, stage 4. A: The conchal graft is taken from the posterior conchal wall of the contralateral ear. B: An L-shaped incision is made and the graft is inserted with the skin surface down. C: The graft healed nicely. (Reproduced with permission of Charles H. Thorne, MD. Copyright Charles H. Thorne, MD.)



FIGURE 30.18. Fabrication of ear framework from rib cartilage. Nagata technique, stage 1. A: In a manner similar to Brent, the base and its details are carved from the synchondrosis of two adjacent ribs. B: The four pieces of cartilage that make up the cartilage framework are seen and numbered. The base and helical rim are present as they are for the Brent technique. There is an additional antihelix-triangular fossa piece and an additional tragus-antitragus piece that are unique to the Nagata procedure. (Reproduced with permission of Charles H. Thorne, MD. Copyright Charles H. Thorne, MD.)

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D

FIGURE 30.19. Insertion of the cartilage framework. Nagata technique, stage 1. A: The incision is designed, robbing most of the skin on the medial surface of the lobule that will be necessary to line the concha. B: The pocket is dissected, leaving an intact “pedicle” at the caudal end of the flap. C: The framework is inserted. D: Appearance of the framework after stage 1. Suction drains are in place to coapt the skin to the underlying cartilage. (Reproduced with permission of Charles H. Thorne, MD. Copyright Charles H. Thorne, MD.)


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C

FIGURE 30.20. Elevation of framework. Nagata technique, stage 2. A: The auricle is elevated, the scalp is advanced into the sulcus (arrows), the cartilage graft is wedged into the sulcus, and the graft is covered with a temporoparietal flap and skin graft. B: The skin graft is in place. Nagata described the use of split-thickness skin but this author has noted tremendous shrinkage of the thin grafts and recommends full-thickness graft. C: Cross-section showing the cartilage graft in place providing projection as well as the temporoparietal flap covering the temporoparietal flap. (Reproduced with permission of Charles H. Thorne, MD. Copyright Charles H. Thorne, MD.)

of other scars, the Brent technique is used because of its safety and reliability. The other issue involves the chest donor site. The Nagata technique requires harvesting twice as much cartilage as the Brent technique. While Nagata harvests all cartilage subperichondrially, no detailed study has been performed comparing the chest wall deformity created by the Nagata technique at age 10 years with the deformity created by the Brent technique at age 6 years. Although the donor site is an issue not to be ignored, it tends not to be an issue regardless of which technique is used. Patients simply do not complain about the chest unless they are extremely thin. Proponents of the composite alloplastic/autogenous reconstruction using Medpor cite the lack of chest donor-site scars/deformity as an advantage. Although that is true, these same reports fail to mention the scars/deformity that replace the chest deformity. For example, the composite technique robs the contralateral normal ear of all the skin behind it, resulting in obliteration of the sulcus or a skin graft donorsite scar if the retroauricular defect is replaced with partialthickness skin. Additionally, this technique requires a scalp scar to harvest the temporoparietal flap. These scars are frequently hypertrophic and/or associated with thin strips of alopecia, which may be more troublesome to the patient than a chest wall scar.

Severe Facial Asymmetry Placing the reconstructed ear in the best location is straight forward if the face is symmetrical or near symmetrical. In cases of significant asymmetry, however, compromises must be made. The surgeon cannot rely on measurements from landmarks such as the lateral canthus or oral commissure, because the entire side of the face is so much smaller than the other side. If such measurements were used, the ear would be placed far too posteriorly, and would appear strikingly abnormal. Of equal importance, however, the ear must not be place too low or too anterior. The author attempts to place the ear in the correct

craniocaudal position so that the earlobes are at the same level and then determines the anteroposterior positioning based on the relationship to the sideburn. No ear will look normal unless there is a sideburn in front of it.

Acquired Deformity versus Microtia Total auricular reconstruction of the acquired deformity differs from congenital microtia. There is always less skin available. In microtia, removal of the cartilaginous remnant provides some supple, unscarred skin to supplement the retroauricular skin. In the acquired situation, there may be no residual ear skin and the presence of scarring from the traumatic or surgical removal of the ear restricts the skin pocket. In many cases, a temporoparietal flap with skin graft is required in addition to the native skin. The flap provides an unlimited amount of vascularized tissue, but the combination of the flap and the skin graft never has the definition or color match of the native skin. In addition, the presence of an external auditory meatus limits the access incisions, the extent of the skin pocket and the risk of infection. The canal is colonized with bacteria, frequently Pseudomonas species, which adds additional problems not encountered in microtia cases.

SPECIAL SITUATIONS Acute Auricular Trauma and Cauliflower Ear A hematoma may result from trauma and frequently occurs in wrestlers. Unless evacuated, the blood tends to become cartilaginous, resulting in the so-called cauliflower ear. Once fully developed, the cauliflower ear is extremely difficult to correct. Hematomas may require repeated aspirations or an incision to fully evacuate. Suturing gauze bolsters to the auricle to


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A,B FIGURE 30.21. Management of an acute othematoma. A: Recurrent conchal hematoma. B: Throughand-through bolster sutures, after evacuation of the hematoma. C: Appearance of ear after the compression dressing has been removed at 10 days. (Courtesy of Burt Brent, MD.)

compress the skin against the cartilage usually prevents reoccurrence (Fig. 30.21).

Amputated Ear Most attempts to replace an amputated ear will fail, resulting in additional incisions/scars and “burning bridges” that may be useful for secondary reconstruction. The patient, however, will not easily accept the decision to discard the amputated part without an attempt at replacement. There is no easy answer. Replantation of amputated ears has been reported and some excellent results have been obtained. The vessels are small, however, and failure is common. Any attempt at replantation must consider that success is unlikely and may result in scars that limit later reconstructive attempts. Incisions for exposure of recipient vessels are kept to a minimum. Reattaching large pieces of auricular tissue as composite grafts is doomed to failure. The good news is that such an attempt does not disrupt the surrounding tissues, does no harm, and makes the patient feel that “something” is being done. Removing the skin from the cartilage and burying it beneath retroauricular skin is a poor choice. The thin, delicate cartilage will not maintain its shape sufficiently against the forces of scar contracture. An alternative is to cover the de-skinned cartilage with a temporoparietal flap. The esthetic result will be poor for the reasons mentioned above and this useful tissue will not be available for secondary reconstruction. Several successful cases have been reported in which the posteromedial skin was removed from the amputated part, the cartilage was “fenestrated,” retroauricular skin was excised, and the part was placed on the healthy bed. The anterolateral auricular skin is vascularized through the cartilage fenestrations by direct contact with this healthy, vascularized bed. In the opinion of the author, the ideal scenario for an amputated ear is an attempt at microvascular replantation through the available wound, without additional incisions. If unsuccessful, secondary reconstruction with rib cartilage grafts is performed, with or without a temporoparietal flap. If replantation is not an available option, the part should be replaced as a composite graft (knowing it will fail), or the part should be discarded.

Acute Auricular Burns Acute burns may result in chondritis. Characterized by tenderness, erythema, warmth, and induration, chondritis usually occurs several weeks after the initial injury. Once chondritis is diagnosed, aggressive steps are taken to eradicate the infection and prevent subsequent deformity. Drainage and placement of an irrigation system is an appropriate first step. If this therapy fails, the involved cartilage must be debrided. When the latter becomes necessary, incisions are planned judiciously to minimize the effect on secondary reconstruction.

Skin Cancer/Malignant Melanoma Cutaneous malignancies of the helical rim can be excised and closed with helical advancement as described above (Fig 30.7). Lesions in the concha or over the antihelix can usually be excised and skin grafted. If the cartilage is involved, it can be excised and the graft placed directly on the posterior skin. Malignant melanomas should be excised with the same margins as melanomas of the equivalent depth in other parts of the body. Melanoma in situ does not require a full-thickness excision. These lesions are excised with a 5-mm margin, preserving the perichondrium, and skin grafted. Invasive melanomas of the helical rim require wedge resection to achieve adequate margins, eliminating helical advancement as an alternative for closure. These defects may be large and require secondary reconstruction as in Figure 30.11.

Earring Complications While ingenious techniques have been described to reconstruct traumatic clefts in the lobe caused by earrings, the most reliable method is to excise and close the defect in one stage and re-pierce the ears 6 weeks later, or whenever the induration subsides. Another complication of earrings is keloid formation. Small keloids can be excised and closed primarily and may not recur.


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If the patient is truly prone to keloids, then excision, triamcinolone injection, and pressure earrings are warranted. If the keloid recurs, excision with immediate irradiation offers the best chance of avoiding recurrence. Finally, piercing through the cartilage in the upper portion of the ear can result in severe infections. While not common, chondritis can lead to severe, permanent disfigurement of the auricle. Infections therefore are treated aggressively. If cartilage requires debridement, it is performed early to limit the deformity and incisions are planned carefully to minimize these deformities.

Suggested Readings Al-Qattan MM, Hashem FK. An alternative approach for correction of Stahl’s ear. Ann Plast Surg. 2004;52(1):105. Antia NH, Buch MS. Chondrocutaneous advancement flap for the marginal defect of the ear. Plast Reconstr Surg. 1967;39:472. Brent BD. Technical advances in ear reconstruction with autogenous rib cartilage grafts—Personal experience with 1,200 cases. Plast Reconstr Surg. 1999;104:319. Davis J. Reconstruction of the upper third of the ear with a chondrocutaneous composite flap based on the crus helix. In: Tanzer RC, Edgerton MT, eds.

Symposium on Reconstruction of the Auricle. St. Louis: Mosby; 1974: 247: 51. Demir Y. Correction of constricted ear deformity with combined V-Y advancement of crus helices and perichondrioplasty technique. Plast Reconstr Surg. 2005;116(7):2044. Firmin R. Ear reconstruction in cases of typical microtia. Personal experience based on 352 microtic ear corrections. Scand J Plast Surg. 1998; 32:35. Gault DT, Grippaudo FR, Tyler M. Ear reduction. Br J Plast Surg. 1995; 48:30. Gosain AK, Recinos RF. A novel approach to correction of the prominent lobule during otoplasty. Plast Reconstr Surg. 2003;112(2):575. Harris PA, Ladhani K, Das-Gupta R, et al. Reconstruction of acquired sub-total ear defects with autologous costal cartilage. Br J Plast Surg. 1999;52(4):268. Janis JE, Rohrich RJ, Gutowski KA. Otoplasty. Plast Reconstr Surg. 2005;115(4):60e. Matsuo K, Hayashi R, Kiyono M, et al. Nonsurgical correction of congenital auricular deformities. Clin Plast Surg. 990;17(2):383. Nagata S. A new method of total reconstruction of the auricle for microtia. Plast Reconstr Surg. 1993;92:187. Noguchi M, Matsuo K, Imai Y, et al. Simple surgical correction of Stahl’s ear. Br J Plast Surg. 1994;47(8):570. Thorne CH, Brecht LE, Bradley JP, et al. Auricular reconstruction: Indications for autogenous and prosthetic techniques. Plast Reconstr Surg. 2001;107(5):1241. Vogelin E, Grobbelaar AO, Chana JS, et al. Surgical correction of the cauliflower ear. Br J Plast Surg. 1998;51(5):359.


PART IV ■ HEAD AND NECK

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CHAPTER 31 ■ SOFT TISSUE AND SKELETAL INJURIES OF THE FACE LARRY HOLLIER, JR. AND PATRICK KELLEY

The treatment of the facial trauma patient continues to evolve with progress in imaging, bone fixation technology, and the application of microsurgical reconstructive techniques and distraction osteogenesis. Many of the principles of access and fixation remain constant, but the application of these principles has been greatly facilitated with improvements in instrumentation and osteosynthesis technology. Facial trauma continues to be treated by a variety of specialists, including plastic surgeons, otolaryngologists, and oral surgeons. Plastic surgeons, however, are uniquely trained to handle the full range of issues present in the trauma patient.

INITIAL MANAGEMENT Facial injuries themselves are rarely life-threatening, but are indicators of the energy of injury. Initial care of all trauma patients should focus on the algorithmic protocol of ATLS (Advanced Trauma Life Support). Facial injuries should alert the examiner to the possibility of airway compromise, cervical spine injuries, or central nervous system injuries.

Airway Airway compromise is the result of either direct laryngeal injury, foreign bodies (including aspirated teeth and bone fragments), or excessive bleeding from an upper airway source. Treatment of the compromised airway is complicated by the likelihood that 10% of facial trauma patients have cervical spine injuries. Often upright positioning with cervical spine protection will improve airway function compromised by excessive bleeding or foreign bodies. Foreign bodies can be mechanically removed by the finger-sweep technique. Airway compromise can also occur when the floor of mouth and tongue lose support from a comminuted mandible fracture and can be alleviated by simple anterior traction on the mandibular symphysis. The trauma team should have a low threshold for definitive airway protection via endotracheal intubation. The use of blind nasal intubation should be carried out with caution. Nasal intubations can exacerbate nasal and nasopharyngeal bleeding. Additionally, the tube may be inadvertently placed ultracranially in the obtunded patient with a skull-base fracture. Endoscopic nasal or oral intubation improves safety by avoiding the cervical spine manipulation; it further provides immediate confirmation of tracheal intubation. Emergent tracheotomy is considered in the unusual circumstance of laryngeal fracture or inability to secure an upper airway route to intubation. Tracheotomy performed in the controlled environment of the operating room is far superior to either emergent tracheotomy or cricothyrotomy. There should be a low threshold for a controlled, temporary tracheotomy

in the patient with significant soft-tissue trauma to the floor of mouth and tongue, especially the base of tongue. These injuries are more commonly penetrating in nature and initially misleading in that there may be minimal signs of distress. The swelling in the first 24 to 48 hours, however, may be significant enough to compromise the airway, forcing tracheotomy under less-than-favorable circumstances.

Hemorrhage The dense vascularity of the head and neck can cause significant blood loss from soft-tissue injuries. Fortunately, most of these injuries allow sufficient access for direct pressure to control hemorrhage. The control of bleeding vessels should be accurate and directed. A number of critical structures can become collateral victims by clamping sources of bleeding with poor exposure and visualization. Bleeding that cannot be controlled with direct pressure requires packing. Packing in the nasal cavity is usually effective and only rarely requires augmentation with a transnasal balloon catheter in the nasopharynx. Nasopharyngeal balloon catheters only serve to impede blood from entering the oropharynx where it can more easily enter the lungs. Massive hemorrhage should be approached with emergent intubation followed by packing and direct pressure. The source of bleeding is most commonly a branch of the external carotid system, which is most appropriately controlled with angiographic embolization. The radiologist usually requires the assistance of the surgeon to remove the packing so that the source of bleeding can be more readily identified. Type-specific blood should be readily available. Surgical ligation of the external carotid artery will not control bleeding from its injured branches because of the robust collateralization present and should not be attempted (Fig. 31.1).

Central Nervous System Neurologic injury is commonly associated with severe facial trauma. In a series of 1,068 patients with facial fractures, 79.4% were associated with some form of traumatic brain injury (1). Patients with facial trauma rarely die from facial injuries, but can die from associated injuries of the central nervous system. As part of a complete trauma evaluation most patients with facial trauma undergo computed tomography (CT) scanning to rule out head injury. The most widely accepted method for expressing the degree of neurological injury is the Glasgow Coma Score (GCS). This evaluates the motor, verbal, and eye-opening responses of the patient on initial evaluation, rating the patient from a lowest score of 3 to a highest score of 15 (Table 31.1). As a general rule, concomitant head injury is not a contraindication to facial fracture repair assuming the neurologic

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facial trauma patients. Cervical spine precautions are mandatory until the spine is cleared both clinically and radiographically. For the obtunded patient, the cervical spine is best evaluated with a CT scan, although a negative exam does not rule out unstable ligamentous injury. These patients require additional examination when the sensorium is clear, and possibly flexion/extension radiographs or magnetic resonance imaging (MRI) to definitively evaluate the cervical spine.

FACIAL TRAUMA EVALUATION History Use of the AMPLE acronym (allergies, medications, past history, last meal, events surrounding the accident) facilitates a complete trauma history.

Head and Neck Examination

FIGURE 31.1. Hemorrhage treated by embolization. Patient with gunshot wound to mandible requiring embolization of lingual artery (note coil) to prevent exsanguination. Segmental defect is treated with a distraction device.

injury is stable and not in the process of evolution. In the event of acute brain injury, surgical repair of facial fractures generally is delayed to avoid the fluid overload associated with surgery and, most importantly, to avoid undetected decline of neurologic function during the period of general anesthesia when clinical neurologic examination cannot be performed. Once the central nervous system injury and concomitant swelling have stabilized, facial fracture repair can generally be undertaken safely. Ten percent of patients with facial trauma suffer some form of cervical spine injury. Suspicion for injury and vigilant care of the cervical spine are key elements in the care of

TA B L E 3 1 . 1 GLASGOW COMA SCALE Eye opening

Verbal response

Motor response

Glasgow Coma Score (Total)

Spontaneous To voice To pain None Oriented Confused Inappropriate Incomprehensible None Obeys commands Localizes Withdraws (pain) Flexion Extension (pain) None

4 3 2 1 5 4 3 2 1 6 5 4 3 2 1 3–16

A thorough head and neck examination serves as the starting point and is performed in a logical and consistent manner to avoid missing something. The examiner should not be distracted by the more impressive injuries because of the likelihood of overlooking less obvious but potentially significant problems. In the acutely injured patient with facial trauma, the physical exam is greatly impaired by facial swelling. Asymmetries that are secondary to fractures are usually concealed. Additionally, it may be difficult to elicit tenderness because of simultaneous distracting injuries. The examiner carefully assesses the face for neurologic deficits, including the trigeminal and facial nerves. Sensory disturbances in the forehead, cheek, and lower lip should be well documented as should any deficits in facial nerve function. Undocumented preoperative nerve injuries may be attributed postoperatively to surgical intervention. Lacerations, contusions, and abrasions of the skin may focus the exam by indicating which nerves are at risk. A complete ocular examination includes the evaluation of ocular history, acuity, light and red light perception, ocular motility, pupillary exam, and examination of the conjunctiva and eyelids. Each eye requires assessment individually to prevent confusion to the patient and examiner. Much of the long-term morbidity of facial trauma is associated with ocular and orbital injury. Although there should be a low threshold to involve the ophthalmologist, the physician treating facial trauma should be well versed in the ocular examination. Examination of the oral cavity is essential, especially in the obtunded patient who may have loose teeth, bone fragments, or foreign bodies. Identification and removal of prosthetics (e.g., dentures) is essential. The occlusion and intercuspation is carefully evaluated, as both mandibular and maxillary fractures can result in malocclusion. Patients are capable of sensing the slightest change in their occlusion. Even in patients with unusual bites, careful analysis of the wear facets may enable the surgeon to determine if an underlying malocclusion is present. Proper record keeping of facial injuries includes rough sketch drawings in the medical chart and photographs to document injuries. These photographs may prove invaluable in the treatment of secondary deformities and can also be beneficial in medicolegal disputes. As such, photographic consents should routinely be obtained as part of the treatment consent upon entrance to the emergency department.


Chapter 31: Soft Tissue and Skeletal Injuries of the Face

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A

B FIGURE 31.2. Fracture missed by Panorex. A: The mandible appears normal on panoramic radiograph. B: CT scan of same patient revealing complete fracture. Although panoramic radiographs provide valuable information about the mandible and dentition, distortion in the image can conceal fractures.

Imaging Most patients presenting to the emergency department with a history of facial trauma will undergo a facial trauma series consisting of plain radiographs (anteroposterior [AP], lateral, Caldwell, and Water views). This is a useful screening tool for the emergency room physician when the index of suspicion is fairly low; however, plain radiographs do not give the degree of information regarding the fracture in terms of severity and displacement that is required for the surgeon. In most patients with significant facial impact, CT scanning should be performed. With modern helical CT scanners, it takes a few additional minutes to scan the face. In a busy emergency room, this approach saves both time and expense. Facial CT scans are not only extremely sensitive and specific in their evaluation of the facial skeleton, the cost is comparable to that of a full series of plain radiographs. Additionally, a complete radiographic facial trauma series requires cervical spine clearance for completion. This is unnecessary with modern helical CT scanners. The CT scan should be performed with axial cuts no greater than 3 mm apart, from the top of the cranium through the bottom of the mandible. Although older models of CT scanners could only perform coronal imaging by hyperextending the neck (requiring cervical spine clearance), most scanners are now capable of rotating their plane of imaging so as to eliminate the need to manipulate the patient’s head position and mobilize the neck. This capability is a tremendous asset in the sense that the scan can be performed immediately at the time of the head and abdominal CT scans, which are usually performed quickly and prior to the time of cervical spine clearance. When coronal cuts cannot be taken, most scanner software now provides for digital reconstructions of the coronal plane from the axial images. Additionally, in cases of complex facial trauma, it may be helpful to have a three-dimensional reconstruction of the facial skeleton formatted so as to provide for a better overall orientation. As a general rule, the CT scan is acceptable for the diagnosis of essentially all facial fractures. The one area where this exam may not be entirely sufficient is the mandible. Although the CT is essentially 100% sensitive and specific for the fractures, it does not give detailed information about dental structures. This is most critical in the region of the mandibular angle with respect to the condition of the third molars. Information re-

garding root damage and tooth position relative to the fracture is critical in the planning and treatment of angle fractures. When using CT scanning for mandible fractures, complications can be related to this factor. As such, a panoramic radiograph is helpful in the evaluation of mandibular fractures. Certain imaging equipment allows the patient to be supine, whereas the more common equipment requires upright positioning and cervical spine clearance. These radiographs place an entire image of the mandible, condyle to condyle, on a single film. They provide excellent detail of the condyles and dentition. Care must be taken when interpreting fractures based solely on a panoramic radiograph of the mandible, especially the symphysis and parasymphysis, as distortion of these regions can be misleading. A supplemental posteroanterior (PA) film of the mandible complements the panoramic image by providing additional detail of the region. Lateral radiographs and CT scans can provide additional information about the regions posterior to the parasymphysis (Fig. 31.2).

TREATMENT OF SOFT-TISSUE INJURIES Preparation and Anesthesia Facial injuries frequently involve contaminated wounds. The most important initial responsibility of the surgeon is to convert the contaminated wound to a clean one and then perform wound closure. Wounds should be closed as soon as possible. Although facial wounds can usually tolerate up to a 24-hour delay in repair, the longer the wound is open, the greater chance of infectious complications. Cleansing of wounds is best performed with a mild surgical soap with the light use of a scrub brush. More extensive wounds or those with a great deal of contamination should be irrigated with a pulsed lavage system. All foreign debris must be removed from the wound prior to closure. Adequate cleansing usually requires total anesthesia of the region of concern and a cooperative patient. These are the primary factors that dictate the method of anesthesia necessary. Although general anesthesia may be necessary for some wounds, many facial wounds can be repaired under a regional nerve block. If regional blockade is impractical, a field

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block may be necessary to avoid direct infiltration of excessive amounts of local anesthetic, distorting anatomic landmarks that may be useful in restoring the tissues to their anatomic positions. Only 1 to 2 mL of anesthetic at the site of the nerve trunk is needed to provide complete anesthesia for the respective region. Often multiple regions require blockade. We recommend 1% lidocaine with 1:100,000 epinephrine solution mixed at a 9:1 ratio with 8.4% sodium bicarbonate solution (e.g., 9 mL lidocaine with epinephrine and 1 mL of bicarbonate solution). The bicarbonate solution neutralizes the pH of the lidocaine, which has two important benefits. First, it minimizes the pain of the injection. Second, the lidocaine more effectively crosses the neural membrane to affect its sodium ion channel in the neutral state and, therefore, has a quicker onset of action. Topical cocaine (4%) is an excellent choice for anesthesia in the nasal cavity as it also stimulates vasoconstriction of the nasal mucosa providing for a painless and bloodless field.

Traumatic Wounds Traumatic wounds can be variously described as lacerations, punctures, contusions, abrasions, and crush injuries. The wound configuration, whether linear or stellate, is much less important to the final result than the degree of crush, contusion, and vascular compromise of the tissues. The importance of wound cleansing prior to closure cannot be overemphasized. Removal of all foreign bodies is essential as they are the source of a prolonged inflammatory response and possibly infection. Abrasions with residual foreign bodies will form a traumatic tattoo when not properly debrided. When tissue laxity allows removal of crushed tissue margins, a judicious sharp debridement of the wound margins is undertaken. Clearly devitalized tissue is excised. Freshening the wound margins contributes to rapid healing and improves the final result. Perhaps the most important step in repair of skin lacerations is excellent approximation of the deep dermal layer. By placing the tension of the closure deep to the skin the resulting scar is improved. A good choice of the suture material for this deep layer is poliglecaprone 25 (Monocryl, Ethicon, Somerville, NJ). Because of the monofilament nature of this suture, it may have a lower likelihood of suture contamination and extrusion. It also maintains tensile strength for a sufficient period of time to allow for uncomplicated wound healing. The choice of suture for the skin depends a great deal on the patient. Assuming a good deep dermal layer has been placed, the skin suture serves only to more accurately approximate and evert the skin edges. In children, it is beneficial to avoid a permanent suture to obviate the need for suture removal. An excellent choice in this case is 5-0 or 6-0 fast-absorbing gut suture. This suture type dissolves so rapidly that suture marks are not left on the face. It provides very little tensile strength, however, requiring the use of adhesive strips. If a skin adhesive is chosen in the pediatric population, one must take great care not to place any within the wound itself, as placing any within the wound may cause a profound inflammatory response, resulting in breakdown of the closure. A subcuticular skin suture is also an option in the face. If this is to remain in place, Monocryl is again a good suture material choice. Should one desire to remove the suture, polypropylene tends to be the best choice as it slides out of the skin easily. Skin edges under a greater degree of tension are usually best closed using interrupted nylon or Prolene. In heavily contaminated wounds the use of interrupted sutures or running sutures in short segments can be used. This allows for removal of focal areas of suture in the case of infection, avoiding a complete wound dehiscence. As a general rule, sutures in the face can be removed by 5 to 7 days when they are load bearing. When

a layer of reliable deep dermal sutures are in place, superficial skin sutures can be removed as soon as 3 days to avoid suture marks.

Injuries to Special Facial Regions Eyelids The most important aspect of evaluating trauma to the eyelids is ensuring that injury to the globe has not occurred. A thorough ocular examination is an essential element. It is important to remember that the Bell phenomenon results in an upward and lateral rotation of the globe. As such, one may find penetrating injuries to the globe in locations that do not intuitively correspond to the eyelid injury. Often a general anesthetic is required to provide sufficient anesthesia to explore eyelid injuries and allow for adequate exploration of the globe. General anesthesia is particularly recommended in the pediatric population where additional damage can be caused by working with sharp needles and instruments around the orbit in an uncooperative child. Direct injuries to the globe warrant urgent ophthalmologic consultation. Perhaps the most critical step in suturing the eyelid is to place an everting stitch along the lid margin. This not only facilitates proper anatomic alignment, but also prevents notching of the lid margin. The suture in the lid margin can be left long and taped down to the cheek to prevent the suture ends from irritating the eye. In general, all layers of the eyelid (inner, middle, and outer lamellas) should be repaired. Although the conjunctiva will heal well without sutures, injuries associated with significant deformity should be sutured with plain gut suture, paying careful attention to bury the knots so as to avoid irritation of the globe. The middle lamella, including the tarsus, should be sutured with a resorbable suture. Following this, the skin of the eyelid should be sutured. Sutures should be removed within 5 days. Depending on the magnitude of the injury, it may be helpful to place a Frost suture to support the lid position during the healing, especially in injuries to the lower lids.

Ears Ear lacerations can usually be sutured in one layer, addressing the skin only. It is typically unnecessary to place a separate layer of sutures within the cartilage. The firm adherence of the skin to the underlying cartilage framework of the ear ensures that skin approximation accurately aligns the cartilage. The two most prominent concerns in ear injuries are hematoma and chondritis. Collections of blood in proximity to the cartilage can result in cartilage resorption or a reactive chondrogenesis, which ultimately leads to the cauliflower ear deformity. Hematomas must be evacuated as quickly as possible to avert this adverse sequela. Hematoma can be easily drained through incisions in the overlying skin, making an effort to conceal incisions if possible. Because of the robust perfusion to the auricular skin, a bolster is often required to prevent re-accumulation of the hematoma. Alternatively, a small suction drain or Penrose-type drain may be used. A compression dressing should be employed regardless of the type of drainage technique employed. Following treatment of significant lacerations, one should line the convolutions of the ear with antibiotic-impregnated gauze and place a light head wrap, providing gentle compression of the ear. One should warn the patient regarding significant pain following these injuries. As a general rule, ear trauma is not terribly painful. The development of pain in the posttreatment period usually signifies the development of a hematoma or infection. Therefore, the delayed onset of pain warrants



immediate inspection of the ear. Chondritis is a serious complication of these injuries. As cartilage has such poor blood supply, it is difficult to treat these infections with oral antibiotics. These patients typically require admission for intravenous antibiotics and possibly debridement. It is rare to develop a significant chondritis without concomitant pain.

Nose Soft-tissue injuries of the nose are somewhat different from auricular trauma. When lacerations involve the underlying cartilaginous support system of the nose, all layers should be repaired after appropriate anatomic reduction. Simple reapproximation of the overlying skin does not necessarily align the underlying cartilage. As such, any lacerations or transections of the upper or lower lateral cartilages should be separately addressed. Because of the difficulty in achieving adequate anesthesia and control of bleeding with the use of local anesthetic alone, general anesthesia is warranted to maximize patient comfort and control.

Lips The most important consideration in repairing soft-tissue injuries involving the lips involves accurate re-approximation of the injured structures, especially the vermilion. A discrepancy in alignment of the vermilion border as little as 1 mm is noticeable at conversational distance. As such, prior to infiltration of any local anesthetic, the location of the vermilion border on either side of a laceration should be tattooed using a needle with methylene blue. The vermillion should be accurately re-approximated using a 6-0 nylon or similar suture. Great care must be taken to separately reapproximate the underlying orbicularis oris muscle. Failure to do so will result in bunching of the muscle on either side of the laceration with attempted animation, and typically results in a shortened scar with an exaggerated notching of the lip. Mucosal lacerations are repaired using a resorbable suture such as chromic or Vicryl (Ethicon, Somerville, NJ). A careful examination is performed to rule out underlying damage to the dentition. Any loose or damaged teeth are documented. Particularly unstable teeth may benefit from a bridle wire securing them to adjacent stable teeth. Panoramic radiographs or periapical images may help to better delineate underlying dental trauma.

Facial Nerve Soft-tissue injuries to the face involving the facial nerve are particularly devastating. In examining the patient with facial soft-tissue injury, particularly penetrating wounds, facial motion is examined carefully. One should specifically test elevation of brow, forced closure of the eyes, voluntary smile, and eversion of the lower lip. Eversion of the lower lip is not very well tested by asking a patient to purse the lips; rather, it is best seen in attempted full-denture smile. Deficits in the presence of a penetrating injury likely represent transection of a facial nerve branch. As a general rule, all such injuries should be explored operatively. The exception may be suspected injuries to the buccal branches medial to the lateral cantus of the eye. As a consequence of the extensive arborization of the nerve at this level, most such injuries will undergo spontaneous reinnervation over a 3- to 6-month period. Injuries lateral to this and any deficit in brow elevation, eye closure, or lower lip depression should be explored. Timing is of importance in these situations. The ability to identify the distal transected nerve end is facilitated by stimulating with a facial nerve stimulator and detecting the facial motion. After approximately 48 to 72 hours, the distal nerve end can no longer be stimulated, greatly complicating accurate

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identification because of the small size of the nerve and the inflammatory response in the surrounding tissues. These injuries should be repaired using microscopic magnification and 9-0 or 10-0 nylon epineural sutures. The time to recovery for a repaired nerve can be approximated by measuring the distance between the site of injury and the target muscle. Nerve regeneration typically occurs at a rate of 1 mm per day after a 1-month lag (Chapter 9).

Parotid Gland/Duct Injuries The most significant concern in parotid injuries is the possibility of facial nerve injury. The facial nerve separates the parotid into a superficial and deep lobe, and lacerations in this region frequently injure both the parotid gland and facial nerve. A parotid gland injury does not require intervention unless the underlying parotid duct is involved. Involvement of the Stensen duct will result in a parotid fistula unless corrected. These injuries may be difficult to identify and may only be seen following repair of a skin lacerations with subsequent accumulation of saliva. Duct injuries should be repaired over a stent to allow healing. It may be easiest to repair the duct through the open wound in the cheek. Identification and access to the distal segment of the Stensen duct can also be facilitated by cannulating the papilla opposite the maxillary second molar with a blunt parotid or lacrimal probe. The ends of the duct should be freshened and repaired over a stent. We often employ a 5French pediatric feeding tube brought through the papilla and secured intraorally to prevent accidental displacement during the healing period.

FACIAL FRACTURES Orbital Fractures Orbital Examination In any patient presenting with facial trauma involving the orbit, a thorough examination of the globe and associated structures is mandatory. Unrecognized trauma to any of the orbital contents can be disastrous. There is a great deal of information that can be ascertained from examination in the emergency department. A focused history and examination begins by determining if the patient has had any previous history of iatrogenic globe penetration, such as cataract surgery or radial keratotomy. This substantially increases the risk for globe rupture following trauma. A careful assessment is also made of the contralateral, uninjured eye. A visual examination is performed on every patient. This can be combined with a visual fields exam by having the patient close one eye with the examiner closing the corresponding eye. That is, if the patient is asked to close his left eye, the examiner, facing the patient, should close her right eye. The exam should be performed using a light source at 90 degrees to the visual axis of the examiner and examinee. This is a good assessment for both gross vision and visual fields. Visual field assessment is important, as any damage to the optic nerve may manifest first as a limitation in the visual field rather than a significant change in gross acuity. Additionally, one should test for color desaturation. Perhaps the first indication of optic nerve compression is red color desaturation. The easiest way to test this in the emergency department is to dim the lights and hold a pen light up to the finger. The light through the skin appears red. The patient should be asked with alternate eyes closed whether there is any difference in the intensity of the red color between the two eyes.

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Direct and consensual pupillary responses are elicited to determine the function of the second and third cranial nerves. Anisocoria may be an indication of second or third nerve damage, or direct trauma to the iris. A relative afferent pupillary defect (APD) is indicative of optic nerve injury that can be elicited by a swinging flash light test. Range of motion testing of each eye will determine the function of the third, fourth, and sixth cranial nerves. Restrictions in the range of motion of the globe should be confirmed with a forced duction test to determine if the restriction is caused by mechanical entrapment or by injury to the nerves or muscles. These emergency department maneuvers, although potentially quite informative, are no substitute for a thorough dilated exam by an ophthalmologist. Ophthalmologic consultation should be considered in every case of orbital trauma.

Indications for Surgery: Orbital Floor Indications for repair of orbital fractures are an area of great controversy. There are, however, several well-established indications. The most significant is evidence of mechanical entrapment of an extraocular muscle causing diplopia. This may be demonstrated on forced duction testing or on imaging studies. A second is evidence of enophthalmos. With the initial swelling present secondary to the trauma, any enophthalmos that is manifest indicates a significant deformity as it would be expected to worsen with the resolution of swelling. Deferring surgery will complicate the eventual repair that is required. Defect size is the most controversial parameter in determining the indication for surgery. Various authors have used different guidelines (2). Many believe that any defect greater than 1 cm2 benefits from surgical repair because of the likelihood of subsequent enophthalmos. Other authors have tried to quantitate, via CT imaging, the actual increase in orbital volume compared to the uninjured side. This volume is then used to assess the risk for postinjury enophthalmos. Currently, there are no firm data confirming the usefulness of this approach. There is some benefit, regardless of the indications for surgery, in delaying surgery until there is a modest improvement in swelling. As a successful outcome in these injuries is dependent on reestablishing the proper anteroposterior projection of the globe, it is helpful to have most swelling largely resolved. Because the surgical exploration of the floor evokes some degree of swelling, the cumulative effect can make it difficult to gauge the degree of correction necessary. However, whether the surgery is performed early or late (early, 1 to 3 days; late, 7 to 10 days), the operated eye is overcorrected so that it projects a little farther than the uninjured eye immediately following surgery.

Incisions/Technique The most common complication from incisions used to access the orbital floor is lower eyelid retraction. This may result in ectropion or entropion. The subciliary approach, so often used for blepharoplasty, clearly has the highest risk of associated retraction when one examines the literature. The transconjunctival approach has consequently gained popularity. One may approach this dissection in either the preseptal or postseptal plane. Avoiding dissection of the skin and orbicularis diminishes the risk of postoperative retraction. Although some authors believe that a lateral canthotomy is unnecessary, there is no question that detaching the lateral canthus improves exposure. If a lateral canthotomy is performed, a canthopexy must be performed at the conclusion of the case in order to reestablish the appropriate position of the lateral canthal ligament.

Maxillary sinus

FIGURE 31.3. Identification of posterior ledge in orbital floor fractures. Technique of safely identifying the posterior limit of an orbital floor defect. The elevator is placed into maxillary sinus and used to identify the posterior ledge by sweeping upward and forward.

The subtarsal incision can also be employed, especially in older patients with prominent lower lid rhytides within which the incision can be concealed. This incision is the most direct access to the orbital floor and avoids dissection of the lower lid proper. Consequently, it is very unlikely to cause lower lid retraction. Dissection of the lower lid should be directed toward exposing the periosteum of the infraorbital rim and incising it on the outer margin of the rim. This affords a greater degree of control and ensures that the proper plane is obtained prior to entering the orbit. A periosteal elevator is then used to dissect posteriorly. The infraorbital nerve is encountered within the orbital floor, usually about halfway back. The nerve is protected and kept down with the bone. The orbit is conically shaped with a superior-medial slant toward the orbital apex. The goal of the dissection is to identify the portion of the floor that is still intact and contiguous with the orbital apex. Whatever material is used to reconstruct the floor must be suspended on this posterior ledge to ensure accurate anatomic reconstruction. At times, the posterior ledge can be difficult to identify in the subperiosteal plane. In these cases, it can be safely identified by placing the elevator straight posteriorly into the maxillary sinus and gently walking the elevator superiorly (Fig. 31.3). The posterior floor is then encountered. The anterior ledge of the intact posterior floor can be safely identified by working the elevator anteriorly until the defect is encountered. Once the margins of the defect are defined, reconstruction can proceed.

Floor Implants In the past, there was a general consensus among maxillofacial surgeons that bone was the best implant for reconstruction of the floor. Classically, this was harvested from the outer table of the skull. Although this is clearly a reliable option, it does entail a longer operative time, potential donorsite morbidity, and some degree of resorption of the graft postoperatively. Alloplastics enjoy several advantages over bone grafts, including immediate availability and no risk of resorption. The disadvantage is obviously the potential risk of implant infection and extrusion, which is a rare complication. Among the implants available are titanium mesh, high-density porous



polyethylene, and resorbable materials. Very large orbital defects, particularly those involving the medial wall, are best reconstructed using titanium mesh because of the support provided and the ease of contouring. Resorbable implants may be useful in smaller defects, particularly in children, where there is some reluctance to use permanent implants because of growth concerns. Silastic, although used commonly in the past, is best avoided as a floor implant because of a relatively higher risk of late extrusion and infection.

Complications The most common complications following surgery for orbital fractures are lower-eyelid retraction and enophthalmos. As was previously discussed, lower-eyelid retraction can be minimized by appropriate choice of incision. This should be an uncommon complication if the subciliary incision is avoided. It may also be helpful postoperatively to place a Frost suture maintaining the lower eyelid in an elevated position for 24 hours following the procedure. If retraction is noted in the early postoperative period, the patient should begin aggressive lowereyelid massage and forced eye-closure exercises. This resolves the problem in the vast major of cases. Early operative intervention for lid retractions should be avoided unless the patient is experiencing problems with corneal exposure as indicated by constant irritation of the eye. In the absence of this, operative intervention for lid retraction should only be considered after failure of conservative measures for 4 to 6 months. Regardless of the initial incision, patients with postoperative lid retraction should be approached through the transconjunctival approach. The typical cause is scarring of the middle lamella. This should be released and a spacer such as hard palate mucosa placed. Enophthalmos is particularly resistant to secondary correction and is most frequently caused by inaccurate reconstruction of the orbital floor and excessive orbital volume. As a result of the superior incline of floor, placement of the floor implant must be directed superiorly to anatomically reconstruct the defect. Dissecting straight back rather than cephalically results in the implant being placed within the maxillary sinus (Fig. 31.4). This maintains the expansion in the orbital volume and results in subsequent enophthalmos. One must also remember that appropriate reconstruction of the orbital floor results in the operated eye being slightly proptotic in the early postoperative period when compared to the uninjured side. Failure to achieve this at the time of surgery is an almost certain guaran-

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tee of enophthalmos when the swelling resolves. Although fat atrophy may also increase orbital volume somewhat postoperatively, the contribution of this mechanism to enophthalmos is likely not significant. The most direct approach for correction of this problem is accurate and anatomic reconstruction of the orbital floor. Secondary reconstruction is much more difficult. However, established postoperative enophthalmos never improves and, if bothersome to the patient, will require reoperation. Persistent diplopia may also be seen following repair of orbital fractures. This is most troublesome if it is in the primary field of gaze or in downgaze, as walking may become problematic. In avoiding this complication, it is very important to perform a forced duction test at the termination of the operation to ensure that implant placement has not resulted in a mechanical interference with globe movement. In the event that the patient complains of new-onset diplopia in the immediate postoperative period, a CT scan should be performed to evaluate this possibility. If no mechanical impedance is appreciated, the patient should be followed conservatively with ophthalmologic consultation to assist with care. Although this problem is usually a result of low-grade neurapraxia, muscle contusion, or swelling, which resolves spontaneously within several months, rebalancing of the extraocular muscles may ultimately be required.

Orbitozygomatic Fractures Diagnoses/Examination The physical examination in orbitozygomatic fractures is important, but often misleading. Swelling from the injury frequently conceals the malar recession and any evidence of enophthalmos. Anesthesia in the distribution of the infraorbital nerve is common and should be documented on initial examination. Additionally, severely displaced fractures may cause trismus secondary to impingement of the coronoid process on the mandible by the displaced posterior aspect of the zygomatic arch. The orbital aspect of these injuries necessitates careful ophthalmologic examination and is perhaps the most important aspect of the preoperative work-up. The decision to operatively reduce an orbitozygomatic fracture is largely dependent on the CT scan data, as swelling often precludes accurate determination of the degree of deformity. When evaluating the CT scan, it is most useful to look at the lateral orbital wall on the axial cuts, which represents the articulation of the zygoma with the greater wing of the sphenoid. This broad articulation will manifest any displacement present and determine the degree of deformity. One must also assess four other articulations for displacement, including the infraorbital rim, the zygomaticomaxillary buttress, the zygomaticofrontal suture, and the zygomatic arch. Nondisplaced fractures may be safely managed with a nonchew diet and close clinical follow-up. A nonchew diet will prevent the activation of the masseter from displacing the fracture segment. Displacement of the fracture is a definitive indication for operative reduction and fixation, as the results of early operative repair far exceed those of delayed repair. Repositioning of a displaced fracture in a delayed setting requires osteotomy of all buttresses and extensive craniofacial exposure. It is best to reduce and fixate fractures anatomically in the acute setting.

Operative Techniques FIGURE 31.4. Incorrectly placed orbital floor prosthesis. Orbital floor implant misplaced directly posteriorly into the maxillary sinus. Note the flat lie of the implant, which should incline superiorly.

The operative treatment of orbitozygomatic fractures depends largely on the degree of displacement and comminution. The majority of patients can be accurately reduced and fixated

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using incisions in the upper gingivobuccal sulcus, lower eyelid (transconjunctival), and the lateral extent of the supratarsal fold of the upper eyelid. The coronal incision is necessary only when the zygomatic arch must be exposed and reduced as a guide to appropriate alignment of the zygoma. This is typically only necessary when there is so much comminution of the infraorbital rim and zygomaticomaxillary buttress that these cannot be used as an accurate guide to reduction. In practice, only three of the four buttresses require reduction as long as the zygoma is a single, large, fracture segment. As a general rule, the intraoral incision is typically performed first. In lower-energy fractures, it is occasionally possible to elevate the displaced zygoma using an instrument placed behind the zygomatic arch. If the fracture reduces with this maneuver, a plate may be placed across the zygomaticomaxillary buttress and the operation terminated. Even if this does not allow anatomic reduction of the fracture, it is still beneficial in that it moves the zygoma to a more anatomic location, facilitating the lower-eyelid dissection of the orbital rim. As with orbital fractures, the subciliary incision is typically best avoided. Generally, either the transconjunctival or subtarsal incision is best. If a coronal incision has not been used, the zygomaticofrontal suture requires exposure through the lateral extent of the supratarsal fold. Although eyebrow incisions have been used in the past, these may leave prominent scars and provide less-direct access to the suture. Once all of the articulations of the zygoma have been visualized, they should be aligned and the fracture stabilized. It is very useful to first align the zygomaticofrontal suture using either a wire or a 1.0-mm plate. This sets the vertical height of the zygoma while still allowing rotation and further alignment at the level of the rim and the zygomaticomaxillary buttress. Once this suture is stabilized, the surgeon should anatomically reduce the other two buttresses. Reduction may be facilitated by using a Carol-Gerard screw placed through the lower-eyelid incision into the body of the zygoma (Fig. 31.5). It acts like a joystick and allows easy control of the fracture fragment in three dimensions. A 1.5-mm plate is typically placed along the superior aspect of the infraorbital rim rather than anteriorly to avoid either visibility or palpability by the patient postoperatively. The buttress that provides the most stability to the reduced fracture is the zygomaticomaxillary. A 2.0- or 1.5-mm L-plate is most commonly used at this buttress. In the most severe fractures, when the arch has to be exposed to align the zygoma, this is

FIGURE 31.6. Incorrect reduction of the zygomatic arch. CT scan of a zygomatic arch that was inappropriately reconstructed as an arch. The normal arch lies in an almost straight anteroposterior direction, as can be seen on the normal side.

best plated first with a 2.0-mm plate to reestablish the width and projection of the zygoma. It is not necessary to provide three or four points of fixation for every zygoma fracture. Although this number of plates is commonly used, it is usually a result of the sequence of steps used in aligning the fracture. Although three or four plates may be necessary in high-energy injuries, many fractures can be adequately fixated using a single 2.0-mm L-plate along the zygomaticomaxillary buttress. When the zygomatic arch is significantly displaced and comminuted it requires full exposure and reconstruction. There is a tendency for surgeons to view the arch as an arch when in reality it is much more of a straight anteroposterior structure. If reconstructed as an arch it will result in excessive facial width and prominence to the region relative to the contralateral side. In addition, the malar eminence will not be projected as far forward as it should. This is an especially important factor when there is significant destruction to the malar and arch complexes bilaterally and the surgeon must reestablish facial width in proportion to facial height without the benefit of an internal reference (Fig. 31.6).

Arch Fractures

FIGURE 31.5. Carol-Gerard screw. This instrument can be used to gain control of the zygoma in orbitozygomatic fractures. It can be placed either through an intraoral incision or percutaneously.

Isolated fractures of the zygomatic arch are treated differently from true orbitozygomatic injuries. Isolated arch fractures frequently do not require operative reduction. Operative treatment of these fractures is indicated for severe depression of the arch causing either a cosmetically significant contour depression or impingement on the coronoid process and trismus. The fracture may be approached intraorally through an upper buccal sulcus incision or an incision in the temporal scalp. The intraoral approach, although more difficult, avoids an external scar. The scalp incision, commonly referred to as the Gillies approach, allows more direct access to the fracture site. The incision is placed vertically within the temporal hairline and dissection is carried directly through the temporoparietal fascia and deep temporal fascia. The elevator is then placed in plane between the deep temporal fascia and the temporalis muscle and advanced to a position deep to the arch. Any resistance to sliding the arch inferiorly usually indicates that the plane of dissection is too superficial. Outward pressure



on the arch forces the fracture into an anatomically reduced position. Occasionally, arch fractures essentially snap back into position and are stable. In the majority of cases, however, the fracture is unstable in the reduced position. In such situations, it is helpful to splint the reduced arch using permanent sutures placed transcutaneously and encircling the arch. The suture is tied over a metal eye shield to provide constant upward and outward traction. Typically two sutures are required to hold the arch in position. Excessive tension on the sutures may lead to skin necrosis at the margins of the eye shield.

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ment, particularly in high dorsal deviations. Extensive septal mobilization, resection, and scoring may be necessary. Airway compromise should also be a focus of the subsequent rhinoplasty.

Maxillary Fractures Diagnosis

Nasal Fractures

Fractures of the maxilla have been classically described as Le Fort I, II, and III patterns. These patterns, by definition, are fractures that detach the maxilla from the skull base. The maxilla is mobile and may result in malocclusion. Although it is not uncommon in facial trauma that the anterior wall of the maxillary sinus, and even the zygomaticomaxillary and nasomaxillary buttresses, are fractured, injury to these structures alone does not constitute a true Le Fort injury. The fracture must extend through the pterygoid plates to create a complete Le Fort fracture (Fig. 31.7). The Le Fort I injury classically passes through the maxilla transversely, somewhere between the tooth roots and the infraorbital rims, with preservation of the integrity of the infraorbital rims. The Le Fort II fracture extends through the infraorbital rim and nose and is sometimes referred to as a pyramidal fracture. The Le Fort III fracture involves the zygomatic arch, lateral orbital wall, and the nasofrontal region. Le Fort fractures rarely exist in pure form. More commonly, patients will present with a combination of injuries such as a Le Fort I on one side and a Le Fort III on the contralateral side. Preoperative evaluation should be focused on the occlusal relationship. Any sign of malocclusion should be evaluated carefully. Correction of the occlusion to the preinjury state will guide the appropriate anatomic reduction.

Diagnosis/Examination

Operative Technique

The diagnosis of a nasal fracture is clinical. Patients presenting with a history of acute trauma with evidence of a deviated nose have an underlying nasal fracture. Radiographs, although frequently obtained, are superfluous. When examining a patient with a suspected nasal fracture, an intranasal inspection is mandatory to identify a septal hematoma. Untreated septal hematomas may lead to resorption of the cartilaginous septum and result in a saddle nasal deformity. Septal hematomas should be expeditiously evacuated. Reaccumulation can be prevented with the use of either septal quilting sutures or intranasal splints.

Le Fort I injuries can be adequately exposed through an upper gingivobuccal sulcus incision and maxillary degloving. Le Fort II injuries often require a lower lid incision. As in orbital fractures, a transconjunctival incision is preferred over a subciliary incision. In older patients, a subtarsal incision can be concealed in a lower-lid crease. Le Fort III injuries may be approached through a combination of buccal sulcus and lower-lid incisions in low to moderate impact injuries. More severe injuries require a coronal approach for exposure of the nasofrontal and medial orbital regions and the zygomatic arch. Following mobilization of all of these fractures, the patient should be placed in maxillomandibular fixation and the zygomaticomaxillary and nasomaxillary buttresses stabilized with plates.

Complications The most common complication following repair of orbitozygomatic fractures is enophthalmos. This results from malreduction of the fracture. As in orbital floor injuries, displaced orbitozygomatic fractures almost always expand orbital volume, as the zygoma constitutes a large portion of the orbital floor and lateral wall. Both the increased orbital volume and the malar recession must be addressed in the treatment of the malreduced fracture. To address this, the zygoma is best osteotomized, repositioned in its appropriate anatomic location, and secured with plates. Occasionally, the malar recession is not significant and treatment can be directed at correction of the orbital volume alone. As in an orbital floor fracture, additional alloplast may be placed in the floor or along the wall of the orbit to diminish volume and correct the enophthalmos. Maxillary sinusitis and persistent numbness in the infraorbital nerve distribution may complicate orbitozygomatic fractures less frequently.

Treatment Treatment of nasal fractures can be divided into early and late phases. If one sees a patient with nasal fracture immediately following the injury, it is beneficial to perform a closed reduction. This may be done in the emergency department using local anesthesia and an intranasal vasoconstrictor. Although closed reduction can be performed any time in the first 2 to 3 weeks, the swelling may be so severe as to camouflage the magnitude of the deformity and complicate accurate reduction. Swelling usually improves significantly 10 to 14 days after injury facilitating closed reduction. The late phase is defined as a period where sufficient bony union has taken place such that osteotomy is required to anatomically reduce the fracture fragments. Correction in the late phase should be viewed as a complete rhinoplasty. The contribution of the septum to the deviation should be appreciated and addressed. Simply performing osteotomies is unlikely to correct the deformity in the face of septal involve-

Nasoorbitoethmoid Fractures Diagnosis and Examination Fractures of the nasoorbitoethmoid (NOE) region involve the medial orbit, nasal bones, septum, and nasofrontal junction. On examination, patients with nasoorbitoethmoid injuries may exhibit substantial loss of dorsal nasal support. Additionally, telecanthus may be present secondary to lateral displacement of the bone fragments bearing the medial canthal tendon. These patients demonstrate an increased distance between the medial canthi and rounding of the medial canthal angle. The CT scan is the most helpful radiologic tool in determining the location of the injury and the degree of comminution— the two factors critical to determining the appropriate treatment. Analysis of the axial cuts should focus on the lacrimal

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B

A FIGURE 31.7. Incomplete Le Fort I fracture. A: Three-dimensional CT demonstrating a midface fracture that appears to be present at the Le Fort I level. B: Axial CT scan of the same fracture revealing intact pterygoid plates. This fracture was completely stable on examination under anesthesia and thus does not require stabilization.

fossa and the start of the nasolacrimal duct. This region identifies the level of insertion of the medial canthal tendon. A great deal of comminution at this level may require transnasal fixation of the bone fragments bearing the medial canthal ligaments. Bilaterally mobile medial canthal tendons represent a significant challenge to reconstruction as there is no normal frame of reference with which to judge preoperative location of the medial canthi. On occasion, it is difficult to definitively make the diagnosis of nasoorbitoethmoid injury. Definitive diagnosis can be made by examination under anesthesia by placing a hemostat in the nose to the level of the medial canthus. With a finger palpating externally over the medial canthus and outward pressure on the internally positioned hemostat, one can determine the degree of mobility, and consequently the need for operative stabilization.

Operative Technique The majority of nasoorbitoethmoid injuries should be exposed through both coronal and lower-eyelid incisions. As the fracture is dissected, one must take great care not to strip the insertion of the medial canthal tendon off of the fracture fragments. Markowitz et al. (3) have devised a classification scheme based on the relation of the insertion of the medial canthal tendon to the fracture. Type 1 fractures involve a very large bone fragment to which the medial canthal tendon is inserted. These injuries may be treated essentially by fixation of the bone fragment to adjacent surrounding bone. Type 2 fractures involve more extensive comminution; however, the medial canthal tendon is still attached to a bone fragment that can be stabilized directly. When the fragment is too small for fixation, transnasal wiring can be used to position the fragment and medial canthal tendon appropriately. Additional bone grafting may be required. Type 3 injuries involve avulsion of the medial canthal tendon from its skeletal insertion. In addition to appropriate reduction of bone fragments and bone grafting, these patients require transnasal fixation of the medial canthal tendon. When transnasal medial canthoplasty is necessary, it must be performed so that the direction of pull on the canthal tendon is posterior and superior. A common mistake is to reattach the canthal tendon too anteriorly, resulting in persistent telecanthus. The procedure is performed by drilling from the contralateral side through the nasal bones with the exit

point planned at approximately the level of the superior aspect of the lacrimal fossa. This is an appropriate vector for pull on the tendon. The medial canthal tendon is grasped either from the underside of the coronal incision, or looped from an anterior incision medial to the medial canthal angle. The wire or permanent suture is then placed through the drill hole using a wire-passing drill bit toward the contralateral side. The suture or wire can be affixed to a screw placed on contralateral side. Many of these injuries involve substantial loss of nasal support that cannot be restored by direct plating. In these situations onlay bone grafting of the nasal dorsum will reestablish the appropriate projection and width of the nasal radix. Multiple techniques have been described to stabilize bone grafts in this region including miniplates, lag screws, and K-wires. A soft-tissue bolster over the medial canthal valley is also often necessary to restore the normal contour to this region. The medial canthal valley is a unique region of the face where the skin is intimately adherent to the underlying skeleton. The soft-tissue bolster prevents the subcutaneous accumulation of blood and fluid that interferes with the healing of the skin directly to the underlying bone. These bolsters are usually left in place for 7 to 10 days. The skin underlying the bolster should be watched carefully for necrosis and the bolster should be tied in such a way to allow for adjustment of tension postoperatively. The most common complication following nasoorbitoethmoid fractures is telecanthus. This is a very difficult problem to correct secondarily. Once it is established, the area must be approached in a similar fashion, the scar contractures completely released, bone grafts placed to reestablish contour, and transnasal canthoplasties performed. The results of secondary repairs are always disappointing when compared to accurate acute repair.

Frontal Sinus Diagnosis and Examination Patients with frontal sinus fractures may present with obvious contour deformities of the forehead, but often the swelling



FIGURE 31.8. Axial CT scan of the frontoethmoidal region revealing complete obliteration of the nasofrontal duct by bone fragments. The frontal sinus requires obliteration in the case of a nonfunctioning duct to avoid development of a mucocele.

associated with the injury blunts the degree of deformity. Injury to the frontal sinus is commonly associated with injury to the central nervous system, and early evaluation should focus on this possibility. Axial cuts of the CT scan are useful in determining the degree of injury and involvement of anterior table, posterior table, and the nasofrontal duct. These three structures are used in the classification of frontal sinus fractures as well as subsequent treatment. Isolated anterior table fractures may be treated simply by reduction and plate fixation via a coronal incision or through existing cuts in the forehead. The function of the nasofrontal duct should be kept in mind at all times. In many cases, involvement of the nasofrontal duct is obvious from the CT scan (Fig. 31.8). This is particularly true for fractures located inferior and medially in the sinus, where the meatus typically originates. During operative exploration, direct instillation of dye (fluorescein) into the region of the nasofrontal duct within the sinus cavity can be used to test the function of the duct. The presence of dye on pledgets placed intranasally indicates a functional duct system. Any compromise of this drainage requires frontal sinus obliteration. The first step in frontal sinus obliteration is removing the anterior table entirely. The limits of the sinus may not be obvious based on direct examination, particularly in small fractures. Placing one arm of a bayonet forceps into the sinus until the limits of the sinus are reached can help delineate the margins so that the sites of the antrostomy can be determined. Additionally, the operating room lights may be turned down and a light source placed within the sinus, defining the margins of the sinus. Finally, a 1:1 posteroanterior radiograph of the skull may be used to obtain a template of the shape and location of the sinus. This may be cut out from the radiograph, sterilized, and used as a guide for antrostomy. Once the anterior table is removed, all mucosa must be removed from the sinus. Because of small mucosal invaginations into the bone, termed the vascular crypts of Breschet, a burr should be used to ensure complete mucosal obliteration. Once this has been accomplished, the nasofrontal drainage system must be plugged to prevent ingrowth of the mucosa from the ethmoid sinus and nose below. This may be accomplished with a graft of muscle, bone, fat, or a pericranial or galeal flap. At this point, many surgeons fill the sinus cavity with graft material, most frequently fat. This has been challenged by some on the basis of the concept of osteoneogenesis. Mickel and

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FIGURE 31.9. Pericranial flap. This tissue is often used to interrupt the communication between the ethmoid sinuses and nose with an obliterated frontal sinus.

Rohrich (4) demonstrated spontaneous obliteration by bone in cat frontal sinuses that were surgically burred out and not filled with graft material. This technique has been used by the authors for years without evidence of any increase in complication rates over those published in the literature. From a conceptual standpoint, one must question the superiority of filling a bone cavity with nonvascularized material over simply not filling it at all. In reality, the pericranial or galeal flap used to obliterate the nasal communication may in itself completely fill smaller sinus cavities (Fig. 31.9). Fractures of the posterior table of the frontal sinus place the patient at risk for acute meningitis and late intracerebral mucocele formation. Fractured fragments of the posterior table may develop trapdoor-type phenomena leaving small bits of mucosa within the cranial cavity. These areas of trapped mucosa are at risk for mucocele formation. Evaluation of the axial cuts through the frontal sinus will reveal displacement of the posterior table within the cranial cavity. Any significant posterior displacement or the presence of a cerebrospinal leak is considered an indication to cranialize the sinus. Cranialization involves performing a frontal craniotomy and removing the entire forehead as a bone flap. The posterior table is then removed and the mucosa of the anterior table burred out. As in obliteration, the nasal communication is eliminated using a pericranial or galeal flap. The bone flap is then plated back into position and the brain is allowed to expand into the space previously occupied by the sinus.

Complications The most significant complications related to frontal sinus fractures are infectious in nature. In cases in which the frontal sinus has been preserved, one must give consideration to serial CT scans in the postoperative period to assess adequate drainage of the sinus. Failure of the sinus to clear radiographically may indicate impaired drainage that may lead to infection. Evacuation of a poorly draining sinus should be achieved with aggressive medical therapy, including topical and systemic decongestants and mucolytics, or via an endoscopic or open surgical drainage procedure. Mucocele formation may be a late complication of these fractures (Fig. 31.10). Unfortunately, most mucoceles and infections present very late following these injuries. It is not uncommon for this to occur years following the injury or surgery. Such delayed presentation makes accurate data regarding the success of the various treatment options difficult to obtain.

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Diagnosis and Examination

patient’s preinjury occlusion. Stable mandible fractures with no evidence of malocclusion can occasionally be treated with a nonchew diet for a period of 4 to 6 weeks, depending on the age, state of dentition, and compliance of the patient. For the most part, this is the exception and not the rule, as patients suffering mandible fractures tend to be young, male patients notorious for their noncompliant demeanor. Because of the constant motion of the lower jaw in normal daily function, mandible fractures tend to be painful until stabilized. Some of the immediate discomfort is relieved by temporary immobilization of the fracture with a wire joining the teeth adjacent to the fracture site. This must be done carefully to avoid dislodging the teeth, which may be destabilized by the fracture. Careful documentation of mental nerve function is performed. Mental nerve neurapraxia often indicates involvement of the body of the mandible between the mental foramen and the mandibular foramen. Because of the likelihood of further neurapraxia related to surgical correction, it is wise to discuss the condition of the nerve and its clinical course prior to undertaking the operative repair. As with all facial fractures, radiographic evaluation is mandatory. An excellent single test for mandibular fractures is the panoramic radiograph. This requires that the patient be able to sit upright with a mobile neck, so cervical spine clearance is obligatory. The panoramic radiograph places the entire mandible on one film. It provides an excellent evaluation of the condyles and dental anatomy. Because of the nature of the technique in which it is taken, there can be significant distortion in the region of the symphysis, which may conceal fractures in this region (Fig. 31.2). The symphysial region is best evaluated with a plain, posteroanterior radiograph of the mandible. The CT scan, which is frequently obtained in the emergency center to evaluate facial trauma, is very sensitive and specific in detecting mandibular fractures. On the other hand, it provides a very little information about the dental anatomy, especially in the region of the mandibular angle. The relationship of fractures in the region of the mandibular angle to the surrounding teeth, particularly the third molars, is critical to successful treatment and is best evaluated with a panoramic radiograph. We routinely obtain a Panorex radiograph as an adjunct to the CT scan when the CT scan has already been obtained in the emergency department and indicates a mandible fracture.

Mandible fractures typically result in some degree of malocclusion. As patients are capable of detecting even the slightest degree of change in their occlusion, a complaint of malocclusion is a reliable indication of a mandible fracture. Care must be taken in the evaluation of mandible fractures to determine the effect on the occlusion that the fracture has caused. Because the goal of treatment is to restore the mandibular arch to its preinjury occlusal state, as much information as possible must be obtained from the patient history, including orthodontic treatment and any history of dental extraction. The wear facets of the dentition are perhaps the most valuable indicators as to the

Choice of fixation must be predicated on the specifics of each fracture. One must choose between rigid fixation (loading bearing) and what one might term functionally stable fixation (load sharing) (5). When internal fixation was first applied to the mandible, it was generally felt that absolutely rigid stabilization was required. Since then it has become appreciated that not all fractures require this, and may indeed do just as well with less-rigid stabilization (Table 31.2).

FIGURE 31.10. Frontal sinus mucocele. Axial CT scan of a mucocele several years following a frontal sinus obliteration with bone cement.

Mandible Fractures

Fixation

TA B L E 3 1 . 2 STABILITY OF FIXATION FOR MANDIBLE FRACTURES (5) Rigid fixation

Functionally stable fixation (nonrigid)

Reconstruction bone plate ( ± arch bar) Two bone plates (miniplates, compression plates, or combinations of these) ( ± arch bar) Two lag screws ( ± arch bar) One bone plate plus one or more lag screws ( ± arch bar) One 4-hole 2.4-mm compression plate + arch bar One 6-hole 2.4-mm compression plate ( ± arch bar)

One 4-hole 2.4-mm compression plate without arch bar One 2.0-mm miniplate + arch bar One lag screw + arch bar One 2.0-mm miniplate without arch bar for angle fracture


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A

B

FIGURE 31.11. Champy’s lines of osteosynthesis.

Rigid fixation typically implies plates that accommodate screws that are 2.4 or 2.7 mm in diameter. Functionally stable fixation most often uses plates accommodating screws 2.0 mm in diameter or smaller. The decision as to the type of fixation should be determined largely by the fracture pattern and its intrinsic stability. Patients with severely displaced fractures or with multiple mandible fractures have lost more of the intrinsic stability of the mandibular arch and may require fixation that is more rigid and bears more of the functional mandibular load. Additionally, patients at high risk for poor healing, such as those with atrophic mandibles or established infection, usually benefit from absolutely rigid fixation. Uncomplicated, isolated mandible fractures heal uneventfully using smaller plates and screws placed along the lines of osteosynthesis as delineated by Champy (Fig. 31.11).

Operative Technique Symphysis/Parasymphysis Fractures. As with most mandible fractures, the operative procedure should begin by reestablishing the patient’s occlusion using maxillomandibular fixation. In severely displaced fractures, it may be beneficial to expose the fracture first to achieve some degree of initial reduction. If the arch bars are applied initially without some degree of reduction, the arch bar itself will essentially lock the arch into a malreduced position and consequently a malocclusion. Displaced symphysis fractures typically require internal fixation. Maxillomandibular fixation does not usually achieve sufficient immobilization and stabilization of symphysial fractures because of the lack of intercuspation of the anterior dentition in most patients. These fractures may be adequately stabilized with either large or small plates. Placement of a single, large plate (≥ 2.4 mm) along the inferior border using bicortical screws is sufficient. It should be noted, however, that contouring a 2.4-mm plate to the acute curvature of the symphysial or parasymphysial region can be difficult and timeconsuming. Equally rigid fixation can be achieved by placing a 2.0-mm plate with bicortical screws at the inferior border and a 2.0-mm tension band with monocortical screws just below the root apices. A well-placed arch bar can take the place of the tension band and be left in place until bone union. We prefer the use of a tension band as we use it to assist with reduction prior to placing the inferior border plate. After the patient is placed into maxillomandibular fixation, two small holes are drilled into the inferior border on each side of the fracture to accommodate a reduction clamp. With the bone aligned and

the patient in occlusion, the monocortical tension band plate is applied. With this in position, the bone reduction clamp may be removed without impacting the reduction, and the inferior border plate placed onto a relatively stable platform. Most of these fractures may be treated via an intraoral incision. External incisions are typically reserved for only the most severe fractures in this region (multiple fractures and comminuted fractures). Body Fractures. Mandibular body fractures are treated with either maxillomandibular fixation alone (for 4 to 6 weeks) or internal fixation. Most practitioners prefer to perform an open reduction and internal fixation in these cases. As with symphysial and parasymphysial fractures, a single 2.4-mm inferior border plate or two 2.0-mm plates may be used. Care must be taken to avoid the mental nerve with the screws when treating these injuries. As with symphysial fractures, all but the most severe fractures are treated using an intraoral incision. Angle Fractures. Mandibular angle fractures are associated with the highest risk for infection and postoperative complications. The presence of a partially erupted or impacted third molar is the cause of the majority of complications. Partially erupted or impacted third molars predispose the angle region to fractures by weakening the bone in the region. The fracture site is frequently described as open secondary to its direct communication with the third molar socket. Although the decision to remove or retain the third molar is controversial, it may be generally believed that any significantly damaged or diseased third molar should be removed, as should any third molar that prevents reduction. Mandibular angle fractures have been treated with a variety of fixation techniques. Ellis et al. (6) advocate using a single miniplate along the external oblique ridge of the mandible along the lines of Champy. When comparing this to all other forms of fixation, the authors found their complication rate to be the lowest. Additionally, the fracture may be plated along the buccal cortex using a single 2.4-mm plate or two 2.0-mm miniplates. Intraoral exposure and plating is preferred in the majority of patients with simple angle fractures. A small incision in the cheek is required for placement of the screws. However, in complicated or comminuted fractures consideration should be given to an external incision. The external incision provides much greater exposure and control over the fracture. Subcondylar Fractures. No area of the mandible is as controversial as this region in terms of appropriate treatment. The literature is confusing with regard to terminology in the condylar/subcondylar regions. Injury may occur at the level of the

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condylar head, the condylar neck, or the region below the sigmoid notch, the subcondylar region. Condylar head injuries are intra-articular and for the most part are not amenable to internal fixation techniques. They are at very high risk for ankylosis. Condylar neck fractures are defined as those that occur between the head and the sigmoid notch. Historically, most of these injuries have been treated using maxillomandibular fixation for a period of 2 to 6 weeks. Although this results in excellent functional occlusion in many patients, it rarely reduces the fracture into anatomic alignment. Rather, the patient essentially develops a functional occlusal adaptation to the malreduction. Patients frequently continue to deviate to the fractured side with maximal opening and lose some of the contour of the mandibular border on the fractured side. Many authors advocate open reductions and internal fixation. The concern of many surgeons regarding this is the potential risk of damage to the facial nerve. Although most published series have demonstrated a very low risk of permanent injury to the facial nerve, even neurapraxia is a distressing complication. In an effort to avoid this, endoscopic instrumentation has been developed to fixate these fractures largely through an intraoral incision with small trochar sites externally (7,8). Zide and Kent (9) published a list of absolute and relative indications for open reduction and internal fixation of condylar fractures. This list has been modified by the body of literature over the years. As a general rule, internal fixation is considered in cases where maxillomandibular fixation is contraindicated (e.g., poorly controlled seizure disorder), fractures in which an acceptable occlusion cannot be reestablished, and bilateral fractures in the panfacial injury (to reestablish appropriate facial height). When maxillomandibular fixation is chosen as the treatment, the period of fixation varies, depending on the age of the patient and the fracture pattern. Patients with uncomplicated clinical healing should usually be maintained in maxillomandibular fixation for 2 to 3 weeks, followed by an additional 2 to 3 weeks of nonchew diet. As a general rule, the primary determinant of the period of treatment is the occlusion. Patients with no significant occlusal change may not even require maxillomandibular fixation. Additionally, high condylar fractures may have a greater risk of ankylosis and should be immobilized for shorter periods of time. The same can be said of children in whom maxillomandibular fixation is limited to 2 weeks. Many surgeons advocate the use of elastics rather than wire to guide the occlusion in the postoperative period. This approach should only be attempted in the highly reliable patient. Using elastics provides control of the patient’s occlusion while still allowing constant mobilization of the mandible, avoiding the problems inherent in maxillomandibular fixation.

Complications The most common complications after mandibular fracture repair is malocclusion, usually secondary to maladaptation of the plate used for fixation. Inappropriately contouring the plate (especially a large plate such as the 2- to 4-mm system) results in the mandible shifting to adapt to the plate. This shift promotes malreduction and, consequently, malocclusion. It is less commonly seen when miniplates are used, as the plates tend to adapt to the bone instead of the reverse. This phenomenon is less likely with locking plates. These are plates designed with threads within the screw hole. As the screw head approaches the plate, it locks into the plate. As such, the screw does not continue to tighten until the head is pulled up to the plate even if the plate is maladapted and is sitting above the plane of the bone. The screw stops when it reaches to the plate.

Once fixation has been applied to a mandibular fracture, maxillomandibular fixation is released and the patient’s occlusion carefully assessed. Malocclusion at this point mandates removal of the fixation and recontouring of the plate. One never relies on postoperative maxillomandibular fixation or elastics to correct a malocclusion secondary to a malreduction. Infection is also a common complication of mandibular fractures, most often as a consequence of mobility at the fracture site or because of loose hardware. During the exploration of an infected fracture that had been previously repaired, the operative site is thoroughly irrigated and the stability of the fixation assessed. In patients in whom the fixation has not failed and continues to provide stabilization of the fracture, the plates and screws are left in place, the wound cultured, and closed over drains. Culture-specific antibiotic therapy is instituted after an appropriate operative culture in obtained. If, on the other hand, the fixation is loose, it is removed and a more rigid fixation applied to ensure stable fixation of the fracture site.

SECONDARY DEFORMITIES IN FACIAL TRAUMA Enophthalmos Enophthalmos is defined as posterior displacement of the globe within the orbit. Clinically, it is noticeable when the displacement is 2 mm or greater. Inferior displacement is termed hypoglobus. Often there is some element of both enophthalmos and hypoglobus in the presence of malreduced or unreduced orbital injuries. Failure to reestablish the correct orbital volume is the most common mistake in the repair of these fractures, resulting in late enophthalmos. This occurs if the orbital implant is not appropriately angled superiorly toward the anterior edge of the remaining intact orbital floor but is placed straight back into the maxillary sinus. Some suggest that correct placement of the implant or bone graft should be confirmed with an endoscope placed into the maxillary antrum. Delayed enophthalmos is evaluated with a maxillofacial CT scan with 1.0-mm cuts through the orbits. Sagittal and coronal reconstructions are useful adjuncts to the orbital analysis and comparison to the normal contralateral side is extremely helpful. Thorough examination of the eye is performed by the ophthalmologist to assess abnormalities in vision or extraocular movement. The most common finding in patients with enophthalmos is diplopia, more often in peripheral than central gaze. Diplopia is most frequently related to disorders of the nerves or muscles controlling ocular motility, but may be related to malposition of the globe. The central nervous system can accommodate a significant degree of ocular displacement before diplopia becomes evident. Correction of enophthalmos should be directed toward correction of the orbital volume. In the case of fractures of the orbital floor or medial wall, placement of bone grafts or an alloplastic implant in the deficient areas will correct the displacement. We often use titanium mesh, which can be easily molded and contoured, to reconstruct larger and more complex defects. Porous polyethylene is useful in the reconstruction of isolated floor fractures. The orbit is typically approached through a transconjunctival incision in much the same way that it is approached in primary repair. If the problem with globe positioning is strictly one of posterior displacement (enophthalmos) with no vertical component, and there is no well-defined defect to reconstruct, the implant is typically placed posterolaterally in the orbital cone. This achieves forward displacement of the globe without changing the vertical dimension. It is also


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Malocclusion

FIGURE 31.12. Porous polyethylene implant used to treat temporal hollowing. The implant is placed in the subperiosteal plane and larger than the anticipated defect.

important to perform a thorough subperiosteal dissection of the orbital cone to prevent the globe from being tethered posteriorly by scar. A slight degree of overcorrection is warranted in these cases to compensate for swelling that occurs during the dissection. Enophthalmos secondary to malunion of an orbitozygomatic fracture requires careful evaluation. When the malar eminence is displaced in the presence of enophthalmos, corrective osteotomies of the entire zygomatic complex are performed at the level of the zygomaticomaxillary buttress, infraorbital rim, arch, zygomaticofrontal buttress, and sphenoid articulation within the orbit. This is accomplished through the coronal, lower lid, and buccal sulcus incision. Bone grafting is often required to compensate for the inevitable loss of bone that occurs from the original injury.

Malocclusion is a very difficult problem to correct secondarily once bone union has occurred. It is far easier to avoid it in the first place. Although malocclusion can be related to malunion of maxillary, palatal, or mandible fractures, it is most commonly associated with poorly treated mandible fractures. It cannot be emphasized enough that the occlusion seen following plating of the fractures must be meticulously evaluated. Any discrepancy seen in intercuspation and alignment of wear facets must be corrected. Removal and replacement of hardware is a minor inconvenience when compared to the inconvenience to both the surgeon and patient of a postoperative malocclusion. To fully assess the corrected occlusion it is vital to release the patient from maxillomandibular fixation at the conclusion of the plating. Maxillomandibular fixation can displace the condyles or bone fragments enough to give the appearance of a good bite. When checking the occlusion at the conclusion of the procedure, the surgeon should use only gentle upward pressure on the symphysis to check the occlusion. Because of the relatively lax configuration of the mandibular articulation with the skull, it requires only a mild degree of force to dislocate the condyles and force the patient into an occlusal state that appears normal, but is not centric. Centric occlusion is seen when the condyles are seated within the articular fossae. The challenge is to ensure that the occlusion at the end of the case is equal to centric occlusion. When malocclusion is discovered in the immediate postoperative period, Panorex and plain radiographs can often determine if the condition is amenable to operative correction. Minor tooth interferences can be addressed by burring down teeth at the points of contact. Orthodontics is a powerful tool to address less-significant degrees of malocclusion. Orthodontics is often more useful in the malaligned alveolar fracture or segmental fractures of this nature. The vast majority of postoperative malocclusions, however, should be taken back to the operating room for exploration, removal of hardware, appropriate reduction, and stabilization. If internal fixation cannot

B

A FIGURE 31.13. A and B: Shotgun wounds. Shotguns cause both extensive soft-tissue and skeletal destruction, often resulting in severe comminution of the facial skeleton.

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B

A

D C

E

FIGURE 31.14. Complete phases of treatment of facial shotgun wound. A: Initial injury B: Three-dimensional CT scan of initial injury revealing degree of skeletal destruction. C: Reconstruction of the zygomatic complex with extensive primary bone grafts fixed with miniplates. D: Soft-tissue reconstruction with a combination of local flap advancement from cheek and radial forearm free flap for the central region. Stable soft-tissue reconstruction is critical to bone graft survival. E: Two-year follow-up.



be achieved for some reason, then the fail-safe maneuver is 4 to 6 weeks of maxillomandibular fixation. In the case of malunion, where bone fragments are no longer mobile, osteotomies must be made. This approach requires the fabrication of models and mock surgery. The models are cut to correct the malocclusion, and an occlusal or lingual splint is fabricated to guide the repair. Although reproducing the initial fracture often suffices, in late cases in which there has been some degree of dental compensation, sagittal split and Le Fort I osteotomies may be required.

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anteriorly. It should always be remembered that it is difficult to overcorrect patients with this deformity. Redraping the soft tissue of the medial canthal valley is a significant challenge. Transnasal wiring or suturing can be used to set the correct position of the medial canthus, but does little to ensure that the overlying soft tissues adhere down to the bone. It is useful in this regard to employ a soft-tissue bolster to compress the skin to the bone. It is best to use a technique that allows for adjustment of tension on the bolster postoperatively to avoid tissue necrosis. The bolster helps eliminate dead space and evacuate blood so that hematoma formation does not impede soft-tissue adherence.

Temporal Hollowing Temporal hollowing is caused by injury and subsequent loss of volume within the temporal fat pad. The temporal fat pad lies between the two layers of the deep temporal fascia (the thick layer of fascia immediately superficial to the temporalis muscle) that encompass the fat pad and insert onto the zygomatic arch. In dissection of the temporal region, some surgeons believe it is important to dissect deep to the superficial layer of the deep temporal fascia as one approaches the zygomatic arch in an effort to protect the temporal branch of the facial nerve. This results in some degree of trauma to the fat pad, which may result in devascularization and some loss of volume in this region. Although elevating this fascia does provide protection to the nerve (which runs deep to the temporoparietal fascia), nerve injuries are usually the result of excessive traction, which is not necessarily prevented by this fascial layer. To minimize the risk of devascularization and temporal hollowing, the authors prefer to dissect just on top of the superficial layer of the deep temporal fascia (or temporoparietal fascia) with a moist sponge using a sweeping motion. The dissection should elevate the superficial temporal fascia off of the deep temporal fascia, ensuring that the nerve is raised with the flap, and avoids the fat pad altogether. Once temporal hollowing has occurred, one effective treatment is placement of a porous polyethylene implant in the subperiosteal plane and secured to the temporal fossa. Because of the deep placement of the implant below the temporalis muscle, the size of the implant is frequently larger than one would anticipate relative to the defect (Fig. 31.12). Porous polyethylene offers several advantages, including availability, permanency, and tissue ingrowth. It can also be stabilized with screws to the temporal region to prevent displacement. For smaller volume defects, autologous fat grafts are also an option.

Gunshot Wounds and Panfacial Fractures Gunshot wounds can cause any combination of soft-tissue injury and fracture within the craniofacial skeleton. With most gunshot injuries to the face, the entrance wound tends to be inconspicuous relative to the degree of skeletal injury. The exit wounds are more variable and depend to a large degree on the caliber (energy) of the weapon. Shotgun wounds, on the other hand, almost universally impart a great deal of soft-tissue injury along with a significant degree of underlying skeletal injury (Fig. 31.13). This difference is extremely important with respect to how these injuries are treated. The goal of skeletal reconstruction must first be the restoration of the anteroposterior projection and width of the face. Primary bone grafting has proven a reliable technique in the face of bone loss and severe comminution (10,11). Although the order in which the craniofacial skeleton is addressed is somewhat controversial, the zygomatic arch serves as a useful guide and should be plated early in the sequence. Correct positioning of the arch essentially establishes the proper facial width, framing the face. Failure to accurately reconstruct the arch results in the remainder of the reconstruction being set to the incorrect frame. When a large soft-tissue component is also present, as occurs with shotgun wounds, soft-tissue reconstruction is an early priority. Stable soft-tissue coverage is vital to restoration of the skeleton, especially when bone grafting is required (12). Additionally, damaged and devitalized tissue can lead to significant scar contractures that ultimately can limit facial form and function. Although debridement of soft tissues in the facial region should be tempered with the goal of preservation of critical structures, all efforts should be made to achieve complete soft-tissue coverage and wound healing within 1 to 2 weeks in an effort to avert scar contractures. At times, this goal can only be achieved with free tissue transfer (Fig. 31.14).

Telecanthus Telecanthus is even more difficult to resolve secondarily than it is primarily. The most common findings are tenting of the soft tissues of the medial canthus, lateral displacement of the canthus, and rounding of the medial canthal angle. The goal of revisional surgery is to correct all of the above deformities and ensure that the skeletal contour in the region is correct. Because of the nature of soft tissue in the region, most deformities in bone contour are readily visible. Exposure is obtained most frequently through a coronal and lower lid incisions. The entire soft-tissue envelope is mobilized and scar tissue resected or released. The correct position of the insertion of the medial canthal tendon is at the posterosuperior aspect of the lacrimal fossae. If this area has been distorted, it should be reconstructed to the appropriate contour, using the uninjured side to guide the reconstruction. The same is true for positioning of the medial canthus. The typical error is in reinserting the canthus too

References 1. Martin RC 2nd, Spain DA, Richardson JD. Do facial fractures protect the brain or are they a marker for severe head injury? Am Surg. 2002;68(5): 477. 2. Manolidis S, Weeks BH, Kirby M, Scarlett M, et al. Classification and surgical management of orbital fractures: Experience with 111 orbital reconstructions. J Craniofac Surg. 2002;13(6):726; discussion 738. 3. Markowitz BL, Manson PN, Sargent L, et al. Management of the medial canthal ligament in nasoethmoidal orbital fractures. Plast Reconstr Surg. 1991;87:843. 4. Rohrich RJ, Mickel TJ. Frontal sinus obliteration: In search of the ideal autogenous material. Plast Reconstr Surg. 1995;95(3):580. 5. Ellis E. Selection of internal fixation devices for mandibular fractures: How much fixation is enough? Semin Plast Surg. 2002;16(3):229. 6. Ellis E. Treatment methods for fractures of the mandibular angle. Int J Oral Maxillofac Surg. 1999;28(4):243. 7. Martin M, Lee C. Operative controversies: Thoughts on an intraoral

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endoscopic assisted method of condylar fracture repair. Semin Plast Surg. 2002;16(3):251. 8. Lee C, Mueller RV, Lee K, et al. Endoscopic subcondylar fracture repair: functional, aesthetic, and radiographic outcomes. Plast Reconstr Surg. 1998;102:1434, discussion 1444. 9. Zide MF, Kent JN. Indications for open reduction of mandibular condyle fractures. J Oral Maxillofac Surg. 1983;41(2):89. 10. Manson PN, Crawley WA, Yaremchuk MJ, et al. Midface fractures: ad-

vantages of immediate extended open reduction and bone grafting. Plast Reconstr Surg. 1985;76:1. 11. Gruss JS, Mackinnon SE, Kassel EE, et al. The role of primary bone grafting in complex craniomaxillofacial trauma. Plast Reconstr Surg. 1985; 75:17. 12. Gruss JS, Antonyshyn O, Phillips JH. Early definitive bone and soft-tissue reconstruction of major gunshot wounds of the face. Plast Reconst Surg. 1991;87:436.


CHAPTER 32 ■ HEAD AND NECK CANCER AND SALIVARY GLAND TUMORS PIERRE B. SAADEH AND MARK D. DELACURE

The intricate anatomy of the head and neck and its myriad of specific afflictions combine to present powerful treatment challenges with tremendous functional and aesthetic consequences. Several texts comprehensively discuss these topics (1–3). The vast majority of malignant tumors of the head and neck are squamous cell carcinomas, heterogenous in behavior, arising from the mucosal lining of the upper aerodigestive tract. Chapter 16 discusses tumors of the skin and adnexa. Salivary gland tumors are a diverse group of pathologic entities addressed later in this chapter. Successful reconstruction is contingent on communication between members of a multidisciplinary team, familiarity with the anatomy of the region, an appreciation of the terminology used to quantify the severity and prognosis of disease, an understanding of the natural history of the disease process and its treatment goals, a sense of the expected deficit requirements, and a logical approach to reconstruction.

HEAD AND NECK TEAM The modern standard of care for the treatment of patients with head and neck tumors requires a collaborative effort among the ablative, reconstructive, radiologic, oncologic, radiotherapeutic, dental, speech and swallowing therapy, and psychosocial services.

HEAD AND NECK ANATOMY AND STAGING A systematic, standardized approach to head and neck anatomy facilitates discussion and treatment. The primary site/subsite approach currently used for head and neck cancer reflects both unique regional tumor behavior and specific treatment-related considerations (functional, reconstructive, etc.). This section of the chapter focuses on sites with the greatest incidence of pathology and on subsites with specific reconstructive challenges. Primary tumor sites include the oral cavity, the nasopharynx, the oropharynx, the hypopharynx, and the larynx (supraglottis, glottis, subglottis). The tumor, node, metastases (TNM) classification developed by the American Joint Committee on Cancer (AJCC) in 2002, is the standard system used to establish stage grouping and to facilitate determination of both prognosis and treatment. Because T stage definitions vary depending on primary site location, these definitions are included with the primary site figures.

Nasopharynx Table 32.2 defines the primary site locations of the nasopharynx. Figure 32.2 demonstrates the anatomy and T staging of the nasopharynx.

Oropharynx Table 32.3 defines the primary site locations of the oropharynx. Figure 32.3 demonstrates the anatomy and T staging of the oropharynx.

Hypopharynx and Cervical Esophagus Table 32.4 defines the primary site locations of the hypopharynx and cervical esophagus. Figure 32.4 demonstrates the anatomy and T staging of the hypopharynx.

Larynx Table 32.5 defines the primary site locations of the larynx. Figure 32.5 demonstrates the anatomy and T staging of the larynx.

Nasal Cavity and Paranasal Sinuses Table 32.6 defines the primary site locations of the nasal cavity and paranasal sinuses. Figure 32.6 demonstrates the anatomy and T staging of the nasal cavity and paranasal sinuses.

Neck Table 32.7 defines the primary site locations of the neck. Figure 32.7 demonstrates the anatomy and T staging of the neck. To facilitate and standardize discussion of neck metastases and neck dissection, the neck has been divided into nodal group levels.

STAGING

Oral Cavity Table 32.1 defines the primary site locations of the oral cavity. Figure 32.1 demonstrates the anatomy and T staging of the oral cavity.

Figure 32.8 outlines head and neck TNM staging as defined by the American Joint Committee on Cancer. (Figures 32.1 through 32.7 correlate the anatomic site to the respective T stage.)

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TA B L E 3 2 . 1 PRIMARY SITE LOCATIONS OF THE ORAL CAVITY Lip

Skin–vermilion junction to oral mucosa and including the commissures. Mucosal lining extending from the pterygomandibular raphe forward. The Stensen (parotid) duct arises next to second maxillary molar. Gingival mucosa anterior to retromolar trigone. Mucosa behind the last mandibular molar tooth extending superiorly to the maxillary tuberosity. Bounded by the superior alveolar ridge and the junction of the soft palate. Bounded by the inferior alveolar ridges and the tongue. Wharton (submandibular) ducts arise in the midline. Extends anteriorly from the circumvallate papillae and bounded by the floor of mouth. Motor innervation of the tongue is via the hypoglossal nerve (cranial nerve [CN] XII) whereas sensory innervation is via the lingual nerve (branch of CN V3).

Buccal mucosa Alveolar ridge Retromolar trigone Hard palate Floor of mouth Anterior (two-thirds) tongue (oral tongue)

Lip

HEAD AND NECK CANCER

Alveolar ridge

Hard palate

Retromolar trigone Buccal mucosa Oral tongue Floor of mouth

Alveolar ridge

Although head and neck cancers are a devastating group of diseases, site- and stage-specific survival reveal that many locally advanced tumors exhibit 50% overall 5-year survivals (Table 32.8). Although a major cause of morbidity and mortality worldwide (500,000 cases in 2001), the incidence of squamous cell carcinoma of the head and neck has been decreasing in the United States, paralleling a decrease in smoking rates (Fig. 32.9). However, it remains the fifth leading cause of cancer incidence and sixth leading cause of cancer death in the United States. Cumulative DNA alterations caused by the synergistic effects of cigarette smoking and alcohol use are thought to underlie a majority of mucosally derived head and neck squamous cell carcinomas. Of note, a link has been identified between oropharyngeal tumors and human papillomavirus (HPV) DNA. As a result of “field cancerization” (7), the entire upper aerodigestive tract mucosa is at risk for both synchronous (5%) and metachronous (5% to 15%) second primary malignancies. The surgical treatment of other oral malignancies (e.g., salivary gland, sarcoma), which account for less than 10% of the malignancies in this region, is generally similar to squamous cell carcinoma and is outlined below.

Lip

Oral Cavity

T1 < 2 cm

Precancerous lesions of the oral cavity include the leukoplakia, which is common among smokers, and erythroplakia. Dysplastic leukoplakia and erythroplakia require, at minimum, close

T2 2–4 cm T3 > 4 cm T4 Invades adjacent structures (cortical bone, inferior alveolar nerve, floor of mouth, muscles of tongue, skin); superficial erosion of bone by gingival primary is insufficient for T4 classification

TA B L E 3 2 . 2 PRIMARY SITE LOCATIONS OF THE NASOPHARYNX

FIGURE 32.1. Anatomy and T staging of oral cavity.

Hollow cavity delimited by oropharynx, hard palate, skull base, spine, and nasal cavity.


Chapter 32: Head and Neck Cancer and Salivary Gland Tumors

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Lip

Nasopharynx

Oropharynx

Hypopharynx

Squamous cell carcinoma of the lip comprises approximately 30% of oral cavity malignancies and the vast majorities of these occur on the lower lip. The majority of tumors of the upper lip are basal cell carcinomas. Unlike the remaining squamous cell carcinomas discussed in this chapter, sun exposure is thought to play a major role in its pathogenesis. Furthermore, although occult metastatic spread is unusual for most lip tumors, the commissures are associated with a 20% risk. In situ lesions may be treated with shave excision, topical 5fluorouracil (5-FU), or imiquimod (Aldara, 3M, St. Paul, MN; non-FDA approved as of this writing), whereas later-stage lesions require assessment of possible mandibular and/or mental nerve involvement prior to excision with adequate margins. Because of the difficulty reconstructing the commissure, malignancies of this area may be treated with radiotherapy. Larger lip lesions warrant evaluation of the neck and possible selective neck dissection. Upper lip and commissure malignancies may drain to periparotid nodes, which require evaluation and possible superficial parotidectomy, in selected cases. Lip reconstruction is discussed in Chapter 36.

Anterior (Oral) Tongue

T1 Tumor confined to nasopharynx T2 Tumor extends to soft tissues T3 Tumor involves bony structures and/or paranasal sinuses T4 Tumor with intracranial extension and/or involvement of cranial nerves, infratemporal fossa, hypopharynx, orbit, or masticator space FIGURE 32.2. Anatomy and T staging of nasopharynx.

serial observation. Additionally, treatment options include either chemoprevention (isotretinoin), or ablation with cryotherapy, electrocautery, or surgery. Because of the accessibility of the oral cavity, and the morbidity of radiation-induced xerostomia, early tumors of this area (T1 and T2) are generally treated surgically. Locally advanced lesions (T3 and T4) are typically treated with combination therapy.

The anterior tongue is the site of malignancy in 25% to 50% of oral cavity cancers, with the midlateral aspect most frequently affected. Because of the lack of anatomic barriers to spread, tongue cancer has a propensity for diffuse, infiltrative involvement, which is often difficult to gauge clinically. Curative resection, therefore, mandates an adequate cuff (generally 1 cm) around the lesion. T1 or T2 lesions are usually amenable to transverse wedge excision. Larger T2 and posteriorly situated lesions are treated with paramedian mandibulotomy, which provides access for both tumor excision and, if indicated, in-continuity neck dissection. Smaller resections are treated with primary closure or skin-grafting, whereas larger defects generally require free tissue transfer (which may be sensate) to maintain tongue mobility and optimize oral function. All patients with tumors thicker than 3 to 5 mm and clinically negative necks should be treated with supraomohyoid neck or postoperative adjuvant radiotherapy dissection because of the relatively high risk of occult metastasis (up to 60%). Lymphoscintigraphy and sentinel node dissection may play a role in further refining the approach to occult neck disease.

Floor of Mouth Floor of mouth cancer accounts for 30% of oral cavity malignancies and may extend locally into the tongue or the

TA B L E 3 2 . 3 PRIMARY SITE LOCATIONS OF THE OROPHARYNX Soft palate Tonsil Lateral pharyngeal wall

Posterior pharyngeal wall Posterior (one-third) tongue (base of tongue)

Extends from the hard palate junction to the uvula posteriorly and anterior tonsillar pillars laterally. Bounded by the tonsillar pillars (faucial arch). Extends from posterior tonsillar pillar to posterior pharyngeal wall. The internal carotid artery, internal jugular vein, vagus and sympathetic nerves, and cranial nerves (CN) IX to XII are located in the parapharyngeal space, which is immediately lateral to the lateral pharyngeal wall. Bounded by lateral pharyngeal walls and extending from the level of the hard palate superiorly and the hyoid bone inferiorly. From circumvallate papillae to epiglottis (vallecula).

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Soft palate Tonsils

Pharyngeal wall Base of tongue

agement of the mandible, therefore, is an essential aspect of floor of mouth cancer treatment. Surgical guidelines include 1-cm margins, which results in marginal mandibulotectomy for tumors intimately related to the mandible. Radiologic evidence of cortical invasion mandates segmental mandibulotectomy with bone cuts about 1 cm away from the soft-tissue portion of the malignancy and evaluation of inferior alveolar nerve margins. Preplating the mandible may facilitate reconstruction. Larger tumors that do not require segmental mandibulotectomy may be resected in continuity with planned neck dissection through a transcervical route. This subsite also has a propensity for occult neck metastasis which may be bilateral.

Retromolar Trigone Tumors of this subsite are generally difficult to treat because of challenging access and because of their locally aggressive nature, which often requires segmental mandibular resection and inferior alveolar nerve sacrifice.

Alveolar Ridge Malignancies occur in this subsite uncommonly and are treated according to the principles outlined above. Occult metastases are rare. There is an increasing trend towards free bone/soft tissue transfer in the reconstruction of anterior maxillary defects.

Hard Palate

T1 < 2 cm T2 2–4 cm T3 > 4 cm T4 Invades adjacent structures (larynx, deep muscles of tongue, pterygoids, hard palate, pterygoid plates, skull base), surrounds carotid artery FIGURE 32.3. Anatomy and T staging of oropharynx.

mandible in the alveolar region. Dentition plays an important role, both as a relative barrier to mandibular invasion by tumor and in the maintenance of alveolar height. Irradiated mandibles lose the characteristic of alveolar invasion and are at greater risk of direct cortical involvement. After cortical breach, tumor infiltrates the cancellous space and may track in a perineural fashion if the alveolar canal is entered. Loss of alveolar height in the edentulous patient places the alveolar canal in proximity to the mucosal surface and affords portal of entry via empty tooth sockets. Oncologically sound man-

The hard palate is an uncommon subsite for oral cavity malignancy. Up to a third of tumors in this area may be of minor salivary gland origin. Principles of resection are similar to those described above and occult neck metastases are rare. Depending on tumor size and location, resection may be performed perorally, through a transoral midface degloving approach, or through a Weber-Ferguson approach. Reconstruction of the hard palate (to maintain speech, feeding, and the separation of the oral cavity from the nasal cavity), restoration of nasal lining, and, occasionally, reconstruction of the inferior orbital wall may be required. Small defects may be addressed with local flap closure or prosthodontics, but larger defects require free tissue transfer and/or maxillofacial prosthodontics.

Buccal Mucosa Although also uncommon, buccal mucosal malignancies are locally aggressive and have a propensity to metastasize. Resection of these lesions may result in large, full-thickness soft-tissue deficits with significant cosmetic consequences. Free tissue reconstruction is frequently required.

TA B L E 3 2 . 4 PRIMARY SITE LOCATIONS OF THE HYPOPHARYNX AND CERVICAL ESOPHAGUS Hypopharynx Postcricoid region Posterior pharyngeal wall Pyriform sinus

Cervical esophagus

Arbitrarily divided into three anatomically contiguous regions. Extends from the arytenoids superiorly to the cricoid cartilage inferiorly. Anterior to retropharyngeal space and extends from the level of the epiglottis to the level of the cricoid cartilage. Pyramidal in shape with a base superiorly and an apex inferiorly. Extends from the oropharynx superiorly to the laryngeal ventricles inferiorly. The medial border is the lateral cricoid cartilage while the lateral border is the medial thyroid cartilage. The posterior border is bounded by both the lateral and posterior pharyngeal walls. Extends from the cricoid level to the sternal notch.



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[CNs] III, IV, V1 , and VI [commonest]). The primary treatment for this highly radiosensitive tumor is chemoradiation with surgery reserved for recurrent disease (8).

Oropharynx Pharyngeal wall Pyriform sinus

Pharyngoesophageal (postcricoid area)

T1 < 2 cm and limited to one subsite T2 2–4 cm without fixation of hemilarynx or invades more than one subsite T3 > 4 cm or with fixation of hemilarynx T4 Invades adjacent structures (thyroid/cricoid cartilage, hyoid bone, thyroid gland, esophagus, central compartment soft tissue, prevertebral fascia), encases carotid artery, or involves mediastinal structures FIGURE 32.4. Anatomy and T staging of hypopharynx and cervical esophagus.

Nasopharynx Rare in the United States, tumors of the nasopharynx are much more common in China and have an association with EpsteinBarr virus and nitrosamine-containing foods. Although still a factor, cigarette smoking is thought to play a minor etiologic role in squamous cell carcinoma of this subsite. Locally advanced disease with (bilateral) neck involvement is a common presentation. Growth into local structures including the oropharynx, nasal cavity, sphenoid sinus, orbit, spine, or skull base can occur. Skull base extension into the cavernous sinus may present with associated neural involvement (cranial nerves

TA B L E 3 2 . 5 PRIMARY SITE LOCATIONS OF THE NASOPHARYNX Consists of the supraglottis, glottis, and subglottis. Supraglottis Includes the epiglottis, arytenoids, aryepiglottic folds, and false cords. Glottis Consists of the true vocal cords, the anterior commissure, and the posterior commissure. Subglottis Region below the glottis extending to the inferior margin of the cricoid cartilage.

Functional outcomes take on greater importance in this subsite as a result of the proximity of the digestive and respiratory tracts to one another. Tumors in this region are characterized by their relatively small size compared to much larger neck metastases (clonal heterogeneity), the propensity of near midline lesions for bilateral neck involvement, and the possibility of retropharyngeal nodal metastasis. Although most tumors are squamous in origin, the higher concentration of lymphatic tissue yields a proportionally higher incidence of lymphomas (mucosal-associated lymphoid tissue [MALT] tumors), which are exquisitely radiosensitive. Sixty percent of patients present with a mass in the neck, as the primary site is usually asymptomatic or has nonspecific symptomatology. However, CN IX or X involvement may present with referred otalgia and/or ipsilateral soft palate paresis. CN XII invasion can manifest as wasting and ipsilateral deviation of the tongue. In light of functional considerations, early lesions (T1 and T2) that cannot easily be resected are often best treated with radiation therapy. Advances in organpreservation chemoradiation protocols are increasingly relegating surgery to advanced lesions (T3 and T4) and to salvage for treatment failure or recurrence (9). The base of the tongue is most frequently affected and, similar to the oral tongue, infiltrative spread is common. While most base-of-tongue tumors are presently treated with chemoradiation and/or brachytherapy, there are multiple approaches to this area. Surgical access, depending on the lesion’s location and size, includes transoral excision, lateral pharyngotomy, supra/transhyoid pharyngotomy, lip splitting, and paramedian mandibulotomy. The latter approach implies a larger tumor, which generally mandates advanced reconstruction. Similarly, locally advanced pharyngeal wall tumors require advanced access, laryngopharyngectomy, and reestablishment of digestive continuity. Tumors close to or involving the mandible (ramus: tonsil, pharyngeal arches, lateral pharyngeal wall) require marginal or segmental mandibulectomy, usually with reconstruction, as outlined in the section on oral cavity tumors. Consideration of tracheostomy and/or gastrointestinal feeding tube should be part of the preoperative plan of any extensive resection/reconstruction of the oropharynx. Except for early lesions of the soft palate and posterior pharynx, the propensity for neck metastasis by tumors of the oropharynx mandates treatment of the neck.

Hypopharynx and Cervical Esophagus Malignancies of the hypopharynx most frequently involve the pyriform sinus with dysphagia and palpable neck disease as frequent presenting complaints. Referred otalgia from tumor invasion of the tympanic branch of the CN IX is also a common symptom. Locally advanced hypopharyngeal tumors have the highest rate of distant metastases (usually to the lungs). Tumors of the cervical esophagus are characterized by submucosal infiltration. Traditional surgical treatment of hypopharyngeal cancer commonly involves laryngopharyngectomy because of the proximity of tumor to the larynx and the limited ability to preserve function. There has been a shift in the treatment of hypopharyngeal tumors to concurrent chemoradiation protocols, similar to those used in the treatment of oropharyngeal cancer, which offer the hope of larynx preservation. This remains, however, an area of both controversy and of active

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Anterior commissure Vocal cords

Supraglottis Glottis Subglottis

Supraglottis T1 Limited to one subsite (mobile vocal cords) T2 Invades mucosa of more than one adjacent subsite (mobile vocal cords) T3 Limited to larynx with vocal cord fixation and/or invades: postcricoid space, pre-epiglottis, paraglottic space, and/or minor thyroid cartilage erosion T4 Invades through thyroid cartilage and/or tissues beyond larynx

Glottis T1 Limited to vocal cord(s) with normal mobility T2 Extends to supraglottis or subglottis, and/or with impaired vocal cord mobility T3 Limited to larynx with vocal cord fixation and/or invades paraglottic space, and/or minor thyroid cartilage erosion T4 Invades through thyroid cartilage and/or tissues beyond larynx

Subglottis T1 Limited to subglottis T2 Extends to vocal cords with normal or impaired mobility T3 Limited to larynx with vocal cord fixation T4 Invades cricoid or thyroid cartilage and/or invades tissues beyond larynx FIGURE 32.5. Anatomy and T staging of larynx.

investigation. Surgical treatment is indicated in selected earlystage patients, in patients with extensive, bulky disease, and in chemoradiation failures. Small localized lesions of the pyriform sinus may be treated by partial laryngopharyngectomy (PLP) that typically results in a hemicircumferential defect of the

hypopharynx, whereas total laryngopharyngectomy results in complete disruption of gastrointestinal continuity. Reconstructive options usually favor free tissue reconstruction with fasciocutaneous flaps for resurfacing of hemicircumferential defects and intestinal interposition flaps for complete defects. Total

TA B L E 3 2 . 6 NASAL CAVITY AND PARANASAL SINUSES Nasal cavity

Four paired sinuses Maxillary sinus Frontal sinus Ethmoid sinus Sphenoid sinus

Extends superiorly from the walls of the ethmoid sinus anteriorly and the sphenoid sinus posteriorly down to the hard palate anteriorly and nasopharynx posteriorly. Lateral margins are the medial walls of the maxillary sinus and the nasal cavity is bisected sagittally by the septum. Bounded superiorly by the orbital floor, inferiorly by the hard palate, posteriorly by the pterygoid plates and pterygopalatine fossa, and laterally by the pterygoid muscles and mandibular ramus. Above and along the anterior aspect of the ethmoid sinus. Between medial orbits, superior to nasal cavity. Skull base, posterior to ethmoid sinus.



Frontal sinus Ethmoids

Sphenoid sinus

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ryngectomy, speech may be reestablished through esophageal speech, tracheoesophageal puncture, or with an electrolarynx. Early neck metastases with a propensity for bilaterality warrant an aggressive approach to the neck.

Nasal cavity

Larynx

Ethmoids

Nasal cavity

Maxillary sinus

Maxillary sinus T1 Limited to sinus mucosa without bone invasion T2 Bone invasion excluding posterior sinus wall and/or pterygoid plates T3 Invasion of posterior sinus wall, subcutaneous tissues, orbital floor, pterygoid fossa, ethmoid sinuses T4 Invades orbit, skin of cheek, nasopharynx, pterygoid plates, skull base, dura, brain

Nasal cavity and ethmoid sinuses T1 Restricted to one subsite, with or without bony invasion T2 Invades two subsites in a single region or extends to involve an adjacent region within the nasoethmoidal complex, with or without bony invasion T3 Extends to medial/floor orbit, maxillary sinus, palate, cribiform plate T4 Invades orbit, skin of cheek, nasopharynx, pterygoid plates, skull base, dura, brain FIGURE 32.6. Anatomy and T staging of nasal cavity and paranasal sinuses.

esophagectomy is reconstructed with gastric pull up. Pectoralis major flaps are generally reserved for poor free flap candidates, as adjunctive coverage, or for salvage. Complications specific to hypopharyngeal/esophageal reconstruction include fistula, stenosis, and dysphagia, which vary according to the selected reconstructive option. In patients who have undergone la-

Treatment considerations for carcinoma of the larynx center on tumor ablation, local control, and organ/voice preservation. The disease is generally divided into early and late laryngeal cancer. Early laryngeal cancer (defined as stages I and II) usually involves the glottis and represents 60% of laryngeal cancers. Early glottic tumors generally have a good prognosis with 90% 5-year patient survival for T1 lesions. Because of limited lymphatic drainage, the neck is rarely affected. Historically, single-modality therapy with radiation therapy has been the standard treatment. Treatment options for T1 lesions include transoral laser ablation and other partial laryngectomy procedures. Controversy persists regarding both adequate evaluation and treatment of lesions involving the anterior commissure. Open vertical partial laryngectomy is generally reserved for T2 tumors, radiation failure, or limited local recurrence. Another operative option of increasing interest is supracricoid subtotal laryngectomy. Early supraglottic cancer is similarly treated with radiation, transoral endoscopic approaches, or open surgery. However, because the rate of neck involvement in the clinically negative neck exceeds 20%, elective treatment of the neck (bilateral for midline or larger lesions) is advocated, usually with the same modality as the primary site treatment. Radiation therapy is most effective in the treatment of smaller volume, superficial lesions without cartilage destruction. Open surgery typically involves horizontal supraglottic laryngectomy and is an effective treatment of both T1, T2, and select T3 tumors. Involvement of the anterior commissure is a similar subject of controversy. Early subglottic laryngeal carcinoma is very rare, and is amenable to the treatments indicated above. Because of similar outcomes between the various treatment modalities, albeit with some compromise between voice quality and local control rates, the treatment decision must often be made with patient performance status and preferences in mind. Treatment of patients with advanced laryngeal carcinoma (stages III and IV) has undergone considerable change in the last two decades (10). Although survival has not changed appreciably, newer chemoradiation protocols have dramatically increased laryngeal preservation rates, reserving surgery (usually total laryngectomy) for salvage. Management of the N+ neck depends on the primary modality employed either with surgery performed after radiation or radiation therapy performed depending on clinicopathologic analysis of the surgical specimen. Free flap reconstruction (commonly radial forearm free flap with palmaris tendon) of the vocal cord deficit in vertical partial laryngectomy defects has increased the predictability of the functional result in conservation laryngectomy (less than total) salvage procedures (11).

Nasal Cavity and Paranasal Sinuses Similar to the nasopharynx, sinonasal tract squamous cell carcinoma occurs infrequently and has a relatively low association with cigarette smoking. The maxillary sinus is most frequently affected and tumors can grow considerably before becoming symptomatic. Tumors located below the Ohngren line (which extends from the medial canthus to the angle of the jaw) have a better prognosis than tumors located above it. Treatment

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TA B L E 3 2 . 7 SUMMARY OF THE REGIONAL NODAL GROUPS FROM THE MOST RECENT NECK DISSECTION CLASSIFICATION SYSTEM (4) Level (nodal groups)

Anatomy

Likely primary site

Level I

Submental: nodal tissue superior to the hyoid bone and between the anterior bellies of the digastric muscles (sublevel 1A). Submandibular: nodal tissue between the mandibular border and the digastric muscles, including the submandibular gland (sublevel 1B). Nodal tissue along the upper aspect of the internal jugular vein extending from the skull base to the hyoid bone (clinical landmark) or the carotid bifurcation (radiologic landmark). Extends superiorly to the border of the sternohyoid muscle and inferiorly to the lateral border of the sternocleidomastoid muscle. Sublevel IIA represents tissue anterior to the spinal accessory nerve whereas sublevel IIB tissues are located posterior to the spinal accessory nerve. Nodal tissue along the middle aspect of the internal jugular vein extending from the lower limit of level II the cricothyroid membrane (clinical landmark) or the omohyoid muscle (radiologic landmark). Anterior and posterior borders are the same as level II. Nodal tissue along the lower aspect of the internal jugular vein extending from the lower limit of level III to the clavicle. Anterior and posterior borders are the same as level III. Nodal tissue along the posterior course of the spinal accessory nerve. Triangle is defined by the lateral border of the sternocleidomastoid muscle, the trapezius muscle, and the clavicle. Nodal tissues delimited by the hyoid bone superiorly, sternal notch inferiorly, and common carotid arteries laterally.

Floor of mouth, anterior oral cavity/alveolar ridge, lower lip Submandibular gland, oral/nasal cavity, midfacial soft tissues

Level II

Level III

Level IV

Level V

Level VI

of malignancies of this area is generally surgical and consideration must be given to possible involvement of surrounding structures, including the remaining sinuses, the nose, the orbital floor and orbit, and the anterior and middle cranial fossae. The functional and cosmetic deformities resulting from tumor extirpation with uninvolved margins present significant reconstructive challenges, including restoration of hard palate continuity, reconstruction of the orbital floor, dead space elimination, and prevention of cerebral spinal fluid leak. Postoperative radiation is usually indicated.

Management of the Neck The prognostic and therapeutic implications of nodal neck metastases mandate a standardized approach to both the description of neck anatomy, as outlined previously, and to options of management. The traditional radical neck dissection involves unilateral removal of lymphatic groups I to V and sacrifice of the spinal accessory nerve, internal jugular vein, and sternocleidomastoid muscle. Numerous modifications of this operation have been described in an effort to limit morbidity or to more specifically target occult metastases (Table 32.9 and Fig. 32.7). Neck dissections are classified as comprehensive (radical, modified radical), or selective, based on the nodal levels dissected and nonlymphatic structures preserved.

Oral/nasal cavity, nasopharynx, oropharynx, hypopharynx, larynx, parotid

Oral cavity, nasopharynx, oropharynx, hypopharynx

Hypopharynx, cervical esophagus, larynx, thyroid Oropharynx, nasopharynx, posterior scalp and neck Thyroid, glottic/subglottic larynx, piriform sinus apex, cervical esophagus

The proliferation of the various neck dissections is largely based on the observation that cervical metastases in previously untreated patients proceed in a predicable fashion depending on the site of the primary tumor. In the N0 neck, treatment includes surgery or radiotherapy, generally depending on the treatment modality selected for treatment of the primary tumor (“split-modality therapy” describes treating the primary tumor with surgery and the neck with radiation or vice versa). Elective treatment is further dependent on the location of the primary tumor. Occult metastases of oral cavity tumors have been correlated with increasing T stage (T3 or T4) and tumor thickness (>3 mm) and such patients should undergo elective treatment, surgical treatment of which generally involves supraomohyoid neck dissection. Tumors of increasing stage of the oropharynx, hypopharynx, and supraglottic larynx have a high incidence of occult cervical spread and elective treatment of the neck is recommended, surgical treatment of which involves lateral neck dissection. However, because access to the oropharynx often necessitates a mandibulotomy, consideration to an anterolateral neck dissection should be given. Elective surgical treatment of the neck is also indicated in unreliable patients and if the approach of surgical treatment of a primary tumor involves a neck approach (either for extirpation or reconstruction). Treatment of the N+ neck generally involves comprehensive neck dissection with an effort to spare structures depending on



FIGURE 32.7. Anatomy of regional nodal groups.

tumor involvement. Selective neck dissection may be appropriate in many cases because of the rarity of level V involvement (except in nasopharyngeal malignancies) in the absence of multilevel involvement or level IV adenopathy. As implied above, radiotherapy compares favorably to surgery in the elective treatment of N0 necks with regards to locoregional recurrence. Although there remains some controversy regarding the timing of radiation, radiotherapy is generally indicated in the treatment of N+ necks, particularly in the presence of multiple nodes or extracapsular extension.

Recent and Future Developments Diagnostic, staging, and surveillance strategies of head and neck cancer are increasingly incorporating positron emission tomography (PET), which exploits the tendency of tumor cells to preferentially take up a radiolabeled glucose analog (fluorodeoxyglucose). PET is particularly useful in detecting recurrence, where traditional anatomically based imaging is limited by postoperative and radiation induced tissue derangements. Additionally, PET has demonstrated usefulness in the localization of occult primary tumors; detecting synchronous, metachronous, or late metastases; and improving the diagnostic accuracy of computed tomography (CT) when used with newer CT-PET fusion technology. Radiation therapy has evolved. The most significant innovation is three-dimensional conformational radiotherapy (also referred to as intensity-modulated radiation therapy [IRMT]) planning and delivery, sparing radiation-induced damage to normal, uninvolved tissue. Furthermore, standard fractionation schedules have, in many cases, been supplanted by hyperfractionation or accelerated fractionation schedules. Hyperfractionation delivers smaller does of ionizing radiation over an unaltered timeframe, resulting in higher overall radiation doses as a consequence of lowered tissue toxicity. Accelerated fractionation shortens the delivery period of radiation, thereby limiting both duration of therapy and tumor doubling time. These therapies have improved locoregional control by up to 15%. Mucositis remains a significant side ef-

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fect, exacerbated, sometimes severely, by chemoradiation protocols. Other significant developments include paradigm shifts in reradiation schemes (now accepted and increasingly aggressive) (12) and increasing roles for neoadjuvant and combination modality protocols (10). Implant brachytherapy and intraoperative radiotherapy continue to have roles in selected patients. Although there have not been any dramatic changes in chemotherapeutic agents, the use of these agents in combination with radiation, based on their radiosensitizing characteristics, has dramatically altered the treatment of locally advanced head and neck cancer (13). Chemotherapy can be administered as induction therapy (before other treatments), concurrent with radiation (most common), or as adjuvant therapy (after other treatments). Current clinical trials are evaluating the potential of antiangiogenic agents, such as the antivascular endothelial growth factor agent bevacizumab (Avastin, Genentech, South San Francisco, CA) in the treatment of head and neck cancer. As in so many other areas of medicine, an improved understanding of the molecular and genetic derangements associated with head and neck cancer will likely play an ever more important role in its diagnosis and management. Disease progression is closely associated with the loss of tumor-suppressor genes p16 (80%) and p53 (50%, more common in smokers), and the elaboration of epidermal growth factor receptor (>90%), which may allow both earlier detection of cancer and the development of novel chemotherapeutic strategies. The discovery of biomarkers will likely aid in the identification of otherwise occult or early-stage tumors and has the potential to improve the prognostic accuracy of staging systems. Additionally, significant research efforts to attenuate or reverse the aforementioned molecular derangements via monoclonal antibodies, tyrosine kinase inhibitors, or even adenovirally mediated p53 gene delivery offer the hope of novel medical therapies for head and neck cancer.

SALIVARY GLAND TUMORS Neoplasms of the salivary glands are a unique and rare (3% to 6% of all adults) subset of head and neck tumors. Their varied histology and infrequent occurrence, as well as their relationship to critical surrounding structures (facial nerve, mandible), often present a diagnostic and therapeutic challenge. There are three paired major salivary glands (parotid, submandibular, sublingual; Fig. 32.10) and 600 to 1,000 minor salivary glands distributed primarily throughout the oral cavity (concentrated in the soft palate) and upper aerodigestive tract. Whereas the output of the parotids is primarily serous, that of the submandibular and sublingual is mucous and that of the minor glands mixed. This fact, in addition to the antigravitational anatomic arrangement of the submandibular duct, is responsible for the frequent involvement of that gland in chronic inflammation (sialadenitis) and sialolithiasis (stone) formation, the most common surgical condition of the submandibular gland. In aggregate, the major and minor glands produce 500 to 1,500 mL of saliva daily. Seventy percent to 85% of all adult salivary gland tumors occur in the parotid gland, 8% to 15% in the submandibular, and 5% to 8% in the minor salivary glands. Sublingual neoplasms are extremely rare (9 cm Free tissue transfer offers a one-step solution for resurfacing large scalp defects and produces surprisingly good results, especially in patients with preexisting alopecia (1,8). Because the area to be covered usually exceeds the size of any myocuta-

neous flap that can be harvested with primary closure of the donor site, muscle-only free flaps along with nonmeshed splitthickness skin grafts are used, and lead to very acceptable outcomes. The superficial temporal vessels are frequently available as recipient vessels, although the vein is occasionally inadequate or absent, in which case interpositional vein grafting to the neck is necessary. Alternatively, the transferred muscle’s pedicle can be lengthened by an intramuscular dissection, leaving portions of remaining muscle in the preauricular region to reach the neck without vein grafts. This skin-grafted muscle may be secondarily thinned, but this often is not necessary because of significant spontaneous atrophy. Traditionally, a latissimus dorsi muscle flap has been used to cover large defects of the scalp because of its consistent vascular pedicle and its large muscle (Fig. 35.10). A rectus abdominis muscle flap, covered with a skin graft, is also useful for this purpose. The serratus anterior muscle free flap has a longer pedicle that can reach the neck vessels without the need for vein grafts, and is a good choice for smaller defects. Fasciocutaneous flaps, such as the anterolateral thigh, can also be used, but if

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A

C

B

FIGURE 35.9. Free latissimus dorsi flap reconstruction of scalp defect. A: Large scalp defect following angiosarcoma resection, radiation therapy, and unsuccessful skin graft placement. B: Latissimus dorsi free flap placed on defect with anastomoses to superficial temporal vessels. C: Postoperative result with satisfactory contour.

their donor sites are to be closed primarily, these flaps will not cover substantial defects. A large omental flap can be used, covered with a skin graft, but this flap often becomes thin over time and may not be suitable for long-term durable coverage. The superficial temporal vessels can serve as recipients for free tissue transfer in many cases. These vessels are easily found through a preauricular incision with elevation of the skin flap to the location of the palpable pulse of the artery. The depth of these vessels decreases as the incision advances superiorly, such that they are quite superficial in the temporal region and lie within the parenchyma of the parotid gland more inferiorly. The vein is occasionally located at a distance from the artery or may not be detectable at all. Occasionally, the occipital vessels can be used as recipient vessels. Free tissue transfer works very well for scalp defects, but may not be appropriate for all clinical situations. Subtotal scalp flaps have been used successfully for defects approaching 50% of the surface area of the scalp in these circumstances. Some lower scalp defects can also be reconstructed with regional pedicled flaps such as the trapezius myocutaneous flap or the latissimus dorsi myocutaneous flap (9). Preliminary delay of these flaps should be considered to enhance vascularity and maximize flap success.

FOREHEAD RECONSTRUCTION Soft-Tissue Defects Small defects of the forehead can be closed primarily, but because the forehead is more visible than much of the scalp, incision placement is critical for an aesthetic result. Although there are preferred locations to place incisions in the forehead, there really are no anatomic subunits per se to preserve. Incisions oriented transversely and placed along the eyebrows or anterior hairline lead to the best results. Distortion of the brows and hairline should be avoided when possible, and in some cases, complete replacement of the entire forehead unit with a full-thickness skin graft may yield a better result than gross eyebrow malposition following primary closure. If primary closure is not possible or desired, local flaps should be used for defects of up to 40% (Fig. 35.10). A rotation-advancement flap can be designed based on the supratrochlear and supraorbital vessels, with the superior incision skirting the anterior hairline. Another approach is to advance the remaining forehead in a V-to-Y fashion to close the defect, basing the flap on or both supraorbital and supratrochlear vessels. An “H” flap can be also used by creating parallel


Chapter 35: Reconstruction of the Scalp, Calvarium, and Forehead

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ble depression. If additional dead space exists, the temporalis muscle, which can comfortably reach the anterior orbital roof and apex, is used. Free tissue transfers have revolutionized the repair of skull base defects, especially if the region has been or will be irradiated. Fasciocutaneous flaps, such as the free radial forearm flap, have great utility in and around the orbit, because the long pedicle can often obviate vein grafting. Free muscle flaps with skin grafts on the exposed portions are also useful for delivering bulky soft tissue and well-vascularized tissue to support a dural reconstruction. Muscle is particularly helpful in this regard, because even with a “watertight” closure of the dura, cerebrospinal fluid may leak. In cases where an established cerebrospinal fluid leak is identified, the muscle of the flap may assist in spontaneous closure of the leak over time. The bone of the skull base rarely needs to be replaced, even in the orbital roof, where “pulsatile” enophthalmos rapidly resolves absence of bony repair. FIGURE 35.10. Reconstructive choices for forehead defects with local flaps. Solid lines, “H” flap advancement; dashed lines, rotation advancement.

transverse incisions from the superior and inferior aspects of the defect and advancing the tissues medially. The Burrow triangles may need to be resected if redundancy is excessive. Sometimes a rotation-advancement flap oriented obliquely and stair-stepped along the hairline is successful. Lateral defects near the eyebrows can be addressed with superficial temporal artery-based hair-bearing flaps. The anterior hairline can be preserved, at least partly, by transfers of hair-bearing scalp flaps, but recognize that any postoperative radiation therapy will cause alopecia and ruin the effect . Near or total forehead defects can also be resurfaced with free radial forearm or groin flaps. Central defects are harder to close with forehead tissue, and consideration should be given to leaving such a defect to heal secondarily, as one would the donor site of a paramedian forehead flap. Central defects can be closed vertically, but the eyebrows may be positioned too close to each other. Tissue expansion can also be used to recruit enough tissue to replace a poorly healed scar or a temporary skin graft. In some instances, tissue expansion of adjacent forehead provides adequate coverage and is appropriate for removal of large congenital nevi or burn scars in this location. Sometimes, a forehead defect should be considered as just a specialized scalp defect, and large scalp rotation flaps can be used to rotate large parcels of hair-bearing and non–hairbearing scalp to resurface the defect. Care must be taken to preserve the hairline when moving the scalp and forehead as one unit. Hairstyle changes can camouflage some hairline aberrations. Lateral forehead defects can sometimes be reconstructed by elevating cheek skin upward along with the sideburn area, recruiting excess facial tissue to fill in temporal deficiencies. An extended paramedian flap that includes immediate subjacent scalp can resurface lateral and temporal defects.

SKULL BASE RECONSTRUCTION The goals of skull base reconstruction include separation of intracranial contents from the external environment and, for anterior defects, from nasal secretions (see Chapter 42) (10). The pericranial or pericranial–galeal flap is first harvested during a craniotomy and is placed over the exposed dura or dural repair. All remnants of sinus mucosa are ablated to reduce the incidence of late mucocele. The galeal flap may be better vascularized than the pericranial flap but its use leaves a visi-

CALVARIAL RECONSTRUCTION The two questions that must be answered regarding calvarial reconstruction are (a) should it be done and (b) if it should be done, what material should be used. The goals of reconstructing defects of the calvarium include protection of the underlying contents and restoration of the overlying contour. These can be accomplished with a variety of materials, including nonvascularized autogenous bone grafts (calvarial, split rib, or iliac crest), vascularized autogenous bone grafts, and alloplastic materials (e.g., methylmethacrylate, calcium phosphate cements, and titanium). Many factors influence whether to perform a cranioplasty, such as the size of the defect, cleanliness of the wound, age of the patient, and prognosis. If calvarial reconstruction is contemplated, autogenous bone is the most reliable material especially when craniofacial growth is anticipated or bone is also advantageous if there is any contamination of the wound. Alloplastic cranioplasty has its place, however, especially if the defects are very large. Of autogenous materials, iliac crest bone grafts, split-rib grafts, and calvarial bone grafts, can be used. Most commonly, these grafts are used as nonvascularized free grafts, but vascularized grafts are also available. Split-rib grafts can be harvested via an anterolateral incision centered over the seventh rib. Subperiosteal elevation of the bone may allow for bony regrowth of the rib donor site in smaller children. It is advisable to minimize rib harvest to three ribs per side, choosing alternate ribs in order to minimize the contour deformity of the donor site. The ribs are then split longitudinally with an osteotome, curved with a rib bender, tightly packed into the defect, and immobilized by wire, suture, or plate fixation. Bone graft incorporation is generally successful with split-rib grafts, but the final result is a washboard contour, making it less suitable for defects anterior to the hairline. Calvarial bone grafts allow for better contouring and can be harvested from the same operative field. These grafts are ideally harvested as full-thickness bone and split ex vivo. In situ harvest with a curved osteotome is adequate for small grafts. The skull is thickest in the parietal region, just posterior to the coronal suture, and graft harvest from this region minimizes the risk of violating the inner table or dura. Vascularized versions of calvarial bone and rib grafts exist and are usually chosen in the setting of an irradiated recipient bed or the presence of infection. A vascularized calvarial bone graft can be transferred based on the superficial temporal vessels, maintaining attachment to the superficial temporal fascia and pericranium (3). For rib grafts to be vascularized, microsurgical anastomoses need to be performed. In this situation, a few slips of serratus anterior muscle are harvested with one or

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more ribs as a composite free flap in order to deliver bone that can heal more promptly without reliance on vascular ingrowth from a compromised wound bed. Bone chips, paste, or other bone substitutes can be inserted in the small gaps that may remain after reconstruction with either rib or calvarial bone. Rib grafts can also be vascularized by wrapping them with a soft-tissue free flap such as a rectus abdominis flap. A variety of alloplastic materials have been used for cranioplasties, ranging from metal alloys to biocompatible acrylics and, more recently, “smart” moldable pastes. Metals such as vitallium (cobalt-chromium alloy), titanium, and stainless steel have the advantage of being easy to apply but are prone to infection, are radiopaque, and conduct heat and cold. Polymethylmethacrylate (PMMA), a quick-setting polymer, has been widely used for restoring bony defects because it is easy to apply, is relatively inexpensive, and has a long record of biocompatibility. However, PMMA has a complication rate as high as 23% in the pediatric population and can reach temperatures as high as 100◦ C (212◦ F) as it sets up (11). Calcium phosphate cements in conjunction with titanium mesh have also been used for cranioplasty. Fast-setting calcium phosphate cements with favorable handling properties are gaining popularity as cranioplasty material because during curing these materials are less exothermic than similar products, and some of the formulations can harden under wet conditions. The choice of cranioplasty material, however, is ultimately based on the surgeon’s preference, material handling characteristics, type and size of

the defect, age of the patient, cleanliness of the wound, and reliability of the overlying scalp tissue (see Chapter 7).

References 1. Hoffman JF. Management of scalp defects. Otolaryngol Clin North Am. 2001;34(3):571–582. 2. Zide BM, Jelks GW. Surgical Anatomy of the Orbit. New York: Raven Press; 1985:13–20. 3. McCarthy JG, Zide BM. The spectrum of calvarial bone grafting: introduction of the vascularized calvarial bone flap. Plast Reconstr Surg. 1984;74(1):10–18. 4. Horowitz JH, et al. Galeal-pericranial flaps in head and neck reconstruction. Anatomy and application. Am J Surg. 1984;148(4):489–497. 5. Molnar JA, et al. Single-stage approach to skin grafting the exposed skull. Plast Reconstr Surg. 2000;105(1):174–177. 6. Worthen EF. Transposition and rotation scalp flaps and rotation forehead flap. In: Strauch B, Vasconez LO, H.-F.E. J., eds. Grabb’s Encyclopedia of Flaps. Boston: Little Brown and Company; 1990. 7. Orticochea M. New three-flap reconstruction technique. Br J Plast Surg. 1971;24(2):184–188. 8. Hussussian CJ, Reece GP, W. U.S.L.M.O.U.S.A. Division of Plastic Surgery. Microsurgical scalp reconstruction in the patient with cancer. Plast Reconstr Surg. 2002;109(6):1828–1834. 9. Mustoe TA, Corral CJ, N.U.M.S.U.S.A. Department of Surgery. Soft tissue reconstructive choices for craniofacial reconstruction. Clin Plast Surg. 1995;22(3):543–554. 10. Langstein HN, et al. Coverage of skull base defects. Clin Plast Surg. 2001;28(2):375–387, x. 11. Taggard DA, et al. Successful use of rib grafts for cranioplasty in children. Pediatr Neurosurg. 2001;34(3):149–155.


CHAPTER 36 ■ RECONSTRUCTION OF THE LIPS SEAN BOUTROS

The lips are the primary aesthetic feature of the lower central face, with functional requirements that include speech, containing oral contents, and kissing. A hallmark of the lips is their mobility, which is critical for natural appearance and function. Reconstruction of lip defects is simple in that reconstruction, in most cases, is feasible, but complex in that a natural-appearing, dynamic reconstruction is often elusive.

ANATOMY The lip consists of four basic components: the skin and subcutaneous tissue, the muscle, the mucosa, and the vermilion. Each of these structures has unique characteristics that must be considered when planning the reconstruction. The skin of the lips is typical of facial skin. It is hair bearing with the hair being mostly vellus in women and children, with a downward direction of growth. The skin is of intermediate thickness for facial skin and is rich in sebaceous and sweat glands. The skin thickness and the number of appendages decrease with age. Deep to the skin is a significant amount of subcutaneous fat that makes up the bulk of lip thickness (Fig. 36.1). The external landmarks of the lips are the philtral columns and the Cupid’s bow. The philtral columns are musculocutaneous ridges that diverge slightly in their course from the base of the columella to the vermilion border. The philtral columns merge with the white roll, another ridge formed by the orbicularis muscle. The orbicularis fibers form the philtral dimple in the central lip between the paired philtral columns. There is a low point between the two peaks of the Cupid’s bow, which is referred to as the depth of the Cupid’s bow (Fig. 36.2). The primary muscles of the lip are the orbicularis oris muscles. They are paired, mostly horizontally oriented muscles that originate just lateral to the commissure at the modiolus. The modiolus is a crossroads of several other facial muscles, including the levator anguli oris, the risorius, and the depressor anguli oris. The two orbicularis oris muscles join in the midline of the lower lip in a raphe. In the upper lip, it crosses the midline and inserts into the opposite philtral column. The orbicularis also sends fibers to the skin at the base of the ala, nasal sill, and septum, and is the most important muscle for oral competence. It also provides for pouting and eversion of the lip, and some elevation of the lower lip. The buccal branches of the facial nerve innervate the orbicularis muscles. The second most important, and least understood, lip muscles are the paired mentalis muscles. The mentalis muscles are the main elevators of the lower lip, and this elevation is required for lower-lip positioning and lip competence. These muscles are inaccurately depicted in most anatomy texts, where they are shown as small, striplike muscles. In fact, they are large trapezoidal/pyramidal-shaped muscles that originate from the mandible just below the attached gingiva and insert horizon-

tally and inferiorly into the chin pad below the labiomental fold. The superior extent of the muscles defines the labiomental fold. They travel horizontally and inferiorly from the mandible to the skin of the chin. Contraction of the mentalis muscles elevates the lower lip in order to strongly coapt the upper and lower lip or to push contents out of the gingivobuccal sulcus. The marginal mandibular branch of the facial nerve innervates the mentalis muscles. The depressors of the lip include the depressor anguli oris (also called the triangularis), the depressor labii inferioris, and, to some degree, the platysma. The marginal mandibular branch of the facial nerve innervates these muscles, with the exception of the platysma that is innervated by cervical branches. The elevators of the upper lip include the levator anguli oris, the zygomaticus major and minor, and the levator labii superioris. They elevate the commissure, the lateral aspect, and the central body of the upper lip respectively. The zygomatic and buccal branches of the facial nerve innervate theses lip elevators. The inside of the lip is lined by mucosa, which is nonkeratinized epithelium that is rich in minor salivary glands. The mucosa is distinct from vermilion in its color and appearance. Vermilion, on the other hand, is the visible portion of the lip inside the white roll. It is duller than mucosa in its appearance. It has a unique light reflection and is nearly impossible to duplicate. The wet–dry line is the junction of the wet vermilion and the dry vermilion. Close observation will show that the vermilion tissue extends for a few millimeters beyond where the lips meet in natural mouth closure. It is in these few millimeters that the vermilion transitions to mucosa. The sensory innervation of the lip is provided by the mental and infraorbital nerves. The mental nerve is the terminal branch of the inferior alveolar nerve which is, in turn, a branch of the mandibular division of the trigeminal nerve (V3). The mental nerve exits the mandible between the first and second premolars. It divides into several branches, some of which can be seen intraorally. The upper lip receives its sensibility from the inferior orbital nerve, which is a branch of the maxillary division of the trigeminal nerve (V2). It exits the skull through the foramen rotundum, passes through the inferior orbital fissure and travels along the orbital floor before diving into the maxillary sinus and emerging from the bone through the infraorbital foramen. It provides sensation to the upper lip, ala, and nasal sidewall. These two distinct nerves allow for local anesthesia to be easily and quickly established for lip procedures. Low volumes of solution, placed accurately, will give complete anesthesia. Intraoral injections have the advantage of being less painful, and simpler to achieve complete blockade as they are based on bony landmarks (teeth) and the entire path of the needle parallels the bone. The mental nerve is injected by placement of the needle at the depth of the gingivobuccal sulcus in line with the canine. The needle is advanced for 1 cm and a depot of 1 to

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the periparotid nodes. Both of these nodal regions subsequently drain to the ipsilateral jugulodigastric nodes. The drainage is primarily ipsilateral, although there can be some crossover in the midline. The lower lip also drains to the ipsilateral submandibular nodes with the exception of the midline lip, which drains into the submental nodes. These are prone to cross the midline. The submental nodes subsequently drain into the submandibular nodes.

FUNCTION

FIGURE 36.1. Cross-section of the lip from the vermilion to the labiomental fold. Note the labial artery (arrow) just below the junction of the wet and dry vermilion and the significant amount of subcutaneous tissue making the bulk of the lip.

2 mL of lidocaine is injected. If sharp pain or paraesthesia is felt, the needle is backed out a few millimeters and the remaining volume deposited. The infraorbital nerve is also injected at the height of the gingivobuccal sulcus in line with the canine. The needle is advanced approximately 2 cm along the bone directed towards the lateral commissure of the eye. Again, a depot of 1 to 2 mL of lidocaine is injected, with care to avoid injection if a sharp pain or paraesthesia is felt. The vascular supply of the lips is both significant and redundant. The main arterial supply is from the labial arteries, which are branches from the facial artery and form a 360degree loop, allowing for various flap designs. The arteries lie just deep to the orbicularis muscle and can be found in cross section approximately at the wet–dry line (Fig. 36.1). They provide numerous perforators through the orbicularis muscle to the overlying skin. Although it is advised that flaps in the area contain the labial artery, the blood supply is so rich in this region that many authors have described survival of local flaps based only on a segment of mucosa. The venous drainage of the lips does not follow the arterial supply. A dense venous network coalesces in the area of the major names arteries to form the larger veins. The lymphatic drainage of the lips is important for oncologic considerations. The upper lip drains primarily to the submandibular nodes with some drainage from the commissure to

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5 6 7 FIGURE 36.2. Topographic anatomy of the lips. 1, Philtral columns. 2, Philtral groove or dimple. 3, Cupid’s bow. 4, White roll upper lip. 5, Tubercle. 6, Commissure. 7, Vermilion. (Redrawn after Zide BM. Deformities of the lips and cheeks. In: McCarthy JE, ed. Plastic Surgery. Philadelphia: Saunders; 1990:2009.)

The lips serve many functions that are accomplished as a result of their unique anatomy, especially the sphincteric muscle anatomy. The muscular content of the lips allow for their tone. Without this muscular support, the tissue would simply lose its support and become ptotic, as seen in patients with facial palsy who inevitably develop lower-lip laxity and lowerincisor show. Similarly if the upper lip was without muscular tone, the normal upper incisor–upper lip relationship would be lost. The sphincteric function of the lips allows for oral competence in eating and drinking, speech and sound production, forceful blowing, and kissing. The loss of this function with many lip reconstructions is frequently frustrating. Many reconstructions, especially those involving nonlip tissues, may look fine at rest, but appear abnormal in the living, moving patient.

ETIOLOGY The etiology of most lip defects is tumors or trauma. Lip tumors are either congenital or acquired. Congenital tumors are most often vascular malformations and hemangiomas. Acquired tumors are usually basal cell carcinoma in the upper lip and squamous cell carcinoma in the more sun-exposed lower lip. Melanoma is also quite common on the lip. Other tumors or pathologies are rare. Traumatic defects are different in that they occur in young, health patients.

LIP DEFECTS When analyzing a lip defect, the most important assessment is the amount of remaining lip vermilion. Vermilion, if present, carries with it muscle that can be used to maintain the sphincteric function of the lip. All methods of vermilion reconstruction by using other tissues are suboptimal. Buccal mucosa and tongue look like buccal mucosa and tongue. They do not take lipstick in the same way, have different light reflection, and have different color. Remaining lip skin is also important, but in general, this tissue can be replaced more easily than vermilion. When deciding on the operative plan, one must decide whether the lip can be reconstructed with lip tissue, which is preferable, or if the defect will require nonlip tissue. Lip tissue not only replaces “like with like,” but most lip reconstruction using lip tissue with orbicularis muscle will eventually have some element of neurotization. This will allow for functional reconstruction that provides a natural appearance both at rest and in conversation. It also allows for the replacement of precious vermilion tissue. Direct lip closure, or closure with sliding lip tissue, is always the first choice. Flaps such as the Abbe and reverse Abbe flap also satisfy the principle of reconstruction of “lip with lip.” These flaps are lip-switch flaps that do not move the commissure. As a result, a normal appearance at the commissure can be expected. The insertion of the muscles at the modiolus is preserved and


Chapter 36: Reconstructionof the lips

a more normal dynamic appearance is likely. They also have the distinct advantage of tightening the donor lip, which helps provide balance with the tightened reconstructed lip. The Abbe flap’s disadvantages are that it is a two-stage procedure and that it has no way to directly preserve innervation of the transferred orbicularis muscle. Other lip reconstructive flaps such as the Estlander, Gilles, and Karapandzic flaps, slide lip elements around the commissure. The upper lip is recruited to the lower lip as the commissure moves medially and a new commissure is created. These flaps have the advantage of not requiring a secondary flap division and inset. The Karapandzic flap has the advantage of maintaining innervated muscle. These other flaps, however, often require secondary revisions to establish a more normalappearing commissure. With the exception of the Estlander flap, they do not directly shorten the donor lip and instead move the modiolus and the corresponding muscles from the normal location to the defect. Some defects are simply too large to allow for reconstruction with lip tissue. In general, if a defect involves more than 40% of the total available upper- and lower-lip area (or greater than 80% of either lip), reconstruction with lip tissue will result in microstomia that is too significant and creation of a new lip must be considered. The Webster-Bernard, McGregor, Nakajima, and free flap reconstructions are examples of reconstructions that create new lip tissue from nonlip tissue (cheek and forearm). Although they are occasionally necessary reconstructions using nonlip tissue result in an unnatural dynamic appearance. In addition, the establishment of lip competence is more difficult.

Vermilion Because of its importance in lip appearance, the anatomy of the vermilion deserves special attention. The vermilion is a thin layer of nonkeratinized epithelium that is devoid of sebaceous glands and hair follicles. It gets its unique color and spongy nature from the underlying dense capillary network. Beneath this capillary network is the orbicularis muscle. The vermilion is bordered by the white roll, which is a myocutaneous ridge that sits just outside the vermilion border. The upper-lip vermilion is thickest directly below the high points of the Cupid’s bow. Below the depth of the bow, the vermilion often forms a tubercle. This is most obvious in children. The vermilion tapers off toward the commissure where the white roll becomes less prominent. The lower-lip vermilion is thickest in the midline and is usually more prominent than the vermilion in the upper lip. It tapers slightly until the lateral one-third of the lower lip, where it tapers rapidly. Alignment of the vermilion is a key element in any lip procedure, from simple lacerations to complex reconstructions with flaps. Stepoffs in the vermilion of 1 mm are noticeable at conversational distance. Note that it is impossible to accurately identify the vermilion or the white roll after injection of local anesthetic solutions. The pressure of the anesthetic solutions or vasoconstriction of the epinephrine distorts the distinct vermilion color and obscures the white roll. Therefore, the vermilion or white roll is marked prior to infiltration of anesthetic solutions. Consequently, the aforementioned nerve blocks are useful for lip procedures. They have the advantage of complete anesthesia without local deformation of tissues. A useful technique is tattooing of the vermilion border or white roll with a needle dipped in methylene blue. This will provide a reference that can be realigned accurately. Alternatively, a single fine suture can be placed at the white roll or vermilion border prior to infiltration of local anesthesia.

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Small, superficial vermilion defects can usually be closed primarily without elevation of flaps. Care must be taken to evert the edges to prevent notching. Lateral, superficial defects more than 2 to 3 mm from the white roll can usually be left to heal by secondary intention. This is less successful centrally where there can be a depression or a notching at the site. Alternatively, V-to-Y advancements from inside the vermilion will result in minimally noticeable scars. For larger vermilion defects that do not involve the white roll, flaps are indicated. These can include vermilion flaps (lip flaps) or mucosal and tongue flaps (nonlip flaps). Vermilion flaps are best suited for defects that are close to the white roll. They replace vermilion with vermilion and scars in the vermilion itself usually heal well. Techniques include vermilion advancements or vermilion switches from the opposite lip. Vermilion advancements are best suited for central defects. They are robust flaps based on the labial vessel. The external incision is made directly on the vermilion border and the intraoral incision is made well inside the lip (Fig. 36.3). These flaps have a distinct advantage, especially in central defects in that the normal vermilion taper is preserved. This advantage is lost in more lateral defect. For more lateral defects, the distance from the vermilion border to the wet–dry line is measured on both sides of the defect. The taller side is tailored so that the vermilion will not show a significant step off at the wet–dry line. Vermilion switch flaps are extremely useful. The vermilion is cut exactly as in a vermilion advancement, but is inset in the opposite lip (Fig. 36.4). The reconstruction of the donor lip is with vermilion advancement at the time of flap division. These flaps, like all lip flaps, are divided at 10 days. It is best not to delay division too long, as significant secondary healing will make tailoring and inset time more difficult, especially in the donor lip. Mucosal advancements are useful for broad defects that are remote from the vermilion border, as these defects will have enough normal appearing vermilion spared. As mucosal flaps contract and retract, they will result in a thinner lip, and this

FIGURE 36.3. Vermilion advancement flap. Proper eversion of the sutured edges will prevent notching. The height of the vermilion should be tailored in closure of lateral defects. (Redrawn after Zide BM. Deformities of the lips and cheeks. In: McCarthy JE, ed. Plastic Surgery. Philadelphia: Saunders; 1990:2016.)

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For central defects involving up to half of the distance between the philtral columns, primary closure is the best option. This will shift the philtrum in most cases, and will result in a narrow central lip. For defects that include greater than half of the central lip, an Abbe flap will give the best result. The remainder of the central lip, that is, from philtral column to philtral column, should be excised. This excision can, of course extend past the philtral column, knowing that this may result in slight asymmetry. With elevation and inset of the Abbe flap, certain principles must be followed (Fig. 36.5). The flap is harvested based on the labial artery. As the venous drainage does not follow the

FIGURE 36.4. Vermilion switch flaps can be performed using a portion of the vermilion (as shown here) or the entire vermilion. If the entire vermilion is used, the donor site is closed with vermilion advancement flaps. (Redrawn after Zide BM. Deformities of the lips and cheeks. In: McCarthy JE, ed. Plastic Surgery. Philadelphia: Saunders; 1990:2029.)

should be expected. These bipedicled flaps are elevated just below the minor salivary glands and advanced to fill the defect. The donor site is treated with a mucosal graft. Tongue flaps are another method of reconstruction. The anteriorly based lateral tongue flap is a useful tool as it can provide significant bulk. It, like all other nonvermilion flaps, does not leave a normal-appearing lip and is therefore best reserved for lateral defects. It is elevated from the lateral surface of the tongue, avoiding the papillary tongue. Closure of the donor site is important as the lingual nerve may be exposed in larger flaps.

Upper Lip Superficial defects of the upper lip must be categorized by their location and size. These defects have the advantage of intact orbicularis and lip bulk. As a result, the reconstruction can often be simplified and still give a good aesthetic result, even with larger defects. Central defects between the philtral columns can be repaired primarily or with a wedge resection if they involve less than half of the central lip segment. The orbicularis muscle must be accurately repaired for normal lip movement. If the superficial defect involves more than half of the central lip, but does not cross or just crosses the philtrum, a full-thickness skin graft from the preauricular area is a reasonable option. This technique has the advantage of hair growth that can often improve the aesthetic appearance. For lateral, superficial defects, wedge resection is usually a good option except for cases where there is greater than half of the lateral lip involved. For these cases, full-thickness grafting will often give an acceptable result. Full-thickness defects are defects that include significant amounts of the subcutaneous fat and the orbicularis muscle. Treatment is based on their size and location in the upper lip. Defects up to one third will do well with primary closure with local tissue rearrangement and advancement. This local tissue rearrangement will often include perialar crescentic excisions and medial advancement of the nasolabial fold.

FIGURE 36.5. Abbe flap. Top: The Abbe flap is elevated from the central lower lip. For central upper defects, it is elevated to the labiomental fold. For lateral defects, it continues through the central chin pad. Middle: It is inset onto the columella, above the columellar base with the extensions to the nasal sill. Bottom: The flap is divided and inset at two weeks.



arterial supply, it is best to maintain a several-millimeter cuff of labial mucosa for venous drainage. The Abbe flap should be harvested from the central lower lip. One must remember that the orbicularis muscle is paired. The Abbe flap should include the central raphe so as to leave neurotized orbicularis on both sides of the closure. Whenever possible, the Abbe flap should be in the exact center of the lower lip. Central lip incisions will leave the best donor scar on the lip and chin. The base of the Abbe can be closed with two Burrow triangles on either side so as to leave a small horizontal scar at the labiomental fold. It is rare that the Abbe flap needs to be extended beyond the labiomental fold. This is true because most lateral defects of the upper lip should be treated with concomitant medialization of the cheek and thus the nasolabial fold. This decreases the superior extent of the defect. In cases where the Abbe flap must be extended beyond the labiomental fold, it should be kept directly in the midline. This will avoid disrupting the balance of the paired mentalis muscle and usually leaves an acceptable scar. When the Abbe flap is inset in the upper lip, it should be sutured on the columella, just above the medial footplates. If it is inset below the medial footplates, there will be loss of the normal meniscus that exists between the columella and the upper lip. The Abbe flap can also be used to replace lateral lip defects larger than a third. This is the preferred technique if the commissure is intact. It is best to combine the Abbe flap with perialar excision and lip advancement. This allows for the tip of the Abbe flap to be inset at the alar base and the cheek tissue to be advanced to fill the lateral portion of the defect. The nasolabial fold is thus advanced medially such that it begins at the alar base, and not at the lateral ala. The remaining lip defect is closed via medial advancement of the lateral lip. This will shift the philtrum slightly and the patient should be forewarned. For even larger defects, those up to 80% of the upper lip or 40% of the total available lip tissue, the Abbe flap is simply made larger. It is designed with a bilateral Schuchardt advancement because it will allow for medial advancement of the lower lip and closure of the large donor side. This is also combined with bilateral perialar crescentic excision. Overall, this will leave a microstomia, and secondary lip stretching will be necessary. Remember that a balance in the length of the upper and lower lip is important and the tissue should be near equally shared by the two lips. Subtotal (greater than 80%) and total upper lip defects are rare, and reconstruction is basically a salvage operation. Most patients with these defects have lived with deforming tumors for years without seeking care. The exceptions, and most difficult cases, are traumatic lip loss and these patients have higher demands. As mentioned above, procedures employing nonlip tissues rarely appear natural at rest, and even more seldom in the living, moving patient. Functional reconstruction is not as critical in the upper lip as in the lower lip. A static upper lip can allow for competence if the lower lip is normal. The radial forearm free flap is a useful tool for subtotal or total lip defects. It can provide adequate bulk of tissue and a reasonable color match. It is often folded to provide both intraoral and external tissue. Care should be taken to avoid a lip that is too long, as the new lip will become ptotic with time. The vermilion can be reconstructed with either tattooing or with buccal mucosal grafting. If grafting is used, the forearm flap is de-epithelized in a second stage and buccal mucosa placed. In male patients, good results can be expected with the free occipital flap. It results in a hair-bearing upper lip that allows for camouflage of the nonmobile, poor-color-match lip. The inside of the lip is reconstructed with a thick split-thickness graft. This is advantageous as it will give some stiffness to the lip as the graft contracts.

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Lower Lip Lower-lip defects should be divided into those involving the commissure (or approaching the commissure) and those of the central lip. The lower lip can tolerate wedge excision for the majority of defects encountered. This includes most superficial defects, which, unlike the upper lip, are treated in the same fashion as full-thickness defects. The only exception is the rare superficial defect of greater than 50% of the lower lip for which a skin graft is appropriate. For defects that are not amenable to straight wedge excision, the Schuchardt procedure is the next option (Fig. 36.6). This is a sliding-lip reconstruction that advances the lower lip with an inferior incision along the labiomental fold to the mandibular

FIGURE 36.6. The Schuchardt procedure rotates and advances the cheek and lip to provide closure. The skin folds are removed as crescents (top) or submental triangles (bottom). (Redrawn after Zide BM. Deformities of the lips and cheeks. In: McCarthy JE, ed. Plastic Surgery. Philadelphia: Saunders; 1990:2017.)

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border. Intraorally, the incisions are on the labial side of the gingivobuccal sulcus. The lip is advanced centrally. It is performed on the side of the lower lip with the greatest amount of tissue as this allows for the greatest advancement. It avoids complex reconstructive procedures and leaves minimal scarring. This technique can be applied to most lower-lip defects as it is easily combined with many of the lip-switching procedures. Lip-switching procedures are often necessary. The workhorse flap is the reverse Abbe flap, which can be used for either lateral or midline lower-lip defects. These include either the lateral or the central reverse Abbe flaps. The lateral Abbe flap is usually based off the medial labial artery. It differs from the Estlander flap in that it does not move the commissure. The lateral aspect of the flap, and thus the vermilion, is kept medial enough so that it is of sufficient height to match the medial defect of the lower lip. The tip of the Abbe is the perialar crescentic excision in order to allow for primary closure of the upper lip. This is most useful for lateral lower lip defects that cannot be repaired with the Schuchardt alone. It does shift the philtrum towards the Abbe closure. The central reverse Abbe flap is used for central lower lip defects. This differs from the lateral reverse Abbe flap in that the perialar crescents are not part of the flap, but are discarded in the closure of the upper lip. It also differs in that the vascular pedicle is lateral and not medial. The medial incision for the Abbe flap is at the philtral column and the lateral extent is just at the lateral aspect of the ala. It can be performed as a double central reverse Abbe flap for large lower-lip defects (Fig. 36.7).

FIGURE 36.8. Bilateral Karapandzic flaps for closure of a large lowerlip defect. The Karapandzic techniques preserves the nerves to the orbicularis muscle. (Redrawn after Zide BM. Deformities of the lips and cheeks. In: McCarthy JE, ed. Plastic Surgery. Philadelphia: Saunders; 1990:2023.)

FIGURE 36.7. Double central reverse Abbe flap for closure of large lower-lip defects. This is especially useful as it distributes the total lip tissue without distorting the commissure. (Redrawn after Zide BM. Deformities of the lips and cheeks. In: McCarthy JE, ed. Plastic Surgery. Philadelphia: Saunders; 1990:2019.)

With this, bilateral central reverse Abbe flaps are used along with lower lip medial advancement. For these cases, precise measurements are necessary as the goal is to evenly distribute the lip tissue between the upper and lower lip. Again, this can be used for up to 80% defects of the lower lip. The total lip area will be reduced by 40% and secondary stretching will be beneficial. The sliding lower-lip reconstructive procedures are the Karapandzic and the Estlander flap. The Karapandzic flap is essentially a Gilles flap that maintains the nerve supply to the lower lip and has replaced the Gilles flap (Fig. 36.8). This flap is a rotation-advancement flap along the nasolabial fold that pivots at the commissure and upper lip. The Estlander is a lip-switching flap that involves the commissure and pivots the upper lip to the lower lip (Fig. 36.9). Of these flaps, the Karapandzic is the most useful. Bilateral Karapandzic flaps can be employed for up to 80% defects. The advantage is that the lip is innervated, while the disadvantage is the microstomia, rounding of the commissure, and the misplacement of the modiolus that is inevitably produced.



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FIGURE 36.9. The Estlander flap rotates the upper lip to the lower lip. It results in a round commissure and loss of the normal taper of the vermilion. (Redrawn after Zide BM. Deformities of the lips and cheeks. In: McCarthy JE, ed. Plastic Surgery. Philadelphia: Saunders; 1990:2022.)

For larger defects, nonlip techniques must be employed. The Webster-Bernard operation has stood the test of time (Fig. 36.10). It involves medial advancement of the cheek tissue to create a new lower lip. Excision of tissue at the nasolabial fold allows for this advancement. The vermilion is reconstructed with a bipedicled mucosal sliding flap. The mucosal flap should be brought well outside the lip as it inevitably contracts. It can give good results, although it does result in significant facial scarring. The free radial forearm, as in the upper lip, is a reasonable option. The palmaris tendon can be included with the flap and used to suspend the lower lip. This allows the lower lip to be placed high and provides for oral competence. Hair transplantation to the free radial forearm flap can greatly improve the result. Even if the hair is shaved, it provides texture to the skin that gives a more normal appearance.

Other Reconstructive Tools Lip reconstructions often require reversionary procedures. Lipsharing procedures result in some element of microstomia. Because of the superiority of the techniques employing lip tissue, some degree of microstomia is preferable to a reconstruction using nonlip tissues. Established microstomia can be treated with serial stretching. For millennia, the Mursi tribes in presentday Ethiopia have practiced lip stretching by serial placement of larger lip disks (Fig. 36.11). Several techniques have been described for lip expansion and the simplest devices are often the best. Self-retaining spring dental retractors are easy for patients to obtain and can be used at night. These devices are also useful for remodeling the commissure in cases of commissural burns.

FIGURE 36.10. The Webster-Bernard flap advances the cheek skin medially to replace the lower lip. The vermilion is reconstructed with a mucosal flap. (Redrawn after Zide BM. Deformities of the lips and cheeks. In: McCarthy JE, ed. Plastic Surgery. Philadelphia: Saunders; 1990:2020.)

Hair transplants are also very useful. They can camouflage the scars of lip reconstruction and can provide normal texture to the new lip skin even if shaved. They are especially useful in free tissue transfers as they hide nonmobile tissue.

KEY POINTS 1. The mentalis muscles are required for lower lip position and lip competence. They are large trapezoidal/

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2.

3. 4.

5. 6. 7. 8. 9.

and inferiorly into the chin pad below the labiomental fold. When analyzing a lip defect, the most important assessment is the amount of remaining vermilion. Lip vermilion carries orbicularis muscle that allows for movement of the lip. The lip vermilion is distinct from mucosa in its color and appearance. The vermilion or white roll is marked prior to infiltration of anesthetic solutions because it is difficult to accurately identify the vermilion or the white roll after injection of local anesthetic solutions. A balance in the length of the upper and lower lip is desirable. With larger reconstructions, total lip tissue should be near equally shared by the two lips. Functional reconstruction of the upper lip is not as critical as in the lower lip. The lower lip can tolerate wedge excision for the majority of defects encountered. Lip-switching procedures have the distinct advantage of simultaneously shortening the normal lip along with reconstructing the opposite lip defect. The Abbe and reverse Abbe flaps have the advantage of not moving the commissure.

Selected Readings

FIGURE 36.11. A Mursi tribeswoman with large lip disk in place. Note how the vermilion tissue is truly expanded.

pyramidal muscles that originate from the mandible just below the attached gingiva and insert horizontally

Berkovitz BKB, Moxham BK, Brown, MW, et al. A Textbook of Head and Neck Anatomy. London: Wolfe Medical; 1988:154. Dupin C, Metzinger S, Rizzuto R. Lip reconstruction after ablation for skin malignancies. Clin Plast Surg. 2004;31(1):69. Langstein HN, Robb GL. Lip and perioral reconstruction. Clin Plast Surg. 2005;32(3):431, viii. Sultan MR, Hugo NE. Basic principles of reconstruction of the lip, oral commissure, and cheek. In: Georgiade GS, Riefkhol R, Levin LS, eds. Plastic, Maxillofacial, and Reconstructive Surgery. 3rd ed. Baltimore, Md: Williams and Wilkins; 1997. Zide BM. Deformities of the lips and cheeks. In: McCarthy JE, ed. Plastic Surgery. Philadelphia: Saunders; 1990:2009.


CHAPTER 37 ■ RECONSTRUCTION OF THE CHEEKS BABAK J. MEHRARA

The cheeks represent the largest surface area of the face and frame the central facial units. This anatomic arrangement exposes the skin of the cheek to trauma and to the effects of sun exposure, and, in turn, the frequent need for reconstructive surgery. Reconstruction must be planned carefully and executed meticulously to restore the natural contours, maintain hair patterns, and camouflage scars. The face can been divided into units based on a number of characteristics, including skin color, skin texture, hair, contour, relaxed skin tension lines, and boundaries between anatomic structures. The cheek, however, is less amenable to “aesthetic unit” analysis. Zide has divided the cheek into three overlapping zones: suborbital, preauricular, and buccomandibular based on reconstructive needs (1). Similarly, Jackson, has divided the cheek into five areas based on reconstructive techniques and anatomic characteristics (lateral, lower, malar, superomedial, and alar base-nasolabial) (2). These classification systems are helpful for planning reconstruction, but principles used for subunit reconstruction in other areas (e.g., resurfacing entire units, discarding remaining tissues of entire units if more than 50% of a unit is missing, using contralateral side to make exact templates) are less applicable to cheek reconstruction.

ANATOMY The cheek is bounded by the preauricular fold laterally, the zygomatic arch and lower eyelids superiorly, the nasal sidewall and nasolabial fold medially, and the mandibular border inferiorly. The sensory innervation of the cheek is provided by the maxillary and mandibular divisions of the trigeminal nerve, as well as a small contribution from the anterior cutaneous nerve of the neck and the great auricular nerve, both of which arise from the cervical plexus. Motor innervation of the superficial facial muscles is provided by the facial nerve and its main branches. The masseter and temporalis muscles are innervated by the trigeminal nerve. The facial nerve is located deep to the parotid masseteric fascia and is protected by the superficial lobe of the parotid gland anterior to the ear. The arterial supply of the cheek is provided by branches of the external carotid artery including the facial artery, the superficial temporal artery, and the transverse facial artery. Venous drainage follows the arteries and is abundant. The lymphatic drainage of the cheek is provided by lymphatic channels within the parotid nodes and along the facial vessels to the submandibular nodes.

(simple) and include only the skin and subcutaneous tissues, or may be more complex and include muscle, parotid gland, facial nerve, mucosa, and bone. Ideally, surgical incisions are placed at the cheek margins or within established skin rhytides to camouflage the resulting wound. Care is taken to avoid, if possible, placement of hair-bearing skin into non–hair-bearing areas. Similarly, rotation of non–hair-bearing skin into male beard lines and distortion of sideburns is avoided. Contour deformities and color mismatches are avoided whenever possible by careful planning. Distortion of surrounding structures such as the lower eyelid and upper lip is disfiguring and is an important consideration in planning the surgical approach to reconstruction. According to Zide and colleagues, vertical incisions placed medial to a line drawn from the lateral canthus remain obvious on frontal view and instead should be replaced by incisions along the nasolabial fold or by blepharoplasty incisions (3). Defects involving the full thickness of the cheek can occur from invasion of more superficial cancers, from extensive trauma, or as a result of advanced intraoral cancers. Appropriate reconstruction of all layers, while maintaining reasonable contour, are planned if possible. A successful reconstruction will recreate the missing tissues using the most similar replacement tissues. Thus, as with nasal reconstruction, plans for lining, support, and coverage are developed individually. Secondary revisions for contour may be necessary, particularly for complex reconstructions, and should be described to the patient prior to initiation of therapy. Facial nerve reconstruction is ideally performed as a planned procedure with the ends of the nerve stimulated and tagged at the time of resection since identification of nerve ends after tumor extirpation is tedious. In addition, nerve transection is performed sharply to avoid cautery damage at the site of neurorrhaphy. Nerve grafts may be harvested from the neck (ansa cervicalis, great auricular nerve) or from distant sites (e.g., sural nerve). For any given defect, more than one reconstructive option is usually available. The best option is determined based on the relationship of the defect to the surrounding structures, hairbearing status, skin laxity, natural wrinkles, previous surgical scars, and relaxed skin tension lines. Contaminated wounds undergo serial debridement and dressing changes until bacterial content is reduced to an acceptable level before definitive reconstruction is accomplished. A history of previous radiation therapy may prohibit local flap reconstruction.

RECONSTRUCTIVE OPTIONS

DEFECT ANALYSIS

Healing by Secondary Intention

Analysis of the defect or anticipated defect is a critical part of any reconstructive procedure. Defects may be superficial

The simplest method of closure is healing by secondary intention. Unfortunately, the indications for this technique are

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limited as large wounds may result in contour irregularities, distortion of surrounding structures, and unstable coverage. This technique may be useful for small (7 cm) and below or lateral to the expander pocket; expanders are filled intraoperatively to safest maximal amount to avoid seroma/hematoma; postoperative expansion should be delayed for 10 to 14 days; overexpansion by 30% to 50% is recommended; the capsule is incised and capsulectomy is avoided at the time of flap transposition.

fects (Fig. 37.12). Multiple skin islands may be designed along the length of the flap and the flap may be de-epithelized or thinned to allow soft-tissue contouring. A short segment of the radial bone may be harvested as vascularized bone with the flap. The main drawbacks of this flap include donor-site scarring and color/texture mismatch with local tissues. In addition, the flap may be hair-bearing in some men.

Parascapular Flap

Microsurgical Reconstruction Microsurgical reconstruction is an important option for complex defects involving multiple tissue layers. These techniques are also useful for resurfacing massive skin resections and in patients in whom local flaps may not be available (e.g., previous neck dissection, facial burns) or advisable (contaminated wounds, history of radiation therapy). Resurfacing of extensive intraoral or through-and-through defects and contour deformities are additional potential indications for the use of microsurgical tissue transfer. Although a number of flap options have been described, the radial forearm, parascapular, rectus abdominus, anterolateral thigh flap, and free fibula flap have been the most useful in our experience. The choice of free flap is dependent on the amount of external skin, intraoral lining, and soft-tissue contour requirements. In addition, the availability and location of the recipient vessels must be carefully determined.

Radial Forearm Flap The radial forearm flap is a fasciocutaneous flap based on the radial artery. The flap is an excellent source of thin, pliable skin with a long, reliable pedicle. The flap has a dual venous drainage with the cephalic vein and radial vena comitans. Sensate reconstructions may be performed using the lateral antebrachial cutaneous nerve. The forearm flap is an excellent choice for defects requiring a thin coverage of skin (Fig. 37.11). In addition, the flap may be folded upon itself to provide more bulk or to provide coverage of through and through cheek de-

The parascapular flap is also a fasciocutaneous flap based on the circumflex scapular vessels. This flap has more bulk than the radial forearm flap and is useful in reconstruction of composite resections such as radical parotidectomy (Fig. 37.13). The flap may be harvested with a segment of scapular bone (up to 14 cm). In addition, the latissimus dorsi muscle can be harvested on a common pedicle, resulting in a large amount of soft tissues useful in reconstruction of massive defects. In general, this flap has a better color match with facial skin than most other microvascular flaps and is associated with minimal functional deficits, although the donor-site scar tends to widen if large flaps are designed. The flap is not usually useful for through-and-through defects and its pedicle length is shorter and more difficult to dissect than the radial forearm flap. In addition, parascapular and scapular flap dissection requires lateral positioning of the patient, making simultaneous flap harvest and tumor resection difficult.

Rectus Abdominus Flap The rectus abdominus myocutaneous flap is a workhorse flap for facial reconstruction. The use of this flap for cheek reconstruction is more limited, however. The flap is usually designed with a vertical skin paddle and its primary indications are reconstruction of complex defects including multiple layers. The pedicle vessels are the deep inferior epigastric artery and vein and are highly reliable. Pedicle length may be lengthened through intramuscular dissection and may be as long as 14 to 15 cm. The flap may be bulky, particularly in obese patients, and secondary revisions with liposuction and direct excision


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A,B

C

D,E

F FIGURE 37.10. Cervicopectoral rotation flap. Preoperative (A, B), intraoperative (C, D), and postoperative (E, F) photographs of cervicopectoral rotation flap for large cheek defect resulting from basal cell cancer excision. The flap is elevated in the subcutaneous plane until a point approximately 2 cm below the angle of the mandible at which point the platysma is included with the flap (dark arrow in C). A small skin graft was necessary below the hairline to obtain tension-free closure (arrow in D). Note good contour and acceptable final scar.

may be required. The flap can be folded upon itself for reconstruction of through-and-through defects of the cheek, but is likely to be too bulky in most patients. The amount of muscle harvested with the flap can be tailored to fit the defect and is particularly useful for obliterating radical resections involving the maxillary sinus and the overlying cheek skin. Recently, perforator flaps (deep inferior epigastric perforator flap) that include only perforating vessels without harvesting rectus muscle have been described for head and neck reconstruction. These flaps have the advantage of being less bulky and may be associated with less donor-site pain and abdominal wall laxity or hernias. The potential drawbacks to the use of the rectus flap for cheek reconstruction include donor-site complications and bulkiness of the flap necessitating secondary revisions.

Anterolateral Thigh Flap The anterolateral thigh flap is a fasciocutaneous flap based on the perforating vessels of the descending branch of the lateral

circumflex femoral artery and vein. The flap may be thin and pliable, depending on the patient’s body habitus, and is useful for providing a large amount of skin together with a variable amount of vastus lateralis muscle to fill complex defects (Fig. 37.14). The flap may be thinned somewhat at the time of flap harvest, however, aggressive thining may be associated with partial flap necrosis. Alternatively, secondary revisions with liposuction and direct excision may be required. Thin patients may be good candidates for reconstruction of through-andthrough cheek defects based on dissection of multiple perforating branches. Pedicle dissection is more difficult than the radial forearm flap because of anatomic variability; however, large-caliber vessels are available in most instances. Dissection of the pedicle vessels to their origin can result in a lengthy pedicle that enables microvascular anastomosis to the neck vessels while avoiding vein grafting. The advantages of this flap include more favorable donor-site scarring than the radial forearm flap, potential for simultaneous flap harvest and tumor ablation, and the ability to tailor the thickness of the flap by altering the amount of vastus lateralis muscle resection. Knee

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C

A,B

D

E

FIGURE 37.11. Radial forearm free flap. Intraoperative (A, B, C) and postoperative (D, E) photographs of a free radial forearm flap used for reconstruction of deep, wide, central cheek defect resulting from resection of a desmoplastic melanoma. The flap was folded upon itself medially to correct the volume deficiency. Note postoperative ectropion (D) despite intraoperative canthoplasty and flap suspension.

A,B

D

C

FIGURE 37.12. Folded radial forearm flap. Preoperative (A) and intraoperative (B, C, D) photographs of a folded radial forearm flap for intraoral and external coverage of a complex cheek defect. Note that lip continuity was restored using lip rotation flaps (right, Karapandzic; left, Estlander) thereby avoiding interposition of the radial forearm flap in the lip defect.


Chapter 37: Reconstruction of the cheeks

C,D

A,B

E

387

F

FIGURE 37.13. Parascapular flap. Postoperative (A) and intraoperative (A, B, C, D) and postoperative (E, F) photographs of a free parascapular flap for reconstruction of a complex cheek defect resulting from resection of a recurrent malignant melanoma of the right parotid gland. Facial nerve repair was performed using sural nerve grafts. Postoperative photographs were taken 1 year postoperatively without further revision. Note good color match and contour.

C

A,B

D,E

F FIGURE 37.14. Anterolateral thigh flap. Preoperative (A), intraoperative (B, C, D, E), and postoperative (F) photographs of a massive cheek and neck defect resulting from resection of osteoradionecrosis and infection of the right mandible. The patient had a previous parotid tumor treated with wide resection, radical neck dissection, and maximal doses of external beam radiation therapy. Note severe atrophy of the surrounding tissues. A thin anterolateral thigh flap together with a small portion of the vastus lateralis muscle (D) was used to cover the cheek defect and close the small intraoral defect resulting from resection.

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FIGURE 37.15. Summary of reconstructive technique for acquired cheek defects. See text for details. FTSG, fullthickness skin graft.

extension is rarely affected unless there is inadvertent injury to the femoral nerve. Color match to facial skin is poor, however, as is the hair patterns.

Fibula Osteocutaneous Flap The fibula osteocutaneous flap (Chapter 41) is an excellent source of vascularized bone (up to 30 cm) and a variable amount of skin and soft tissues. Portions of the soleus muscle and flexor hallucis longus muscle can be harvested as vascularized muscle. The flap is based on the peroneal vessels and is useful for reconstruction of segmental mandibular defects that include external skin resections. The flap may be harvested at the time of tumor ablation, and the skin paddle may be folded upon itself to provide both intra- and extraoral lining. The fibula skin paddle is most reliable in the distal portions of the leg where the perforating vessels tend to follow a septocutaneous pattern. Care must be taken during flap harvest to avoid injury to the neurovascular structures of the lower extremity and to preserve adequate bone proximally and distally to avoid knee and ankle instability, respectively. In addition, the vascular supply of the leg should be carefully evaluated preoperatively, either by physical examination or in combination with radiologic studies, to avoid lower extremity ischemia.

CONCLUSION Reconstruction of cheek defects requires careful planning and execution. Although the choice of surgical options must be individualized, an overall guide for the practitioner is summarized in Figure 37.15.

References 1. Zide B, Longaker, M. Cheek surface reconstruction: best choices according to zones. Oper Tech Plast Reconstr Surg. 1998;5:26. 2. Jackson I. Local Flaps for Head and Neck Reconstruction. St. Louis, Quality Medical Publishing, 2002. 3. Longaker M, Glat P, Zide BM, et al. Deep-plane cervicofacial “hike”: anatomic basis with dog-ear blepharoplasty. Plast Reconstr Surg. 1997;99:16. 4. Chadawarkar R, Cervino A. Subunits of the cheek: an algorithm for the reconstruction of partial-thickness defects. Br J Plast Surg. 2003;56:135–139. 5. Al-Shunnar B, Manson P. Cheek reconstruction with laterally based flaps. Clin Plast Surg. 2001;28:283. 6. Kroll S, Reece G, Robb G, et al. Deep-plane cervicofacial rotationadvancement flap for reconstruction of large cheek defects. Plast Reconstr Surg. 1994;94:88. 7. Antonyshyn O, Gruss J, Zuker R, et al. Tissue expansion in head and neck reconstruction. Plast Reconstr Surg. 1988;82:58. 8. Wieslander J. Tissue expansion in the head and neck. Scand J Plast Reconstr Hand Surg. 1991;25:47.


CHAPTER 38 ■ NASAL RECONSTRUCTION FREDERICK J. MENICK

Life is about choices and compromises. For a nasal reconstruction to be successful, the problem must be analyzed, options identified, limitations appreciated, and the best solution chosen to achieve the desired outcome.

THE NOSE Anatomically, the nose is covered by external skin, supported by a mid layer of bone and cartilage, and lined primarily by mucoperichondrium. If missing, each layer must be replaced. Aesthetically, the nose is a central facial feature of high priority. To appear normal, it must have the proper dimension, position, and symmetry. Its surface can be divided into aesthetic subunits—adjacent topographic areas of characteristic skin quality, border outline, and three-dimensional contour— the subunits of the dorsum, tip, columella, and the paired sidewalls, alae, and soft triangles (Fig. 38.1). Restoration of these “expected” characteristics permits a reconstruction to “appear normal” (1–3). Functionally, the nose must allow unobstructed breathing.

PLANNING Thoughtful consideration of the patient, the wound, and the available donor materials helps to identify the most appropriate treatment.

The Patient Most patients want the wound healed and their appearance restored to its preoperative condition. In some cases, however, age, associated illness, or patient desire may dictate a less complicated, quicker repair with minimal surgery or stages. A nasal wound can be allowed to heal by secondary intention. If full thickness, the cover and lining can simply be sutured to one another, accepting a permanent deformity. If a more complex repair is indicated, the surgeon must be aware that previous surgical treatments for skin cancer, radiation, trauma, or rhinoplasty add scars, may interfere with blood supply, impair healing, or preclude a specific flap option. Operative time, anesthetic requirements, hospitalization needs, the number of stages, and time to completion must be considered.

The Wound The site, size, depth, and wound condition influence the reconstructive approach. Frequently, the wound is distorted and does not reflect the true tissue loss. It may be enlarged by edema, local anesthesia, gravity, or resting skin tension or diminished by

wound contracture due to secondary healing. A preliminary operation may be needed to release an old scar, reposition normal to normal, or open the airway. In all circumstances, missing tissues must be replaced in the exact amount. If too little is replaced, adjacent landmarks will be distorted, collapsing underlying cartilage grafts. If too much is resupplied, adjacent landmarks will be pushed outward, distorting the external shape or pushing the lining inward, obstructing the airway. A superficial defect with residual well-vascularized subcutaneous tissue will accept a skin graft. However, exposed cartilage or bone without perichondrium or periosteum will not. The skin of the dorsum and sidewall is thin, smooth, pliable, and mobile. The skin of the columella and alar rim is thin but adherent. The skin of the tip and ala is thick and stiff, pitted with sebaceous glands. Skin grafts, even when taken from a donor site of similar skin quality, will appear shiny and atrophic. Skin grafts are best used within the thin skin of the dorsum or sidewall or the alar rim or columella rather than within the thicker skin of the tip and ala, where they will blend poorly and may appear as a patch. Local flaps because of skin laxity and mobility are most easily used within the dorsum or sidewall. The nasal bones and cartilage support the nose, impart a nasal shape to the soft tissues both of lining and cover, and brace any repair against the force of the myofibroblast contraction. If missing, support must be replaced. The normal ala is shaped by compact fibrofatty soft tissue and contains no cartilage, but cartilaginous support must be placed along the new nostril margin to maintain shape and projection when an alar rim is reconstructed. In the past, bone and cartilage grafts have been placed secondarily, months after the initial reconstruction. Unfortunately, once the soft tissues have healed in place, they become scarred and can rarely be re-expanded and reshaped by cartilage grafts at a later date. In almost all circumstances, support should be resupplied prior to the completion of wound healing. Local flaps do not add skin to the nose. They rearrange the residual skin and redistribute it over the entire nasal surface. Under the tension of local skin rearrangement, local flaps may collapse newly positioned cartilage grafts. If cartilage must be replaced, therefore, a regional flap from the cheek or forehead to resurface the nose will be required. In summary, nasal defects may be classified as small and superficial or large and deep. A small, superficial lesion is one that is less than 1.5 cm in size, with an intact underlying cartilage framework. If a vascularized bed of perichondrium or periosteum is present, a skin graft may be placed or the defect resurfaced with a local nasal flap. If the defect is greater than 1.5 cm, there may not be enough residual skin over the nose to spread over its entire nasal surface without distorting the tip or alar rims. A large, deep defect is one that is greater than 1.5 cm or one requiring the replacement of a cartilage framework or lining. A regional flap from the forehead or cheek will most often be employed for nasal resurfacing.

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are best employed for deeper wounds requiring replacement of soft tissue bulk in convex areas.

GENERAL PRINCIPLES OF REPAIR

A

Alar lobule

Dorsum

Soft triangle B

Tip

FIGURE 38.1. Aesthetic units and aesthetic junction lines of the nose. A: Lateral wall subunit. B: The nasal lobule and its aesthetic subunits.

Most often, a failure in repair results from a shortage of lining. If the defect is full thickness, lining replacement must be vascular enough to support the early replacement of cartilage grafts, supple enough to conform to their proper shape, and thin enough that it neither stuffs the airway nor distorts the external shape. Infection or tissue ischemia may preclude immediate reconstruction. Soft tissue foreign bodies, such as injectable or implantable silicone or other allografts, increase the risk of infection, fibrosis, and later extrusion.

The Donor Site Defects require replacement of variable amounts of cover, support, and lining. Each donor material is chosen by evaluating the quality of the material needed, the available excess (which can be shared from the donor site to recipient site), and its ability to be transferred as a skin graft to a vascular bed or by a pedicle with an adequate arc of rotation. Covering skin must match the face—only skin from above the clavicle will suffice. Skin grafts lie flat, rarely pincushioning, whereas flaps may trapdoor. The fibroblast contraction under a flap will enhance the repair of a convex surface unit such as the ala but distort the flat sidewall. Skin grafts are best used for superficial defects involving a planar or concave surface. Flaps

1. Establish a goal. The objective may be a healed wound or the reestablishment of normal appearance. Priorities must be set, stages identified, and materials and techniques planned. 2. Visualize the end result. The normal is described in terms of skin quality, outline, and three-dimensional contour. Materials and methods are chosen to achieve this end. 3. Create a plan. Nothing happens by chance. The operative steps and, if necessary, the surgical stages required to transfer tissues for cover, lining, and support are determined. 4. Consider altering the wound in site, size, depth, or position if this will assist the repair. Although all patients have a fear of scars, most nasal wounds heal with minimal scarring. Scars interfere with success only when they distort the expected subunits. If a defect of the convex tip or alar subunit will be covered with a flap and the wound encompasses greater than 50% of that subunit, consider discarding adjacent normal skin within the subunit and resurfacing the entire subunit, rather than just patching the defect. Inevitable trap door contraction (along with cartilage grafts) then contributes to restoration of the expected convexity. If residual tissues are distorted by the old scar, the remaining normal landmarks are returned to their normal position first. 5. Use the ideal or contralateral normal as a guide. Fresh wounds may not represent the true size or shape of the tissues that are actually missing due to the distortion of edema, tension, or gravity. A template of the contralateral normal is made to create a mirror image of the true defect or subunit. 6. Replace the missing tissue exactly to avoid overfilling or underfilling of the defect. 7. Choose ideal donor materials. Covering skin must be thin and conform to the underlying subcutaneous architecture while matching the face in color and texture. Cartilage and bone grafts must be thin but supportive. A nasal framework must extend from the nasal bones superiorly to the alar margin inferiorly and from the tip anteriorly to the maxilla posteriorly. If missing, the support framework must be replaced. Such a reconstruction supports the repair against gravity, shapes the overlying cover and underlying lining, and braces the repair against later scar contraction. Each support graft is carved to create a subsurface framework, which will be reflected through thin, supple covering skin. Lining materials must be vascular enough to support the positioning of early cartilage grafts and supple enough to conform to the shape of the overlying support grafts yet thin enough that they neither stuff the airway nor bulge outward, distorting the external shape. 8. Ensure a stable platform. A composite facial wound that involves nose and adjacent cheek and lip may require a preliminary step. The lip and cheek are repaired before the nose. A shifting lip/cheek platform that has pulled a reconstructed nose inferiorly and laterally under the influence of edema, gravity, and tension will ruin an otherwise beautiful result. Therefore, composite defects are usually reconstructed in stages.


Chapter 38: Nasal Reconstruction

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Correct Submuscular plane Alar cartilage

90-100˚

Pivot point Incorrect Subcutaneous plane Muscle Submuscular undermining Trim

A

Excise

B

FIGURE 38.2. Bilobed flap. A: The skin of the superior two thirds of the nose is mobile and in slight excess, whereas the skin of the tip and ala is adherent and tight. The excess in the superior nose is transferred in one stage to the tip with a bilobed flap. The defect created by the first flap is closed with a second lobe, which can be primarily sutured without distortion. B: The flap is elevated in the areolar plane above the perichondrium and includes the fat and nasalis muscles with the skin. C: Temporary quilting sutures are useful to close dead space.

C

SURGICAL TECHNIQUES Cover: Small, Superficial Defects Small, superficial defects that lie on planar or concave surfaces and do not border adjacent mobile landmarks that might be distorted by wound contraction can be allowed to heal by secondary intention. Defects less than 0.5 cm can be closed primarily within the more mobile skin of the dorsum or sidewall. Full-thickness skin grafts from the forehead, postauricular, or supraclavicular areas are useful within the thin skin zones of the upper two thirds of the nose. Although unpredictable in color and texture, the smooth and atrophic surface of a skin graft tends to blend within these smooth, thin skin zones. Skin grafts are immobilized with a light bolus dressing for 48 hours and must be placed on a well-vascularized bed. The principle of subunit excision is not used when a defect is resurfaced with a skin graft. Composite chondrocutaneous grafts from the helix, rim, or ear lobe can be used to repair small defects (less than 1.5 cm) along the alar rim and columella. Composite grafts consist of variable amounts of cartilage positioned in a sandwich of an outer and inner layer of skin. Any portion of the graft greater than 5 mm distant from the vascular recipient bed may not survive. So the larger the “skin-only” extension of a composite graft overlapping adjacent vascularized soft tissue, the more likely it is that the composite graft will be successful. Initially, they appear white, but over the next 24 hours, they become blue and congested as vascular flow increases. Over the next 3 to 7 days they become pink as the blood supply is established. Postoperative cooling for the first 36 hours may decrease the

metabolic rate of the skin graft until vascularization occurs and improve “take.” Except as a temporary wound dressing, split-thickness skin grafts are rarely employed. Split-thickness skin grafts provide no bulk, contract significantly, and usually hyperpigment. Single-lobe transposition flaps (banner) provide an excellent color match. For defects less than 1.5 cm in the lax mobile skin of the upper one third, they are an alternative to skin grafts. Their 90-degree arc of rotation makes them unreliable within the thick, stiff skin of the tip or ala due to dog-ear and vascularity concerns (4). The geometric bilobe flap is useful for defects up to 1.5 cm in the thick skin zones of the tip and ala (Fig. 38.2) (5). Rules for its design are as follows: 1. Allow no more than 50 degrees of rotation for each lobe. 2. Excise the triangle of dog-ear between the defect and flap pivot point. 3. Undermine widely above the perichondrium on both sides of the incision. 4. Make the diameter of the first lobe equal to the defect. The second lobe may be reduced in width to ease primary closure of the secondary defect. Dorsal and tip defects can also be resurfaced with a rotationadvancement flap of the residual dorsal skin (6). The dorsal nasal flap (Fig. 38.3) provides good coverage of defects up to 1.5 to 2 cm in size that lie at least .5 cm above the alar rims and no lower than the tip defining points. It has been used with and without a glabella extension. A superiorly based, single-stage, nasolabial flap can be designed as an extension of a sliding cheek advancement flap (Fig. 38.4). It is useful to resurface defects of the sidewall and ala. A Burow’s triangle is excised at the superior pivot point toward

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arc of rotation are limited, and it is not useful to recover the tip, dorsum, or a heminasal defect. When greater than 50% of the ala subunit is missing, residual normal skin is discarded. An exact foil template based on the contralateral normal ala is positioned along the nasolabial crease. The flap is elevated distally with a few millimeters of subcutaneous fat, maintaining a proximal deep superior subcutaneous base, perfused by perforators from the facial and angular arteries. A primary cartilage graft is positioned on residual or repaired alar lining, and the flap is transposed medially to resurface missing alar skin. The donor defect within the nasolabial fold is closed primarily. A few weeks later, the pedicle is divided, the inset is partially re-elevated and excess soft tissue sculpted, and the flap inset is completed. The two-stage nasolabial flap can achieve aesthetic alar subunit reconstruction.

The Forehead Flap

FIGURE 38.3. Dorsal nasal flap. Residual skin and soft tissue of the superior nose is transferred to the dorsum and tip. A Burow’s triangle excision in the glabella or nasal root may be needed on closure.

the inner canthus. Periosteal sutures recreate the nasofacial sulcus and minimize tension on the transposed flap. Rather than just redistributing residual nasal skin, this flap adds additional skin from the cheek and avoids the risk of alar rim or tip distortion associated with many of the other local flaps.

Cover: Large, Deep Defects Two-Stage Nasolabial Flap A moderate amount of excess skin is available within the nasolabial fold for reconstruction of the ala (7). Although occasionally used as a simple advancement flap to resurface sidewall defects, nasolabial tissue is most commonly transferred in two stages to resurface the ala as a subunit (Fig. 38.5). Its size and

Undermine cheek Incision should not go higher than alar remnant

A

The forehead is acknowledged as the ideal donor for nasal reconstruction due to its superb color and texture match, vascularity, and ability to resurface all or part of the nose. Supplied by a vast arcade of vessels from the supraorbital, supratrochlear, superficial temporal, postauricular, and occipital arteries, the forehead skin has been transposed on numerous pedicles (Fig. 38.6). Most of these designs have only occasional application. Most commonly, a vertical paramedian flap based on a single supratrochlear artery is designed extending from the brow to the hairline. The pivot point can be lowered by incising across the medial brow towards the medial canthus. The flap can be lengthened by including hair-bearing scalp. Hair follicles are later removed by depilation if necessary. Traditionally the forehead flap is transferred in two stages (8). The forehead is thicker than nasal skin. Initially, the distal flap is thinned by excising frontalis and subcutaneous fat before transposition to the nose. Two weeks later, the pedicle is divided and the proximal aspect debulked while completing the inset. In smokers or in patients with major defects, the flap is best transposed in three stages. Initially, the flap is transposed without thinning (9). Three weeks after the first operation, the flap is elevated off its bed at a superficial subcutaneous level. The underlying excess bulk of frontalis and subcutaneous fat is excised from the recipient bed. The thin forehead skin is then returned to cover the sculpted recipient site. The pedicle is divided 3 weeks later (6 weeks after the initial transfer). The three-stage method ensures maximal vascularity, precise thinning and soft tissue sculpturing,

Deep sutures to contour nasofacial sulcus

B

FIGURE 38.4. The one-stage nasolabial flap. A: Defects of the sidewell and ala can be resurfaced by advancement of a cheek flap with a skin extension from cheek excess adjacent to the nasolabial fold. Extra skin may be excised inferior to the defect if does not extend to the rim to hide the scar along the rim. Prime support is placed to brace and suppor the repair. B: Deep buried sutures preserve the nasofacial contour.



Cartilage C Defect

NL fold

A

Flap design

B

D

E

F

FIGURE 38.5. The two-stage nasolabial (NL) flap. A: The ala is best resurfaced with a two-stage flap as a complete alar subunit. Residual normal adjacent skin is discarded with the subunit if the defect is greater than 50% of the subunit. Lining is supported with a primary ear or septal or rib cartilage graft. B: Based on an exact pattern of the opposite ala, a template is positioned precisely along the nasolabial fold. Distally the flap is tapered to permit excision of the dog-ear on closure. Proximally, the skin pedicle should be tapered to keep the final scar of closure off the nose while maintaining a wider vascular subcutaneous base during flap elevation. The distal flap is thinned, maintaining 2 to 3 mm of subcutaneous fat. C, D: At the first stage the flap is transposed to resurface the entire. The cheek donor site is closed by advancement. E, F: Three weeks later the pedicle is transected. The proximal inset is re-elevated, sculpting excess subcutaneous fat and scar into an alar shape, and the skin is trimmed to precisely resurface the lateral alar defect. Excess soft tissue is excised in the medial cheek and the donor closure completed.

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Corrugator frontal crease Supraorbital a. Subcutaneous

Supratrochlear a. Infratrochlear a.

Subfrontalis Subperiosteal

Axial dermal vessels preserved

Angular a. Dorsal nasal a. A

B FIGURE 38.6. Forehead flap. A: Blood supply is abundant in central forehead. B: Paramedian flap design. In the traditional two-stage technique, the frontalis is left on the forehead and skin only is transferred to the defect, as shown here. In the three-stage technique, the full thickness of the forehead is often transferred and thinned at an intermediate stage. A, artery.

and, most important, the useful application of skin grafts or a folded distal extension of the forehead flap for a nasal lining. The forehead donor defect, although traditionally skin grafted, is best left to heal by secondary intention. Preliminary forehead skin expansion has been recommended to allow primary closure of the forehead defect. However, skin expansion delays the repair, may be associated with secondary late contraction, and has little advantage. It may be useful in secondary nasal reconstruction or in patients with very limited vertical forehead height, less than 3 to 4 cm.

nasal repair, the shape of soft tissue becomes distorted permanently by scar. Ideally, the support framework should be placed prior to flap division. Supportive grafts are designed to replace the missing nasal bones, upper lateral cartilage, and tip cartilages. Alar reconstructions include cartilage grafts to prevent rim collapse. In extensive midline defects the septum may be absent. A strong central midline support must be re-established to

Distant Transfers Multiple flaps can be taken from the forehead donor site without significant deformity. However, if the forehead is unavailable and the nasal defect too large for repair by a skin graft or local flap, replacement tissue can be brought from distant sites. Arm flaps, cervical flaps, abdominal tube pedicles, and deltopectoral flaps are largely of historical interest. Free flaps, principally the radial forehead flap, have been employed. Unfortunately, distant tissues provide poor color and texture match to adjacent facial skin. The future of free flap nasal reconstruction lies in their use to restore missing lining in the massive, irradiated or cocaine nose, not in its use for nasal cover.

Sidewall brace

Dorsal buttress

Septal cartilage Ethmoid bone

Columellar strut Alar margin batten

Support If missing, a supporting framework must be replaced to reestablish support, shape, and resist scar contraction. Each graft is fashioned to mold the overlying skin (and the underlying lining) into the expected nasal shape: a dorsal buttress, a sidewall brace, tip grafts for projection and definition, and an alar batten (even though the ala normally contains no cartilage) (Fig. 38.7). Septal and ear cartilage and rib costicartilage grafts are most commonly used. Traditionally, support grafts have been placed only to support the bridge (cantilever dorsal graft) or alar rim (composite prefabricated rim grafts). Months after the

Auricular cartilage Septal and auricular cartilage FIGURE 38.7. Primary or delayed grafts of cartilage or bone must be placed before the completion of reconstruction to shape and support the soft tissue against gravity and scar contracture. Support must be present or must be restored to all nasal subunits. (Redrawn after Burget G, Menick F. Nasal support and lining: the marriage of beauty and blood supply. Plast Reconstr Surg. 1989;84:189, with permission.)



prevent soft tissue collapse of the tip and dorsum. Several methods are useful, often in combination. When the septal composite lining flap is pivoted anteriorly, both lining and central support are positioned simultaneously. This creates a basic platform on which to rest other grafts. A cantilever dorsal graft of rib or cranial bone can be fixed with wire or a screw to the nasal bones (which are first lowered to avoid excessive radix augmentation). This graft extends from the nasal bones to the tip. A rib cartilage or bone graft in the shape of an “L” can be positioned from the nasal bones to the maxilla, but they tend to create an excessively wide columella.

Lining Ideally, lining should be thin, supple, and vascular.

Local Hingeover Lining Flaps If a full-thickness defect is allowed to heal, external skin and scar bordering the defect can be turned over to supply lining, based on the scar along the border of the defect. Such lining flaps are thick and stiff and risk necrosis if greater than 1.5 cm in length. The airway, at the point of the hingeover, is often constricted. Although useful for limited rim defects or in salvage cases, they are not a first choice (10).

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branches of the superior labial artery, which perfuse the right and left septal mucoperichondrial lining leaves (11,12). In smaller unilateral defects, residual vestibular skin lying above the defect can be incised as a bipedicle flap 6 mm wide, based laterally at the alar base and medially on the septum. This flap is advanced inferiorly to line the alar rim. The defect that remains above is filled by another method (a contralateral septal lining flap or a skin graft). In larger heminasal defects, a contralateral septal flap (Fig. 38.8) can be hinged and transposed laterally to line the lower vestibule and alar margin. A second mucoperichondrial flap, based dorsally on the anterior ethmoid vessel, is hinged laterally to line the upper vault. (This dorsal flap can be used alone to reconstruct an isolated defect of the sidewall or be combined with the bipedicle vestibular flap). In some cases an anteriorly based septal mucoperichondrial flap composed of the entire septum can be advanced out of the pyriform aperture based on branches of the right and left superior labial arteries located near the nasal spine (Fig. 38.9). This flap simultaneously supplies dorsal support and bilateral leaves of septal perichondrium, which can be reflected laterally to line the dorsum and vestibules. Intranasal lining flaps are thin, vascular, and supple and allow the primary placement of cartilage grafts. They are associated, however, with moderate to significant intranasal manipulation and the associated morbidity of bleeding and crusting.

Prelaminated Skin Graft and Cartilage for Lining of the Forehead Flap During a preliminary operation, several weeks before transfer, composite grafts from the ear or septum or separate pieces of skin and cartilage can be placed under the distal end of a forehead flap. These preinstalled lining grafts can create a satisfactory alar margin but may not create an ideal nasal shape after transfer. The technique is most useful for smaller defects in elderly patients in which less complex procedures are indicated due to health concerns.

Intranasal Lining Flaps Residual nasal lining, although not apparent at first glance, remains within the residual nose and pyriform aperture. The nose is perfused by branches of the anterior ethmoid artery along the dorsum and the angular artery at the alar base and from septal

Skin Grafts for Lining Simultaneous placement of the skin graft on the undersurface of a forehead flap at the time of its transfer has traditionally been unsuccessful. Cartilage grafts are precluded. As the skin graft shrinks, late collapse and distortion follows. However, a full-thickness skin graft of postauricular skin will survive on the deep surface of a forehead flap. Three weeks after transfer, the skin graft becomes integrated into the adjacent normal lining and is no longer dependent on a covering flap. Excess soft tissue can be excised during an intermediate operation, and cartilage grafts are placed. In this manner, a complete cartilage support structure is positioned prior to flap division in a delayed primary fashion, thus preventing significant shrinkage. The simplicity and the avoidance of intranasal manipulation

Septal cartilage removed for later support framework

A

B

C

FIGURE 38.8. The contralateral mucoperichondrial flap. Defects of the midvault can be lined with a dorsally based contralateral mucoperichondrial flap perfused by the anterior ethmoid arteries. A: Sidewall defect. B, C: The flap is passed through a dorsal slit in the ipsilateral septum and will provide lining for the midvault. Septal cartilage is harvested for primary cartilage grafts, which will support and shape the reconstructed midvault. The repaired lining and cartilage flaps are covered with a vascularized flap of cheek or forehead skin.

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placement of primary support. The resultant alar rim remains thick, shapeless, and unsupported. However, realization that such folded skin becomes revascularized by adjacent lining and is no longer dependent on the covering flap for blood supply permits the elevation of the covering flap, leaving the folded lining in place. Three weeks after transfer, the skin covering aspect of the folded flap is incised along the planned alar rim during an intermediate operation and elevated with 2 to 3 mm of subcutaneous fat. Underlying excess soft tissue is excised from the reconstructed lining, creating thin, supple, and wellvascularized lining. Delayed primary support grafts are placed to support the ala and sidewall as needed. In this way, a complete support framework is positioned prior to pedicle division without intranasal manipulation. Unilateral defects of up to 2.5 cm are readily repaired. This folded technique may become the workhorse for modern nasal repair of full-thickness defects. The technique is simple and can produce excellent results.

References

FIGURE 38.9. Septal composite flap. In subtotal nasal loss, the residual septum often remains and can be transposed out of the pyriform aperture based on the right and left septal branches of the superior labial arteries. Fixed superiorly to the residual dorsum, each leaf of the septal mucoperichondrium can be swung laterally to provide lining to the midvault and anterior vestibule.

make this an excellent option for defects less than 1.5 cm along the alar rim.

Folded Forehead Flap for Lining Although the distal end of a forehead flap can be folded to supply lining, traditionally the technique has precluded the

1. Burget GC, Menick FJ. Subunit principle in nasal reconstruction. Plastic Reconstr Surg. 1985;76:239. 2. Menick F. Artistry in facial surgery: aesthetic perceptions and the subunit principle. In: Furnas D, ed. Clinics in Plastic Surgery, Vol. 14. Philadelphia: WB Saunders, 1987;723. 3. Millard DR. Principlization of Plastic Surgery. Boston: Little Brown, 1986. 4. Elliot RA Jr. Rotation flaps of the nose. Plast Reconstr Surg. 1969;44: 1a47. 5. McGregor JC, Soutar DS. A critical assessment of the bilobed flap. Br J Plast Surg. 1981;34:197. 6. Marchac D, Toth B. The axial frontonasal flap revisited. Plast Reconstr Surg. 1985;76:686. 7. Herbert DC. A subcutaneous pedicle cheek flap for reconstruction of ala defects. Br J Plast Surg. 1978;31:79. 8. Menick FJ. The aesthetic use of the forehead for nasal reconstruction— The paramedian forehead flaps. In: Tobin G, ed. Clinics in Plastic Surgery. Philadelphia, WB Saunders, 1990;607. 9. Menick FJ. Ten-year experience in nasal reconstruction with the three-stage forehead flap. Plast Reconstr Surg. 2002;109:1839. 10. Millard DR. Aesthetic reconstructive rhinoplasty. Clin Plast Surg. 1981; 8:169. 11. Burget GC, Menick FJ. Nasal reconstruction: seeking a fourth dimension: Plast Reconstr Surg. 1986;78:145. 12. Burget GC, Menick FJ. Nasal support and lining: the marriage of beauty and blood supply. Plast Reconstr Surg. 1989;84:189.


CHAPTER 39 ■ RECONSTRUCTION OF THE EYELIDS, CORRECTION OF PTOSIS, AND CANTHOPLASTY MARTIN I. NEWMAN AND HENRY M. SPINELLI

EYELID ANATOMY AND PHYSIOLOGY The eyelids are comprised of an upper and lower lid, a fold of complex, mobile tissue anterior to the globe. Closure of the eyelids affords protection to the globe. Opening of the eyelids is facilitated primarily by elevation of the upper lid and creates the resultant palpebral fissure. The lower lid remains essentially stable, but retracts appreciably on downward gaze. When the upper lid is open, it folds upon itself, creating a furrow or superior sulcus, superior to the globe and inferior to the supraorbital rim. Disruption of the supporting structures of the upper lid, such as levator dehiscence (see Correction of Eyelid Ptosis Section), may elevate or obliterate this fold. The upper and lower eyelids meet at angles known, respectively, as the medial and lateral canthi or palpebral commissures. In the normal, youthful, or aesthetically pleasing eye, the lateral canthus is inclined 10 to 15 degrees cephalad to the medial canthal tendon. The punctum lacrimale are appreciated at the apex of the lacrimal papilla on the margins of both lids with the lower lying more lateral than the upper. Arranged in double or triple rows at the margins of eyelids are the eyelashes or cilia. Juxtaposed to the cilia are the openings of the numerous vertically oriented sudoriferous ciliary glands of Moll and sebaceous glands of Zeis (1–4). The eyelid may be thought of as a three-layered structure: skin on the outside, a mucosal lining on the inside, and structural elements bridging the space between (Fig. 39.1). The skin of the eyelid is extremely thin. In places, the upper lid can measure 1 mm thick, less than 10 cell layers across, and is considered by many to be the thinnest in the body (1,4). The mucosal lining is the palpebral conjunctiva. The conjunctiva forms an uninterrupted layer as it arises from the skin at the free edge of one lid and extends over the globe to the free edge of the other. It forms the posterior wall of the lids, folding back upon itself to then form the anterior covering of the globe, the bulbar conjunctiva. The apexes of the folds are known as the superior and inferior fornices. The function of the conjunctiva is to provide a smooth surface facilitating near friction-free movement of the lids over the globe (1,3,4). Many surgeons consider the elements of the lid between the skin and conjunctiva to form a bilamellar structure. The anterior layer is contiguous with the soft tissues of the face and scalp, and the posterior layer is contiguous with the structures of the orbit. Separating the anterior and posterior lamella is the tarsofascial layer. This layer arises from the orbital rim and begins proximally as the orbital septum, formed by the confluence of the periosteum of the orbit and the periosteum of the facial bones. As it proceeds distally, the tarsofascial layer continues

as a dividing plane between the anterior and posterior lamella. Distally, the orbital septum fuses with the lid-retracting membrane. In the upper lid, this is the levator palpebra aponeurosis; in the lower lid, it is the capsulopalpebral fascia. The tarsofascial layer serves as a complete anatomic boundary between the anterior lamella (skin and muscle) and the deeper structures (1–4). The anterior lamella is composed of skin, subcutaneous tissue, and orbicularis oculi muscle. The subcutaneous tissue is sparse and areolar. The orbicularis oculi is composed of three concentric oval portions: the innermost pretarsal portion, the middle preseptal portion, and the outermost orbital portion. Together, the pretarsal and preseptal portions form the palpebral portion, which contribute to the anterior lamella of the eyelid (1–4). In the upper lid, the levator palpebra aponeurosis continues distally to fuse with the orbital septum anteriorly and the tarsal plate posteriorly. Deep to the levator palpebra aponeurosis is the Mueller muscle proximally and the tarsal plate distally. On the lower lid, the structures posterior to the tarsofascial layer include the inferior tarsal muscle proximally and the tarsal plate distally (1–4). The tarsal plates are the dense cartilaginouslike structures that provide vertical support and rigidity to the eyelids. Composed of dense connective tissue, they measure approximately 2.0 mm in depth and 2.5 cm in length. The superior tarsus is larger, semilunar in shape, and 8 to 10 mm in the vertical dimension at the center. The proximal edge of the plate serves as the insertion for the Mueller muscle, which is innervated by the sympathetic nervous system. Sympathetic stimulation of this muscle provides an additional 1 to 2 mm of upper lid excursion. The inferior tarsus is smaller, elliptical in shape, and has a vertical diameter of 4 to 6 mm. The proximal edge of the inferior plate serves as the insertion for a membrane formed by the confluence of the capsulopalpebral fascia and inferior orbital septum. Here, the capsulopalpebral fascia should be thought of as a structure analogous to the levator palpebral aponeurosis and serves as the lower eyelid retractor. With an origin on both the inferior oblique and rectus muscles, the capsulopalpebral fascia serves to coordinate an unobstructed line of sight on downward gaze. Along the medial and lateral margins of the palpebral fissure, the tarsal plates become confluent with their respective palpebral ligaments or canthal tendons. The lateral canthal tendon is formed by the confluence of the upper and lower crura, which arise off their respective tarsal plates and create a complex structure known as the lateral retinaculum, inserting onto the Whitnall tubercle. This key anatomic bony prominence lies 2 mm within the lateral orbit, below the lacrimal fossa. Also contributing to the lateral retinaculum is the lateral horn of the

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Orbicularis septum

Fat

Orbicularis oculi muscle

Mueller muscle

Levator aponeurosis

Tarsal plate

Subaponeurotic space

Conjunctiva

FIGURE 39.1. Structural elements of the upper lid in cross section.

levator aponeurosis, the Whitnall ligament, which is formed by the fascial condensation of the levator aponeurosis. It helps to direct the forces of the levator palpebral muscle vertically to facilitate lid retraction and serves as a sling providing support to the globe. The Lockwood ligament is the lower-lid analog of the Whitnall ligament. Medially, the tarsal plates give rise to the upper and lower crura of the medial canthal tendon, which, in turn, gives rise to the medial canthal complex, a tripartite composite structure with posterior, anterior, and superior limbs that insert onto the medial orbital margin and nasal bones. The most distal portion of the plates contribute to the free edge of the lids. There, just posterior to the cilia, they are pierced by the ducts of the Meibomian glands. The Meibomian glands, also known as the tarsal glands or glandulae tarsales, are sebaceous. They secrete an oillike substance onto the conjunctiva, which facilitates gliding of the lid over the globe. The glands, which number approximately 10 to 20 on the lower lid and 20 to 40 on the upper lid, may be the site of pathologic inflammatory processes, which may be acute (hordeolum or stye), chronic (noncaseating granulomas, chalazia), or postsurgical (meibomianitis or blepharitis) (1–4). The vascular system of the eyelid is rich and consists of overlapping contributions from numerous adjacent vessels. The lacrimal system functions to bathe with and drain the globe of tears (Fig. 39.2). It consists of the lacrimal gland and microscopic accessory glands, which secrete the tears, and the lacrimal ducts or canaliculi, the lacrimal sac, and the nasolacrimal duct, which provides nasal drainage. Tears form a trilaminar fluid layer composed of a deep mucoprotein layer, a middle aqueous layer, and a superficial lipid layer. Together, these layers act in concert to preserve a moist antimicrobial environment. This layer also serves to bend incoming light before it strikes the cornea and has up to 0.5 diopter of refractile power (1–5). The lacrimal gland proper is composed of two lobes: the main orbital lobe and the smaller palpebral lobe. They are situated in the lacrimal fossa of the superolateral orbit and upper lateral eyelid, respectively. They are separated from each other

by the lateral horn of the levator palpebral superioris and the Whitnall ligament. The ducts of the palpebral lobe empty into the upper lateral half of the superior fornix. The ducts of the orbital lobe pass through the palpebral lobe before exiting. In response to stimuli the lacrimal gland elaborates fluid analogous to that of the serous salivary glands. The process of blinking distributes the trilaminar fluid layer across the globe medially where it reaches the puncta and drainage system (1–5). Tears reaching the medial aspect of the palpebral fissure are drained, or rather pumped, into the nasal cavity by an intricate system of soft tissue consisting of the puncta, canaliculi, lacrimal ducts, muscle fibers of the orbicularis oculi, the lacrimal sac, and, eventually, the nasolacrimal duct. The flow of tear film from the palpebral fissure begins as the fluid passes through the lacrimal ducts, also known as the ductus lacrimalis, lacrimal canals, or canaliculi via the puncta lacrimali located at the apex of the papillae lacrimales, as described above. Both the upper and lower lids contain canaliculi at their medial aspect that dilate along their course into ampullae that are enveloped by deep fibers of the orbicularis. The canaliculi come together to a common canaliculus and then empty into the lacrimal sac. The sac sits within the bony lacrimal fossa that lies posterior to the insertion of the medial canthal tendon. The lacrimal sac represents the dilated origin of the nasolacrimal duct. Like the lacrimal ducts, the lacrimal sac is enveloped by fibers of the orbicularis muscle, and contraction of the orbicularis, as in blinking, drives the pumping mechanism that both draws the fluid tear film into the lacrimal ducts through the puncta and propels it forward through the canaliculi and lacrimal sac into the nasolacrimal duct where it drains. The nasolacrimal duct is approximately 18 mm in length and receives the efflux from the lacrimal canaliculi and lacrimal sac. It directs flow inferiorly into the nasal cavity through the inferior meatus of the nose. It runs within a bony canal formed by the maxilla, the lacrimal bone, and the inferior nasal concha. The terminal end of the nasolacrimal duct expands into an imperfect mucosal

FIGURE 39.2. The lacrimal system is composed of the lacrimal gland, microscopic accessory glands, lacrimal ducts or canaliculi, the lacrimal sac, and the nasolacrimal duct.


Chapter 39: Reconstructionof the Eyelids, Correction of Ptosis, and Canthoplasty

valve known as the plica lacrimalis, which is formed by a fold of mucous membrane (1–4).

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EYELID RECONSTRUCTION Eyelid defects may result from congenital anomalies, neoplastic processes, ablative surgical procedures, or trauma. Regardless of the etiology, however, the skin, muscle, supporting structures, and conjunctiva must be assessed and, if absent or deficient, reconstructed. The quality and quantity of local, regional, and distal tissues is evaluated, as is the patient’s overall health, comorbid conditions, and personal goals. For congenital defects, it is critical to rule out or identify and treat associated anomalies. If the defect in question follows an ablative surgical procedure, it is necessary to be familiar with the histologic diagnosis and surgical pathology of the underlying neoplastic process. Defects created by the ablation of, for example, a sarcoma may not be amenable to immediate reconstruction, but may better be reconstructed after permanent pathology confirms adequate margins. Any plan for adjuvant treatment, such as radiation therapy, should be considered when planning reconstruction. Finally, lid defects that result from traumatic causes rarely occur in isolation. In these instances, it is important to ensure that all associated injuries have been properly identified and accounted for in the overall treatment plan. Once the above concerns are addressed, evaluation and treatment of eyelid defects are best approached by dividing the region into zones, each with its own anatomic, functional, and aesthetic considerations (Fig. 39.3) (6). Evaluation of defects with respect to location or zone, and the extent to which each zone is affected (partial or full thickness) may also be predictive of possible postreconstructive complications. With these concepts in mind, and all others factors being equal, defects at risk for postoperative complications should be reconstructed with the most durable techniques available (6). The following principles serve as guidelines (2,4,7,8). ■ ■

All reconstructions should begin with a through evaluation of the defect and function of the lid. Components that have been compromised as well as those that remain viable including elements of skin, muscle, tarsus, and conjunctiva should be properly identified and documented.

I

V

IV III

II V FIGURE 39.3. Periocular zones, each with individual anatomic, functional, and aesthetic considerations. (Adapted from Spinelli HM, Jelks GW. Periocular reconstruction: a systematic approach. Plast Reconstr Surg. 1993;91(6):1017–1024, with permission.)

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When feasible, a complete and thorough preoperative ophthalmologic examination, including visual acuity and field testing, as well as a Schirmer test, should be performed and documented. In acute situations, when the luxury of a preoperative evaluation is not possible, ophthalmologic consultation should be considered. The eyelids are the focus of much aesthetic attention. Consideration of this detail is important when composing the reconstructive plan. Transverse incisions will help to camouflage scars, and symmetry with contralateral structures should be preserved whenever possible. Vertical incisions should be avoided so as to obviate contracture and distortion of eyelid function. Debridement of nonviable tissue should proceed, and when doing so, reconstructive goals should be kept in mind. When approximating lid margins, alignment of all layers must be achieved. Failure to do so may result in significant functional and/or aesthetic problems. Suture material and knots should be placed in an effort to avoid direct contact with the surface of the cornea and globe. Even the finest suture materials can cause extensive irritation and corneal abrasions. Ultimately, as in all reconstructive scenarios, the principles of the reconstructive ladder should be appreciated and applied in eyelid reconstruction.

Upper Eyelid Reconstruction: Zone I Although the structural components of the upper and lower eyelids are analogous, the two differ anatomically and functionally in a few important ways. The upper lid is taller in height, more lax, more mobile, and is the major facilitator of closure. Zone I defects are considered partial-thickness defects when they involve only skin or skin and muscle (external lamina). Full-thickness defects include loss of the tarsus and conjunctiva as well. It is helpful to divide partial-thickness defects of the upper lid into two categories: those involving less than 50% of the lid length and those involving more than 50% of the lid length. Full-thickness defects of the upper lid are best considered in three categories, defects less than 25% of lid length, defects measuring 25% to 75% of lid length, and defects measuring greater than 75% of upper-lid length. Partial-thickness defects of the upper lid that measure less than 50% of lid length are, in the author’s opinion, best repaired by primary closure with local tissue advancement (Fig. 39.4). The laxity of the upper lid skin facilitates primary closure provided appropriate myocutaneous flaps are raised and advanced appropriately. When possible, scars should be oriented in a transverse direction. In general, vertical scars may result in contracture and related functional and aesthetic problems (6). Partial-thickness defects of the upper lid that involve more than 50% of the lid length provide a greater challenge (Fig. 39.4). In all likelihood, simple primary closure with local tissue advancement would place too much tension on the underlying tarsus, causing the wound to dehisce, inappropriately scar, or, in extreme cases, buckle the tarsus and disrupt function. For this reason, a tension-free closure is advocated. In our opinion, this is best achieved with a full-thickness skin graft from the contralateral upper lid. A full-thickness graft harvested from the contralateral upper lid provides an excellent match for color and texture and a superior aesthetic result. A composite graft consisting of orbicularis muscle and skin can also be used, however, the added tissue may compromise graft viability. One should note however, that the upper lid is

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PT

FT FT 50%

Sliding tarso-conjunctival flap, levator recession or composite graft

FTSG from opposite upper lid

FT >75% Lower-lid switch flap for very large defects

Zone I

All: Routinely probe and intubate the lacrimal system

All: Lateral canthal support procedure

Zone III

Zone IV

Medially based myocutaneous flap from upper lid

Cheek advancement flap OR

Zone II

Other local flaps

Skin graft

PT PT 50% FTSG from opposite upper lid

FTSG

FT FT 50% Sliding tarso-conjunctival flap with skin graft

FT >75% OR myocutaneous transposition flap from same upper lid

Composite graft with cheek advancement

FIGURE 39.4. Reconstructive algorithm based on periocular zones. FT, full-thickness defect; FTSG, fullthickness skin graft; PT, partial-thickness defect. (Adapted from Spinelli HM, Jelks GW. Periocular reconstruction: a systematic approach. Plast Reconstr Surg. 1993;91(6):1017–1024, with permission.)



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A

A

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D

FIGURE 39.5. Modified Cutler-Beard advancement flap.

critical to eyelid function and should a donor-site complication arise, the consequences could be devastating. For this reason, some authors recommend avoiding the upper lid as a donor site unless other options are unavailable, suggesting instead using the postauricular region for the full-thickness skin donor site. Proponents for the use of postauricular skin cite its simplicity of harvest, its large available size providing enough skin to cover a canthal-to-canthal defect, and a cosmetically hidden donor site scar. We prefer contralateral upper lid skin donor sites whenever functional compromise can be avoided (2,8,9). Full-thickness defects of the upper lid should be divided into three categories, those involving less than 25% of the lid length, those involving 25% to 75% of the lid length, and those measuring greater than 75% of lid length. Full-thickness defects of the upper lid measuring less than 25% of the upper lid length may be reconstructed primarily (Fig. 39.4). The smallest of these defects may be closed applying the principles set forth by Ross and Pham, debriding the wound edges to approximate a pentagon with its apex pointing away from the lid margin. In this manner, dog-ears and notching can be avoided or minimized. Larger defects in this category may also be closed primarily, but might require local myocutaneous flap advancement, canthotomy, and/or cantholysis (2,4,6,9,10). Full-thickness defects of the upper lid measuring between 25% and 75% are usually not amenable to primary closure (Fig. 39.4). These, we believe, are best reconstructed by either composite grafts or by a sliding tarsoconjunctival flap. Composite grafts, whether they are used to reconstruct upper or lower lid defects, must include a posterior mucosal layer, a structural support layer, and a well-vascularized covering. There are a host of composite grafts described for eyelid reconstruction (2,4,6,8). One of the best choices for a composite graft

reconstruction is to combine a nasal septal cartilage–mucosal graft for the posterior conjunctival-tarsal layer and a transposition myocutaneous flap from an adjacent area for the anterior lamella. Benefits of using the nasal septal mucosal–cartilage for the posterior layer include the pre-existing relationship between the mucosal and cartilaginous layers, and the thinness and pliability of septal cartilage compared to other donor sites. We advocate the use of a pedicled skin–muscle flap for coverage over a composite graft based on its superior blood supply. A full-thickness skin graft may be used as external coverage over a transposition flap of internal lamella structures, providing an excellent functional and cosmetic result. An equally effective option for reconstructing a 25% to 75% full-thickness defect of the upper lid is the Hughes sliding tarsoconjunctival flap from the lower lid. This is accomplished by elevating tarsus and conjunctiva off the remaining lid segment as a proximally based transposition flap and covering it either with a full-thickness skin graft or myocutaneous flap. In general, the skin graft appears and functions more naturally. Another option for repair of full-thickness defects of the upper lid measuring between 25% and 75% is the Cutler-Beard advancement flap. As originally described, reconstruction is carried out by first creating a full-thickness advancement flap from the lower lid, below the tarsal plate, leaving the margin of the lower lid intact (Fig. 39.5). The pedicled flap is then advanced superiorly into the upper lid defect and inset. Division of the pedicle is delayed for 6 to 8 weeks, allowing for maximum ingrowth of local vasculature. The obvious disadvantages to this technique are that (a) the eye must remain closed until division of the pedicle is carried out; (b) the reconstructed portion of the upper lid remains without a supporting structure (e.g., tarsal plate or cartilaginous graft analog); and (c) alteration of lower lid

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structure and function secondary to full-thickness and longterm scarring. Since its introduction in the 1950s, modifications to the Cutler-Beard advancement flap have been offered, but the need for the eye to remain closed during flap “take,” as well as irreversible alteration of lower-lid structure and function, remain major drawbacks to its use. Full-thickness defects of the upper lid that are greater than 75% of the lid length present a challenge in that donor options are limited (Fig. 39.4). Of the described techniques, our preferred method of reconstruction is a simultaneous lower-lid switch flap with a cheek rotation–advancement as necessary. The lower-lid switch flap was modified for the upper lid by Mustardé (8). This flap uses an intact lower lid to recreate the upper lid by raising the lower-lid tissue as a bilaminar flap based on the marginal artery and rotating it around the medial or lateral palpebral fissure. Closure of the upper-lid defect is achieved by first reducing the size of the defect, up to 25%, by simple advancement of the wound margins, and then by rotating the lower lid to complete the reconstruction. The cheek flap is advanced as length is needed (2,6,8). On occasion, upper lid defects may extend beyond zone I and involve adjacent periocular tissue. For example, to achieve adequate margins during the excision of a medial upper eyelid neoplasm, ablation of medial canthal tissue (zone III) may be necessary. Large traumatic defects, too, may result in disruption of the upper eyelid in conjunction with nearby adjacent tissue. When faced with these more extensive defects, importation of local tissue should be considered using full-thickness glabella skin or temporoparietal fascia as indicated. The glabella flap is based on the supratrochlear blood supply and is discussed below in relation to medial canthal (zone III) defects (6,7). As an interpolation flap, it can be tailored to meet the needs of a wide variety of defects, especially those involving multiple zones. An example of this is the split-finger graft that uses full-thickness glabellar skin to reconstruct a combined defect involving zones I, II, and III (Fig. 39.6). The temporoparietal fascia flap is useful for extensive upper-lid defects that include a lateral perior-

FIGURE 39.6. The split-finger graft is an interpolation flap that can be tailored to meet the needs of a wide variety of defects. (Redrawn after Jackson IT. Eyelid and canthal region reconstruction. In: LocalFlaps in Head & Neck Reconstruction. St. Louis: Quality Medical Publishing, 2002.)

bital component. In these scenarios, the fascia can be harvested through a hemi-coronal incision, tunneled anteriorly, and tailored to meet the needs of the defect. It can be covered with a split-thickness skin graft. A cartilaginous graft can be added to provide support when needed (6,7).

Lower Eyelid Reconstruction: Zone II As discussed above, the upper and lower lids are analogous in many ways, but each possesses some distinct and specialized anatomic structures and function. For example, the lower lid is shorter in height, less mobile, and contributes only minimally to closure. However, the lower lid is most important in its contribution to passive corneal coverage. Considerations for reconstruction of the lower lid should include lash preservation, appropriate lid position (i.e., avoidance of entropion or ectropion and/or lid retraction), lid tone, marginal notching and irregularities, and overall aesthetic outcome (6). Similar to defects of the upper lid, we consider defects of the zone II (lower lid) based on the thickness and size of the defect. Partial-thickness defects of the lower lid should be viewed as either those involving less than 50% of the lid length or those involving more than 50% of the lid length. In distinction, full-thickness defects of the lower lid should be further broken down into those less than 50% of lid length, defects measuring 50% to 75% of lid length, and, finally, defects measuring greater than 75% of lid length. Partial-thickness zone II defects measuring less than 50% of the lid length are best repaired with primary closure, adding local tissue advancement as necessary (Fig. 39.4). As with partialthickness zone I defects, reconstruction of skin or skin–muscle deficits must provide coverage to the underlying tarsus. Simple primary closure may be adequate when defects are small, but tension-free closures are usually best facilitated by advancement of local, adjacent tissue. Vertical incisions should be avoided if at all possible. This method of reconstruction provides the best color and texture match along with a superior functional and cosmetic result. Partial-thickness zone II defects that measure greater than 50% cannot be closed primarily without placing, as stated above, undue tension on the tarsus below (Fig. 39.4). For this category of defects, we recommend either a full-thickness skin graft from the contralateral upper lid or a myocutaneous transposition flap from the ipsilateral upper lid. A full-thickness skin graft from the contralateral lid can provide a fairly large amount of coverage as needed. Fullthickness grafts provide superior coverage, contract less than split-thickness grafts, and offer excellent cosmetic and functional results. If contralateral upper-lid skin is unavailable or undesirable, postauricular skin is an excellent second choice for full-thickness harvest (6,9,10). Another reconstructive option for repair of partial-thickness zone II defects measuring greater than 50% are local myocutaneous transposition flaps from the ipsilateral upper lid. The two most commonly used examples of these local myocutaneous transposition flaps in lower-lid reconstruction include the unipedicled Fricke flap and the bipedicled Tripier flap. The Fricke flap (Fig. 39.7) is a unipedicled myocutaneous transposition flap composed of the skin and preseptal portion of the orbicularis oculi muscle of the upper lid. The pedicle can be placed either medial or lateral to the palpebral fissure. If a myocutaneous transposition flap is raised on both the medial and lateral pedicle, a bipedicled myocutaneous transposition flap (Tripier) is generated (Fig. 39.8). When constructing either the unipedicled Fricke flap or the bipedicled Tripier flap, inset is performed at initial operation. The unilateral flap will adequately cover defects of the lower lid up to and beyond the midline. For defects requiring a greater length, a bipedicled flap



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the posterior lamella of the upper lid, including the tarsus and the conjunctiva, is advanced to fill the defect of the lower lid. The Mueller muscle can be included in the conjunctival pedicle as it adds increased vascular reliability. The anterior lamella of the lower lid is covered with a full-thickness skin graft or local advancement flap. Donor sites include the contralateral upper lid and postauricular skin. The flap is left on its pedicle for several weeks and later divided. The donor site of the upper lid is not affected as long as 3 to 4 mm of distal tarsus remains intact to ensure upper lid stability. One must recess the upper lid levator by undermining at the second stage division and insetting to avoid upper lid retraction from the advanced upper lid retractors (2,6). Zone II defects of full-thickness measuring greater than 75% of the lower lid length require a more aggressive approach. In these cases, restoration of the anterior layer can be completed with a cheek flap, and reconstruction of the posterior layer performed by using a composite graft of nasal septal cartilage and lining (2,6,8). This full-thickness cutaneous rotation– advancement flap can be harvested to include the superficial musculoaponeurotic system and provides an excellent color and texture match for zone II defects. Principles to keep in mind when raising a cheek flap include dermal anchorage to the inferior orbit to ensure tension-free closure, superolateral curvature of the incision line to prevent “shortening,” and incorporation of a Z-plasty when necessary (2,4,6,8,9,11). Cervicofacial flaps may be used in place of cheek rotation flaps and, when properly executed, provide excellent coverage of not only of zone II defects but also of defects that extend beyond zone V (12).

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FIGURE 39.7. The unipedicled myocutaneous Fricke transposition flap. (Redrawn after Jackson IT. Eyelid and canthal region reconstruction. In: Local Flaps in Head and Neck Reconstruction. St. Louis: Quality Medical Publishing, 2002.)

is usually necessary. Advantages of the Tripier flap include its ease of performance, lack of distal donor sites and facial scars, and maintenance of the visual field. Disadvantages of the Tripier flap include the extremely rare compromise of the upper lid donor site. In general, these myocutaneous transposition flaps are hardy but provide notable bulk that sometimes requires late minor revision procedures for conturing (7). Full-thickness defects of zone II should be viewed in three distinct categories based on lid length: less than 50%, 50% to 75%, and greater than 75% of lid length. We recommend one of two excellent reconstructive options for repair of fullthickness defects less than 50% of lid length: (a) primary closure with lateral canthotomy, cantholysis, and local tissue advancement (Fig. 39.4), or (b) Hughes tarsoconjunctival flap with skin graft or myocutaneous coverage. Unlike partialthickness zone II defects, full-thickness defects of up to several millimeters can repaired primarily and dog-ears and notching can be avoided by following the principles set forth by Ross and Pham, debriding the wound edges to approximate a pentagon with its apex pointing away from the lid margin. Some surgeons argue that defects as large as 25% to 33% of the lower lid can be closed in this manner; however, for defects larger than a few millimeters, we find that the addition of lateral canthotomy, cantholysis, and local tissue advancement provides a superior cosmetic and functional result. Of course, this depends on the patient’s age and amount of horizontal laxity present (2,4,6,8). A sliding tarsoconjunctival flap with a skin graft is a versatile technique that can be used to reconstruct zone II defects of less than 50% of lid length, as well as defects that fall into the 50% to 75% category. In this procedure, a superiorly based flap of

Medial Canthal Reconstruction: Zone III Zone III, the medial canthal region, is the most anatomically and physiologically complex of the periocular zones. The lacrimal papilla, puncta, canaliculi, plica semilunaris, caruncula lacrimalis, and tripartite insertion of the medial canthal tendon are all located within this square centimeter of tissue. Procedures in this zone are associated with a high incidence of complications involving the lacrimal canalicular system and/or medial canthal tendon (6). For this reason, routine lacrimal stenting by silicone tube intubation, as well as measures to insure medial canthal tendon support, are recommended when performing procedures in zone III. Defects of the anterior layers are reconstructed with a medially based, myocutaneous flap from the upper lid based on branches of the infratrochlear vessels. Acceptable alternatives include other local flaps such as the V-Y glabellar flap, and healing by secondary intention (2,6). Measures to ensure that the medial canthal tendon support remains intact may be simple or complex, depending on the nature of the defect. If the tendon is intact but minor laxity is appreciated, simple plication is recommended. In this procedure, the inferior arm is “tucked” under the canthus. As with all procedures in zone III, care must be taken not to compromise the lacrimal system (10). If the insertion of the tendon is not intact, canthopexy is recommended. In this case, the medial aspects of the upper and lower tarsal plates can be sutured to the nasal periosteum taking care to place the point of fixation below the anterior lacrimal crest. Alternatively, if the tendon is simply avulsed, it can be secured with a wire loop, which is passed and anchored in a transnasal fashion (6).

Lateral Canthal Reconstruction: Zone IV The critical structure in zone IV, underlying the lateral palpebral fissure, is the lateral canthal tendon. Partial or complete

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FIGURE 39.8. The bipedicled myocutaneous Tripier flap. (Redrawn after Jackson, IT. Eyelid and canthal region reconstruction. In: LocalFlaps in Head & Neck Reconstruction. St. Louis: Quality Medical Publishing, 2002.)

C

ablation or injury to this structure can result in laxity of the lower lid, or, in extreme cases, medial displacement and rounding of the lateral canthus with a shortened horizontal fissure (6,10). For these reasons, we recommend that all reconstructions performed in zone IV include a canthal support procedure or canthopexy. Complete disruptions of the canthus require a canthoplasty. In addition, laxity of the lateral canthus, even when corrected, has a tendency to recur over time. Thus, a slight overcorrection should be the goal (6,10). Options for reconstructing the superficial component of these defects include a cheek advancement flap or full-thickness skin graft. Simple disruptions of the lateral canthal tendon may be repaired primarily, reattaching the severed portion to the stump as indicated. More significant disruptions, with loss of the lateral aspect, may be reconstructed by anchoring the medial end of the remaining ligament to either the periosteum at the level of the Whitnall ligament or to the bone directly, using small drill holes in the orbital rim (6,10). When the upper portion of the tendon is intact, a lateral canthal sling is used to provide support and tighten an otherwise lax lower lid (6). Finally, when completely obliterated, the lateral canthal ligament can be reconstructed via a lateral tarsal strip procedure. The tarsal plates are sutured to a strip of orbital periosteum raised for this purpose (6,10). Canthopexy and canthoplasty are discussed under Lower Eyelid Reconstruction: Zone II section. The loss of the superficial components of zone IV defects should be reconstructed with either a local cheek advancement flap or with a full-thickness skin graft. Cheek flaps, as described for zone II defects, may be rotated into defects and provide an excellent color and texture match. Unlike the local advancement cheek flap described above, however, the quan-

tity of tissue required to reconstruct lateral canthal defects is usually minimal. For this reason, flaps may be designed with either superolateral or inferolateral incisions (10). If one elects to reconstruct a zone IV defect with a graft, it should be fullthickness and harvested from a site as close to the recipient bed as possible. Full-thickness grafts provide the necessary texture with less contracture than split-thickness grafts, and postauricular skin provides an excellent color and texture match with minimal donor-site morbidity.

Reconstruction of Periocular Defects: Zone V Zone V defects are defined as those outside of but contiguous with zones I to IV (6,10). Although Zone V defects do not involve the eyelids or canthi directly, they are relevant to this discussion in that they can affect lid position and function. Normal eyelid form and function results from a fine equilibrium, or balance, between support forces and the counterproductive distraction forces (4,6). Disruption of these forces, by loss or manipulation of the surrounding tissue, can have manifestations within zones I to IV, as discussed in Lower Eyelid Reconstruction: Zone II section. For example, reconstruction of an infraorbital cheek defect following Mohs micrographic surgery without attention to the principles outlined previously can result in ectropion or scleral show (4,6,11). Zone V defects should be reconstructed with attention to the proper functioning and appearance of the lids and canthi in all four of the periocular zones. When necessary, adjuvant procedures, such as lateral canthoplasty and/or canthopexy, should be performed when addressing zone V defects.



Cervicofacial flap reconstruction of the entire cheek illustrates this point. In this example, the patient’s lower eyelid (zone II) may lie in a functional anatomic position only until the inferior distraction forces of the flap are applied by way of zone V. Anticipating this, the surgeon should support the lower lid, and the flap, by way of a medial and lateral canthopexy with or without bone fixation, and the flap should be supported independently. In this manner, the lower lid is insulated from the distraction forces of an unsupported flap in zone V.

CORRECTION OF EYELID PTOSIS Anatomy and Physiology of Eyelid Elevation The natural state of the upper eyelid is closed. Eyelid elevation in the waking state is mediated primarily by the action of the levator palpebrae superioris muscle with a less-significant contribution made by the Mueller muscle. Together, the levator palpebrae superioris muscle, the levator aponeurosis, and the Mueller muscle form the levator complex responsible for eyelid elevation. In distinction, the action of eye closure and blinking is mediated by the orbicularis oculi muscle (1,3,4). The levator palpebrae superioris muscle originates from the bony orbit, just superior and anterior to the optic foramen. It courses anteriorly, above the superior rectus muscle, following the curve of the globe. As it crosses the Whitnall ligament, the levator muscle fibers dissipate, giving rise to the levator aponeurosis, which continues forward, first fusing with the orbital septum and eventually terminating by inserting fibrous connections into the tarsal plate posteriorly and the orbicularis anteriorly (see Eyelid Anatomy and Physiology above) (Fig. 39.1). The fusion of the levator aponeurosis with the orbicularis fibers gives rise to the upper eyelid fold. Disruption at this level—as seen with “levator dehiscence”—results in blunting of the upper eyelid fold, a common characteristic of the senescent eye. The levator palpebrae superioris is innervated by the occulomotor nerve (cranial nerve [CN] III). The Mueller muscle arises from the inferior surface of the levator superioris muscle at the level of the Whitnall ligament. From there, it courses anteriorly to insert on the superior margin of the tarsal plate. The Mueller muscle is innervated by sympathetic fibers that arise from the cervical sympathic ganglion and course through the sympathetic trunk along the internal carotid plexus. In the normal lid, contraction of the levator muscle results in elevation of the upper eyelid. Full excursion of the lid approximates 10 to 15 mm. An additional 1 to 2 mm of elevation is provided by the action of a well-functioning Mueller muscle (1–4).

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TA B L E 3 9 . 1 GRADES OF PTOSIS AND LEVATOR FUNCTION Ptosis

Levator Function

Mild: 2–3 mm Moderate: 3–5 mm Severe: >5 mm

Good: 10–15 mm Fair: 6–9 mm Poor: 6 mm). For these reasons, levator advancement is our procedure of choice for individuals with ptosis secondary to involutional, senescent, traumatic, and certain forms of congenital ptosis. Additionally,

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it may be performed with or without concomitant blepharoplasty. As with all lid procedures, levator advancement should begin with tetracaine drops and injection of local anesthetic. When injecting the local anesthetic, care should be taken not to distort the natural anatomy and landmarks. Voluntary muscle function should be preserved whenever possible. A protective corneal shield is inserted. A transparent shield is preferred that allows visualization of the pupillary aperture. The lid is then incised through the orbicularis muscle fibers and the levator aponeurosis is identified. Dissection, using needle-tip electrocautery, continues superiorly past the orbital septum, which is divided at its junction with the aponeurosis. Further cephalad, dissection identifies the preaponeurotic fat. Dissection is next performed inferiorly to just beyond the aponeurotic–tarsal junction. Here, the levator aponeurosis is separated from the tarsal late along its superior margin, and the levator is lifted superiorly. When possible, the Mueller muscle is left behind, lying on the conjunctiva, while elevating the aponeurosis from below. Once the free edge of the levator aponeurosis is mobilized, dissection continues medially and laterally and the horns of the levator aponeurosis are released. Next the aponeurosis is grasped and advanced anteriorly and inferiorly, pulling it like a window shade over the tarsal plate to which it will eventually be resecured. The degree of advancement depends on the degree of ptosis and levator function. In most cases, 1 mm of advancement will provide 1 mm of correction, but as levator function decreases, greater advancements may be necessary to achieve the same results. This is especially true in cases of congenital ptosis where the levator function is, at best, fair. Regardless of the degree of advancement, however, the position of the lid should be evaluated after the first suture is placed intraoperatively in all cooperative patients. This is achieved by advancing the aponeurosis and securing it to the tarsal plate with absorbable suture in temporary fashion. The operating lights are directed off the field to minimize reflexive squinting, and the patient is placed upright and asked to look straight ahead. The cooperative patient is then asked to look up and down in order to assess function and the degree of lagophthalmos. The position of the lid is evaluated with respect to the ideal. The lid should fall halfway between the pupillary aperture and the corneoscleral junction at a vertical line approximating the pupillary nasal margin. Generally, a slight overcorrection by 1.0 to 1.5 mm is necessary to compensate for epinephrine-induced Mueller muscle stimulation. However, one must remember that undercorrection is easier to correct than overcorrection and is usually better tolerated by the patient. Once the degree of advancement and lid position is determined, the aponeurosis is secured to the superior aspect of the tarsal plate with absorbable sutures. Excess levator tissue is amputated and, if necessary, the skin is secured to the supratarsal levator to recreate the lid fold. The lid incision is then closed with a running intracuticular permanent pullout suture in a medial-to-lateral fashion. If necessary, skin and orbicularis fibers may be excised, thus performing a concomitant blepharoplasty prior to closing the incision. However, it should be noted that, in our experience, resection of skin often is best deferred until a second procedure, after resolution of edema allows for a more accurate evaluation. This is especially true in the previously operated lid. If significant skin excess is left in place, however, a prominent lid fold, distortion of the lash line, or entropion may result. In summary, the advantages of levator advancement include its broad application and its ability to be performed with or without blepharoplasty. It is technically more demanding, and has a steeper learning curve. However, once mastered, the levator advancement procedure is the most widely useful procedure. It allows adjustments intraoperatively and, most im-

portantly, directly addresses the underlying pathophysiology in most cases (2,4).

Tarsal Conjunctival Mullerectomy The tarsal–conjunctival mullerectomy (Fasanella-Servat procedure) is indicated for patients with good levator excursion and mild ptosis. In this procedure, a portion of the posterior lamella, including the superior margin of the tarsal plate, the inferior portion of the Mueller muscle, and the associated conjunctiva is removed en block. Anesthesia is provided by instilling topical tetracaine drops and subcutaneous injection of lidocaine with epinephrine, avoiding distortion of the anatomic layers. A minimum of 7 minutes is allowed to elapse for the hemostatic effects of epinephrine to take effect. The lid is everted, presenting the conjunctival surface and underlying cephalic aspect of the tarsal plate and the Mueller muscle. A portion of the posterior lamella, including the superior margin of the tarsal plate extending cephalad, is secured in a pair of identical mosquito clamps, as illustrated in Figure 39.11, leaving a 3- to 4-mm cuff of posterior lamella exposed. It is critical to adjust the placement of the matched clamps so that they parallel the natural curve of the lid. Eccentric clamp placement will result in an unbalanced resection and a “tented” or “pinched” lid. Next, a running, horizontal mattress, monofilament nonabsorbable suture is the brought through the skin on the medial aspect and run laterally under the clamps, exiting through the lateral eyelid skin. Using a scalpel, the tissue above the clamps is amputated and the clamps are removed. The palpebral conjunctiva is smoothed over with the back end of a forceps and the eyelid is reverted to its natural position. The suture tails are tied to each other, and a Steri-Strip is placed as shown. The suture is removed in approximately 1 to 2 weeks—sooner if overcorrection is suspected, and later if undercorrection is supposed. Disadvantages of this procedure include a variable tarsal plate contour, inability to provide graduated tension, a decreased wetting surface, and an increased risk for corneal abrasions in the postoperative period secondary to suture irritation. In contrast to levator advancement, there is little room for flexibility and adjustment intraoperatively with the tarsal conjunctival mullerectomy. Consequently, the individual tailoring aspect of this procedure is somewhat limited (2,4).

Levator Plication The levator plication, or the levator tuck, is indicated for patients who have mild to moderate ptosis (1 to 5 mm) and good levator function in whom a minimal dissection is desired and required. Plication may be performed with or without other aesthetic or functional procedures such as blepharoplasty or brow lift. Unlike the tarsal conjunctival mullerectomy, the levator plication uses an anterior approach. After anesthetic drops are placed, local anesthesia is administered. A simple curvilinear incision or elliptical upper blepharoplasty incision is made, depending on whether or not skin and orbicularis fibers are to be removed. After identifying the levator aponeurosis, dissection is carried out inferiorly to the tarsal plate and superiorly through the orbital septum exposing the preaponeurotic fat medially and laterally to the margins until the levator aponeurosis is defined. The levator aponeurosis is plicated such that each millimeter of plication results in an equal correction of the ptosis. Some surgeons prefer to correct more so for each millimeter of ptosis, but we have found that a 1:1 ratio is sufficient in patients with fair to good levator function. On the other hand, 2:1 or even 3:1 correction may become necessary when performing this procedure in patients with poor levator function. The patient can be positioned upright and the plication can be adjusted, intraoperatively, accordingly. The first plication suture is placed in a vertical line approximating the nasal pupillary margin, the medial most aspect of the pupillary



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TARSAL CONJUNCTIVAL MULLERECTOMY

Mild upper lid ptosis, 1–2 mm

Cross-section of suture placement Running suture (full thickness) behind clamps, lateral to medial

Trim excess clamped tissue

Closure—suture tied on skin surface and covered with Steri-Strip

aperture. Because the degree of correction required will vary from patient to patient, indeed even from the left to right eyelid, we assess the lid position in the sitting position prior to completing the plication and closure. As in all levator procedures, we err on the side of overcorrection by 1.0 to 1.5 mm in individuals with a competent muscle to compensate for epinephrineinduced Mueller muscle stimulation. After the level of plication is determined, additional plication sutures are placed, medially

FIGURE 39.11. The tarsal–conjunctival mullerectomy (Fasanella-Servat procedure) is indicated for patients with good levator excursion and mild ptosis. (Reproduced from Spinelli HM. Ptosis and upper eyelid retraction. In: Spinelli HM, ed. Atlas of Aesthetic Eyelid and Periocular Surgery. Philadelphia: Elsevier; 2004; 100, with permission.)

and laterally, to complete the tuck. The cuff of levator tissue between our sutures is then assessed. If it is determined that leaving the tissue in place will distort the overlying skin of the lid, it is amputated; otherwise, it is left in place. At this point in the operation, some authors advocate reapproximation of the overlying skin to the levator aponeurosis to recreate the upper lid sulcus. This is especially true in patients in whom the lid height is to be altered. Finally, the skin is closed as in a

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standard blepharoplasty. The advantages of this procedure are its relative technical ease and the ability to adjust the plication sutures to the correction required. Its disadvantages include its limited application and an inability to be applied to a wide array of ptosis cases (2,4).

Frontalis Sling When intrinsic levator function is poor (5,000 mL of total aspirate) is performed, or when liposuction is combined with a significant open surgical procedure(s), hospital admission or 24-hour observation in a hospital setting is necessary. Attention to perioperative fluid management is imperative when significant volumes are suctioned. Approximately 70% of the injected subcutaneous fluid will be absorbed and must therefore be taken into account when calculating intraoperative intravenous (IV) fluid. Anesthesiologists unfamiliar with liposuction may not be aware of this fact and excessive fluids may be administered. When the superwet technique is used (see Wetting Solution below) the following guidelines for fluid resuscitation are recommended: (a) for volumes 5 L are planned. When liposuction is combined with an open surgical procedure, or when large-volume liposuction is performed, compression hose and/or sequential compression device (SCD) boots for deep vein thrombosis (DVT) prophylaxis are recommended.

WETTING SOLUTION Liposuction was first practiced as a “dry” technique, meaning that nothing was done to prepare the fat prior to suctioning it from the subcutaneous plane. As one might expect, hemorrhagic complications were common. Illouz is credited for developing the “wet” technique, which he described as a “dissecting hydrotomy,” wherein he instilled normal saline, water, and hyaluronidase in the hope of creating a weak hypotonic solution to lyse the adipocyte cell wall (8). Hetter is credited with adding lidocaine and dilute epinephrine to the wetting solution (9). Jeffrey Klein, a dermatologist, developed and coined the term tumescent technique, which is now used for the infiltration of large-volume, dilute lidocaine with epinephrine solution for the purpose of performing liposuction with low blood loss (10). The importance of infiltration of wetting solution cannot be overstated. The superwet technique is defined as a 1:1 ratio of the volume of wetting solution infused to the volume of aspirate. The term tumescent technique was classically described as a ratio of 2 or 3:1. Technically, the tumescent and the superwet techniques differ in the ratio of volume infused to volume of aspirate; however, both involve infusion of wetting solution to the point of tissue turgor or a “peau d’orange” of the overlying skin. Practically, the term tumescent liposuction is used as a generic term for liposuction using wetting solution. Wetting solution has a number of advantages. It provides a mechanism for delivery of anesthetic and vasoconstricting agent, thereby providing a component of intraoperative anesthesia, decreasing blood loss and postoperative bruising, and also providing postoperative analgesia. Administration of wetting solution eases the passage of the cannula through the tissue, and minimizes fluid requirements during and after surgery. Some surgeons believe that magnification of the area to be suctioned is an advantage, whereas others believe that distortion of the area is a disadvantage. It is my opinion that “final contour” is an end point that comes with experience, and infiltration of wetting solution is a necessary part of the equation for the student to master. Table 52.1 describes my standard wetting solution recipes. The total amount of lidocaine infused per patient should not exceed the maximum recommended subcutaneous dose of 35 mg/kg (Chapter 11) (11). The maximum dose for each patient should be calculated preoperatively and the case should be planned accordingly. If more infiltrate is needed once the maximum dose has been reached, lidocaine can be left out of

TA B L E 5 2 . 1 STANDARD WETTING SOLUTION Local anesthesia

General anesthesia

1 L lactated Ringer solution 1 mL epinephrine 50 mL 1% Xylocaine

1 L lactated Ringer solution 1 mL epinephrine 30 mL 1% Xylocaine

the final bags when general anesthesia is used (see the discussion of lidocaine toxicity in Risks and Possible Complications below). The actual infiltration technique is especially important. An uneven infiltration of wetting solution increases the chances of an uneven final result. Infiltration is begun in the deepest plane of the area to be suctioned and proceeds in a systematic fashion from deep to superficial. Each level, or “plane,” should be evenly infiltrated before slowly moving a bit more superficial. The infiltrated fat should be evenly firm, and there should be no disproportionate bulges in the skin at the end of the infiltration process. The wetting solution should be “feathered” at the edges of the target area, just like the suctioned fat is feathered.

ASPIRATION OF FAT The wetting solution is allowed 7 to 10 minutes for maximal vasoconstrictive effect. Aspiration is performed through various small incisions, the location of which depends on the area being suctioned. Every attempt should be made to hide incisions in anatomic creases or Langer cleavage lines, when appropriate, although most liposuction cannulas are small enough that the eventual scars are almost imperceptible. As a general rule liposuction is performed using the dominant hand, making even strokes in a systematic fashion. For instance, one can approach the lateral thigh through a gluteal crease incision with the patient in a prone position. If the surgeon is right handed, the surgeon may stand on the left side of the patient and insert the appropriate cannula into right or left gluteal crease incision. The cannula is inserted into the deep plane first. Using even in-and-out strokes, the cannula is moved back and forth in a fanlike pattern, with the incision as the fulcrum. The cannula is moved more superficially as fat is removed. The nondominant hand is kept over the area being suctioned to provide tactile feedback as to the depth of the underlying cannula and the amount of remaining fat. Cross-tunneling (suctioning an area from a second incision at right angles from the first incision) is recommended for most areas to avoid contour deformity (Fig. 52.3). The end point of aspiration is determined by a number of factors. Contour of the patient is the most important factor, but determining it can sometimes be confusing because of infused wetting solution. The aspirate volume should also be considered. Additionally, a comparison of sides when bilateral areas are suctioned is helpful. When UAL is used, the amount of time that ultrasonic energy is applied should be recorded and considered when determining the end point and can be helpful when attempting to obtain symmetry between sides. The pinch test is also helpful. The pinch test is performed by gently pinching the patient’s skin and subcutaneous fat between the thumb and forefingers to assess the thickness and smoothness of the underlying subcutaneous tissue and for comparing preoperative with postoperative thickness. Simply pinching or rolling the tissue between one’s thumb and index finger helps in the assessment of irregularities. When all is said and done, it doesn’t matter what is removed; what matters is what you leave behind! Final contouring is routinely done at the end of the liposuction procedure. The surgeon may use saline to wet the skin and glide his or her hand over the surface to assist in finding small irregularities. Usually smaller diameter cannulas (2.5 or 3.0 mm) are chosen to do the final contouring and feathering. The old adage “the enemy of good is better” should be kept in mind. Overresection is more difficult to fix than underresection, so it is better to err on the side of underresection. Liposuction may not be difficult, but is time-consuming and requires meticulous attention to detail.


Chapter 52: Liposuction

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B FIGURE 52.3. Cross-tunneling. Cross-tunneling is a technique used to enhance smoothness and to decrease risk of contour irregularity. The patient is in the prone position with her head on the left side of the picture. A: The liposuction cannula is inserted into the gluteal crease incision (black arrow) to suction the left lateral thigh, and into the parasacral area to suction the left posterior hip. B: A second incision is made and the same areas are suctioned from a separate incision in the midaxillary line (at approximately a right angle from the first “line” of suction).

BODY AREAS TREATABLE WITH LIPOSUCTION Numerous body areas are amenable to liposuction given the plethora of equipment now available. Today’s patient can be treated from head to toe (Figs. 52.4–52.7). The face and neck can be successfully treated with liposuction, although fat injection instead of aspiration is increasingly popular. The trunk, including the abdomen, back, breast, and posterior hips (flanks), and the lower extremity, including the knees, calves, and ankles, have all been successfully treated with liposuction. In my experience, treatment of gynecomastia is particularly amenable to UAL (12). The upper arm is also well suited for UAL or SAL when the skin is not too loose. The buttocks can be successfully treated but should be approached with some degree of caution. Creation of a flat or ptotic buttocks is not only unsightly, but usually requires excisional measures to repair.

POSTOPERATIVE COURSE Incisions for cannulas larger than 3.0 mm are generally closed with a 5-0 nylon suture. Some surgeons recommend leaving smaller incisions open to allow wetting solution to drain. The patient is dressed in a compression garment that covers the areas that have been suctioned. I believe that compression foam (e.g., Topi-Foam, Byron Medical, Tucson, AZ) under a garment decreases early bruising and edema, which seems to speed recovery. An abdominal binder can be used when only the hips or abdomen were treated. If thigh suction was also done, a girdle is preferable. The patient will experience copious serosanguineous drainage from incision sites for approximately 24 to 36 hours, which can be alarming to family and friends if they are not informed in advance. Showering is permissible on postoperative day 1 or 2 and if the patient is instructed to replace the compression foam over the suctioned areas. Drains are recommended for gynecomastia and when >2,000 mL lipoaspirate is removed from the abdomen alone. They are left in place until drainage is less than 25 to 30 mL in a 24-hour period. Ideally, foam padding is left in place for 3 to 5 days. Compression garments are generally encouraged

24 hours per day for 4 to 6 weeks if circumferential thigh suctioning is performed. Postoperative follow-up visits are scheduled at 5 days to remove sutures; 2 weeks to make sure that bruising is subsiding normally and to advance the patient’s activity; 6 weeks to make sure that edema is subsiding normally and to assess the early result; 3 months to assess early result; and 6 months to assess final result. Maximal swelling can be expected at postoperative days 3 to 5. In my experience, 60% to 80% of the swelling subsides by 6 weeks postprocedure, and it takes a full 4 to 6 months for 100% of the swelling to resolve, depending on the extent of the procedure. Patients should begin ambulating on the day of surgery. Oral fluids and a high protein diet are encouraged. Physical activity should be low for the first week to discourage edema, followed by a gradual increase in activity during the second week, depending on the amount of suction that was done. At the end of the first week, most patients can return to work and should be encouraged to begin light exercise, such as brisk walking on a treadmill (with compression garments on!). At 3 to 4 weeks, if edema and bruising are resolving appropriately, the patient should be advancing to full activity, and may “wean” him- or herself out of the compression garment over the course of a week. These are general guidelines for patients undergoing average volume liposuction (lipoaspirate 2,000–5,000 mL) and must be tailored to the individual patient. Large-volume liposuction and circumferential thigh patients will need a more restrictive postoperative regimen.

RISKS AND POSSIBLE COMPLICATIONS Any surgical procedure has risks. Fortunately, serious complications are rarely associated with liposuction procedures. The most common undesirable sequela after liposuction is contour irregularity, which is directly related to inexperience and lack of attention to detail. Contour irregularities generally fall into four categories: (a) overcorrection, (b) undercorrection, (c) failure of skin retraction or abnormal skin retraction, and (d) complex deformities consisting of combinations of a, b, and c (13). Revisionary procedures should be performed only after all the swelling has completely subsided. Generally, the treatment of undercorrection is removal of more fat; the


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A

B

C

D FIGURE 52.4. Ultrasound-assisted liposuction of a 27-year-old woman shown before (A, C) and 12 months after (B, D) UAL of the abdomen, posterior hips, and circumferential thighs. A total of 4,700 mL of wetting solution was infiltrated and a total of 4,775 mL of lipoaspirate (fluid and fat) was removed: 575 mL from the abdomen, 475 mL from each posterior hip, and 1,625 mL was removed from the each thigh circumferentially.


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A

B

C

D FIGURE 52.5. Ultrasound-assisted liposuction of a 50-year-old woman. She was treated with UAL to the abdomen, posterior hips, and lateral thighs. A total of 1,250 mL, 600 mL, and 700 mL of wetting solution was infiltrated into the abdomen, hips and lateral thighs, respectively. A total of 1,300 mL, 900 mL, and 925 mL of lipoaspirate, respectively, was removed from each area. The total infiltrated was 3,850 mL, and the total aspirated was 4,950 mL.


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A

B

C

D FIGURE 52.6. Power-assistedliposuction of the breast in a 47-year-old man with gynecomastia. The patient is shown before (A, C) and 4 months after (B, D) PAL of the breast. A total of 650 mL of wetting solution was infiltrated into each breast and 575 mL of lipoaspirate (fluid and fat) was removed from each breast.

A

B, C FIGURE 52.7. Suction-assisted lipoplasty of the neck in a 53-year-old woman shown before (A, B) and after (C) SAL of the neck. Superior results can generally be obtained with liposuction of the neck in the younger population; however, this woman had very good skin retraction for her age. Careful preoperative assessment of skin quality and thorough preoperative counseling with this type of patient is imperative. In this case, incisions were made in the submental area and behind each ear in order to allow contouring along the jawline.



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TA B L E 5 2 . 2 LIDOCAINE TOXICITY Early signs

Later signs

Late signs

Plasma concentrations 3–6 μg/mL Lightheadedness Restlessness Drowsiness Tinnitus Slurred speech Metallic taste in mouth Numbness of lips and tongue

Plasma concentrations 5–9 μg/mL Shivering Muscle twitching Tremors

Plasma concentration >10 μg/mL Convulsions CNS depression Coma

treatment of overcorrection is fat injection; the treatment of loose skin is skin excision; and the treatment of complex deformities is beyond the scope of this chapter. The best way to “treat” contour irregularity is to avoid it. Other risks, including unusual bleeding, which could result in unusual ecchymosis or permanent skin discoloration, hematoma, seroma, infection, dysesthesia, fat embolism, thromboembolism, fluid imbalance, lidocaine toxicity, skin necrosis, perforation of viscera, and death, fortunately, are rare. Lidocaine toxicity deserves special mention because according to the Physicians’ Desk Reference, the maximal recommended dose of subcutaneous lidocaine HCl when used in combination with epinephrine is 7 mg/kg in an adult, yet numerous studies have documented the safety and efficacy of larger doses of lidocaine for the purposes of liposuction (11). Table 52.2 lists the signs and symptoms of lidocaine toxicity.

CONCLUSION Liposuction is an extremely popular cosmetic procedure in today’s body-conscious society. Technically, it is a relatively easy procedure to perform adequately; however, it requires strict attention to detail and a keen aesthetic eye to perfect the art of liposuction. Sucking fat is easy, whereas sculpting the

human body by removal of the perfect amount of fat, and leaving behind the perfect amount of fat, is an art.

References 1. Fournier P. Popularization of the technique. In: Hetter GP, ed. Lipoplasty: The Theory and Practice of Blunt Suction Lipectomy. 2nd ed. Boston: Little Brown; 1990: 35–38. 2. Hughes CE. Patient selection, planning and marking in ultrasound-assisted lipoplasty. Clin Plast Surg. 1999;26:279. 3. Markman B, Barton FE. Anatomy of the subcutaneous tissue of the trunk and lower extremity. Plast Reconst Surg. 1987;80:248. 4. Rohrich RJ, Kenkel JM, Janis JE, et al. An update on the role of subcutaneous infiltration in suction-assisted lipoplasty. Plast Reconstr Surg. 2003;111:926. 5. Pitman GH, Teimourian B. Suction lipectomy: complications and result by survey. Plast Reconst Surg. 1985;76:65. 6. Kenkel JM, Robinson J, Beran SJ, et al. The tissue effects of ultrasound assisted lipoplasty. Plast Reconst Surg. 1998;102:213. 7. Ablaza VJ, Gingrass MK, Perry LC, et al. Tissue temperatures during ultrasound assisted lipoplasty. Plast Reconst Surg. 1998;102:534. 8. The wet technique. In: Illouz YG, DeVillers YT, eds. Body Sculpturing by Lipoplasty. New York: Livingstone Churchill; 1989: 124. 9. Hetter GP. The effect of low dose epinephrine on the hematocrit drop following lipolysis. Aesthetic Plast Surg. 1984;8(1):19. 10. Klein JA. The tumescent technique for liposuction surgery. Am J Cosmetic Surg. 1987;4:263. 11. Klein JA. Tumescent technique for regional anesthesia permits lidocaine doses of 35 mg/kg for liposuction. J Dermatol Surg Oncol. 1990;16:248. 12. Gingrass MK, Shermak, MA. The treatment of gyncomasta with ultrasoundassisted lipoplasty. Persp. Plastic Surgery. 1999;12(2). 13. Gingrass MK, Hensel JM. Secondary liposuction. In: Mathes SJ, Hentz VR, eds. Plastic Surgery. 2nd ed. Philadelphia: Saunders/Elsevier. In press.


CHAPTER 53 ■ ABDOMINOPLASTY AND LOWER TRUNCAL CIRCUMFERENTIAL BODY CONTOURING AL ALY

Body contouring of the lower trunk region is an integral part of the plastic surgeon’s armamentarium. The lower trunk is a circumferential structure that begins at the inferior border of the breasts and ends at the pelvic rim. Although this is a convenient unit, it is difficult to separate from surrounding structures such as the thighs and the upper truncal unit, or thorax. Deformities in the lower truncal region are variable in nature and require different approaches for their treatment. Recent advances in bariatric surgery have resulted in a large population of weight loss patients, which has led to an emphasis on the evaluation and treatment of lower truncal contour deformities. This chapter will focus on excisional procedures, with or without liposuction, in the treatment of lower truncal deformities. Problems that can be ameliorated by liposuction techniques alone are covered in Chapter 52.

PATIENT PRESENTATION Patients with lower truncal complaints demonstrate a variety of deformities on a continuum from minimal lipodystrophy to circumferential fat and skin excess accompanied by abdominal wall laxity (1) (Table 1). Weight is the first important factor that affects the presentation of patients with lower truncal deformities. Because absolute weights can be misleading, body mass index (BMI), which relates weight to height, is the most commonly used parameter. It is calculated in the following manner: Body mass index = weight in kilograms/(height in meters)2 Body mass index = weight in pounds/(height in inches)2 × 703 Patients who present for lower truncal contouring span the range of BMI from normal to obese. The upper limit of normal BMI is 25; 26 to 30 is considered overweight; and 30 and above is considered obese. A variety of surgical approaches is required to treat patients in different BMI ranges. A second factor that affects the presentation of patients is the fat deposition pattern, which is genetically controlled. Women typically deposit fat in the infraumbilical abdomen, lateral thighs, hips, and medial thighs. Men tend to deposit fat in the flanks, the infraumbilical abdomen, and intra-abdominally (2). Although these patterns are common, even within the same gender, dramatically different patterns of fat deposition are often present. The quality of the skin-fat envelope is a third factor to evaluate. Women who have had one or more pregnancies tend to have abdominal skin laxity and stretch marks. The skin has been stretched beyond its ability to rebound back to its original elasticity. A similar process occurs with massive weight gain

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and subsequent weight loss in which the skin is overexpanded, leading to a skin-fat envelope that is loose and inelastic.

HISTORY Body contouring procedures early in the twentieth century consisted of dermatolipectomies of hanging abdominal panniculi. In these procedures, excess skin and underlying fat were removed to rid the patient of hanging tissues with minimal attention to aesthetic principles. In the second half of the century, advances in abdominoplasty techniques consisted of improved scar placement, abdominal wall plication techniques, and umbilical transposition. In the 1980s, liposuction was introduced, and it became a tremendous tool in the armamentarium of the plastic surgeon for affecting body contour, replacing a number of excisional procedures. Currently plastic surgeons routinely use both excisional and liposuction techniques, alone and in combination, to improve body contour.

RELEVANT ANATOMY Fat in the lower trunk is organized into superficial and deep layers separated by the superficial fascial system, which pervades the entire body. Anteriorly the superficial fascial system is referred to as the Scarpa fascia (Fig. 53.1). The blood supply of the abdominal skin and fat is important to understand. The skin overlying the rectus muscles is primarily supplied by arteries that originate from the superior and inferior epigastric vessels that run within the rectus muscles. Branches from these vessels perforate the overlying rectus fascia and traverse through the two layers of abdominal fat, finally reaching the skin. This direct blood supply of abdominal skin is interrupted during the elevation of the abdominal flap in an abdominoplasty. A secondary blood supply is derived from lateral intercostal, subcostal, and lumbar vessels that course anteriorly in the fat superficial to the Scarpa fascia (Fig. 53.2). These vessels are the only remaining blood supply of central abdominal skin after flap elevation. Interruption of these vessels by scars such as cholycystectomy incisions can lead to necrosis of inferomedial abdominal flap tissues. The superficial epigastric vessels supply blood to the skin of the lower abdomen but are also divided during abdominoplasty procedures. The lower trunk has fascial attachments between the skin and underlying muscle fascia that act as anchoring points or zones of adherence (3) (Fig. 53.3). These zones of adherence do not allow overlying skin to move during the processes of aging and/or weight fluctuations. Posteriorly the midline has a zone of adherence that overlies the spine. The anterior midline of the abdomen has a less will defined zone of adherence. Three horizontal zones of adherence are located in the inferior aspects of


Chapter 53: Abdominoplasty and Lower Truncal Circumferential Body Contouring

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infraumbilical skin and fat excess are candidates for a miniabdominoplasty. Physical examination of the abdomen in the supine position will demonstrate infraumbilical rectus diastasis, which can be confirmed by the “diver’s test” (Fig. 53.4). These patients are usually young women who have had one or two pregnancies, have good skin elasticity, and are not overweight. They may or may not have localized fat deposits in other areas of the trunk and lower extremity such as the hips and lateral thighs. The goal of surgery in this patient population is to eliminate the infraumbilical abdominal wall laxity and the minimal skin and fat excess.

TA B L E 5 3 . 1 FACTORS THAT AFFECT THE PRESENTATION OF THE PATIENT REQUESTING LOWER TRUNCAL CONTOURING Body mass index. (BMI) at presentation Fat deposition pattern Quality of the skin–fat envelope

the lower trunk; one is located at the inguinal region bilaterally and extends toward the anterior superior iliac spine (ASIS). Another is located just above the mons pubis and is variable in its adherence properties. The third is located bilaterally between the hip and lateral thigh fat deposits. Truncal tissues become lax due to aging, pregnancy, and/or massive weight loss. They descend the greatest distance laterally, caused by a combination of tissue laxity and central tethering of the midline zones of adherence. As tissues descend around the pelvis they also migrate centrally (see Fig. 53.3). The inguinal and mons pubis zones of adherence are responsible for holding the final position of abdominoplasty scars in the lower truncal region. Without their effect, the scars would migrate cephalad, possibly above natural underwear lines.

PATIENT SELECTION Patients who have minimal to moderate subcutaneous fat excess and no abdominal wall laxity are good candidates for liposuction alone. Patients who present with abdominal wall laxity and minimal abdominal skin excess limited to the infraumbilical region are good candidates for mini-abdominoplasty. Patients who present with abdominal wall laxity of both the infraand supraumbilical regions and generalized skin excess limited to the anterior aspects of the lower trunk are good candidates for a full abdominoplasty. As the deformities increase in magnitude and involve the lateral and posterior aspects of the lower trunk, circumferential truncal liposuction and/or dermatolipectomies become necessary. The indications, goals, and a general description of each procedure are given later. Lower truncal body contouring procedures are often long and extensive in nature. Medical problems such as heart disease, diabetes, and lung disease must be under control before surgery is contemplated. Cigarette smoking also has a deleterious effect on blood supply and, when combined with the already compromised vascular supply of the abdominal skin, can lead to significant tissue necrosis.

MINI-ABDOMINOPLASTY Women who present with abdominal wall laxity restricted to the infraumbilical region that is associated with minimal

Technique An incision is marked in the patient’s natural suprapubic crease and angled toward the ASIS. Often the incision can be limited to the width of the pubic hair or just beyond its lateral edges. Intraoperatively the proposed incision is made and the dissection extended to the muscle fascia. An abdominal flap is elevated superiorly to the level of the umbilicus. The infraumbilical rectus muscle diastasis is identified, and rectus fascia plication is performed. Some surgeons prefer a single layer, whereas others favor a two-layer plication (Fig. 53.5). The abdominal flap is advanced inferiorly and tailored to remove the excess skin and underlying fat. This advancement will usually pull the umbilicus down 1 to 3 cm. The closure of this incision, as in all subsequent incisions discussed in this chapter, is performed in multiple layers, with the most important layer being the reapproximation of the superficial fascial system, or the Scarpa fascia (4). Permanent or long-lasting sutures are used in this layer in an attempt to limit widening of the scar in the long run. I prefer to use interrupted monofilament nonpermanent suture in the subcuticular layer to perfectly approximate skin with an overlying layer of medical-grade skin glue. Drains are inserted to identify hematomas and reduce the seroma rate. A compression garment is used in the postoperative period by most surgeons. A variation of this technique can be used in patients who have minimal lower abdominal skin excess, no upper abdominal skin excess, and both infra- and supraumbilical rectus diastasis. To allow access to the supraumbilical rectus diastasis, the base of the umbilicus can be amputated. The abdominal flap is then elevated on either side of the midline in the supraumbilical region, and a supraumbilical rectus plication is performed in continuity with the infraumbilical plication. The umbilical stalk is then resutured to the plication at the appropriate level, and the lower aspect of the abdominal flap is tailored appropriately. It is also possible to use a minimal-incision approach to the supraumbilical plication by making an incision in the superior aspect of the umbilicus and using an endoscope to perform a dissection superior to the umbilicus that is wide enough to allow for the desired supraumbilical plication. In any of the

Skin Superficial fat layer

Superficial fascial system (Scarpa fascia anteriorly) Deep muscular fascia Muscle

FIGURE 53.1. Organization of fat and fascia in the anterior abdomen.


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Superior epigastric a.

Intercostal a. Subcostal a. Lumbar branches

Ascending branch of deep circumflex a.

Inferior epigastric a. Superficial epigastric a.

FIGURE 53.2. The abdominal wall vasculature. a., artery.

Strong zones Variable zones

B

A

C

FIGURE 53.3. Fascial zones of adherence. The zones of adherence control the movement of tissue associated with aging and/or massive weight loss. These fascial attachments result in lateral descent of truncal tissues, which rotate toward the midline.



A

B

FIGURE 53.4. The classic “diver’s test” demonstrates how a bend at the waist will reveal the true extent of abdominal wall laxity.

mini-abdominoplasty techniques discussed, liposuction can be used to decrease the thickness of any part of the abdominal flap that has not been elevated. One of the most difficult aspects of mini-abdominoplasty is avoiding dog-ears because of the short incision.

ABDOMINOPLASTY Generally abdominoplasty is indicated in patients whose laxity involves the supra and infraumbilical regions, limited to the an-

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terior aspects of the lower trunk. The goals of abdominoplasty depend on the presenting deformities. They include creating a flat abdominal contour, eliminating abdominal wall laxity, enhancing waist definition in some patients, and eradicating mons pubis ptosis if present. Stretch marks are common and may be limited to the infraumbilical region or may include both the infra- and supraumbilical skin. Rectus diastasis of the entire vertical extent of the abdomen is present in these patients, with the infraumbilical diastasis usually more extensive because of the position of the uterus during pregnancy. Preoperatively abdominal wall laxity can again be detected by the “diver’s test” and physical examination. Massive-weight-loss patients who reach a near-normal BMI may also present with lower truncal excess limited to the anterior abdomen. However, most often they present with circumferential deformities that require more extensive circumferential excisions. Patients who present with excess intra-abdominal fat that would prevent flattening of the abdominal wall by plication are not good candidates for abdominoplasty. The outer skinfat envelope of the belly always conforms to the shape of an inner balloon whose anterior wall is made up of the abdominal muscle wall. If that wall is rendered convex in profile by virtue of overly abundant intra-abdominal contents, then the final profile of the belly will also be convex. Because abdominal contour flattening is one of the major goals of surgery, these patients are better served by weight loss prior to contemplating abdominoplasty-type procedures. By the nature of an abdominoplasty, where an ellipse of tissue is removed from the lower abdomen, dog-ears can be created at the edges of the ellipse, especially in patients who already have lateral excess. Patients who present with deformities that extend beyond the anterior aspects of the lower trunk may require extending the abdominoplasty excision laterally, liposuction of the lateral and posterior trunk, and/or circumferential dermatolipectomy to attain the best possible contour. Some authors advocate the use of fleur-de-lis or I-type excisions in which an anterior vertical wedge of tissue is resected, as will be discussed later in this chapter. Generally, as circumferential lower truncal dermatolipectomy has become more mainstream in plastic surgery because of the massive-weight-loss population, the indications for isolated abdominoplasty have narrowed.

Technique

FIGURE 53.5. The abdominal flap elevation and rectus fascia plication in a mini-abdominoplasty.

The markings for an abdominoplasty are performed prior to surgery. The proposed excision is marked in the lower abdomen. Centrally the inferior incision line is often marked in the natural suprapubic crease and then carried laterally. Recently many surgeons have adopted the use of a “French bikini/thong pattern” in which the lateral aspects of the proposed inferior incision are angled toward the ASIS, but many variations are described in the literature (5). An attempt is made to avoid the incision beyond the ASIS, but it is more important to avoid dog-ears. With the inferior mark in place the patient is slightly flexed at the waist, and the pinch technique is used to approximate the superior extent of the excision. Ideally the patient should have enough excess abdominal skin to allow excision of the skin from just above the umbilicus to the suprapubic crease centrally. In the operating room a circumumbilical incision is made, and the inferior incision of the proposed excision is made. Abdominal flap is elevated superiorly, around the umbilicus, and up to the xiphoid and costal margins (Fig. 53.6). This type of wide undermining allows the greatest amount of inferior abdominal flap advancement at the time of flap tailoring, but it also leads to the division of more lateral intercostals, and


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FIGURE 53.6. The extent of abdominal flap elevation and fascial plication in a traditional abdominoplasty.

subcostal and lumbar vessels, which make up the remaining blood supply of the flap. Some surgeons prefer a more limited dissection on either side of the midline above the umbilicus, just enough to allow for supraumbilical rectus fascia plication up to the xiphoid. The benefit of the limited dissection is the increased number of the lateral vessels left intact to support the blood supply of the tailored abdominal flap. In some patients, however, the limited dissection will not allow the appropriate advancement of the abdominal flap and reduce the amount of tissue that may need to be resected to create the best contour. As a general rule, flap elevation should be restricted to just what will allow appropriate rectus fascia plication and appropriate flap advancement. Often it is best to limit the initial elevation and then release the tissues incrementally to allow for appropriate contour. After flap elevation, rectus fascia plication is performed. Many patterns have been proposed for plication, but a vertical plication in one or two layers is most common. The patient is then flexed at the waist, and the abdominal flap is advanced inferiorly to facilitate the process of flap tailoring. As the abdominal flap is advanced, the surgeon can control where the greatest tension will be at closure—centrally or laterally. Creating the greatest amount of tension centrally is advantageous in limiting the lateral extent of the final scar but may lead to excessive mons pubis elevation and less waist definition. Lockwood, in his “high-lateral-tension” approach to abdominoplasty, has espoused placing the greatest tension on the lateral aspects of the abdominal closure (6). This is based on the fact that the

greatest laxity in the trunk occurs laterally. However, the increased lateral tension often necessitates extensions of the scar laterally to eliminate dog-ears. This approach leads to better waist definition and improvement in anterior thigh contour. With the tailored abdominal flap approximated to the lower incision, the position of the umbilicus is noted on the flap and a neo-umbilicus is created. The stalk of the umbilicus is brought through the abdominal flap through various types of incisions advocated by different authors. I prefer a simple vertical incision, no defating of the underlying soft tissues, and three, point fixation sutures at 3, 6, and 9 o’ clock. Whatever method the surgeon chooses, the umbilicus should be fairly small, vertically oriented, superiorly hooded, and have a slight hollow around it. The closure of the abdominal incision is accomplished in multiple layers, with the most important layer being the superficial fascial system, or the Scarpa fascia (4). This is accomplished with permanent or long-lasting suture, which, it is hoped, reduces the significant tension that can be generated at closure, prevents acute wound dehiscence, and reduces scar widening in the long run. I prefer to use interrupted monofilament nonpermanent suture in the subcuticular layer to perfectly approximate skin. An overlying layer of medical-grade skin glue is then applied. Drains are placed. A compression garment is used in the postoperative period by most surgeons. Figure 53.7 shows an example of abdominoplasty in an ideal patient. Combining liposuction with traditional abdominoplasty techniques is controversial and often is left to the surgeon’s experience and philosophy (7). Liposuction of the abdominal flap in nonundermined areas is generally considered safe. Liposuction of undermined regions of the flap can potentially lead to flap necrosis because of the compounding effect of liposuction on the already compromised blood supply. Certainly, liposuction of areas outside the bounds of the undermined abdominal flap, such as the hip region or the lateral thighs, can be performed without concern for flap compromise.

CIRCUMFERENTIAL LOWER TRUNCAL DERMATOLIPECTOMY OR CIRCUMFERENTIAL LIPECTOMY As a basic principle of plastic surgery, it is always better to treat an anatomic unit in its entirety whenever possible. Abdominoplasty treats deformities limited to the anterior lower trunk. When deformities involve more than the anterior abdomen, other procedures are required. If the surrounding areas such as the thighs, buttocks, hip, and lower back regions contain excess fat without ptosis, liposuction can be added to abdominoplasty to create a better overall lower truncal contour. However, for patients who present with generalized laxity and/or ptosis of those areas, circumferential lipectomies are required. Massiveweight-loss patients make up the largest group of such patients who require circumferential excisional procedures. They will continue to grow in numbers, given that obesity has been recognized as a major health care issue in the United States and the world. In addition, women who gain moderate weight, 30 to 40 pounds, usually with childbirth and/or aging, and are not able to lose the weight through normal means of exercise and nutritional changes may be candidates. They often present with a desire to eliminate anterior abdominal excess, but careful examination will demonstrate circumferential excess that is best treated with a circumferential lipectomy. Finally, normalweight-range patients who desire remarkable improvements in their lower truncal contour may be candidates.



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FIGURE 53.7. Traditional abdominoplasty. A young woman who presented after two pregnancies desiring an improvement in her abdominal contour. She complained of loose abdominal skin and protrusion of her belly, despite a regular exercise program. Her abdominal wall laxity was more prominent in the infraumbilical region, consistent with her pregnancies. She underwent an abdominoplasty using a Frenchbikini pattern of excision and is shown 6 months after surgery. Because her deformities were limited to the anterior abdomen and she was within the normal weight range, there was no need to combine other procedures with her traditional abdominoplasty.

There is a variety of names used to describe circumferential lower truncal dermatolipectomies: extended or circumferential abdominoplasty, central body lift, torsoplasty, and body lift. I prefer to divide these different variations into two general categories based on what they treat and what they accomplish. The first category is made up of centrally based procedures that mainly treat the lower truncal unit, which will be referred to as belt lipectomies, as espoused by Aly and Cram (8,9). The second category includes procedures that treat the lower trunk and thighs as a unit, which will be referred to as lower body lifts, as espoused by Lockwood (10,11). Each procedure has its benefits and drawbacks. Both should be in the armamentarium of the plastic surgeon who performs body contouring surgery. The choice of procedure is based on the patient’s desires and presenting deformities. Both procedures eliminate a circumferential wedge of tissue from the lower trunk. A belt lipectomy removes a wedge that is more superiorly located than that removed in a lower body lift in its lateral and posterior extents (Fig. 53.8). The final scar after belt lipectomy is located above the widest aspect of the bony pelvic rim, at the junction between the lower back and buttocks, which maybe visible outside of brief undergarments. Because this allows cinching at waist level, more waist definition can be created by this technique. This is often desired in women but may be less desirable in men. Pelvic rim zones of adherence help to prevent the descent of lower truncal tissues as well as inhibit elevation of lower extremity tissues, (see Fig. 53.4). These fascial attachments are interrupted but not completely eliminated during a belt lipectomy, and they prevent extensive lifting of lower thigh tissues. Thus, overall, a belt lipectomy is capable of creating excellent lower truncal contour by accentuating waist definition, delineating the buttocks from the lower back, and lifting the lateral thighs, but it has limited capability in lifting the distal thighs. A lower body lift treats the lower trunk and thighs as a unit. The pelvic rim zones of adherence are intentionally interrupted as completely as possible, which allows inferior thigh tissues down to knee level to be lifted, a fact that leads to a significant reduction in anterior and lateral thigh laxity. The final scar is located on the buttocks proper, which can blunt waist definition (see Fig. 53.8). This is often desirable in men but

may be less so in women. The resultant scar is easily covered by normal undergarments, and the thighs are dramatically improved down to knee level. However, a lower body lift is less efficient in creating waist narrowing and can result in less than ideal buttocks definition because the scar does not respect the natural junction between the lower back and buttocks. The majority of patients undergoing a circumferential lipectomy are massive-weight-loss patients. Often they present with a hanging panniculus, mons pubis ptosis, an ill-defined waist, lower back rolls, hip-fat excess, lateral thigh ptosis, and varying types of buttocks deformity. The goals of surgery include elimination of the hanging panniculus, mons pubis elevation, creation of waist definition (especially in women), decrease or elimination of lower back rolls, lifting of the outer thighs, and increase in buttocks definition.

Techniques Although a circumferential lipectomy is a combination of an abdominoplasty, a lateral thigh lift, and a buttocks lift, the procedure is more complex than simply combining them. The lower trunk of patients who present with circumferential excess has the shape of an inverted cone (Fig. 53.9). A wedge of tissue is marked for proposed excision around the lower trunk. The wedge brings a narrower part of the cone down to the level of a wider part of the cone located at, or near, the pelvic rim (see Fig. 53.9). As previously noted, the wedge to be excised is generally located in a more superior position in belt lipectomy when compared to the wedge to be excised in a lower body lift. In either method, the anterior aspect of the wedge is wider (in vertical distance) than the lateral or posterior aspects. The lateral resection is the next widest aspect so as to reverse the lateral truncal descent (Fig. 53.10). Because of the circumferential nature of the procedure, more than one position is necessary to accomplish the resection in the operating room. No matter what sequence is preferred by a particular surgeon, the abdominal part of the procedure is performed in the supine position. Surgeons who advocate prone/supine or supine/prone positioning cite the single turn


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FIGURE 53.8. Belt lipectomy and lower body lift. Two patients who underwent a belt lipectomy above and a lower body lift below. In a belt lipectomy the scar is placed at the junction between the buttocks and lower back, which helps to frame the natural buttocks contour and accentuate waist narrowing. In a lower body lift the scar is onto the buttocks proper and is overall more inferiorly placed, especially in its lateral and posterior aspects. The combination of eliminating the pelvic zones of adherence and the lower position of the excised wedge allows the lower body lift to elevate the thighs more effectively than in a belt lipectomy.

required in the operating room and the ability to control buttock symmetry as their reasons for choosing the “two-position” sequences. The supine/lateral/lateral or lateral/lateral/supine proponents prefer these “three-position” sequences because they allow for easier lateral thigh liposuction and hip flexion in

the lateral decubitus position, which facilitates maximal lateral resections. The extent of anterior flap elevation in the abdominoplasty portion of the circumferential procedure is based on surgeon preference. The lateral elevation is usually more extensive than

FIGURE 53.9. Truncal deformity in weight loss patients. In the massiveweight-loss patient the presenting lower truncal deformity is in the shape of an inverted cone. In a circumferential lipectomy a wedge of tissue is removed. The diameter of the wedge at its superior edge is smaller than its diameter at the inferior edge.



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FIGURE 53.10. A 31-year-old woman presented after an 80pound weight loss to reach a body mass index of 27.31. (Above) Shown with preoperative markings for a circumferential belt lipectomy. Note the excision laterally is generally aggressive to counteract the lateral descent that occurs with massive weight loss and/or aging. Vertical marks are placed along the circumference of the proposed resection to help alignment at closure. Surrounding areas of the thigh are also marked for liposuction. (Below) The patient 6 months after surgery, demonstrating dramatic waist narrowing, elimination of the panniculus and lower back rolls, and improved buttocks definition.

in an abdominoplasty, which compromises the remaining blood supply to the abdominal flap to a greater extent. Thus it is important that an effort is made to preserve as many lateral feeding vessels as possible. The plication of the rectus fascia is similar to abdominoplasty plication except that it may sometimes require plication distances that far exceed the usual 5 to 7 cm encountered with routine abdominoplasty. Closure of the circumferential wound should include reapproximation of the superficial fascial system with permanent and/or long-lasting suture. During the lateral and posterior resection aspect of the procedure, some surgeons prefer to incise the superior marks first and dissect an inferior skin–fat flap, which is tailored based on tension, whereas others prefer the opposite. Some surgeons incise both the superior and inferior extents and excise a predetermined marked amount. I prefer to incise on one side and tailor based on tension. Some surgeons choose to combine extensive liposuction of the surrounding regions, such as the lower back, the upper back, and thighs, whereas others limit their liposuction to the lateral thighs. A major difference between belt lipectomy and a lower body lift is in the treatment of the pelvic rim zones of adherence. In belt lipectomy these attachments are disrupted by liposuction of the lateral thighs, but they are not completely eliminated. In a lower body lift the pelvic rim zones of adherence are intentionally destroyed by discontinuous undermining of the anterior and lateral thighs down to the knee, which allows significant thigh elevation (10). The results attained from circumferential lipectomies depend to a great extent on the presentation of the patient and the type of procedure chosen (see Fig. 53.10). As a general rule, the lower the BMI of the patient at presentation, the better are the results that can be expected (8,9).

are more likely to develop seromas. Measures that are used to reduce their occurrence include the use of suction drains and compression garments, reduction of activity, and use of deep quilting sutures. When they do occur they can most often be treated with serial aspirations. For persistent seromas, sclerosing agents and seroma catheter insertions may be utilized. Occasionally a pseudo-bursa can result from the prolonged presence of a seroma, which may have to be excised surgically. Seromas are the most common source of infection after lower truncal procedures. Simple cellulitis is fairly uncommon and is usually treated by appropriate antibiotic coverage and close follow-up. Seroma pockets that become infected usually present with overlying cellulitis, fluid collections that may or may not spontaneously drain, fever, and generalized malaise. A diligent effort should be made to find seromas and treat them whenever suspected. Once seromas become infected, aggressive intravenous therapy and appropriate surgical drainage should be instituted. Toxic shock syndrome can occur with any body contouring procedure. Postoperatively, patients who appear toxic with fever, chills, generalized malaise, and elevated white blood cell counts should be investigated. Although there is often no evidence of frank pus or large fluid collection in the wounds, aggressive surgical drainage is urgently required in this group of patients. Wound healing problems can occur with any body contouring excisional procedure because of the high tension created at the wound edges. Most often conservative wound care will allow healing with the possible need for subsequent scar revisions. Wound dehiscences, defined as separation of the wound

TA B L E 5 3 . 2

COMPLICATIONS Table 53.2 lists complications that can occur with lower truncal contouring procedures (12). Circumferential procedures are associated with more complications, but they are often performed on patients with higher BMI. When complications are stratified by BMI, noncircumferential and circumferential procedures have similar rates. Seromas are the most common complications with lower truncal contouring procedures. They are due to large dissection surface areas and can develop anywhere in the surgical field but tend to be located posteriorly in circumferential procedures. Patients who present in the high BMI ranges

COMPLICATIONS ASSOCIATED WITH LOWER TRUNCAL BODY CONTOURING PROCEDURES Seroma Wound-healing problems/dehiscence Infections Tissue necrosis Bleeding/hematoma Thrombotic events (deep venous thrombosis pulmonary emboli) Psychiatric difficulties Scar and contour asymmetry


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at the level of the superficial fascial system, are possible with any of the procedures discussed in this chapter but tend to occur more frequently with circumferential procedures. In procedures limited to anterior resections, mini-abdominoplasty, and abdominoplasty, dehiscences can be prevented by keeping patients flexed at the waist for 5 to 7 days after surgery and educating patients on a slow return to the full upright position over the second week after surgery. Circumferential procedures create competing anterior and posterior tensions, making it difficult to place patients in positions that do not stress at least one aspect of the closure. Avoidance of dehiscences in this patient population entails adjustments of the competing resections to account for opposing tensions, careful ambulation of the patients in the early postoperative period, and education of patients on how to help prevent dehiscences (13). Vascular compromise can occur with lower truncal body contouring procedures, leading to tissue necrosis. Most commonly the necrosis occurs in the inferomedial aspect of the abdominal flap. A number of factors can contribute to this problem, which include excessive tension on the abdominal closure, aggressive thinning of the abdominal flap, overly aggressive liposuction, and anything that may lead to compromising the lateral feeding vessels of the abdominal flap such as open cholycystectomy incisions. Tissues that appear compromised in the early postoperative period may be treated with nitropaste topical application. Once necrosis occurs the wound is treated conservatively and eventually allowed to heal by secondary intention. Eventually scar revision may need to be performed. Bleeding after lower truncal contouring procedures can be extensive because of the surface area within which blood can accumulate prior to detection. Although drains do not prevent hematomas, they can often warn the surgeon of a developing hematoma. Small hematomas that are well evacuated by drains in place can be managed expectantly. Large hematomas should be treated by surgical drainage. Procedures that tighten the abdominal wall can result in an increase of intra-abdominal pressures, leading to a decrease in venous return from the lower extremities. The possible resultant stasis of blood in the deep venous system may cause deep venous thrombosis and/or pulmonary emboli. Measures that are commonly used in the prevention of thrombotic events include early ambulation and sequential compression garments. Some surgeons use subcutaneous low-dose heparin in the perioperative period. Patients who undergo large excisional procedures of the lower trunk, especially massive-weight-loss patients, can have psychiatric difficulties in the postoperative period that may interfere with their recovery. Although this can occur with any surgery, the long recovery period that is required after circumferential procedures makes it wise for the plastic surgeon to actively investigate a patient’s psychiatric reserves and consider obtaining psychiatric clearance prior to surgery. The tendency of massive-weight-loss patients to have life-long psychiatric problems that are not solved by weight loss alone also contributes to the relatively high incidence of these problems. Although careful marking techniques can help to reduce scar and contour asymmetry, it is not possible to eliminate these problems in many patients because of intrinsic skeletal and soft tissue unevenness. It is best for the surgeon to recognize these natural asymmetries and point them out to patients prior to surgery.

FLEUR-DE-LIS OR T-TYPE PROCEDURES A fleur-de-lis or T-shaped excision, whether used as an abdominoplasty pattern or in combination with a circumferential lipectomy, is advocated by some authors. The advantage of the vertical wedge is to eliminate horizontal excess, create more waist definition, and decrease lateral fullness. Traditionally this pattern has not been frequently used because it is difficult to justify a vertical midline incision without a pre-existing scar in that position. Recently, however, it has found more use because many bariatric surgeons use open vertical midline incisions. Even with a pre-existing scar, however, there are major disadvantages to the vertical aspect of the T pattern. There is an increased chance of flap necrosis at the T intersection. Waist definition is frequently not increased with this procedure. When used to treat circumferential excess, a fleur-de-lis resection pattern does not eliminate lateral excess or posterior lower truncal deformities. When the pattern is used in conjunction with a circumferential lipectomy it can create a greater mismatch between the upper and lower circumferences of the inverted cone-shaped edges to be reapproximated (see Fig. 53.9). Finally, the vertical wedge excised will often lead to epigastric fullness secondary to the dog-ear effect created by the excision. Due to these disadvantages, I do not recommend this pattern of excision (12).

References 1. Aly AS. Approach to the massive weight loss patient. In: Aly AS, ed. Body Contouring After Massive Weight Loss. St. Louis: Quality Medical Publishing; 2006: 49. 2. La Trenta GS. Suction-assisted lipectomy. In: Rees TD, LaTrenta 65, eds. Aesthetic Plastic Surgery, 2nd ed. Philadelphia: WB Saunders: 1994: 1180. 3. Aly AS. Options in lower truncal surgery. In: Aly AS, ed. Body Contouring After Massive Weight Loss. St. Louis: Quality Medical Publishing; 2006: 59. 4. Lockwood T. Superficial fascial system (SFS) of the trunk and extremities: a new concept. Plast Reconstr Surg. 1991;87:1009. 5. La Trenta GS. Abdominoplasty. In Rees TD, La Trenta GS eds. Aesthetic Plastic Surgery, 2nd ed. Philadelphia: WB Saunders; 1994: 126. 6. Lockwood T. High-lateral-tension abdominoplasty with superficial fascial system suspension. Plast Reconstr Surg. 1995;96:603. 7. Matarasso A. Abdominoplasty: a system of classification and treatment for combined abdominoplasty and suction-assisted lipectomy. Aesthetic Plast Surg. 1991;15:111. 8. Aly AS, Cram AF. Body lift: belt lipectomy. In: Nahai F, ed. The Art of Aesthetic Surgery. Principles and Techniques. St. Louis: Quality Medical Publishing; 2005: 2302. 9. Aly A, Cram A, Chao M, et al. Belt lipectomy for circumferential truncal excess: the University of Iowa experience. Plast Reconstr Surg. 2003;111: 398. 10. Lockwood TE. Thigh and buttock lift. In: Nahai F, ed. The Art of Aesthetic Surgery. Principles and Techniques. St. Louis: Quality Medical Publishing; 2005: 2424. 11. Lockwood T. Lower body lift. Oper Tech Plast Reconstr Surg. 1996;3: 132. 12. Grazer FM, Goldwyn RM. Abdominplasty assessed by survery, with emphasis on complication. Plast Reconstr Surg. 1977;59:513. 13. Aly AS. Belt lipectomy. In: Aly AS, ed. Body Contouring After Massive Weight Loss. St. Louis: Quality Medical Publishing; 2006: 7.


CHAPTER 54 ■ FACIAL SKELETAL AUGMENTATION WITH IMPLANTS MICHAEL J. YAREMCHUK

The morphology of the facial skeleton is a fundamental determinant of facial appearance. Facial skeletal augmentation is usually done with alloplastic materials. Implants can be used to restore symmetry during reconstruction of posttraumatic or postablative deformities. Most often, facial skeletal augmentation is done electively to improve facial aesthetics (Fig. 54.1).

PREOPERATIVE PLANNING Physical examination is the most important element in preoperative assessment and planning. Reviewing life-size posteroanterior (PA) and lateral photographs with the patient is useful when discussing aesthetic concerns and goals. Although cephalometric radiograph analysis can be helpful in the planning, the size and position of the implant are largely aesthetic judgments. Although often referenced in texts discussing facial skeletal augmentation, neoclassical canons describing ideal proportions of the head and face have a limited role in surgical evaluation and planning because they are arbitrarily determined. When the dimensions of normal males and females were evaluated objectively and compared to artistic ideals, it was found that some theoretic proportions are never found, and others are one of the many variations found in healthy normals, or those determined more attractive than normals (1,2). For these reasons, we have found it more useful to use the anthropometric measurements of normals to guide our gestalt for the selection of implants for facial skeletal augmentation. In planning facial skeletal augmentation it is important to realize that small increases in skeletal projection can have a powerful impact on facial appearance. It should be emphasized to the patient during the preoperative consultation that all faces are asymmetric. If unrecognized preoperatively, an asymmetric postoperative result usually will be attributed solely to the surgeon.

IMPLANTS Materials Virtually all aesthetic facial skeletal augmentation is done with alloplastic implants. The use of synthetic materials avoids donor-site morbidity and vastly simplifies the procedure in terms of time and complexity. Implant materials used for facial skeletal augmentation are biocompatible; that is, they have an acceptable reaction between the material and the host. In general, the host has little or no enzymatic ability to degrade the implant with the result that the implant tends to maintain its volume and shape. Likewise, the implant has a minimal and predictable effect on the host tissue that surrounds it. This type

of relationship is an advantage over the use of autogenous bone or cartilage, which, when revascularized, will be remodeled to varying degrees, thereby changing volume and shape (3). The presently used alloplastic implants used for facial reconstruction do not have a toxic effect on the host (4). The host responds to these materials by forming a fibrous capsule around the implant, which is the body’s way of isolating the implant from the host. The most important implant characteristics, those that determine the nature of the encapsulation, are the implant’s surface characteristics. Smooth implants result in the formation of smooth-walled capsules. Porous implants allow varying degrees of soft-tissue ingrowth, which results in a less-dense and less-defined capsule. Porous implants, the result of fibrous incorporation rather than encapsulation, have less tendency to erode underlying bone, to migrate because of soft-tissue mechanical forces, and, perhaps, to be less susceptible to infection when challenged with an inoculum of bacteria. The most commonly used and commercially available materials today for facial skeletal augmentation are solid silicone, polytetrafluoroethylene, and porous polyethylene. Solid silicone or the silicone rubber used for facial implants is a vulcanized form of polysiloxane, which is a polymer created from interlocking silicone and oxygen with methyl side groups. Silicone is derived from silicon, a semimetallic element that in nature combines with oxygen to form silicon dioxide, or silicone. Beach sand, crystals, and quartz are silica. The advantages of solid silicone are that it is easily sterilizable by steam or irradiation, it can be carved easily with either a scissor or scalpel, and it can be stabilized with a screw or a suture. There are no known clinical or allergic reactions. Because it is smooth, it can be removed quite easily. The disadvantages of silicone implants include their tendency to cause resorption of the bone underlying it, particularly when used to augment the chin, the potential to migrate if not fixed, and the potential for its fibrous capsule to be visible when placed under a thin soft-tissue cover.

Polytetrafluoroethylene Gore-Tex (W.L. Gore, Flagstaff, AZ) has a carbon-ethylene backbone to which are attached four fluorine molecules. It is very chemically stable, has a nonadherent surface, and, because it is not cross-linked, it is very flexible. There is extensive experience with the use of Gore-Tex for vascular prostheses, softtissue patches, and sutures. A variety of preformed implants are available for both subdermal and subperiosteal placement. Preformed implants are made with a pore size between 10 and 30 μm. The porosity allows for some soft-tissue ingrowth, for less fibrous encapsulation, and for less tendency to migrate as compared with smooth-surfaced implants. It is easily sterilizable, smooth enough to be maneuvered easily through soft tissues, and can be fixed to underlying structures with sutures or screws.


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B

A

C

FIGURE 54.1. A 26-year-old male who in two operations had multiple implants placed. Implant augmentation of the infraorbital rim, paranasal, malar, and mandibular body was performed. In addition, rhinoplasty, midface lift, and lateral canthopexy were also performed. A: Preoperative; (B) diagrammatic representation of operation; (C) postoperative. (From Yaremchuk MJ. Facial skeletal reconstruction using porous polyethylene implants. Plast Reconstr Surg. 2003;111:1818, with permission.)

Polyethylene

Positioning

Polyethylene is a simplex carbon chain of ethylene monomer. The high density variety—Medpor (Porex, Newnan, GA)—is used for facial implants because of its high tensile strength. Although chemically similar to polytetrafluoroethylene, polyethylene has a much firmer consistency that resists material compression yet permits some flexibility. Medpor has an intramaterial porosity between 125 and 250 μm, which allows more extensive fibrous ingrowth than Gore-Tex. Soft-tissue ingrowth lessens the implant’s tendency to migrate and to erode underlying bone. Its firm consistency allows it to be easily fixed with screws and to be contoured with a scalpel or power equipment without fragmenting. A disadvantage of Medpor’s greater porosity is that it allows soft tissues to adhere to it, making placement more difficult and requiring a larger pocket than is required for smoother implants for its placement. Soft-tissue ingrowth into the larger pores also makes implant removal more difficult than removal of smooth-surfaced implants.

Although some surgeons prefer to place implants in a softtissue pocket, clinical experience has led me to adopt a policy of strict subperiosteal placement. Placement in a subperiosteal pocket involves a dissection that is safe to peripheral nerves and relatively bloodless. It allows visualization and more precise augmentation of the skeletal contour desired for augmentation. The size of the pockets is determined by the type of implant used and its method of immobilization. The longstanding teaching when using smooth silicone implants is to make a pocket just large enough to accommodate the implant so as to guarantee its position. Porous implants require a larger pocket because they adhere to the soft tissue during their placement. When using smooth or porous implants, I dissect widely enough to have a perspective of the skeletal anatomy being augmented, which allows more precise and symmetric implant positioning.

Immobilization

Requisites of Implant Shape, Positioning, and Immobilization Shape The external shape of the implant should mimic the shape of the bone it is augmenting. Its posterior surface should mold to the bone to which it is applied. Gaps between the bone and implant result in a relative increase in augmentation and a potential site for seroma and hematoma formation. The implant margins must taper imperceptibly into the bone they are augmenting so that they are neither visible nor palpable.

Many surgeons stabilize the position of the implant by suturing it to surrounding soft tissues or by using temporary transcutaneous pullout sutures. Screw fixation of the implant to the skeleton has several benefits. It prevents any movement of the implant and assures application of the implant to the surface of the bone. Because each facial skeleton has a unique and varying surface topography, a nonconforming implant will leave gaps between the implants and the skeleton. Screw fixation also allows for final contouring of the implant in position. This final contouring is particularly important where the implant interfaces with the skeleton (Fig. 54.2). Any step-off between the implant and the skeleton will be palpable and possibly visible in thin-skinned patients.


Chapter 54: Facial Skeletal Augmentation with Implants

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FIGURE 54.2. Representation of a preferred technique for chin augmentation. Through a submental approach a two-piece porous polyethylene implant is fixed to the skeleton with titanium screws. This maneuver immobilizes the implant and obliterates any gaps between the implant and the underlying bone. The implant is being contoured to provide an imperceptible implant-native mandible transition. (From Yaremchuk MJ. Improving aesthetic outcomes after alloplastic chin augmentation. Plast Reconstr Surg. 2003;112:1422, with permission.)

ANESTHESIA Facial skeletal augmentation can be performed under local or general anesthesia. It is routinely done on an outpatient basis. I prefer to perform most facial skeletal surgery under general nasotracheal anesthesia because most facial implants are placed either in the malar midface or along the mandible, usually through a combination of intraoral incisions. Nasotracheal intubation assures protection of the airway and the best possible antiseptic preparation of the oral cavity. Patient positioning and exposure for implant placement are also optimized with nasotracheal control of the airway. The surgical site is infiltrated with a solution containing Marcaine for postoperative pain control and epinephrine to minimize bleeding.

AREAS FOR AUGMENTATION The mid and lower face are the areas most often altered with implants (Fig. 54.3).

Midface Augmentation Implants are specifically designed to augment the malar, paranasal, and infraorbital rim areas.

Malar Patients who seek malar augmentation may have midface hypoplasia or normal anatomy and usually seek greater prominence of their middle malar prominence (5). Malar augmentation can be performed through intraoral, coronal, or eyelid incisions. I prefer to access the malar midface through an intraoral approach. An upper buccal sulcus incision is made far enough from the apex of the sulcus so that sufficient labial tissue is available on either side for a secure two-layer closure. Division of the lip elevators is avoided. Taking care

FIGURE 54.3. Representation of commonly used implants designed to augment various areas of facial skeleton. In the midface, these include the malar, paranasal, and infraorbital rim implants. In the lower face, the chin, as well as the mandibular body, ramus, and angle, may be augmented with alloplastic implants.

to identify the infraorbital nerve, subperiosteal dissection is carried over the malar eminence and onto the zygomatic arch, almost up to the zygomaticotemporal suture. The pocket size should enable precise insertion of the implant to the area of the skeleton desired for augmentation. Surgeons who use smooth silicone implants often assure the position of the implant by using suture suspension fixation. The position of both smooth and porous implants at the time of the placement can be guaranteed with screw fixation of the implant to the skeleton. Patients who are dissatisfied with malar implant surgery frequently complain that the implants are too large, are placed asymmetrically, or are placed too far laterally, increasing midface width.

Paranasal A relative deficiency in lower midface projection may be congenital or may be acquired, particularly after cleft surgery and trauma. Patients with satisfactory occlusion and midface concavity can have their aesthetic desires satisfied with skeletal augmentation. Implantation of alloplastic material in the paranasal area can simulate the visual effect of LeFort I advancement (Fig. 54.4) (6). Paranasal augmentation is done through an upper gingival buccal sulcus incision made just lateral to the piriform aperture to avoid placing incisions directly over the implant. An adequate cuff of mucosa is left to allow layered closure.

Infraorbital Rim Augmentation of this area is useful for patients with severe deficiencies of the midface and infraorbital rim area that result in excessively prominent eyes. Infraorbital rim


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A

B

C

D FIGURE 54.4. A 26-year-old woman underwent an aesthetic rhinoplasty and paranasal augmentation. A,C: Preoperative. B,D: Postoperative.

augmentation can effectively reverse the “negative” vector of midface hypoplasia (7). The infraorbital rim and adjacent anatomy can be exposed sufficiently to assure ideal implant placement, smooth implant facial skeleton transition, and screw fixation. Subciliary skin or skin muscle flap incisions can provide this exposure. A transconjunctival incision alone is inadequate for implant placement or screw stabilization. Use of a transconjunctival retroseptal incision requires its lengthening with a lateral canthotomy or its combining with intraoral or coronal incisions.

Mandibular Augmentation Each of the anatomic areas of the mandible—the mentum, body, angle, and ramus—can be deficient and is amenable to augmentation with alloplastic materials.

Chin There is a consensus among surgeons that the ideal profile relation portrays a convex face with the upper lip projecting approximately 2 mm beyond the lower lip and the lower lip


Chapter 54: Facial Skeletal Augmentation with Implants

projecting approximately 2 mm beyond the chin (8). The projection of the chin should be interpreted in the context of the surrounding facial features, including the projection of the nose, the relationship to the lips, and the depth of the labiomental sulcus.

Implant Design Early implant designs augmented the mentum only and often created a stuck-on appearance as a result of failure of the lateral aspect of the implant to merge with the anterior aspect of the mandibular body. “Extended” chin implants have tapered lateral extensions that enable the chin implant to better merge with more lateral mandibular contours. Myriad designs are available that give great latitude in the desired effect. Flowers (9) and Terino (10) developed extended chin implants that augmented both the central mentum and the mandibular body. This type of implant widened the anterior jaw line, in addition to increasing the projection of the chin. I prefer a two-piece chin implant (11). A two-piece implant allows the inferior border of the implant to follow the inferior border of the mandible. This is usually not possible with a one-piece chin implant.

Submental Incision It is my opinion that ideal results from alloplastic augmentation of the chin are not routinely obtained. Problems result from implants that merge poorly with the mandibular body; implants with posterior surfaces that are inappropriate for the tilt of the anterior surface of the chin; asymmetric implant placement; implant migration; and morbidity from surgical exposure. To avoid these problems, I choose to position two-piece extended implants through submental incisions to assure ideal implant placement and to minimize soft-tissue morbidity. The incision is carried onto the mentum and a subperiosteal pocket is created that avoids disturbing the mentalis muscle origin above and allows easy identification of the inferior alveolar nerves (Fig. 54.2).

Intraoral Incision In patients where a submental scar may be objectionable, an intraoral incision is employed. An approximately 2 cm transverse incision is made 1 cm above the buccal sulcus in the midline. When the mentalis muscles are encountered, these muscles are neither divided nor stripped from the mandible, but are separated in the midline to access the mentum where a subperiosteal pocket is created. Placement of an extended chin implant through a midline intraoral approach alone is difficult. This intraoral exposure may result in division or damage to the mentalis muscles, damage to the mental nerve, and improper positioning of the lateral tails of the implants. To assure implant placement particularly of the lateral extensions, sulcus incisions 1.5 to 2 cm long are made lateral to the mental nerve. The mental foramen usually lies halfway between the top and the bottom of the mandible and directly between the space between the two premolars. Once the implant is positioned, it is immobilized with sutures or screws.

Implant Augmentation versus Sliding Genioplasty Sliding genioplasty involves a horizontal osteotomy of the mandible approximately 4 mm beneath the mental foramen. A now free chin point that can be moved in any direction is positioned as desired, usually anteriorly to increase chin projection. It has two advantages over implant augmentation of the

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chin. First, the chin point can be lowered after osteotomy to increase the vertical height of the chin. Vertical elongation may efface the deep labiomental sulcus affecting some patients. Second, the chin point advancement stretches the attached suprahyoid muscles, thereby decreasing submental fullness and improving submental contour. The major disadvantage intrinsic to sliding genioplasty is the unnatural bony and border contours that accompany the selective movement of the chin point. The contour result is one that has a poor transition, resulting in the stuck-on appearance of the chin—much like a large button chin implant. There are also step-offs at the osteotomy sites along the mandibular body. The notchings or indentations are particularly detrimental to those who have an existing prejowl sulcus. Furthermore, sliding genioplasty requires considerable facility in bone carpentry. Obliquity in a horizontal osteotomy can either lengthen or shorten the vertical height of the chin after advancement.

Ramus and Body Alloplastic augmentation of the mandibular ramus and body can have a dramatic impact on the appearance of the lower third of the face (12). Two patient populations have had their aesthetic concerns satisfied with mandibular augmentation procedures. One group has mandibular dimensions that relate to the upper and middle thirds of the face within the normal range. These patients perceive a wider lower face with a well-defined mandibular border as an enhancement to their appearance. Patients in this treatment group often present with a desire to emulate the appearance of models, actors, and actresses who have a defined, angular lower face. This patient group benefits from implants designed to augment the ramus and posterior body of the mandible, and, in so doing, increase the bigonial distance. The other major group of patients who benefit from augmentation of the mandibular ramus and body are those patients with skeletal mandibular deficiency. Those patients who have their malocclusion treated with orthodontics alone are left with mandibular skeletal deficiencies that may be deforming. The skeletal anatomy associated with mandibular deficiency that can be camouflaged with implants include the obtuse mandibular angle with steep mandibular plane and decreased vertical and transverse ramus dimensions. The addition of an extended chin implant will camouflage the poorly projecting chin.

Operative Technique A generous intraoral mucosal incision is made to expose the ramus and body of the mandible. It is made at least 1 cm above the sulcus on its labial side. The anterior ramus and body of the mandible are freed from their soft tissues. The inferior alveolar nerve is visualized as it exits its foramen to avoid its injury. It is important to free both the inferior and posterior borders of the mandible of soft tissue attachments to allow implant placement. As determined by preoperative assessment, the implant is trimmed with a scalpel prior to its placement on the mandible. To assure the desired placement of the implant and its application to the surface of the mandible, the implant is fixed to the mandible with titanium screws. The incision is closed in two layers with absorbable sutures. Care is taken to evert the mucosal edges.

Implants Used to Camouflage Soft-Tissue Depressions The implants discussed in this chapter are designed to increase the surface projection of the facial skeleton. Certain authors


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have used implants placed on the facial skeleton to disguise overlying soft-tissue volume inadequacy, usually caused by involutional changes brought on by age. These include the submalar, prejowl, and tear trough implants. Augmentation of the skeleton to compensate for a soft-tissue deficiency should be extremely conservative. Skeletal augmentation does not give the same visual effect as the soft-tissue augmentation. Similarly, soft-tissue augmentation beyond 1 or 2 mm provides a different visual effect than skeletal enlargement. For example, a chin point augmented with fat to increase projection by 5 mm reads as a fatty chin pad, not as a more projecting chin.

COMPLICATIONS There is no scientific data to document the complication rate related to facial skeletal augmentation. Prospective studies that control for surgical technique, implant site, patient selection, and follow-up time do not exist. Because all the biomaterials commonly used for facial skeletal augmentation are biocompatible, complications are usually technique related— improper implant size, contour, or placement. Infections are unusual when implants are placed through cutaneous incisions. When infection occurs, the most reliable treatment is implant removal.

CONCLUSION Augmentation of the facial skeleton with alloplastic materials is a powerful way to alter facial appearance. Virtually any area

of the facial skeleton can be augmented. Requisites for success include implants of appropriate size and shape, adequate soft-tissue cover, and careful subperiosteal dissection during exposure and implant placement.

References 1. Farkas L, Hreczko TA, Kolar JC, et al. Vertical and horizontal proportions of the face in young adult North American Caucasians: revision of neoclassical canons. Plast Reconstr Surg. 1985;75:328. 2. Farkas LG, Kolar JC. Anthropometrics and art in the aesthetics of women’s faces. Clin Plast Surg. 1987;14:599. 3. Chen NT, Glowacki J, Bucky LP, et al. The role of revascularization and resorption on endurance of craniofacial onlay bone grafts in the rabbit. Plast Reconstr Surg. 1994;93:714. 4. Rubin JP, Yaremchuk MJ. Complications and toxicities of implantable biomaterials used in facial reconstructive and aesthetic surgery: a comprehensive review of the literature. Plast Reconstr Surg. 1997;100: 1346. 5. Whitaker LA. Aesthetic augmentation of the malar midface structures. Plast Reconstr Surg. 1987;80:337. 6. Yaremchuk MJ, Israeli D. Paranasal implants for correction of midface concavity. Plast Reconstr Surg. 1998;102:51. 7. Yaremchuk MJ. Infraorbital rim augmentation. Plast Reconstr Surg. 2001; 107:1585. 8. McCarthy JG, Ruff JG. The chin. Clin Plast Surg. 1988;15:125. 9. Flowers RS. Alloplastic augmentation of the anterior mandible. Clin Plast Surg. 1991;18:137. 10. Terino EO. Facial contouring with alloplastic implants. Facial Plast Surg Clin North Am. 1999;7:55. 11. Yaremchuk MJ. Improving aesthetic outcomes after alloplastic chin augmentation. Plast Reconstr Surg. 2003;112:1422. 12. Yaremchuk MJ. Mandibular augmentation. Plast Reconstr Surg. 2000; 106:697.


CHAPTER 55 ■ OSSEOUS GENIOPLASTY HARVEY M. ROSEN

Osseous genioplasty is an autogenous method for changing the size, or shape, or both of the mandibular symphysis. Although by strict definition it may involve merely recontouring the chin by burring away bone or by adding bone graft material, the term generally refers to an osteotomy of the anterior mandible in the horizontal (transverse) direction below the mental foramina (Fig. 55.1A). The osteotomy was first described in 1942 by Hofer (1). The procedure remained rather obscure until 1964 when it was popularized by Converse and Wood-Smith (2). It is now the second most commonly performed osteotomy of the facial skeleton for both reconstructive and aesthetic reasons (second only to rhinoplasty). Osseous genioplasty is frequently performed for two reasons: (a) versatility; chin can be moved in any direction— sagittally, vertically, or transversely (Fig. 55.1B-D); and (b) a receding chin or small mandible, or both, are common problems among white North Americans, occurring in approximately 5% of the population (2). When these factors are coupled with the emphasis that Western culture places on aesthetics and the belief that a well-defined jaw line characterizes an aggressive, self-confident individual, it is little wonder that this operation has grown in popularity. The ready availability of alloplastic material such as silastic, however, has prevented osseous genioplasty from becoming an operation that large numbers of plastic surgeons currently employ.

ALLOPLASTIC VERSUS AUTOGENOUS The choice between alloplastic augmentation (chin implants) and osseous genioplasty for correction of the weak chin remains hotly debated among plastic surgeons. The proponents of alloplastic augmentation cite the technical ease, the relatively low risk of complications, and the ability to perform the procedure under a local anesthetic. Those who favor osseous genioplasty point out the extreme versatility of an osteotomy in correcting three-dimensional deformity. In an effort to select the correct procedure, one should simply ask which procedure will provide the best correction for the particular patient. Certain factors are indisputable: (1) Chin implants can adequately correct mild to moderate volume deficiencies of the mandible at the level of the pogonion in the sagittal dimension (2). Chin implants cannot correct vertical excess of the anterior mandible (3). Chin implants are unreliable in correcting asymmetries of the anterior mandible in any plane of space (4). Although chin implants can modestly increase the vertical dimension of the anterior mandible by covering its inferior border, this has significant potential for complications as the soft tissue in this area is relatively thin (5). Provided that chin implants are positioned directly over the symphysis, as they should be, and not over the dental alveolus, the labiomental fold will increase in depth following chin implant placement.

Given these factors, the only appropriate candidates for chin implantation are those with a mild to moderate sagittal deficiency of the chin accompanied by a shallow labiomental fold. All other patients who request surgical alteration of the chin should be considered for osseous genioplasty. One of the least mentioned, yet compelling, reasons to choose osseous genioplasty instead of alloplastic chin augmentation occurs when surgical revision is indicated. Osseous genioplasty is more amenable to revision because the soft-tissue chin has not been degloved and there is no scar capsule (as occurs in smooth implants) with which to contend. As a result, soft-tissue displacement closely follows skeletal displacement. Conversely, the soft-tissue response to removing a smooth implant, or to reducing its size, or to changing its position is unpredictable because the soft tissues have been degloved from the bone. In addition, the dead space created by the implant capsule, which does not fully collapse, fills with blood, creating more scar. Surgical excision of the capsule may cause mentalis muscle disfunction with subsequent lower lip ptosis. Accordingly, the aesthetic consequences of removing or changing smooth chin implants are frequently undesirable. Although a scar capsule may not form with porous implants, these implants can be very difficult to remove because of the soft-tissue ingrowth.

TREATMENT-PLANNING CONSIDERATIONS Preoperative evaluation of the osseous genioplasty patient includes a history and physical examination. The surgeon should ascertain the patient’s specific aesthetic complaints and objectives as they relate to the lower face, including any concerns about the height, the projection, and the symmetry in this area. Specific inquiries should be made into any history of orthodontic therapy, because such therapy may have been used to disguise an underlying class II malocclusion caused by a small mandible. Physical examination should note the following five items: 1. The sagittal position of the pogonion relative to the lower lip and the remainder of the mid and upper face. The lower lip, not the mid or upper facial structures, determines the extent to which the chin should be brought forward (6). Consequently, the chin should not be brought forward any further than a vertical line dropped from the lower lip. When advancing the chin, the ratio of soft tissue to skeletal displacement is generally 1:1. If the lower lip is recessive, as it may be in many individuals with small mandibles who are seeking chin enlargement, one must be willing to accept a residual degree of sagittal weakness of the lower face relative to the mid and upper face. This is aesthetically preferable to a chin that is advanced beyond the lower lip, which invariably results in a bizarre, artificial appearance. Undercorrection


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A B

D

C FIGURE 55.1. A: Standard location and orientation of the advancement osseous genioplasty. Note that the osteotomy is placed well below the mental foramina to avoid injury to the inferior alveolar nerve. The osteotomy extends well posterior to the vicinity of the molar teeth. The angulation of this osteotomy allows forward advancement of the chin without any vertical changes. B: Simultaneous advancement and vertical reduction of the chin. Note that two parallel osteotomies are performed with an intervening ostectomy. C: Simultaneous advancement and vertical elongation of the chin. The interpositional material typically employed are blocks of porous hydroxyapatite. D: Lateral shifting of the symphyseal segment to restore lower-face symmetry.

in the sagittal dimension is always preferable to overcorrection. 2. A qualitative assessment of the height of the lower face as it relates to the midface. In a patient with vertical excess of the lower face, one has the option to reduce the vertical height of the chin. This can be accomplished by two parallel osteotomies with an intervening ostectomy or a steeply oblique bone cut that allows the chin to be advanced and superiorly repositioned. 3. The symmetry of the lower face. Osseous genioplasty presents the surgeon with the perfect opportunity to laterally shift the symphyseal segment either to the right or the left to achieve a symmetric lower face. Similarly, the chin can be vertically elongated or shortened in an asymmetric fashion to correct vertical asymmetry. 4. The depth of the labiomental fold. Sagittal advancement or vertical shortening, or both, of the symphyseal segment results in deepening of the labiomental fold (5). Conversely, vertical lengthening of the chin tends to efface or soften the fold. Accordingly, individuals with a normal or exceedingly deep fold who undergo advancement of the chin also should be evaluated for vertical elongation. This should be considered in a person with

a short lower face and in a patient with normal height of the lower face, but never in a patient with excessive height in the lower face. The individual who has a combination of a long lower face and a deep labiomental fold is never a candidate for chin surgery, and such a patient should be offered a more extensive orthognathic correction (5). 5. Examination of the occlusion. The majority of individuals who request aesthetic enlargement of the chin have class II skeletal deformities secondary to a small mandible (5). This is a tip-off that coexisting problems such as abnormalities of lower face height and labiomental fold depth may be present in addition to a “weak” chin. It is important to remember that prior orthodontic treatment can convert a class II malocclusion into a class I occlusion but this does not correct the underlying skeletal problems. Although the extent of soft-tissue movement closely follows that of skeletal displacement when advancing, shortening, or lengthening the chin, soft-tissue response to posteriorly repositioning of the chin is, at best, 0.5 to 1. Surgical efforts to correct


Chapter 55: Osseous Genioplasty

an excessively prominent chin are not as predictable as those performed to correct a small chin. Radiographic evaluation of the chin should include a Panorex radiograph if periapical pathology of the anterior mandibular teeth is suspected. Any preexisting dental pathology in this area is an absolute contraindication to chin surgery. In addition, one may want to evaluate the vertical dimension between the apices of the incisor roots and the inferior border of the mandible when correcting a short chin. It is important that enough room exists both to perform the osteotomy and to apply fixation devices without risk to the roots of these teeth.

SURGICAL TECHNIQUE Although reports exist describing osseous genioplasty under local anesthesia with intravenous sedation (7), it is best under-

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taken under general anesthesia with orotracheal or nasotracheal intubation and full protection of the airway. Hemostasis is facilitated by infiltration with a dilute epinephrine solution. The soft-tissue incision is placed at least 1 cm away from the depth of the mandibular buccal sulcus onto the lower lip and is 2 to 3 cm in length. The mucosa and submucosa are incised, bringing the mentalis muscle and its median raphe into view. Once these muscles are very superficially incised, the angle of the soft-tissue incision changes so that it is parallel to the mucosa of the lip. This direction is maintained until the anterior mandibular surface is reached, leaving a large amount of mentalis muscle attached to the mandible for later muscle reapproximation. A subperiosteal dissection of the symphysis is performed. The dissection is continued inferiorly only far enough to allow exposure for performing the osteotomy and for applying fixation devises. Complete degloving of the symphysis is not recommended because of the unpredictable

A

B

C

D FIGURE 55.2. A 35-year-old woman with a small mandible and increased lower face height. A,B: There is lip strain, with superior dislocation of the soft-tissue chin pad and a shallow labiomental fold. Surgical correction will effect an 8-mm advancement of the chin and a 5-mm reduction in its height. Simultaneous rhinoplasty will be performed. C,D: Postoperatively, the lip strain has been eliminated and the labiomental fold has been deepened. Note that the chin has been advanced no further that the most anterior position of the lower lip. (From Rosen HM. Aesthetic refinements in genioplasty: the role of the labiomental fold. Plast Reconstr Surg. 1991;88:760, with permission.)


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reattachment of the soft tissues to the bone and the potential risk for development of soft-tissue ptosis, that is, a witch’s chin (8). Exposure is continued laterally so that both mental nerves are identified. Posterior dissection is carried to the inferior border of the mandible directly below the molar roots. Once the soft-tissue dissection is completed, a fissure burr scores a vertical mark in the midline chin, allowing it to be appropriately positioned in the transverse dimension. The reciprocating saw is used to perform the horizontal osteotomy at least 4 mm below the mental foramina to protect the inferior alveolar nerves. As previously mentioned, the osteotomy is carried as far posteriorly as possible to allow for a generous volume of skeletal displacement. This provides for naturallooking results and avoids waist lining and excessive visibility of the inevitable step in the inferior border of the mandible.

Cortical cuts should be completed with the reciprocating saw, avoiding unnecessary prying downward of the symphyseal segment, which may cause fracturing. Following mobilization of the symphysis, it might be necessary to detach the anterior belly of the digastric muscles from the lingual surface if extensive anterior dislocation is anticipated. After full mobilization is achieved, fixation devices are applied to hold the chin segment in the desired location. Although plate and screws are popular, it is perfectly acceptable to use wire fixation. If vertical shortening of the chin is desired, it is usually accomplished by performing two parallel horizontal osteotomies and removing the intervening segment of bone. If vertical elongation is desired, it is most often done by interposing blocks of hydroxyapatite into the osteotomy gaps created by inferior repositioning of the symphysis.

A

B

C

D FIGURE 55.3. A 28-year-old man complaining of a small chin. Physical examination demonstrated a class II malocclusion with deficient sagittal projection of the chin as well as decreased height of the lower face. A,B: In addition, there is a deepened labiomental fold. Surgical planning included a 6-mm advancement and 6-mm elongation of the chin. C,D: The postoperative views demonstrate an increase in the height of the lower face and an apparent decrease in the depth of the labiomental fold. Again, the chin was advanced no further than the most anterior position of the lower lip. (From Rosen HM. Aesthetic refinements in genioplasty: the role of the labiomental fold. Plast Reconstr Surg. 1991;88:760, with permission.)


Chapter 55: Osseous Genioplasty

Following fixation, the wound is copiously irrigated with diluted povidone-iodine (Betadine) solution and closed in layers. The mentalis muscle is repaired using interrupted sutures to help avoid soft-tissue ptosis and subsequent development of a witch’s chin (8). The mucosa is repaired using interrupted 3-0 chromic sutures. By placing the incision well out onto the lower lip, there is sufficient soft tissue to close without tearing the tissues. This helps to minimize subsequent wound contamination and possible infection. No dressings are applied.

PATIENT EXAMPLES The following patient examples illustrate the versatility of the osseous genioplasty.

Patient 1 The patient (Fig. 55.2) is a 35-year-old women with a small mandible, increased lower face height, and a modest component of lip strain. As a result, the soft-tissue chin pad is superiorly dislocated, causing effacement and shallowness of the labiomental fold. Surgical correction involves advancement and vertical shortening of the chin. The segment was advanced 8 mm and shortened 5 mm. A rhinoplasty was also performed. Note that as the chin is advanced the labiomental fold deepens with improved definition. The lip strain has been eliminated. The chin has been advanced no further than the lower lip.

Patient 2 This 28-year-old man (Fig. 55.3) complained of having a small chin. Physical examination demonstrated that he had a small mandible and a class II, deep bite malocclusion. In addition to a lack of projection of the chin, there was decreased height of the lower face relative to the midface and an exaggerated, deepened labiomental fold. Surgical planning involved a 6-mm advancement and 6-mm lengthening of the chin. In the postoperative views, note the softening of the labiomental fold and apparent decrease in its depth. Note again that the chin is advanced no further than the most anterior position of the lower lip.

COMPLICATIONS In a recent report of a large series of patients undergoing osseous genioplasty by three experienced craniomaxillofacial surgeons, the complication rate was low (3). Lower-lip paresthesia

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occurred in 5.5% of the patients. Soft-tissue infection was reported in 3% of patients. Although not reported as a complication, the most frequent problem associated with osseous genioplasty is the undesirable aesthetic result. Such an outcome is caused by errors in both treatment planning and technique. The most commonly committed error in treatment planning is overadvancement of the symphyseal segment, resulting in an unnatural, bizarre appearance, with the chin well in advance of the lower lip. It bears repeating that the osseous genioplasty is a powerful tool and that modest advancement of the chin goes a long way. When in doubt about the extent of advancement, one should err on the side of conservatism and undercorrect in the sagittal dimension. The most commonly encountered aesthetic problem relative to surgical technique is failure to extend the osteotomy cut far enough posteriorly. This can result in an hourglass deformity with excessive tapering of the mandible in the area immediately posterior to the osteotomy. This can be largely avoided if the osteotomy cut is extended back to the molar teeth, as it is placed in an area where abundant soft tissue is present to mask any notching of the inferior mandibular border.

CONCLUSION The osseous genioplasty represents the most versatile procedure that the plastic surgeon has available to enhance the balance and proportion of the lower face. It is a powerful tool that can yield dramatic results if the surgeon performing the procedure knows that it cannot change the sagittal position of the lower lip. It behooves plastic surgeons to become familiar and comfortable with the procedure so that the alternative— alloplastic chin augmentation—will not be used in patients who would benefit more from a skeletal correction.

References 1. Greenberg ST, Pan FS, Bartlett SP, et al. Complications of osseous genioplasty. Proc Northeastern Soc Plastic Surg 1985;92. 2. Converse JM, Wood-Smith D. Horizontal osteotomy of the mandible. Plast Reconstr Surg. 1964;34:464. 3. Hofer D. Die osteoplastiche verlaegerund des unterkiefers nach von Eiselberg bie mikrogenie. Dtsch Zahn Mund Kieferheilkd. 1957;27:81. 4. Bell WH, Proffit WR, White P, eds. Surgical Correction of Dentofacial Deformities. Philadelphia: WB Saunders; 1980:685. 5. Rosen HM. Aesthetic refinements in genioplasty: the role of the labiomental fold. Plast Reconstr Surg. 1991;88:760. 6. Rosen HM. Aesthetic guidelines in genioplasty: the role of facial disproportion. Plast Reconstr Surg. 1995;95:463. 7. Spear SL, Mausner ME, Kawamoto HK. Sliding genioplasty as a local aesthetic outpatient procedure: a prospective two center trial. Plast Reconstr Surg. 1987;80:55. 8. Zide BM, McCarthy JG. The mentalis muscle: an associated component of chin and lower lip position. Plast Reconstr Surg. 1989;83:413.


CHAPTER 56 ■ HAIR TRANSPLANTATION MICHAEL L. REED

State-of-the-art surgical hair replacement using whole donordominant hair follicles from areas of nonbalding scalp to replace lost hair on the crown probably reached its zenith in 2004. Further refinements in ergonomics are likely, but better results await research breakthroughs in tissue-engineering technology using follicular stem cells (1). Modern-day hair transplantation began in the United States in 1959, although micrografting of human scalp hair had been reported in the Japanese medical literature in 1939, and autografting of hair had been done in Germany in the 19th century. Improvements in surgical techniques and instrumentation occurred sporadically until 1993 when surgeons formed The International Society for Hair Restoration Surgery (ISHRS) to share knowledge and advance the field. Much smaller grafts in much greater numbers placed very close together resulted in much more natural-looking transplants. As early as 1984, basic histologic studies of horizontal sections of scalp had revealed that human scalp hairs grow naturally in small compartments (follicular units) containing clusters of one to four follicles surrounded by concentric layers of collagen fibers (Fig. 56.1) (3). Peripheral areas such as the hairline have one and two-hair follicular units (FU), whereas the more dense central regions have more three and four-hair FU (and coarser hair shafts). Toward the end of the 1990s, transplant surgeons realized the significance of the follicular unit as it applied to hair replacement, which has given birth to the follicular unit transplant (FUT) era. The older terms of “micrograft” (one to two hairs) and “minigraft” (three to six hairs) have been replaced by single FU (one to two or three to four hair) and multi FU (two to three unit/two to six hair) grafts. However, some surgeons still use the older terminology and restrict the use of the term follicular unit to the procedure known as the single-FU-only transplant (SFUT). More efficient donor-harvesting methods and better quantitative distribution of hair in the recipient site with adjunctive medical treatment has greatly reduced the use of (and need for) other types of surgery in the treatment of baldness. For these reasons this chapter is restricted to hair transplantation. The reader is referred elsewhere for a discussion of procedures such as alopecia reduction (4).

INITIAL CONSULTATION/SCREENING SESSION The first step in the consultation is to determine whether or not the donor site is adequate to accomplish the patient’s transplant goals. Next, is to give the patient a detailed explanation of the procedure that is optimal based on the patient’s hair and scalp tissue characteristics. Realistic short- and long-term

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goals should be carefully outlined. Because the balding process is progressive and the final results unpredictable, there is always some degree of calculated risk. Over time, the transplanted hair may have to “stand alone.” This end point transplant pattern should be reasonably natural-looking and resemble some variation of either male- or female-pattern hair loss. Patients who appear to be good candidates for surgery based on the findings of the initial exam and discussion of achievable goals must determine for themselves when they are ready and must never be pressured to undergo a procedure. Patients usually like to see before-and-after photos of the results they might expect in one or several sessions. Ideally, they like to speak to, or even meet with, someone like themselves who has had a transplant. However, it must be emphasized that the exact outcome cannot be predicted and patient satisfaction cannot be guaranteed. Despite these caveats, the reality is that the overwhelming majority of patients are pleased with the results of transplantation procedures.

THE PREOPERATIVE PERIOD Prior to the procedure, further communication is essential to optimize the outcome. There should be a specially trained staff member—a “patient care coordinator”—who works closely with the surgeon and is readily available to answer patient questions and address special problems and needs. Many patients experience anxieties, especially with regard to postoperation down time. Patients also receive gratuitous misinformation and misguided counsel from friends and relatives, as well as from other physicians. The coordinator is trained to deal with such problems and assure compliance with preoperation instructions. Patients should be instructed to discontinue medications and diet supplements that can cause bleeding problems such as aspirin, anticoagulants, ibuprofen-type antiinflammatories, vitamin E, garlic pills, fish oil capsules, and herbal supplements, starting 2 weeks prior to surgery. Topical minoxidil (a vasodilator) should be stopped 3 days prior to surgery, and alcohol and caffeine should be minimized 1 day before surgery. Cigarette smoking should be stopped or at least minimized. A written informed consent needs to be read, discussed, and signed, and written pre-/postoperation instruction sheets provided to every patient. Finally, a photo consent is obtained. A planning session with the surgeon is conducted 1 to 2 weeks before the procedure to determine or review and confirm the final surgical plan. The entire procedure, from the time the patient arrives until the patient leaves after the procedure, should be reviewed in detail. In addition, patient plans for activity during the 2 week postoperation period should be discussed. A diagram of the pattern and distribution of grafts, including location and shape of a new hairline, can be given to certain patients. Prescriptions for perioperative medications typically include an oral antibiotic (cefadroxil most commonly)


Chapter 56: Hair Transplantation

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B

A FIGURE 56.1. Follicular units. A: Video microscopic view of single follicular units showing one- to fourhair units. B: Photomicrograph of horizontal section of human scalp showing follicular units with light microscopy.

for 5 to 7 days starting the day of or the day before surgery, a painkiller such as acetaminophen with or without a narcotic analgesic (codeine or hydrocodone) and a 5-day prednisone taper (e.g., a taper protocol of 50 to 40 to 30 to 20 to 10 mg) to reduce postoperation swelling. Because clinical studies have not established a single regimen, there is great variability among medication protocols. Many surgeons do not routinely use prophylactic antibiotics because they believe the risk of an adverse reaction to the drugs is greater than the risk of infection.

THE OPERATION Preanesthesia, Anesthesia, and Photography This is an office-based outpatient procedure that most commonly employs levels I and II sedation. Ativan 2 mg p.o. or Valium 10 mg p.o. are the most commonly used premedications. Some anesthetists also use nitrous oxide, whereas others use intramuscular (or, less often, intravenous) Versed with or without an analgesic such as Demerol or fentanyl. The donor site is shaved to leave 2 to 3 mm of hair shaft for directionality purposes during implantation. The perimeters of the excision site are outlined with a marking pen followed by a BetadinePovidine preparation. Local anesthesia of the donor site is produced initially with plain buffered 1% Xylocaine followed by longer acting 0.25% to 0.5% Marcaine with epinephrine (1:100,000). Normal saline is used to tumesce the donor site to prevent tissue deformation during the excision and to create a fluid-filled space between the hair follicles located in the subcutaneous fat and the underlying galea aponeurotica to minimize blood vessel and nerve transection during excision. An alternative is to use tumescent anesthesia (0.1% Xylocaine with 1:1,000,000 epinephrine). The discomfort associated with local anesthetic injections can be significantly diminished by the use of a mechanical vibrator placed just inferior to the injection site. The recipient site is anesthetized using a local ring block with 1% Xylocaine with 1:100,000 epinephrine followed by infiltration of the recipient site with normal saline with 1:100,000 to 1:150,000 epinephrine. Regional nerve blocks of the supraorbital and supratrochlear nerves in their respective foramina located above the eyebrow can also reduce discomfort at the recipient site. Preoperation photos demonstrating

the intended recipient area(s) from several different views are taken prior to starting the procedure.

THE DONOR SITE The ideal donor site is the region containing hair follicles that are not subject to the gradual miniaturization process that causes baldness (invisible hair). The perimeters of this area are variable, but it is generally described as having an anterior border starting at a line that extends perpendicular to the external auditory canal. The inferior border is typically 4 cm above the hairline at the nape of the neck. The superior border varies according to the final location of the posterior border of the balding zone. This border has been described as typically being 7 cm above the inferior border at the occipital midline, increasing to 8 cm toward the midlateral occiput and narrowing to 5 cm above the ears. Hair density is greatest at the midline and diminishes laterally above the ears and again below the inferior border approaching the nape of the neck. The size of the donor site along with the hair density (hair/cm2 ) and diameter (microns) are the key factors in deciding whether or not the patient is a good candidate, as well as what kind of results should be anticipated. Most experienced surgeons can inspect the donor site and integrate these variables to make a determination. However, it is desirable to have the ability to perform a more quantitative evaluation using a device such as the Russman densitometer, which has a viewing area of 10 mm2 . Hair density and follicular unit density can be calculated at different locations along the donor site. Because hair density and FU density, as well as hair diameter, vary, it is necessary to measure at several points. The three commonly chosen sites are the midocciput over the protuberance, the supra-auricular point above the external auditory meatus, and a spot halfway between over the mastoid. The numbers can be averaged. If only one measurement is done, the midmastoid tends to be intermediate with higher and lower densities at the midocciput and supra-auricular spots respectively. Table 56.1 shows the predicted available hair for transplantation in the average straight-haired patient, assuming that 50% of hair can be harvested before the donor site becomes noticeably depleted. These calculations are useful as a reference point, but it is important to remember that there is great variation among individuals. Hair diameter is the other major factor in determining the coverage achievable with a transplant. The major goal behind


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TA B L E 5 6 . 1 DONOR DENSITY: THE EFFECT OF CHANGES IN DONOR AREA HAIR DENSITY ON MOVABLE HAIR Donor Density (hairs/mm2 )

Total Hair in Permanent Zone

Hair Must Remain in Permanent Zone

Movable Hair

Change in Density

Change in Movable Hair

1.0 1.3 1.5 1.8 2.0 2.2 2.5 2.7 3.0

12,500 16,250 18,750 22,500 25,000 27,500 31,250 33,750 37,500

12,500 12,500 12,500 12,500 12,500 12,500 12,500 12,500 12,500

0 3750 6250 10,000 12,500 15,000 18,750 21,250 25,000

−50% −35% −25% −10% 0 +10% +25% +35% +50%

−100% −70% −50% −20% 0 +20% +50% +70% +100%

Data from Bernsein R, Russman W. The logic of follicular unit transplantation. Dermatol Clin. 1999;17:277–295, with permission.

the frontal zone, especially in the mid postfrontal region, is to see hair rather than scalp. Besides density (hairs/cm2 ), hair volume plays a critical role. Hair volume (hv) is defined in the following formula: hv = π(r)2 (h) (d) (a) In this equation, r is the radius of the hair shaft, h is the hair length, d is the hair density (hairs/cm2 ), and a is the total area covered (cm2 ). It is key to note that a doubling of the radius results in a quadrupling of hair volume, making hair diameter the most important single variable in the coverage achievable in a transplant. It is also the variable that is most beyond our control, at least in male patients. Other factors that affect the final coverage include hair texture and hair/scalp color contrast. Wavy, curly, helical, and spiral hairs improve coverage. A lesser contrast between hair color and scalp color improves the illusion of density. Gray hair on fair skin looks considerably denser than dark hair. The most common technique to harvest donor hair follicles is the single-blade method in which the surgeon uses a no. 10 (or no. 15) blade to remove a long section of scalp that varies

in width from 0.5 to 1.5 cm, and in length from 10 to 25 cm (Fig. 56.2A). Optimal hemostasis is achieved with the Redfield infrared coagulator. Simple running or interlocking 3-0 or 4-0 nylon sutures placed close together and close to the wound edge in the deep dermis/subcutis, which are left in for 10 to 14 days, will usually heal with a fine scar that is not noticeable (Fig. 56.2B). It may be necessary to undermine the galea and place buried absorbable sutures to reduce excessive tension on the wound edges in patients with very fibrotic scalps or with scar tissue from multiple procedures. In ideal circumstances, it is desirable to excise the scar from a previous procedure in a subsequent procedure. However, an attempt to do so may reduce the amount of new donor follicles in the strip or require such a wide excision that the resulting scar becomes unacceptably noticeable. Multiple narrow (2- to 3-mm) scars may be less noticeable than one 1.5-cm scar. Some operators use staples instead of sutures. These can be placed faster, but are more painful to remove. It is also possible to close the wound with surface and/or buried absorbable sutures (Vicryl, Monocryl, cat gut). This method eliminates a visit for suture removal. However, more tissue reaction from absorption may result in a wider scar.

B

A FIGURE 56.2. Scalp donor site for single-strip technique. A: Donor site after excision of scalp using the single-strip technique showing the underlying galea aponeurotica. B: Donor site after closure with a running 3-0 nylon suture. The suture will be removed after 14 days and the site will heal with a pencil-line surgical scar.



The most common alternative to the single-blade method is the multibladed knife, which can be adjusted to remove one or multiple (two to five) “strips” of donor tissue of variable width (1 to 4 mm). These thin strips are then easily microdissected into grafts. However, the ergonomic advantages of a multibladed knife may be offset by loss of viable follicles as a result of follicular transection that occasionally occur even with the most skilled surgeon. The single-blade method allows much better control of the excision when there are multidirectional hairs and when the excision site has unexpected areas of tissue deformation because of incomplete (or lost) tumescence during the harvesting procedure. The newest technique for harvesting is an attempt to improve on the original Orentreich procedure in which a circular punch was used to remove a small cylinder of hair-bearing donor scalp containing multiple follicular units consisting of 10 to 20 hairs per graft. However, instead of using the 4-mmdiameter punch, the surgeon uses a 1-mm punch and attempts to excise individual follicular units. To minimize transection, the punch incision is down to the deep dermis, but not into the subcutaneous tissue as the follicular stem and bulb are located there and tend to splay out in a manner that puts them in a nonparallel position to the cutting edge of the punch. Instead, the punch is removed and tissue-grasping forceps (with or without a tiny, blunt microdissector) is used to “extract” the individual (one- to four-hair) unit. This method is called follicular unit extraction (FUE) (5). The major benefit of FUE is avoiding the linear scar(s) associated with a strip excision. The major disadvantages are (a) follicular bulb “decapitation” caused either by transection during the initial incision or by traction while attempting to dissect or “pluck out” each follicular unit, and (b) a significant increase in time and effort for both patient and operators resulting in considerably smaller transplants than what is achieved with the conventional excision methods. In addition, because not all patients have scalp tissue that will allow extraction without significant traumatic loss, it is recommended to perform a FUE test to determine who is a potential candidate for this method. This test is basically a miniprocedure in which five to ten 1.0-mm grafts are extracted and scored on a 5-point scale for intact tissue. A score of 1 to 2 indicates a potential candidate. In its initial use, the scores obtained found that approximately 60% of patients qualified. More recently, it has been claimed that up to 90% of patients can qualify, probably as a function of increasing surgical expertise (5). Even though transection at the level of the follicular stem leaving the follicular “bulge” region intact may allow survival rates of up to 50%, the new follicles do not achieve their full pretranssection diameters. Nevertheless, FUE with improvements in methodology should be useful in the subset of patients whose donor sites are inadequate for strip excision and in the patient who wishes to avoid potentially visible donor scars if he has to undergo multiple procedures or decides to shave his head.

The Microdissection Procedure (Graft Production) The harvested donor strip obtained using the single-blade excision method is cut into tiny slices that vary from 1 to 3 mm in width, which translates into one to three FU in a typical white/Asian scalp with an average follicular unit density of one FU/mm2 (Fig. 56.3). A typical strip is 1× 20-cm (20 cm2 ) and contains 2,000 units. There are an average of two to three hairs per FU. A dissecting microscope and/or magnification loupes (4×) with backlighting is used for close-up visualization. Single- and double-edge razor blades or no. 11/no. 15

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FIGURE 56.3. A “sliver” produced by sectioning of the donor strip obtained with the single-blade technique showing how the follicular bulbs extend into the subcutaneous fat.

Teflon-coated scalpel blades are employed to cut these sections into grafts. In strictly single follicular unit procedures, it is considered ideal to use a dissecting scope exclusively for best visualization so that the technician can attempt to actually cut around (and then cut out) individual units, a process called slivering. This technique is in contrast to simple straight-cut sectioning, which might have a greater probability of breaking up some follicular units. Depending on the area being transplanted and the color/texture/density of the donor hair, the technician may cut single-only, single and multiple (two to three FU), or multipleonly grafts. There may be an occasional individual with mostly large (three- to four-hair) units and very coarse dark hair who needs a new frontal hairline where an exception must be made to the dictum to avoid breaking up follicular units. Even a single-hair graft may appear unnatural in a frontal line if it is very coarse. For such cases it has been proposed to not only break up large units, but to intentionally injure (transect) follicular bulbs based on the belief that the 30% to 50% of hairs that survive such injury will have a finer texture and thus more natural appearance along the frontal line. The grafts are kept in gauze-lined, chilled, normal saline-filled petri dishes to prevent rapid dehydration (the primary cause of nonviable grafts). The grafts are separated into 10 to 50 graft clusters according to size (one to two hairs, three to four hairs, etc.). If a multibladed knife has been used, it is possible to perform graft preparation using a device called the Mangubat graft cutter. This is a rectangular-shaped, stainless steel base containing a series of parallel, closely spaced (1- to 2-mm) blades. The strip is stretched and placed over these blades so that the hair follicles are parallel to the cutting edges. Next, a wooden tongue blade (“force spreader”) is laid on top of the strip and a rubber mallet is employed to strike (“impulsive force”) the wood surface with several rapid strokes. The entire strip is cut into grafts instantly. This saves a great deal of time for microdissection, but carries an increased risk of splitting follicular units and transecting follicles.

THE RECIPIENT SITE The area to be transplanted, having been anesthetized and prepped with Betadine-Povidine solution that has dried, is carefully marked with a marking pen according to the preoperation plan. The best long-term results are obtained by transplanting from front to back rather than back to front. The frontal line should be as high as the patient finds acceptable.


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B

A

Transplanting the vertex area may eventually result in a “halo head” pattern if the donor site is depleted and hair continues to thin out around the posterior and lateral borders (Fig. 56.4A). A low frontal hairline may over time turn into a “monk’s head” look if the patient has only one procedure or runs out of donor hair prematurely (Fig. 56.4B). It is always best to perform each transplant as if it will be the last one. Ideally, the transplanted hair should be able to stand alone and resemble a variation of naturally occurring male- or female-pattern hair loss. A new hairline will typically have a midline low point 7 to 8 cm above the midglabella in male patients, and 6 to 7 cm above the midglabella in females, although there is a wide range of acceptable hairline shapes and locations. It is better to err on the side of a higher line as it is much easier to move the line forward in the future than to move it backward. The so-called hairline is really a transition zone approximately 0.5 to 1 cm at the midline and 1 to 2 cm in the temporal triangle. Depending on the side to side distance, it takes 200 to 500 single/double hair grafts placed 0.75 to 1.0 mm apart to get an acceptable result. A best result may take two or three sessions, especially in patients with straight, coarse, dark hair and fair skin. Transplanting behind the frontal line is a quantitative challenge because it is theoretically an attempt (at least in the longterm) to use a portion of the estimated 30% of the permanent hairs that reside in the nonbalding areas of the occipitoparietal region to replace the estimated 70% of hairs on the top of the head that are destined to be lost over time. The highest density requirement is in the central postfrontal region. The midscalp and vertex are intermediate in density needs. If the patient has a particular hair style, it can help the plan for density distribution. For example, if the patient combs left to right, it is desirable to place larger grafts closer together on the left side. The donor site density varies from 50 to 350 hairs/cm2 . In most patients 1 cm2 of donor scalp can provide adequate hair for 2 to 4 cm2 of recipient site. A clear plastic baggie can be laid over the marked recipient site and the area outlined with a marking pen. The baggie is then laid on a paper with a large grid marked in 1-cm squares, and the squares inside the perimeter are marked and counted. This gives the total cm2 that need to be covered. In a typical procedure, a frontal/midscalp transplant region of 60 cm2 can be transplanted adequately using a 1×20-cm (20 cm2 ) strip of donor scalp. If the donor site contains an average of 2.3 hairs/FU (range: 1 to 4 hairs/FU) and a total of 2,000 FU (1 FU/mm2 ) it will give the patient 4,600 hairs in 60 cm2 , or an average density of 77 hairs/cm2 (4,600/60).

FIGURE 56.4. A: “Halo head” hair pattern produced by transplanting the vertex area followed by loss of hair in the peripheral regions. B: “Monk’s head” hairline produced by placing the hairline too low in the forehead.

Incisional instruments used to make the recipient site openings include a wide array of needles, miniblades, and micropunches (Fig. 56.5). For one to two hair grafts, the most commonly used instruments are probably an 18-gauge hypodermic needle for coarse hairs and a 19-gauge hypodermic needle for finer hairs. Spearpoint sp90 (1.5 mm) and sp91 (2.0 mm) miniblades are also popular for single- or double-follicular unit grafts, respectively. Nokor needles (16/18 gauge) and 1.5-mm tribevel (Rossati Starr) punches can be used for large (three- to four-hair) single-unit and small (three- to five-hair) double-unit grafts. For larger (two- to three-unit/four- to seven-hair) grafts, 2-mm tribevel (Rossati Starr) punches work very well. Excisional devices, such as round and elliptical/slot (Redfield and Butterfield) punches, are less commonly employed than are incisional devices because they cause more tissue injury and, consequently, more scarring (Fig. 56.5). Also, the grafts must be “cut to fit” the site, which may necessitate breaking up follicular units, causing increased follicular transection. If the grafts are of smaller diameter than the site, there will be a gap between the sides of the graft and the walls of the recipient well. Healing will then occur by secondary intention, which may reduce graft survival. It may also result in “pitting” or even epidermoid cyst formation if the graft “sinks” below the surface and gets “buried alive.” However, it may be necessary to employ these instruments in very fibrotic/inelastic scalps, where it is necessary to remove some tissue in order to place grafts with more than one to two hairs. Elliptical punches have largely replaced circular ones because of superior graft fitting that gives a more natural-looking result. Recipient site incisions are made 0.5 to 2.0 mm apart, depending on the size and location of the grafts. They are put as close as possible along the frontal line and in the central postfrontal areas (so-called dense packing). Most procedures are done with incisional rather than excisional devices to reduce scarring and to avoid having to cut the donor tissue to fit the excision sites (Fig. 56.6). The donor tissue characteristics (density, texture, and color) should determine the type of grafts that are used. Recipient site openings should comfortably accommodate what is inserted with a “snug fit.” This is not a problem for the popular SFUT. However, in patients with lower-density donor sites and finer hair texture with minimal hair/skin color contrast (e.g., women and gray-haired older men), larger grafts may be needed to achieve optimal density with fewer sessions. In such cases, the 1.5- and 2.0-mm tribevel punches are ideal. A small triangular opening that can



567

FIGURE 56.5. Excisional and incisional instruments. Left: A Redfield excisional slot punch. Right: One-mm and 1.5-mm tribevel incisional punches.

be oriented for hair directionality and that is expandable in all directions (360 degrees) is created. The site is able to accommodate variable-sized grafts with the same snug fit up to a maximum diameter of either 1.5 mm or 2.0 mm (Fig. 56.7). Wounds heal by primary intention; if for some reason no graft is placed in the incision site, there is no significant scar tissue generated.

Laser-generated (carbon dioxide or Erbium:YAG) recipient sites enjoyed some popularity during the 1990s, but have declined in use because of problems with delayed wound healing, reduced graft survival, and lateral damage to existing hair follicles in thin-haired (or previously transplanted) recipient sites (6). The only advantage they enjoy over a skilled surgeon using cold-steel devices is that patients are easily

A

B

C

FIGURE 56.6. A: Preoperative view of patient with frontal resection and thin frontal forelock region. B: Intraoperative view showing a series of microincisions. The first two rows were made with 132 incisions using a 1.0-mm tribevel punch; the third to fifth rows were made with 300 incisions using an 18-gauge needle; in the postfrontal region, 263 incisions were made using a 1.5-mm tribevel punch. Single units were placed in the 1.0-mm tribevel punch and the 18-gauge needle incisions, with one to two hairs per graft; two FU grafts containing four to six hairs were placed in the 1.5-mm tribevel punch incisions. C: The patient 7 months postoperation showing the advanced frontal hairline and increased density in the postfrontal area.


568


B

A FIGURE 56.7. A: Patient preoperatively showing extensive frontal hair loss. B: Same patient 7 months postoperation, with 700 two follicular units (four to seven hair grafts, dense packed, in the postfrontal region).

impressed by the high-tech perception associated with laser procedures. The two most common methods for graft placement are (a) simultaneous cut and place and (b) separated cut and place. In the former method, the surgeon makes the incision and an assistant using special, fine-tipped jeweler’s forceps slides the graft into the site either while the instrument is still in the site, using it as a guide, or immediately after removal of the device. In the latter method, all (or most) of the incisions are made before graft placement begins. Both methods achieve the same end result, although each has advantages and disadvantages (7).

THE POSTOPERATIVE PERIOD Postoperation Dressings The traditional dressing is a bilayered protective and absorptive affair with the first layer made from several nonstick Telfa pads covered with a thin layer of an antibiotic such as mupirocin (Bactroban/Centany) cream or ointment. Micropore tape attaches this underdressing to the patient’s forehead. A turbanstyle overdressing made from a Kerlix bandage wrapped over several layers of 4×4-inch gauze pads is constructed and finished off with elastic retainer netting (Surgilast no. gl-705). Some patients greatly prefer a more minimal dressing, or no dressing at all. This is feasible if the patient is able to wait 2 to 3 hours in the office after the surgery before going home. However, the need to prevent graft dislodgement and bleeding must be weighed against the needs of a self-consciousness patient.

Postoperation Sequelae There are a number of expected events that are a normal, albeit unpleasant, part of the transplant experience, such as discomfort/pain lasting several days to a week (primarily at the donor site); forehead/periorbital swelling beginning 2 days after the operation and lasting 3 to 4 days; redness/scab formation (recipient site) that lasts 7 to 14 days; variable degrees of telogen effluvium (shock loss) of native hair (recipient and donor sites) that begins to regrow in 8 to 12 weeks; numbness/paresthesias of the donor region that persists for several months, but (rarely)

may take up to a year to resolve. Very rarely some loss of sensation may persist indefinitely. The transplanted hairs go into a telogen (resting) phase for 2 to 4 months and then begin to regrow. Noticeable regrowth is present by 4 months, but the final results may take as long as a year to be fully manifest. The patient, already selfconscious about hair loss, may look worse for up to 4 months. Women have more difficulty getting through this time period, and in addition to using a variety of cosmetic coverups and styling tricks, may need to use a hair prosthesis (wig/weft) for a time. There will be a linear scar at the site of the donor tissue excision that varies from a fine (1- to 2-mm) pencil line to pencil eraser (4- to 5-mm) width. With multiple procedures, scarring may eventually become visible and problematic, requiring scar revision, transplantation, or camouflage tattooing.

Postoperation Complications The most common complication is the occurrence of variable numbers of inflammatory and noninflammatory lesions (pustules, papules, nodules, and cysts) caused by transplanted tissue becoming trapped beneath the surface in the recipient region. These lesions are usually ingrown hairs or epidermoid cysts formed by buried grafts. They appear 8 to 12 weeks after the surgery and at the same time that normal regrowth occurs. Some lesions resolve spontaneously, some require intralesional Kenalog or incision and drainage. Rarely, a lesion may need to be excised. It is also fairly common to have a small number of grafts extruded in first 24 hours after surgery, with some associated localized bleeding in the recipient site, especially on the vertex. Finally, although most patients heal with 2- to 3-mm scars, some patients heal with wider scars (3 to 4 mm). Other complications are uncommon or rare. Donor-site complications include (a) infection (0.1%) treated with antibiotics and incision and drainage; (b) keloid/hypertrophic scarring treated with intralesional corticosteroids and/or excision; (c) hematoma formation treated by aspiration or incision and drainage; (d) wound dehiscence/necrosis treated with debridement and antibiotic prophylaxis; (e) persistent neuralgia/neuroma formation treated with intralesional corticosteroids (neuralgia) or excision (neuroma); and (f) arteriovenous fistula formation, which usually resolves spontaneously, but may occasionally require surgical ligation of the feeding vessel.



Recipient site complications include (a) change in hair texture usually characterized as being coarser or “frizzy,” which gradually resolves over time; (b) poor graft survival, usually related to problems in tissue handling that cause follicular bulb transection; (c) elevated (“cobblestoning”) or depressed (“pitting”) grafts that occur when grafts do not fit well into excisional recipient sites or are placed below the surface during implantation. This complication is not seen with smaller grafts placed into incisional recipient sites or is minimal and resolves over time; (d) chronic folliculitis caused by bacterial infection or foreign-body type reaction to “spicules” of transected hair shafts left on/in some grafts; (e) postfrontal tissue/graft necrosis caused by inadequate blood supply to the postfrontal region where “dense packing” of grafts is commonly performed to achieve maximum density; (f) hyperfibrotic frontal ridging caused by an overreaction to larger grafts or, perhaps, spicules of transected hairs associated with these grafts. This reaction has not been reported with single (one- to two-hair) FU grafting in the frontal line.

Postoperation Follow-up Visits Patients are seen 1 day after the operation for dressing change to a smaller, lighter bandage (or to no bandage at all). Sutures are removed at 14 days. Typical follow-up visits are scheduled for 8 weeks (wound-healing check), 16 weeks (early regrowth check), and 6 to 12 months (variable final visit for photography). Unscheduled visits are usually for ingrown hairs/cysts that need to be incised or excised.

Postoperation Adjunctive Therapy Most male patients should be on 1 mg of finasteride (Propecia) to slow or prevent further hair loss and thus prevent or delay the need to “chase baldness” with multiple procedures. Sexual side effects (decreased libido/performance) occur in 2% to 4% of patients and are totally reversible if the medication is discontinued. Topical minoxidil (Rogaine) 2% or 5% is also useful to retard hair loss and can be used alone or in combination with finasteride. Even if a patient chooses not to use these medications on a long-term basis, they may be useful in the 6-month postoperation period to assure better recovery from “shock loss”

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and as an aid to earlier regrowth of the transplanted hairs. Finally, these medications may prolong the survival of donor hairs taken from the upper border region that could be subject to miniaturization over time. Female patients may be destined to gradually lose hair diffusely throughout their donor areas. This loss may be at least delayed, if not prevented, with longterm medical treatment. Women who may become pregnant should not receive finasteride, but may use minoxidil prior to pregnancy.

TRANSPLANTATION FOR SPIRAL/HELICAL HAIR TEXTURE Patients of African ancestry with spiral/helical hair texture have generally lower follicular unit densities (0.6 FU/mm2 vs. 1.0 FU/mm2 ). Acute angulation of the follicular stem and bulb make microdissection somewhat more difficult and avoiding bulb transection is more difficult. Leaving more nonfollicular tissue around the follicular unit will usually correct this problem. However, this also means that larger recipient sites may be needed. In addition, many female patients with this hair texture have fibrotic recipient sites as a result of traction alopecia caused by prolonged use of mechanical and/or chemical hair control measures. Excisional instruments are often needed for recipient site preparation in these type of scalps (Fig. 56.8). Although it is more difficult to obtain high density in a single transplant session in such patients, the multidirectionality of the transplanted hairs compensates to some extent for the lower density.

RECONSTRUCTIVE AND CORRECTIVE HAIR TRANSPLANTATION Although the majority of transplants are performed for patients with male- and female-pattern hair loss, the improved transplantation techniques increasingly find application in the field of reconstructive and corrective surgery. Scarring alopecia resulting from many different causes, such as trauma (e.g., burns, automobile accidents), cosmetic surgery

B

A FIGURE 56.8. A: Preoperative patient with helical/spiral hair texture with a 6×8 cm area of traction alopecia. B: Same patient, seven months postoperative, after a transplant using the 2.5 mm. Redfield excisional slot punch with 350 grafts.


570


A

B FIGURE 56.9. A: Preoperation photo of patient with cleft lip repair scar resulting in alopecia of the moustache area. B: Same patient 7 months after surgery with single-hair grafting from donor hair obtained in the submental region.

(e.g., brow, face lift), inflammatory disease (e.g., lichen planopilaris, discoid lupus), and congenital malformations (e.g., cleft lip repair scars), is correctable by transplantation (Fig. 56.9). In addition, old, large-plug transplants that have become unnatural looking can be “finished” by transplanting follicular units in front and between the larger grafts to disguise them (Fig. 56.10) (8,9). If the old grafts are too low on the forehead they can be punch excised and reimplanted in a better location after being bi- or quadrisected (Fig. 56.11). Scar tissue is less vascular, more inelastic, and thinner than normal balding scalp. Despite these potential disadvantages, properly placed grafts survive and grow well in scars. It may be advisable to leave slightly larger spaces between the grafts to compensate for the reduced blood supply. In cases where the scar is very thin and “bound down” to the underlying periosteum, the graft may be too long to fit in the thin scar tissue. In this case, an extra step is required prior to graft placement. After making the incision, the operator uses a pair of curved microforceps to bluntly dissect a small “pocket” or “tunnel” extending from the posterior edge of the incision site. This is achieved by inserting the instrument into the incision and pushing the tips between the dermis and the periosteum. The separation is associated with a “popping” sound and the addi-

tional space created allows the graft to be placed deep enough to stay in and survive (Fig. 56.12).

FUTURE HAIR TRANSPLANTATION SURGERY The idea of obtaining follicular stem cells and using them to create new hair follicles has been around for at least 20 years. The concept is rather simple. First, harvest a small amount of nonbalding scalp normally used in a transplant procedure. Second, microdissect out the stem cells that are responsible for regenerating hair follicles from the telogen (resting) to anagen (growing) phase. Third, multiply these cells in large numbers in vitro (tissue culture). Finally, implant these cells into the balding scalp where they will create new hair follicles that are not subject to the miniaturization process that results in baldness. This procedure would overcome several of the drawbacks that are associated with traditional transplantation, primarily the limited donor supply and scarring from large and multiple donor excisions. The cells responsible for hair follicle induction are generally believed to be the mesenchymal cells located in either the

B

A FIGURE 56.10. A: Preoperative patient with unnatural-looking old plug graft transplant. B: Postoperative view of patient after correction with single unit micrografting.


A

B

C

FIGURE 56.11. A: Hairline from old, large-plug graft procedure located too low on the forehead prior to repair. B: Same patient after excision of plug grafts followed by transverse incisions of scalp between the excisions and a 5-0 running nylon suture. C: Same patient after suture removal and reimplantation of plug graft hairs to a better location.

A

B

C

FIGURE 56.12. A: Preoperative view of severe scarring alopecia resulting from complication after plastic surgery correction of a congenital defect. B: Same patient 6 months after surgery after transplantation with 600 1.5-mm tribevel Starr punch incisions with three to five hairs per graft. C: Same patient 6 months after second procedure to increase density.


571

572


by exposing the cells to epithelial germinative cells from the follicular bulb (11). Dermal sheath cells were shown to induce hair follicles when implanted into forearm skin of a female subject using tissue from an unrelated male donor (12). This use of allogeneic (nonself) cells rather than autologous (self) material reveals that mesenchymal stem cells probably lack surface markers that would cause an immunologic response. Thus, they may be “immunologically privileged.” If this is true, it may be possible (if not desirable) to obtain stem cells from one individual for use in another. Other concerns include whether or not the hair produced by this technology will be cosmetically acceptable and whether such “biologic therapy” will be safe and able to pass the rigorous standards required by the U.S. Food and Drug Administration. Much of the present research is being conducted in a clandestine manner to protect “intellectual property” (i.e., profitability). Nevertheless, it seems likely that the “breakthrough” will occur in this generation, which could make present transplantation methods suddenly obsolete.

References

FIGURE 56.13. Photomicrograph of follicular bulb area showing the spade-shaped dermal papilla, which is continuous with the dermal sheath surrounding the lower portion of the bulb area.

dermal papilla or the dermal sheath that is continuous with it (Fig. 56.13). Hair follicles have been induced in rats using cultured dermal papillae (10). However, a major problem has been that cultured cells seem to lose their ability to induce follicles after several passages in vitro. This problem may be overcome

1. Cooley J. Follicular cell implantation: an update on “hair follicle cloning.” Hair Transpl Forum Int. 2004;14:51–52. 2. Headington JP. Transverse microscopic anatomy of the human scalp. Arch Dermatol. 1984;120:449–456. 3. Alopecia reduction and flaps. In: Unger AP, Shapiro R, eds. Hair Transplantation, 4th ed. 709–830. 4. Rassman W, et al. Dermatol Surg. 2002;28(8):720–728. 5. Rassman W. Follicular unit extraction. Hair Transpl Forum Int. 2004;14(1):9. 6. Unger W. Whatever happened to lasers? Hair Transpl Forum Int. 2003;13(2):285, 292–293. 7. Stough D. Methodology of follicular unit hair transplantation. Dermatol Clin. 1999;17(2):297–306. 8. Bernstein R, et al. The art of repair in surgical hair restoration. Part I: basic repair strategies. Dermatol Surg. 2002;28:783–794. 9. Bernstein R, et al. The art of repair in surgical hair restoration. Part II: the tactics of repair. Dermatol Surg. 2002;28:873–893. 10. Jahoda, CAB, Reynolds, AJ, Oliver RF. Induction hair growth in ear wounds by cultured dermal papilla cells. J Invest Dermatol. 1993;101:584–590. 11. Jahoda CAB, Reynolds AJ. Hair matrix germinative epidermal cells confer follicle-inducing capabilities on dermal sheaths and high passage papilla cells. Development. 1996;122:3085–3094. 12. Reynolds AJ, Lawrence. Trans-gender induction of hair follicles. Nature. 1999;402:33–34.


PART VI ■ BREAST



CHAPTER 57 ■ AUGMENTATION MAMMOPLASTY AND ITS COMPLICATIONS SUMNER A. SLAVIN AND ARIN K. GREENE

No procedure in plastic surgery has been the subject of greater scrutiny and controversy, both scientific and political, than breast augmentation. More than 2 million American women, or 1% of the adult female population, have breast implants. Augmentation mammoplasty is the second most commonly performed cosmetic surgical procedure in the United States, after suction-assisted lipectomy. In 2004, 264,041 patients underwent augmentation mammoplasty. The annual number of breast augmentations has grown exponentially, increasing 676% between 1992 and 2004. Women between the ages of 19 and 34 years old are the largest consumers of cosmetic breast implants (50%), followed by women ages 35 to 50 years (42%). The history of augmentation mammoplasty reflects the search for the ideal implantable material, commencing with 19th century attempts to transplant lipomas into breast defects, followed by the modern era of polymer-based devices. Medical-grade silicone implants became popular after the earlier success of polyvinyl sponge-based implants, known by the trade name Ivalon. Liquid silicone injections were popularized during World War II and afterward in the Far East, but were later banned in the United States because of a high complication rate characterized by recurrent infections, chronic drainage, and granuloma formation. When Cronin and Gerow introduced new, “natural feel” prostheses in 1963, their innovative solid-shell elastomeric device with a gel-filled interior became the prototype for all future devices, including the saline-filled implants. The modern mammary prosthesis is actually a mixture of polymers comprised principally of polydimethylsiloxane that can exist in the form of a solid, liquid, or gel. With the exception of substituting saline for the original silicone gel component, the only attempted modification of the silicone implant elastomeric shell was the addition of an exterior polyurethane coating. However, reports of the carcinogenic breakdown products of polyurethane raised serious health concerns, especially when two specific compounds—toluene 2,4-diisocyanate and toluene 2,6-diisocyanate diamine—were subsequently linked to sarcoma formation in rats. Despite an absence of epidemiologic data connecting polyurethane to an increased incidence of cancer (and to breast cancer in particular) in humans, the Food and Drug Administration (FDA) moved to ban all polyurethanecoated implants from the marketplace in 1991. This edict affected approximately 10% of all breast implant patients (about 200,000 women).

GOVERNMENT REGULATION Few areas of surgery have received greater focus from the government than augmentation mammoplasty. Over the last several years, the FDA hearings regarding the approval of saline and silicone breast implants have received extensive media at-

tention. In 1976, the United States Congress passed the Federal Safe Devices Act, which empowered the FDA to regulate medical devices. Because breast implants were developed prior to 1976, they were “grandfathered” and thus not subjected to FDA approval. However, after reports appeared in the literature in the 1980s describing women with breast implants and connective tissue disorders, the government actively began to investigate the safety of breast implants. Specific concerns of carcinogenicity, autoimmune diseases, product failure, and impaired mammographic evaluation led to a moratorium on the use of all silicone gel implants by the FDA in 1992 (1). Since then saline implants have been available without restriction, and were officially approved by the FDA in 2000. Silicone gelfilled implants, however, have been limited to clinical studies involving both postmastectomy reconstruction and breast augmentation. After banning silicone breast implants in 1992, the government urged plastic surgeons to produce studies validating both the safety and patient satisfaction with breast implants. In response, one study of 112 women demonstrated improved self-image, decreased self-consciousness, and heightened selfconfidence. Overall satisfaction rates approached 86% (2). Since the moratorium on silicone breast implants, several studies have proved that these devices are safe and do not cause connective tissue disease, malignancy, or risk to breast-feeding infants. Although an association between breast implants and systemic disease was disproved, concerns about local complications of silicone implants remained. Specifically, silicone implants were felt to have high rates of capsular contracture, rupture, and infection. However, in April 2005, the results of the prospective Core Study, with a 3-year follow-up of 551 patients after breast augmentation, showed that silicone breast implants do not cause significant local complications. As a result, 13 years after the moratorium on silicone breast implants, the FDA advisory panel recommended approval for Mentor Corporation’s silicone breast prosthesis. The FDA has accepted the recommendations of its advisory panel with conditions that had not yet been made public at the time of this writing.

ANATOMIC CONSIDERATIONS The breast is supplied by a vascular network consisting of perforating branches of the intercostal, internal mammary, lateral thoracic, and thoracoacromial arterial trunks. As a result, devascularization of breast glandular or cutaneous tissues during augmentation mammoplasty is improbable, regardless of incisional site or whether a subglandular or subpectoral position has been chosen. Sensory supply of the breast is far more vulnerable because there are fewer sources of innervation. Sensation is provided chiefly by branches of the fourth (and sometimes the fifth)


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anterolateral intercostal nerve. To a lesser extent, anteromedial branches of the fourth and fifth intercostal nerves also contribute to sensation of the breast. Inframammary and periareolar incisions are more likely to result in injury to these intercostal nerves, especially in the area outside the lateral border of the pectoralis major muscle, whereas transaxillary placement can injure the intercostobrachial nerve (second intercostal nerve) as it traverses the axilla posterior to the usual site of incision. Loss of intercostal innervation of the nipple produces hypoesthesia of varying degrees, or hyperesthesia, depending on the severity of the injury to the nerve. Axillary and posteromedial anesthesia of the upper arm can develop after trauma to the intercostobrachial nerve.

SURGICAL TECHNIQUE Four separate incisional sites—inframammary, periareolar, axillary, and transumbilical—have been used for placement of breast prostheses (Fig. 57.1). Each location has its advantages and disadvantages, depending on the individual surgeon’s experience and the positioning of the implant in either a subglandular, subpectoral, or the more recently described “dual-plane” position (3). Inframammary crease incisions are preferred for patients with a well-developed crease that conceals the scar, particularly when it is placed slightly above the crease on the breast surface. This approach may be suboptimal when the integrity of the inframammary crease ligament has been compromised. In general, the periareolar incision provides excellent access to all portions of the breast. For patients willing to accept a scar on the breast surface, this approach permits meticulous positioning of the implant, particularly along the lower pole. Exposure of the inframammary ligament is excellent with this incision when either lowering of the inframammary crease or reconstruction of supporting ligaments is necessary. Transection of breast ductal tissues is required, however, before the pectoralis major muscle is identified. If subpectoral augmentation is chosen, the pectoralis major muscle is either divided along the obliquity of its fibers or the lateral border of the muscle is elevated. Although unfavorable healing can occur at any operative site, the periareolar incision tends to heal with minimal scarring. The periareolar incision facilitates revisional procedures because it allows easier access to all portions of the breast for capsulorrhaphy or capsulectomy. In addition, the incision may be incorporated into future periareolar mastopexy designs for ptosis as the patient ages.

ENDOSCOPIC APPLICATIONS IN AUGMENTATION MAMMOPLASTY Although the transaxillary technique of subpectoral augmentation has been available for many years, critics have observed difficulty in attaining precise positioning of the implant in the lower pole of the breast. Major advantages have been the absence of any scar on the breast surface, an avoidance of breast ductal transection, and a low probability of sensory nerve injury. One disadvantage of this technique is a minor risk of trauma to the intercostobrachial nerve. Just as minimally invasive surgical techniques have revolutionized the performance of many procedures, endoscopic assistance has enhanced the transaxillary approach by allowing a more accurate placement of the breast implant inferiorly and improved control of the inframammary crease. For the majority of patients, the procedure can be performed through a 2.5- to 3.0-cm incision along the lower axillary crease at the junction of hair-bearing and non–hair-bearing skin (Fig. 57.2). Following blunt dissection at the lateral border of the pectoralis major muscle, the subpectoral space is dissected digitally and with specialized curved retractors similar to a uterine sound. Introduction of a 10-mm 30-degree endoscope expedites division of fibers of the origin of the pectoralis major muscle along the medial and inferior borders of the breast. Scrupulous avoidance of muscle division laterally (at the 6 o’clock to 9 o’clock position on the right and from 3 o’clock to 6 o’clock on the left) protects the intercostal sensory nerve branches. Because of the short length of the axillary incision and its distance from the inframammary crease, it is necessary to deflate and fold the saline implant envelope to create a more rigid and tubular structure before insertion, maintaining the fill tube within the plug-and-strap mechanism of the valve. As the device is filled, it can be positioned bluntly. Hemorrhage that cannot be controlled with specialized endoscopic cautery instruments necessitates conversion to a periareolar incision for more direct open access. Endoscopic transaxillary augmentation mammoplasty usually is performed under general anesthesia because of the necessary blunt elevation and sharp separation of the pectoralis major muscle from its attachments. Meticulous preoperative marking of the breasts is extremely important for accuracy of implant placement and breast symmetry. Implant exchange, capsulorrhaphy, and capsulotomy to treat implant-related complications also can be performed with this technique. Consistent with the concept of minimal scarring, transumbilical augmentation mammoplasty offers an alternate site for placement of saline implants. Using a single infraumbilical incision, this technique uses endoscopic visualization to create a long, subcutaneous tunnel up to the inferior border of the breast, followed by subglandular dissection. Circuitous as it may seem, the technique appears to achieve an accurate subglandular placement of a mammary prosthesis. Although subpectoral placement has been reported with this technique, this approach has not gained wider acceptance because it is more difficult to place implants submuscularly using this incision compared to other approaches. This is a major disadvantage given the preference to place saline implants subpectorally because of their tendency to ripple.

SALINE IMPLANTS FIGURE 57.1. Four different incisional sites have been used for breast augmentation. The transaxillary approach has gained in popularity with the introduction of endoscopically guided placement.

Since silicone gel implants were banned by the FDA in 1992, saline implants have been available for both cosmetic and reconstructive breast surgery. In 1989, the FDA classified saline


Chapter 57: Augmentation Mammoplasty and Its Complications

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FIGURE 57.2. Endoscopic elevation and division of pectoralis major muscle fibers assist the accuracy of positioning near the lower pole and inframammary crease areas of the breast.

breast prostheses as a class III device, the category designated for implantable devices that lack sufficient data to demonstrate safety and efficacy. As a result of this ruling, saline implants underwent extensive governmental and scientific scrutiny. Satisfied that study enrollment levels were met by organized plastic surgery in 1995, the FDA allowed the continued unrestricted use of saline implants until they were formally approved in 2000. An elastomeric solid shell of silicone surrounding a hollow interior is the principal design of current models. Textured implants have been added in an effort to diminish encapsulation, but all available data indicates that smooth-walled saline implants are as efficacious as textured devices in reducing capsular contracture. Because of numerous reports documenting the frequency and severity of encapsulation associated with the use of silicone gel devices, saline implants became an alternative choice with a purported benefit of a lower encapsulation rate. However, an unacceptably high incidence of deflation (approaching 78%) was observed in earlier model devices. Manufacturers altered the design of the implant contour, shell thickness, and valve in an effort to produce a safer device with a low deflation rate. Possible causes of deflation include manufacturing defects, fold flaw failure, encapsulation, capsulectomy, and iatrogenic errors. Fold flaw failure may be the most common mechanism of product failure because most of the defects in the structural integrity of saline implants have been identified adjacent to a fold in the elastomeric shell. Presumably, friction at the fold produces a small opening that allows saline to leak. Valvular failure has been attributed to fibrous tissue ingrowth, resulting in incontinence and subclinical or total deflation. Like any water-filled device, saline implants manifest surface irregularities characterized by waves and ripples. These surface features can be visible clinically, particularly when soft-tissue coverage is inadequate. To avoid this problem, subpectoral placement has been promoted, along with complete filling of the implant. Still newer models have anatomic designs that mimic the lower pole curvature and upper pole fullness of normal breast anatomy and may cause less rippling. Current saline breast implants have a very low spontaneous deflation rate. A multicenter retrospective review used for premarket approval of saline breast implants showed an overall spontaneous deflation rate of 4.3% after 13 years (4). The actu-

arial implant survival, excluding trauma, was 97.9% to 99.5% at 10 years. A risk factor for implant deflation was implant size greater than 450 cm3 . Implant position and underfilling did not influence the deflation rate. Other studies, however, have found that underfilling the implant by more than 25 cm3 significantly increases the risk of implant rupture. Although intraluminal antibiotics and steroids reduce capsular contracture, they also increase the risk of implant deflation and are associated with atrophy of overlying soft tissues.

SILICONE GEL IMPLANTS Silicone, a polymer of dimethylsiloxane, is present throughout nature. Silicone is also found in medications, syringes, heart valves, instruments, and numerous types of implantable devices. The longer the polymer chain of silicone, the greater the viscosity. Both saline implants and silicone implants have an outer shell made of silicone. The first-generation of silicone implants had thick walls and viscous gel, and suffered from high rates of contracture. To reduce the incidence of contracture, second-generation silicone implants developed during the 1970s were designed with thinner shells and a gel of lower viscosity. These implants, however, were found to have high rupture and bleed rates. Third-generation silicone gel implants, developed in the late 1980s, used a thicker shell, a gel of higher viscosity, and a silicone barrier coating on the inner surface of the envelope to decrease silicone bleed and capsule formation. Current fourth-generation silicone implants were developed in the mid 1990s and are similar to the third-generation implants but have high gel cohesiveness that limits silicone leak in the event of implant rupture. Although available in other parts of the world, fourth-generation silicone implants may only be used in the United States under FDA-approved experimental protocols. In contrast to saline implants, rupture of silicone breast implants is often silent because most ruptures are intracapsular. Mentor Corporation’s Core Study presentation to the FDA in April 2005 showed a low rupture rate with current-generation gel implants used in the United States. Using magnetic resonance imaging (MRI), Mentor found a silent rupture rate of 0.5% 3 years after augmentation. Because the rupture rate increases significantly with age, current-generation gel implants imaged prospectively by serial MRI in Danish women have an


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estimated 15% risk of rupture at 10 years (5). Although closed capsulotomy significantly increases the risk of gel rupture and should not be performed, implant position does not affect the rupture rate.

AUTOLOGOUS AUGMENTATION Although much attention has been directed toward the FDA approval process for silicone gel breast implants, several authors have recently described autologous breast augmentation. Autologous tissue eliminates the risk of implant deflation, contracture, infection, exposure, and, ultimately, exchange or removal. However, autologous augmentation has not yet gained wide popularity because of increased operative complexity, donorsite complications and scarring, prolonged recovery, and risk of flap failure. Potential candidates for autologous augmentation include patients unable to have a breast implant, patients after explantation of implants because of complications, or women desiring either abdominal or gluteal contouring in addition to breast augmentation. De-epithelialized pedicled transverse rectus abdominis musculocutaneous (TRAM) flaps have been used for breast augmentation following abdominoplasty. Local perforator flaps from the lateral chest wall also can be used to augment the breasts, which is particularly advantageous when combined with contour surgery in the bariatric patient. Free perforator flaps have been described as potential donors for autologous augmentation. Specifically, deep inferior epigastric perforator (DIEP), superior gluteal artery perforator (S-GAP), and superficial inferior epigastric artery (SIEA) perforator flaps have been used to augment the breast in patients who desired simultaneous excision of abdominal or gluteal tissue.

OVERVIEW OF LOCAL COMPLICATIONS Although much interest has been focused on controversial complications associated with breast augmentation such as capsular contracture or autoimmune diseases, it is important not to ignore the ordinary problems that can occur, including hypertrophic scarring (6.3%), infection (0.5%), hematoma (2% to 3%), and seroma (0% to 1%) (4). Hematoma increases infection rates and frequently leads to capsular contracture. Changes in nipple sensation are estimated to occur in 10% of women after augmentation mammoplasty. Injury to the lateral branch of the fourth intercostal nerve may be reduced with submuscular implant placement. Infection may cause the loss of an implant, either because the device extrudes through a dehisced wound or because removal is necessary for treatment of the infection. Rates of infection for both saline and silicone breast implants are low, ranging from 0.5% to 2.0% (4). Because the lactiferous ducts are in continuity with the skin, they contain bacteria. The most common normal inhabitant is Staphylococcus epidermidis; Propionibacterium acnes is the most frequent nonpathogenic anaerobe; and Staphylococcus aureus is the pathogen usually responsible for implant infection. A consensus does not exist regarding the influence of open versus closed filling systems on the infection rate of saline implants. Management of infection depends on severity and the presence of exposure. Mild infections without implant exposure sometimes can be successfully treated with antibiotics alone.

The most conservative approach for more severe infections or threatened exposure is antibiotic therapy and explantation. However, successful salvage of infected or exposed implants has been described; that is, antibiotic therapy, debridement, capsulectomy, device exchange, primary closure, or flap coverage. In cases of severe infection, the implants cannot be salvaged. Uncommon complications of augmentation mammoplasty include galactorrhea and Mondor disease. Galactorrhea appears to be activated by injury or irritation of thoracic nerves, and in rare instances, can cause a galactocele. Treatment of galactorrhea includes bromocriptine or intercostal blocks. Mondor disease can occur after many types of breast operations. It is caused by thrombosis of veins along the inferior aspect of the breast, resulting in firm cords that are palpable and tender. This problem resolves spontaneously but can be treated on a symptomatic basis with warm compresses and salicylates.

CAPSULAR CONTRACTURE Encapsulation of any breast prosthesis resulting in a firm fibrous periprosthetic shell, or capsular contracture, is the most common complication reported after breast enlargement, occurring in 50% or more patients, depending on the system of grading and the clinical experience of the surgeon (Fig. 57.3). Baker’s classification of capsular contracture, modified to include the results of prosthetic breast reconstruction, is used widely for assessment of clinical firmness following breast enlargement (Table 57.1). This system of classification is subjective, but it identifies both ideal and unfavorable results (6). Multiple causes of clinically evident capsular contracture have been suggested, including migration of silicone gel molecules across the elastomeric outer envelope, foreign-body reaction, autoimmune–connective tissue disorders, a genetic predisposition to form encapsulation, infection or contamination by bacteria, hematoma, and the surface characteristics of the prosthesis. At the cellular level, abnormal fibroblast activity stimulated by a foreign body and a ubiquitous presence of S. epidermidis are popular explanations but unproven causes of fibrous contracture. A prospective, blinded study showed that S. epidermidis was significantly associated with capsular contracture. S. epidermidis was present in 90% of implants removed for Baker grade III or IV contracture, compared to 12% of implants removed for reasons other than contracture (7). Recent multicenter data showed a 20.4% rate of significant capsular contracture (Baker grade III or IV) 13 years after placement of saline implants (4). Although silicone gel implants have historically had higher capsular contracture rates than saline implants, current-generation silicone implants appear to have a similar risk of contracture compared to saline implants. Several studies suggest that submuscular placement, implant size smaller than 350 cm3 , and no drainage of the implant cavity reduce the risk of capsular contracture. Textured implants have shown no advantage. There is no difference in the incidence of contracture between textured and smooth implants. Textured implants do have disadvantages, however, as they are associated with higher rates of rupture, rippling, and malposition. Although the use of textured versus smooth implants remains controversial, there is general agreement that the incidence of severe capsular contracture is reduced by subpectoral placement, regardless of implant texture. Submuscular placement may protect against capsular contracture because the pectoralis muscle moves the implant in the pocket during regular



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A B

FIGURE 57.3. Capsular contracture. A: Bilateral Baker IV contracture, worse on right side, with marked upper pole fullness in a patient with silicone gel implants. B: Bilateral capsular contractures with superiorly retracted implants causing upper pole fullness and lack of inferior pole contour. C: Capsular contracture of a ruptured left silicone breast implant. Intracapsular versus extracapsular rupture may be difficult to determine from either the appearance of the breast or the physical findings.

C

activity. A second hypothesis is that the pectoralis major muscle serves as a protective barrier to bacterial contamination from the nipple and is more resistant to infection compared to skin flaps. It may be the muscle simply disguises the capsule because it is one more tissue layer covering the implant. In a rare consensus, antibiotic therapy in the form of systemic administration and local irrigation is emphasized as a method of encapsulation prevention. In 2000, the FDA warned against breast implant contact with Betadine because of concerns about shell weakening. In response, washing the implant and pocket with a combination of bacitracin, cefazolin, and gentamicin was recommended as a substitute for Betadine (8). A second commonly used strategy to reduce capsular contracture involves moving the implant each day to maintain the pocket size and prevent the developing capsule from tightening around the implant. Calcification can occur within the fibrous capsule of both silicone and saline breast implants, and is related to the du-

TA B L E 5 7 . 1 ORIGINAL BAKER CLASSIFICATION OF CAPSULAR CONTRACTURE AFTER AUGMENTATION MAMMOPLASTY Class I Class II Class III Class IV

Breast absolutely natural; no one could tell breast was augmented Minimal contracture; I can tell surgery was performed, but patient has no complaint Moderate contracture; patient feels some firmness Severe contracture; obvious just from observation

ration of implantation. Calcification is rare before 10 years, but 100% of implant capsules will have calcification after 23 years (9). Calcium adds to implant firmness and complicates the interpretation of mammography. Most mammographers, however, can distinguish accurately between the malignant calcifications of breast cancer and the benign calcifications in the scar tissue surrounding an implant. As a result, pericapsular calcifications do not increase the risk of having a false-positive mammogram (10).

Treatment of Capsular Contracture Women with Baker grade III or IV capsular contracture often require treatment. Closed capsulotomy can improve capsular contracture, even to a Baker grade I contracture. However, several authors have noted a high recurrence rate following closed capsulotomy. In addition, a significant risk of implant rupture, displacement, or hematoma with this technique exists. Because of the high recurrence and complication rates following closed capsulotomy, the Institute of Medicine of the National Academies of Science does not recommend closed capsulotomy to treat capsular contracture. Open capsulotomy or capsulectomy is the treatment of choice for symptomatic capsular contracture. However, a consensus does not exist about the role for capsulotomy versus capsulectomy. Although capsulectomy has a lower recurrence rate compared to capsulotomy, capsulectomy is a more difficult procedure and thus more likely to be associated with complications. Reasonable indications for capsulectomy include a calcified capsule, removal of a ruptured silicone implant, implant infection, explantation, severe contracture (Baker grades III or IV), or implant placement in another location (11).


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FIGURE 57.4. Moderate pseudoptosis corrected by augmentation mammoplasty using a dual-plane approach.

A more recent method of correcting capsular contracture involves repositioning the implant in a dual plane. In this technique, a capsulectomy is performed followed by elevation of the inferior border of the pectoralis major muscle. Approximately the superior two-thirds of the implant is placed submuscularly, while the inferior one-third of the implant is located in a subglandular position (Fig. 57.4).

AUTOIMMUNE AND CONNECTIVE TISSUES DISORDERS Numerous case reports in the 1980s appeared to suggest a linkage between silicone gel implants and connective tissue diseases and symptoms. The principal connective tissue disorders included scleroderma, rheumatoid arthritis, systemic ¨ lupus erythematosus, Sjogren syndrome, dermatomyositis, polymyositis, and polymyalgia rheumatica. In response to these reports, a number of large, population-based retrospective studies were conducted to test the association between silicone breast implants and connective tissue disorders. Although the details of these studies are beyond the scope of this chapter, all studies have concluded that there is no association between silicone breast implants and any connective tissue disease (12).

SILICONE EFFECTS ON PREGNANCY, LACTATION, AND BREAST-FED CHILDREN Currently, there is no scientific evidence that silicone is a mutagen or teratogen. Implants do not interfere with lactation or increase the amount of silicone in breast milk over baseline levels present in women without implants. In fact, cow’s milk and infant formulas contain much greater amounts of silicone than an augmented mother’s milk. Clinical studies conducted by the British Department of Health and the Institute of Medicine of the National Academy of Sciences both demonstrate that

silicone breast implants are safe for pregnancy, lactation, and breast-feeding.

CARCINOGENESIS Two large epidemiologic studies have examined the subsequent risk of breast cancer following augmentation: one based on an implant cohort of 11,676 women in Alberta, Canada, who were followed for 13 years, and a second study in Los Angeles with patients who had had a median of 15.5 years of silicone implant exposure (13,14). These studies concluded that a lower incidence of breast carcinoma was found in augmented patients than in nonimplanted control subjects. Similarly, animal studies also have failed to document an increased incidence of carcinoma after silicone implantation. One possible explanation for the lower risk of breast cancer in augmented women is that augmented women have less volume in which to develop cancer compared to nonaugmented women. A second hypothesis for low rates of breast cancer in augmented women is that silicone may mediate a biologic protective effect against breast cancer.

DETECTION OF BREAST CANCER AND SURVIVAL IN AUGMENTED WOMEN Do women with breast implants who are subsequently diagnosed with breast cancer suffer any delay in diagnosis or have a worse prognosis as compared to breast cancer patients without implants? This important question was raised because implants can obscure mammary lesions on mammography or make physical examination of the breast more difficult. These concerns about mammographic accuracy are especially serious in view of the 13.5% lifetime breast cancer rate observed among white patients in the United States, who also constitute the majority of implant patients. Similar concerns have been



cited repeatedly by the FDA during its investigation into the safety of breast implants. Because saline implants also are relatively radiopaque on mammographic examination (although more radiotransparent than gel devices), these concerns have not abated with the widespread use of saline breast prostheses. The possibility of a missed lesion, hidden by an implant, could lead to a delay in diagnosis and a less-favorable survival. As an outgrowth of these concerns, the American College of Radiology recommends that women with breast implants should not only follow the same screening schedule as those without implants, but also should be evaluated only at accredited mammographic facilities experienced with the special needs of this patient group. In addition, mammography is recommended for women older than 30 years of age before and after augmentation. Although it has been demonstrated that standard mammography shows 56% and 75% of breast parenchyma in subglandular and subpectoral implants, respectively, Eklund et al. recommended four additional “push-back” or displacement views be taken to improve visualization of the entire mammary glandular tissues (15). The Eklund views increased the amount of breast tissue capable of visualization to 64% and 85% in subglandular and submuscular implants, respectively. In asymptomatic women, screening mammography using Eklund views has a lower sensitivity in augmented women (45%) compared to nonaugmented women (66%) (10). Specificity, however, is approximately the same for asymptomatic augmented and nonaugmented women (96% to 97%). Similar trends are found with mammography among symptomatic women. Mammogram sensitivity and specificity for symptomatic women is 73% and 86%, respectively, for women with breast implants, compared to 81% and 87%, respectively, for women without breast implants (10). In addition to mammography technique, the severity of encapsulation and location of the implant also influence the amount of breast tissue visualized by mammography. A Baker III or IV capsular contracture reduces the amount of breast tissue to be evaluated by mammography by 50%. Subglandular implant placement increases the amount of obscured breast tissue with the Eklund technique from 15% in submuscular implants to 36%. Despite the potential interference of breast cancer detection posed by implants, breast implants do not adversely affect breast cancer detection, stage of diagnosis, or survival. A large study in Alberta, Canada investigated 13,246 patients with breast cancer (16). The authors found no difference in the 5- and 10-year survival rates of augmented and nonaugmented patients. Although the tumors were smaller in the augmented group, nodal and distant metastases were similar, as were histologic types of the tumors. Of special interest, all of the breast cancers diagnosed in the augmented population were carcinomas rather than the sarcomas observed previously in implanted animals. A study of the Danish Cancer Registry also concluded that women with and without silicone breast implants were diagnosed with breast cancer at the same stage and had similar survival rates. A recent prospective study showed that in asymptomatic augmented women, cancer stage, tumor size, nodal status, and estrogen-receptor status were the same as for nonaugmented women (10). In symptomatic women, the augmentation cohort had smaller tumor size, lower grade, and greater estrogen receptor-positive status than the nonaugmented group. Augmented women with breast cancer may have superior prognostic factors because of their reduced autologous breast volume. In addition, augmented patients may be more aware of their breast composition or more compliant with breast screening than nonaugmented women. Finally, breast implants may facilitate physical exam detection of breast masses by providing a firm background for palpation (10).

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MANAGEMENT OF AUGMENTED WOMEN WITH BREAST CANCER Because 50% of breast cancer affects women older than 65 years of age, the prevalence of breast cancer will continue to increase as the population of the United States ages. Because the rate of breast augmentation is also rapidly rising, an exponential increase in the diagnosis of breast cancer in augmented women will occur in the future. For those women who develop breast cancer in a breast that contains an implant, breast-conservation therapy is not recommended. The majority of women with implants treated with lumpectomy and radiation will develop complications. Capsular contracture alone has been documented in as many as 65% of augmented women who received conservation therapy for breast cancer. Fifty percent of augmented women after conservation therapy ultimately have completion mastectomy and explantation as a consequence of complications, inability to obtain negative margins, or local recurrence. Although the overall local recurrence rate for breast cancer is 1% per year, some studies suggest that it may be higher in augmented women after conservation therapy. Conservation therapy in augmented women is also problematic for future tumor surveillance. Women with breast cancer are not only at risk for local recurrence, but they have a significantly higher likelihood of developing a second cancer in the same breast or a tumor in the opposite breast. Screening mammography in augmented women after conservation therapy is difficult because it is known that the implant reduces the amount of breast parenchyma visualized on mammogram. In addition, the resulting capsular contracture from the radiation treatment further reduces the accuracy of mammography. Thus conservation therapy in augmented women creates a cohort with a high risk of future breast cancer and serious handicaps to adequate mammography. In addition to radiation complications, difficulty obtaining clear margins, and a high recurrence rate, breast conservation in augmented women also is a poor choice because these women have a higher likelihood of a poor aesthetic outcome compared to nonaugmented patients. Patients with breast implants have small native breast volume and thin skin as a result of implant expansion. Consequently, lumpectomy in these women is more likely to result in significant breast deformity. In addition to the low lumpectomy-to-breast-volume ratio in augmented women, radiation therapy also contributes to a poor aesthetic outcome. The high rate of capsular contracture has caused as many as 100% of patients to end their treatment with a fair or poor cosmetic result. Women with a large amount of breast parenchyma may achieve a satisfactory outcome with explantation, mastopexy, and conservation therapy. However, the safest and most aesthetically acceptable treatment of breast cancer in the majority of augmented women is mastectomy with immediate or delayed reconstruction.

IMAGING OF BREAST IMPLANTS Three modalities—mammography, sonography, and MRI— have been used to detect abnormalities of either the implant or its surrounding capsule. MRI is the most accurate and expensive study, with a sensitivity greater than 95% for a ruptured implant. Shell folding (“linguine sign”) on MRI indicates a rupture implant (Fig. 57.5). Sonographic signs of implant rupture include the “snowstorm” appearance of free silicone in the breast tissue or the “stepladder” sign of linear echoes. Because significant contracture reduces the sensitivity of ultrasonography, MRI is the radiographic study of choice to determine implant rupture in patients with Baker III or IV contracture.


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FIGURE 57.6. Saline implant protruding through the capsule. This condition can be confused with a breast mass. FIGURE 57.5. Magnetic resonance image illustrating shell folding (“linguine sign”) and extracapsular rupture of a silicone implant.

AESTHETIC COMPLICATIONS Implant malposition and an unfavorable shape are the second most common cause, after capsular contracture, of patient dissatisfaction following augmentation mammoplasty (Fig. 57.6). Correction of these types of problems usually involves a combination of techniques, including removal of the implant, capsulotomy, capsulectomy, alteration of the inframammary crease, or selection of a different location. Sometimes, a different size or shape of implant is required. The current availability of both round and more anatomically constructed devices has improved the aesthetic results. Two problems that have been more refractory to correction are residual ptosis and the double-bubble deformity. Resid-

ual ptosis is best treated by recognition of the relationship of the nipple to the inframammary crease and placement of the implant in a subglandular position. When excess skin is observed, a combined mastopexy and augmentation procedure may be indicated. The double-bubble deformity results from distortion or disruption of the inframammary crease (Fig. 57.7). It is commonly noted after attempted correction of a constricted, tubular breast, but it might also occur after subpectoral placement with elevation of the crease or after disruption of the inframammary ligament and inferior displacement of the prosthesis. Surgical correction involves varying combinations of inframammary crease reconstruction, pectoralis major muscle release, and replacement with a smaller implant. Avoiding an unfavorable cosmetic result requires that special attention be directed at preoperative assessment of breast anatomy because even modest differences in position of the inframammary crease or nipples can be magnified after augmentation.

A

B FIGURE 57.7. Double-bubble deformity. A: Severe deformity in a patient with saline implants. B: Demonstration of deformity at operation, illustrating that the implant transgressed the inframammary crease. C: Oblique views of following open repair through a periareolar incision. D: Lateral views of postoperative result.



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C (L)

C (R)

D (L)

D (R) FIGURE 57.7. (Continued.)

Rippling is almost always a complication of saline implants, primarily affecting the upper pole. Risk factors for rippling include underfilling and textured implants. Textured implants have a greater likelihood of causing traction on the skin because of their increased adherent properties. Prophylactic measures to avoid rippling include using a smooth implant, subpectoral placement, and overfilling the implant. First-line treatment of rippling includes conversion to subpectoral placement if previously subglandular, overfilling the implant, changing from a textured to a smooth implant, or converting a saline to a gel implant. Second-line treatment of rippling includes capsulorrhaphy to suture the ripples or partial capsulectomy to tighten the capsule. Other maneuvers include folding the pectoralis major muscle cephalad to add tissue to the upper pole, placing external bolsters, or using allogenic acellular dermal grafts. Allogenic acellular dermal grafts (AlloDerm), when placed between the implant and skin, can improve rippling. Third-line treatment for severe, refractory rippling necessitates the transfer of healthy, well-vascularized tissue to cover the implant. Local pedicled sources of tissue include muscle or myocutaneous latissimus dorsi or rectus abdominus flaps.

ever, like all cosmetic surgery patients, patients seeking breast augmentation have a higher likelihood of impaired body image compared to the general population. Women interested in augmentation mammoplasty, compared to physically similar women, are more concerned about their appearance, report more frequent teasing, and feel that larger breasts are the ideal breast size. In addition, women interested in breast augmentation are more likely to have used psychotherapy compared to control women with similar-sized breasts (17). Although augmentation candidates are more likely to have received psychiatric counseling compared to age- and sizematched controls, some reports have found a higher suicide rate among augmented women. However, a link between implants and suicide cannot be substantiated because augmented women, and cosmetic surgery patients in general, have a greater prevalence of psychiatric disease compared to the general population. In addition, several studies have found that women have a significant improvement in body image after breast augmentation. One interesting report cited an increase in weight among anorexic augmented women, possibly as a consequence of an improved body image after receiving breast implants.

PSYCHOLOGICAL ISSUES

MEDICOLEGAL CONSIDERATIONS

Patient satisfaction with both saline and silicone breast implants is very high, ranging from 93% to 97% (4). How-

Despite a class action settlement and a corporate agreement to provide $4.2 billion to compensate women who claim that


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their health was harmed by silicone implants, litigation related to these devices has not spared plastic surgeons from being named as defendants in suits. Surgeons must navigate between product liability and informed consent laws that hold them accountable for a wide array of health issues, proven and alleged. Consequently, one prerequisite for approval of silicone breast implants set forth by the FDA is a strict, standardized, patient education and consent program. Implant failure or complications create a burden to the patient and thus a potential stimulus for litigation. Currently, both Mentor Corporation and Inamed Corporation will replace deflated implants for the life of the implant with any size or model. In addition, implants from both companies come with either a 5- or 10-year limited warranty that provides $1,200 for surgical expenses not covered by insurance. Extended warranties may be purchased by the patient to cover $2,400 of operating room costs not covered by insurance for 10 years from the time of the augmentation. In addition, these extended warranties also will replace a contralateral implant at no cost.

References 1. Angell M. Breast implants—protection or paternalism? N Engl Med J. 1992; 326:1695. 2. Young VL, Nemecek JR, Nemecek DA. The efficacy of breast augmentation: breast size increase, patient satisfaction, and psychological effects. Plast Reconstr Surg. 1994;94:959.

3. Tebbetts JB. Dual plane breast augmentation: optimizing implant-softtissue relationships in a wide range of breast types. Plast Reconstr Surg. 2001;107:1255. 4. Cunningham BL, Lokeh A, Gutowski KA. Saline-filled breast implant safety and efficacy: a multicenter retrospective review. Plast Reconstr Surg. 2000;105:2143. 5. Holmich LR, Friis S, Fryzek JP, et al. Incidence of silicone breast implant rupture. Arch Surg. 2003;138:801. 6. Spear SL, Baker JL. Classification of capsular contracture after prosthetic breast reconstruction. Plast Reconstr Surg. 1995;96:1119. 7. Pajkos A, Deva AK, Vickery K, et al. Detection of subclinical infection in significant breast implant capsules. Plast Reconstr Surg. 2003;111:1605. 8. Adams WP, Conner WCH, Barton FE, et al. Optimizing breast-pocket irrigation: the post-Betadine era. Plast Reconstr Surg. 2001;107:1596. 9. Peters W, Smith D. Calcification of breast implant capsules: incidence, diagnosis, and contributing factors. Ann Plast Surg. 1995;8:34. 10. Miglioretti DL, Rutter CM, Geller BM, et al. Effect of breast augmentation on the accuracy of mammography and cancer characteristics. JAMA 2004;291:442. 11. Young VL. Guidelines and indications for breast implant capsulectomy. Plast Reconstr Surg. 1998;102:884. 12. Janowsky EC, Kupper LL, Hulka BS. Meta-analysis of the relation between silicone breast implants and the risk of connective tissue diseases. N Engl Med J. 2000;342:781. 13. Berkel H, Birdsell DC, Jenkins M. Breast augmentation: a risk factor for breast cancer? N Engl Med J. 1992;326:1649. 14. Brody G. Silicone implants and the inhibition of cancer [discussion]. Plast Reconstr Surg. 1995;96:519. 15. Eklund GW, Busby RC, Miller SH, et al. Improved imaging of the augmented breast. AJR Am J Roentgenol. 1988;151:469. 16. Birdsell DC, Jenkins H, Berkel H. Breast cancer diagnosis and survival in women with and without breast implants. Plast Reconstr Surg. 1993;92:795. 17. Sarwer DB, LaRossa D, Bartlett SP, et al. Body image concerns of breast augmentation patients. Plast Reconstr Surg. 2003;112:83.


CHAPTER 58 ■ MASTOPEXY AND MASTOPEXY AUGMENTATION NOLAN S. KARP

Mastopexy is a procedure designed to elevate breast tissue and the nipple–areola complex to correct breast ptosis. Mastopexy procedures are derived from breast-reduction procedures except that only skin is removed with little or no parenchymal resection. Breast-reduction surgery is often performed to relieve neck, back, shoulder, and arm pain. The patient receives significant medical and quality-of-life benefits. Although the appearance of the breast is a factor, the medical benefits are often the primary concern of the patient. Mastopexy is almost always a cosmetic procedure. Consequently, the tradeoffs (i.e., scars) are less well tolerated by the mastopexy patient than by the breast-reduction patient. Until recently, the predominant scar after breast reduction was the “inverted T” anchor scar. In most cases, breast-reduction patients will tolerate this degree of scarring. The mastopexy patient, for the most part, will not accept this incision and desires as much benefit as possible with the least amount of scarring. Many patients presenting for mastopexy can be treated with breast augmentation alone or in combination with mastopexy. The most common patient seeking mastopexy alone is happy with her breast size or does not want breast augmentation. The best patients for mastopexy alone have fairly large breasts and ptosis. Usually, these patients desire nipple elevation and correction of glandular ptosis. The best operation for this group of patients is a vertical mastopexy similar in design to a vertical breast reduction. Patients with small (often deflated or empty appearing) breasts, who refuse breast augmentation, are often the worst candidates for mastopexy. The scars in these patients are frequently not worth the benefit of the operation. Breast ptosis was originally staged by Regnault (Fig. 58.1). Minor ptosis (first degree) occurs when the nipple is at the level of the inframammary fold (IMF). Moderate ptosis (second degree) is when the nipple is below the IMF but above the lowest breast contour. Severe ptosis (third degree) is when the nipple is at the lowest breast contour and below the level of the IMF. Glandular ptosis is characterized by a nipple above the IMF with breast tissue hanging below the fold.

MASTOPEXY PROCEDURES The type of mastopexy procedure performed is dictated by the nature of the deformity. Patients with minor degrees of ptosis are frequently treated with periareolar mastopexy procedures. Periareolar mastopexy is also often the procedure of choice when breast augmentation is combined with mastopexy. As the volume of the breast is increased by the implant, the need and degree of the mastopexy procedure becomes less. As the ptosis worsens, vertical mastopexy with a lollipop-type incision or conventional mastopexy with an inverted-T–type incision might be indicated.

Inverted-T Mastopexy Procedures The original procedures for mastopexy involved skin resection using an inverted-T–type incision. There was extensive skin undermining and minimal parenchymal resection. In 1956, Wise described a series of mechanical aids to help mark and plan a skin mastopexy procedure. In 1971, Goulian described a mastopexy procedure designed to reshape the breast by removing excess skin with no undermining. The dermis was folded on the dermis to reshape the breast. There was no surgery on the breast tissue or the chest wall resulting in less postoperative pain. The final scar was an inverted-T. The theory behind this procedure was that keeping the skin and breast in continuity contributed to a longer-lasting result. Whidden was the first to introduce the concept of the tailortack mastopexy. The operation was similar to the Goulian procedure, but rather than mark the breast based on a preconceived pattern, the skin was invaginated and the operation simulated with sutures. The sutures were modified until the desired breast shape was achieved, and a pattern was individually made to guide the de-epithelialization of the skin. After de-epithelialization the breast was closed without undermining or resecting glandular tissue. The “skin-only” mastopexy is frequently followed by recurrent ptosis. Several authors have suggested repositioning and suturing of the breast parenchyma in addition to skin resection as a solution to this problem. These operations were based on the pedicle breast reduction procedures that were becoming popular at the time. Ship et al (1). were the first to describe the creation of double superior pedicle flaps that were sutured over each other and then sutured to the pectoralis fascia. The scar pattern was the standard inverted-T. The authors noted that ptosis and bottoming out of the breast occurred more slowly than in the skin only methods of mastopexy.

Concentric Mastopexy Procedures Because mastopexy is a cosmetic procedure, patient acceptance of the scars has always been a limiting factor. Bartels described the first attempt at concentric mastopexy in 1976. Rees and Aston reported a similar procedure for tuberous breasts at about the same time. These procedures were complicated by poorly shaped breasts, wide scars, and enlarged areola. They never really caught on. The use of purse-string sutures to close a circular wound was first described in plastic surgery in 1985 (2). In 1990, Spear et al. (3) described three rules to mark the patient having concentric mastopexy that seemed to produce more predictable aesthetic results (Fig. 58.2). The three rules are as follows: 1. The outer concentric circle must be drawn not to exceed the original areola diameter by more than the original


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B

C

D

E

FIGURE 58.1. Breast ptosis classification. A: Normal. B: Minor or first degree. C: Moderate or second degree. D: Severe or third degree. E: Glandular ptosis.

areola diameter exceeds the inner concentric circle diameter. 2. The diameter of the outer circle should never be more than twice the diameter of the inner circle. 3. The final areola size should be an average of the inner and outer concentric circles.

Periareolar “Round-Block” Mastopexy Procedures Periareolar mastopexy inevitably flattens the breast. Benelli (4) was one of the first to note that to create an excellent long-

Doutside Doriginal Dinside

FIGURE 58.2. Spear rules. Illustrative markings of the three concentric circles for the Spear rules in mastopexy design. D refers to the diameter of the labeled circles.

lasting breast shape, the surgery on the gland must be separated from the surgery on the breast skin. Similar to older procedures that sutured the breast parenchyma to create better breast contour, Benelli shaped the breast parenchyma by creating multiple flaps within the breast gland that were then criss-crossed and sutured together to create a conical breast shape (Fig. 58.3A– C). The breast was then “laced” with a permanent suture (Fig. 58.3D). The round-block permanent periareolar suture (Fig. 58.3E) was placed in the dermis of the skin and then tied down so that the size of the cutaneous areola matched the size of the actual areola. The breast was sometimes sutured to the chest wall to maintain its shape and location. The skin was allowed to redrape over the newly shaped breast. The best patient for this technique had moderately sized breasts with some hypertrophy. Patients with very loose or very large ptotic breasts were difficult to treat. Patients with tubular breast deformity were also considered good candidates for round-block mastopexy. Brink (5) further defined the round-block periareolar mastopexy. He found the ideal patient to be someone with true ptosis, lower breast pole hypoplasia, or tubular breast deformity. These patients are characterized by normal to high inframammary fold position, normal to short nipple-to-inframammary-fold distance, and downward-pointing nipples. Brink found surgical manipulation of the lower pole breast skin was unnecessary. The patients were treated with purse-string round-block mastopexy without parenchymal manipulation. Spear (6) reevaluated his indications for periareolar mastopexy in 2001 and found that the best patients included those with tuberous breast deformity, small-to-moderate-size breasts with mild to moderate ptosis, and gynecomastia, as well as those having implant explantation. He emphasized the importance of a permanent periareolar blocking suture, particularly when the outer circle of skin resection is oversized. Goes (7) also believed that skin-only mastopexy would not prevent early recurrent ptosis. He performed a periareolar mastopexy that supported the glandular elements of the breast by wrapping the tissue with mesh and suturing the mesh to the chest wall fascia. The periareolar dermis was placed underneath the mesh and the external skin was closed in a blocked manner with permanent sutures over the mesh (Fig. 58.4). Goes found that mixed mesh (absorbable and permanent components) worked better than absorbable mesh alone. His results were longer lasting in patients with mild to moderate ptosis.

Vertical-Incision Mastopexy The periareolar mastopexy techniques are limited by the amount of tissue manipulation and nipple/areola movement that is possible. Some patients require more tissue rearrangement or skin resection than can be achieved with concentric mastopexy techniques. The vertical mastopexy is performed with a periareolar scar and a vertical limb. The vertical limb is on a barely visible part of the breast, usually heals well, and is rarely an issue with the patient. Unlike the inframammary incision, which can often be seen medially or laterally, the vertical is never seen in bathing suits or clothing as long as it is kept above the inframammary fold. Vertical mastopexy procedures are not new; Lassus (8) and Lejour (9) have been performing these procedures since the 1960s. The Lejour and Lassus mastopexy procedures are similar in many ways. In both cases, the blood supply to the nipple is based on a superior pedicle. Skin is resected in the lower portion of the breast, and a central pedicle of tissue is developed based on the superior blood supply. This central tissue is sutured in an elevated fashion to the pectoralis fascia (Fig. 58.5). This process creates medial and lateral pillars that are then sutured together. The procedures only differ in that Lejour undermines the skin flaps more than Lassus. The result


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B A

C

D

E

FIGURE 58.3. Benelli mastopexy. A: The glandular flaps are cut and the nipple–areola blood supply is based on the superior flap. B: The medial flap is rotated and sutured into position. C: The lateral flap is rotated and sutured over the medial flap. D: The conical shape of the breast is supported by full-breast lacing using permanent sutures. E: The round-block purse-string suture is placed.

at the end of the procedure tends to have an overcorrected look that settles down over the first few months after surgery. In the United States, these procedures never really caught on because American patients and physicians have trouble accepting results that are not immediately satisfactory. These procedures do, however, have a role in mastopexy surgery. The result is longer lasting because the breast shape is based on tissue rearrangement and suturing, and not on skin resection alone. Daniel Marchac (10) developed a technique that is similar to that of Lejour and Lassus except that he places a small transverse scar at the bottom of the breast at the end of the case. This scar eliminates some of the excess skin associated with the Lassus and Lejour techniques. The patient’s breast shape is better at the end of the case, but the price is a short transverse scar. In mastopexy surgery, the most difficult problem is maintaining upper pole fullness and preventing recurrent ptosis. Biggs and Graf (11) developed a procedure that creates an inferior chest wall flap that is repositioned in the upper part of the breast. This flap is passed under a loop of pectoralis muscle and sutured in place in the elevated position. The Biggs-Graf technique is performed most commonly with a vertical incision,

but an L-shaped incision or an inverted-T incision can also be used. The blood supply to the nipple-areola is based on a superior dermal pedicle. The inferior chest wall flap blood supply is through the chest wall. The nipple/areola position is marked at the level of the inframammary fold and the superior pedicle is designed. The skin resection is marked as for any other type of vertical breast reduction. The skin is de-epithelialized, and the superior and inferior pedicles are developed (Fig. 58.6A– C). The bottom of the breast is mobilized so that the area is empty when the inferior flap is relocated to the upper part of the breast. The nipple-areola is inset, after which the inferior flap is passed under a loop of pectoralis major muscle. The inferior flap is sutured in place to the pectoralis fascia, and the resulting medial and lateral pillars are sutured together. The skin can usually be closed without tension or gathering. The shape at the end of the case usually looks good with minimal to no overcorrection (Fig. 58.6D, E). The shape of the breast is again based on tissue rearrangement and suturing, not skin resection. The mastopexy techniques that incorporate tissue rearrangement and suturing seem to have longer-lasting


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is allowed to redrape and has no role in the ultimate shape of the breast (Fig. 58.7).

AUGMENTATION MASTOPEXY

FIGURE 58.4. Goes technique. Diagram shows the position of the mesh and purse-string suture.

results than skin resection mastopexy procedures. The principle is to empty the bottom of the breast, and then reposition the tissue in the upper pole of the breast. An empty space is created in the lower pole of the breast that allows pillar sutures to be applied and the breast narrowed and reshaped. The skin

Breast ptosis is caused by a relative excess of skin envelope for the amount of breast tissue that is present. The procedures to decrease the skin envelope and rearrange and reposition the breast volume have been discussed above. Another option is to increase the breast volume with breast augmentation. This will often help to correct the skin–breast volume disparity. Breast augmentation is frequently combined with mastopexy. The augmentation procedure usually decreases the size and scope of the mastopexy procedure. In an augmentation mastopexy procedure, the mastopexy may be as small as a periareolar skin excision to reposition the nipple/areola, or as large as an anchor scar mastopexy with glandular rearrangement. The extent of the procedure depends on the needs of the particular patient. A complete history and physical examination is important in this group of patients. The patients tend to be older than breast-augmentation patients. Prior mammography and personal and family history of breast cancer are discussed. The patient’s goals and desires are clearly delineated. Important issues to be determined are size and shape of the breast desired, the position of the breast on the chest wall, and the amount of upper pole fullness. Patients with Regnault grade 1 ptosis who desire enlargement are frequently treated with breast augmentation alone. Patients with Regnault grade 2 or 3 ptosis usually require mastopexy in

B A

C

D

FIGURE 58.5. Lejour and Lassus method. A: Mobilization of the central pedicle. B: Central pedicle rotated into elevated position. C: Glandular pillars sutured together. D: Configuration of the breast at the end of the case.



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B

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FIGURE 58.6. Biggs-Graf mastopexy. A: Skin markings. B: The inferior pedicle. C: The superior pedicle. D: Preoperative view of patient. E: View just prior to final closure.

addition to breast augmentation. If the patient is happy with her breast size, then mastopexy alone usually suffices. The simplest augmentation mastopexy procedure involves resection of an ellipse (also called crescent) of skin above the areola to raise the nipple/areola position relative to the IMF (Fig. 58.8). The most that the nipple/areola can be raised with this type of procedure is about 2 cm. These patients may have early Regnault grade 2 ptosis. The only real risk to this procedure is a wide scar or an elliptical-shaped areola. If the areola shape is an issue, then the procedure should be converted to a concentric mastopexy to redistribute the tension around the entire areola circumference (12).

When modest skin tightening or repositioning of the nipple/areola is required, the full concentric mastopexy might be indicated. If the two circles of the mastopexy are truly concentric, then there will be no nipple elevation. To elevate the nipple, the outer circle must encompass more skin above than below the nipple (Fig. 58.9). In all augmentation mastopexy cases, the markings are planned preoperatively with the patient standing. In the operating room the nipple areola is cut out with a cookie cutter that is usually between 40 and 45 mm in diameter. The pocket for the implant is created either through the periareolar cut or through part of the mastopexy incision, and the implant is usually placed in the subpectoral


A

B

C

D FIGURE 58.7. A, B: Patient before Biggs-Graf–type mastopexy. C, D: Patient 18 months after BiggsGraf–type mastopexy. Note maintenance of upper pole fullness.

B

A

FIGURE 58.8. Crescent mastopexy. A: Skin resection. B: Insertion implant. C: Final closure.

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FIGURE 58.9. Periareolar mastopexy and augmentation. A: Skin resection. B: Area undermined. C: Insertion implant. D: Final closure.

position. After implant placement, the marks are re-evaluated in the sitting position. Only then are the final incisions opened and the mastopexy performed. In the case of concentric mastopexy, the outer circle markings are confirmed and incised. The guideline for marking concentric mastopexies were established by Spear and discussed above. A nonabsorbable purse-string suture is placed in the dermis of the outer circle. There is usually some pleating in the incision that resolves within 1 to 2 months. The permanent suture helps keep the scar narrow and the areola from enlarging. Vertical-scar augmentation mastopexy is usually used to correct moderate degrees of breast ptosis and allows greater ability to move the nipple areola complex and remove excess skin. Occasionally, a small piece of breast tissue at the bottom of the breast is excised to correct ptosis. Relocation of tissue at the bottom of the breast to the top of the breast is less important than in mastopexy alone because the implant is being used. Vertical mastopexy is more predictable than periareolar mastopexy. The operation offers the ability to better correct asymmetric nipples and wide breasts (Fig. 58.10).

Inverted-T-scar augmentation mastopexy is rarely indicated. In rare cases, the ptosis is so severe and the implant size is not enough to allow adequate skin resection using the vertical or periareolar techniques. This procedure allows maximal control of the nipple/areola position, skin removal, and breast shaping. The major drawback is the scarring. Augmentation mastopexy patients are no different from other aesthetic patients. They desire maximal improvement with minimal scarring. Some patients will accept a lesser result to avoid longer scars. Nipple blood supply is an important consideration in augmentation mastopexy patients. There is rarely a problem with nipple viability in patients undergoing mastopexy alone. In augmentation mastopexy, the effect of the implant position on nipple blood supply must be considered. If the implant is placed in the submammary position and there is substantial soft-tissue dissection, nipple blood supply could be compromised. Subpectoral placement of the implant is less likely to interfere with nipple blood supply. There is a common misconception in augmentation mastopexy patients that the implant should be placed in the


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C

B FIGURE 58.10. Vertical mastopexy and augmentation. A: Skin resection. B: Insertion implant. C: Final closure.

submammary position. This offers the patient less surgery and less postoperative pain. Although subpectoral implant placement is associated with more postoperative pain, the incidence of capsular contracture, implant palpability, and excess upper pole fullness is less. Currently, in this country, augmentation mastopexy patients are allowed to have either saline- or silicone-filled breast implants. Silicone implants placed in the submuscular position have a lower incidence of capsular contracture than those placed in the submammary position. When the implant is placed in the subpectoral position, approximately 50% of the implant is covered with muscle. The partial muscle coverage allows as much flexibility in shaping as does subglandular implant placement. At the same time, mammography is more accurate and the chance of upper pole visibility is less. The augmentation mastopexy population tends to be older and have thinner soft tissue than the breast augmentation population. The ability to perform mammograms and the issues of upper pole fullness are real issues in this group. Augmentation mastopexy is much more challenging than either breast augmentation or mastopexy alone. The patient’s goals and desires need to be carefully addressed, and the scars and limitations of the procedures discussed.

References 1. Ship AG, Weiss PR, Engler AM. Dual-pedicle dermoparenchymal mastopexy. Plast Reconstr Surg. 1989;83:281. 2. Peled IJ, Zagher U, Wexler MR. Purse-string suture for reduction and closure of skin defects. Ann Plast Surg. 1985;14:465. 3. Spear SL, Kassan M, Little JW. Guidelines in concentric mastopexy. Plast Reconstr Surg. 1990;85:961. 4. Benelli L. A new periareolar mammaplasty: the “round block” technique. Aesthetic Plast Surg. 1990;14:93. 5. Brink RR. Management of true ptosis of the breast. Plast Reconstr Surg. 1993;91:657. 6. Spear SL, Giese SY, Ducic I. Concentric mastopexy revisited. Plast Reconstr Surg. 2001;107:1294. 7. Goes JCS. Periareolar mammaplasty: double skin technique with application of Polyglactin 910 mesh. Rev Soc Bras Cir Plast. 1992;7:1. 8. Lassus C. Update on vertical mammaplasty. Plast Reconstr Surg. 1999; 104:2289. 9. Lejour M. Vertical Mammaplasty and Liposuction of the Breast. St. Louis: Quality Medical Publishing; 1993. 10. Marchac D, de Olarte G. Reduction mammaplasty and correction of ptosis with a short inframammary scar. Plast Reconstr Surg. 1982;69:45. 11. Graf R, Biggs TM. In search of better shape in mastopexy and reduction mammoplasty. Plast Reconstr Surg. 2002;110:309. 12. Puckett CL, Meyer VH, Reinisch JF. Crescent mastopexy and augmentation. Plast Reconstr Surg. 1985;75:533.


CHAPTER 59 ■ BREAST REDUCTION: INVERTED-T TECHNIQUE SCOTT L. SPEAR

Reduction mammoplasty represents the clearest example of the interface between reconstructive and aesthetic plastic surgery. Although the avowed goals of this procedure are weight and volume reduction of the breast, aesthetic enhancement is often equally important. Excellent procedures have been described and emphasis has shifted to technical refinements for improved safety and predictable aesthetic results. At the same time, greater importance has been placed on preservation of both sensation and physiologic function. Although there is a fundamental difference between reduction mammoplasty and mastopexy, both operations can follow the design of the techniques to be described for reduction mammoplasty alone (Chapter 58).

ANATOMY AND PHYSIOLOGY Sensory innervation to the superior portion of the breast is supplied by the supraclavicular nerves formed from the third and fourth branches of the cervical plexus. The medial breast skin is supplied by the anterior cutaneous divisions of the second through seventh intercostal nerves. The dominant innervation to the nipple is derived from the lateral cutaneous branch of the fourth intercostal nerve, whereas lateral cutaneous branches of other intercostal nerves travel subcutaneously to and beyond the midclavicular line of the areola and the skin of the breast. Independent confirmation of the importance of the lateral cutaneous branch of the fourth intercostal nerve has led to greater acceptance of techniques that include its course in the vascular pedicle to the nipple. There are three chief sources of blood supply to the breast. The internal mammary artery supplies the medial portion through medial perforators near the sternal border. The variable lateral thoracic artery supplies the lateral portion. The anterior and lateral branches of the intercostal vessels supply the remainder. Although there is a substantial degree of collateralization among these vessels in the breast parenchyma, it has been estimated that the internal mammary artery provides approximately 60% of the total. The lateral thoracic artery is thought to supply an additional 30%, primarily to the upper, outer, and lateral portions. The anterior and lateral branches of the third, fourth, and fifth posterior intercostal arteries supply the remaining lower outer breast quadrant. The variability and overlap between these vascular networks account for the remarkable safety of nipple-bearing pedicles of diverse design based on different vascular supplies. The breast has two major venous drainage systems: one superficial, the other deep. The superficial drainage system is divided into two types: transverse and longitudinal. The transverse veins run medially in the subcutaneous space and empty into the internal mammary veins by multiple perforating vessels. The longitudinal drainage ascends to the suprasternal area to connect with the superficial veins of the lower neck. There

are anastomotic connections across the midline, but only between the superficial systems. The major portion of the deep drainage is through perforating branches of the internal mammary vein. Additional venous drainage is in the direction of the axillary vein. A remaining route of drainage is posteriorly through perforators into the intercostal veins, which carry blood posteriorly to the vertebral veins. The lymphatic pathways draining the breast parallel closely the venous pathways and include cutaneous, internal mammary, posterior intercostal, and axillary routes. Although most lymph flow is through the axillary region, the internal thoracic channels may carry 3% to 20% of the total. Despite an extensive search for underlying metabolic causes of breast hypertrophy and gigantomastia, these conditions remain poorly understood phenomena, the products of end-organ hormonal sensitivity, genetic background, and overall body weight.

REDUCTION MAMMOPLASTY Indications Women seek to reduce the size of their breasts for reasons both physical and psychological. Heavy, pendulous breasts cause neck and back pain as well as grooves from the pressure of brassiere straps. The breasts themselves may be chronically painful, and the skin in the inframammary region is subject to maceration and dermatoses. From a psychological point of view, excessively large breasts can be a troublesome focus of embarrassment for the teenager as well as the woman in her senior years. Unilateral hypertrophy with asymmetry heightens embarrassment.

Inverted-T Techniques Two decisions confront the surgeon: (a) choice of incision (scar) pattern, and (b) choice of pedicle type. The inverted-T scar pattern can be applied to virtually any pedicle, including a superior pedicle, an inferior pedicle, a vertical bipedicle, a central mound pedicle, and a superomedial pedicle. The scar pattern and the pedicle type used in breast reduction are, for the most part, independent variables. Furthermore, there is no absolute cutoff regarding when an inverted-T scar pattern approach is appropriate instead of a vertical technique that avoids attempts to avoid a transverse inframammary scar. At Georgetown University Hospital, we use both vertical techniques as well as inverted-T techniques, depending on (a) the size of the breast, (b) the degree of ptosis, and the (c) patient’s goals. Even when opting for an inverted-T technique, we shorten the transverse scar component because of increasing experience with vertical scar techniques. The distinction, therefore, between vertical


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and inverted-T techniques has become less clear as surgeons add a short transverse scar to their vertical techniques or shorten the transverse scar in their inverted-T techniques. The majority of American plastic surgeons still use an inverted-T scar pattern, most commonly with an inferior pedicle. There are several major advantages to this technique. To begin with, it is reproducible, straightforward, and easily taught. To a large extent, the skin incisions correspond to the glandular incisions that are made on the breast parenchyma itself. In this way, once the lines are drawn on the skin preoperatively, the cutting of the tissues and the closure of the wound proceed along the preoperatively planned lines. This has great advantage in terms of predictability and reliability. In contrast, vertical scar techniques often involve a significant disparity between the skin incisions and glandular incisions beneath the skin. A significant amount of intraoperative adjustment is required both in terms of removing tissue and reshaping tissue to obtain an acceptable result. Finally, the closure of the skin may require adjustment to deal with the excess skin at the caudal end of the vertical incision. Once the decision has been made to perform a breast reduction, the surgeon must choose the orientation of the pedi-

cle. This chapter describes the vertical bipedicle technique, the inferior pedicle technique, a central mound technique, and a superomedial pedicle technique, which is my current preferred technique.

Vertical Pedicle Technique McKissock first described his vertical bipedicle technique for nipple transposition during reduction mammoplasty in 1972. With this technique the central breast is reduced to a vertically oriented bipedicle flap based superiorly on the upper margin of the new areolar window and inferiorly on the inframammary line and chest wall musculature. The flap carries the nipple– areola and, although de-epithelialized, depends primarily on inferior parenchyma for blood supply. With the patient erect, the markings are made in a fashion similar in all breast reductions (Fig. 59.1). The midline is drawn and the breast meridian is established by dropping a line from the midclavicle through the nipple and continuing inferiorly across the inframammary line. The inframammary fold is marked and a tangent to the fold is drawn across the lower thorax and transposed to the anterior breast and marked

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C FIGURE 59.1. Preoperative markings. A: Drawing the basic landmarks, including the midline and breast meridian, for most breast procedures. B: A tangent is drawn from the lower-most portion of the inframammary fold across the midline. C: This tangent is then superimposed onto the surface of the breast. D: The length of the fold is then measured. It is often between 20 and 24 cm long. (Continued)


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FIGURE 59.1. (Continued) E: An arc that is just over one-half the length of the fold is transposed onto the surface of the breast medially. F: A wire keyhole pattern (which is centered around the nipple site) can then be superimposed on the breast such that it crosses the arc line drawn in Figure 59.4. G: The keyhole pattern is completed by making the limbs the desired length, anywhere from 5 to 8 cm long, depending on the size of the breast. It is important to doublecheck that the length of these proposed superiorly based lateral and medial flaps along their cut, free, inferior edge match the length of the fold to which they are to be approximated.

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on the breast meridian. Whereas the initial descriptions set the nipple some 2 cm higher, the best location for the new nipple position is at the inframammary fold level. The entire length of the inframammary fold is measured with a tape measure. In most cases, it is between 20 and 24 cm long. Using a tape, a mark is made in the shape of a short arc on the surface of the breast that measures just over one-half the length of the fold (e.g., for a 22-cm fold, the distance would be 12 to 13 cm). Diverging lines are drawn from the nipple point; they pass as tangents to either side of the dilated areola and meet the arc line drawn from the ends of the inframammary fold. A wire keyhole pattern is then adjusted to a similar angle of divergence and superimposed on the lines, indicating the proper size and location of the new areolar window. A distance of 5 to 6 cm is measured from the window to establish the length of the limbs of the pattern. From these extremities, lines are directed medially and laterally to intersect the inframammary fold. The areola is circumscribed at a diameter of between 42 and 48 mm. The vertical pedicle is outlined by extending the lines of the vertical limbs inferiorly as two parallel lines straddling the breast meridian to the inframammary fold. The entire pedicle, except the reduced nipple-areola, is de-epithelialized. The vertical pedicle is then incised along its medial and lateral margins to the fascia of the underlying musculature, and medial and lateral dermoglandular wedges are resected (Fig. 59.2). A thin layer of breast over the lateral musculature is retained to favor preservation of sensation to the nipple–areola complex. Additional breast tissue is resected from the remaining medial and lateral elements: little to none medially, but a considerable amount, including the axillary tail, laterally. A window of

breast tissue is removed from the upper portion of the bipedicle flap, from the level of the nipple to the height of the keyhole pattern, creating a bucket-handle (Fig. 59.3). This resection must not extend above the upper limit of the areolar window in order to avoid loss of superior breast volume. The flap is folded superiorly on itself, bringing the areola into position within the keyhole pattern. The medial and lateral flaps are brought together over the pedicle, and closure is begun, working from the extremities toward the center (Fig. 59.4). Any central excess of skin is either excised at the vertical closure, or “worked-in” to the closure.

Inferior Pedicle Technique The inferior pedicle technique is the most popular technique among plastic surgeons today. The planning of the inferior pedicle technique is essentially the same as for the McKissock bipedicle procedure, with the desired nipple location determined in the same manner. An inferiorly based dermoglandular pedicle is planned with a base of 4 to 9 cm at the inframammary line that gradually tapers as it ascends to encompass the nipple– areola complex. De-epithelialization with this technique is limited to the zone immediately about and inferior to the nipple–areola (Fig. 59.5). Skin and parenchymal resections are performed medial and lateral to the pedicle, as described above, but also superior to the nipple–areola, up to the level of the keyhole pattern. These excisions are performed leaving a beveled carpet of breast tissue over the muscular fascia, especially laterally. Immediately superior to the 1-cm de-epithelialized cuff about the nipple–areola, the pedicle is


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FIGURE 59.2. McKissock technique. Medial and lateral dermoglandular resections.

terminated and incised down to muscle fascia, taking care not to undercut the inferior vascular base (Fig. 59.6). A pyramidal pedicle of dermis and parenchyma is thus left deep to and inferior to the nipple–areola, based on the chest wall musculature and inframammary line. In the vicinity of the areola, it measures 2 to 4 cm in thickness, and near the base it is 4 to 10 cm. After completion of the breast resection, the nipple–areola is brought to the desired position in the keyhole pattern, and the medial and lateral

flaps are brought together as with the McKissock technique (Fig. 59.7).

Central Mound Technique The central mound technique is a further evolution of the prior two designs. The pedicle is based on central chest wall musculature alone and is not contiguous with any skin boundary. Hence it has no directional base in the sense of traditional skin

FIGURE 59.3. McKissock technique. Central glandular resection produces buckethandle flap for infolding.



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pedicles that may be classified as superior, inferior, or transverse. Preoperative marking is again performed as for the McKissock technique. The skin is de-epithelialized within the entire keyhole pattern, a process continued inferiorly to include the reduced nipple–areola complex (Fig. 59.8). An incision is placed in the inframammary crease and is carried down perpendicularly to the pectoralis fascia. Incisions are now made and beveled around the margins of the keyhole pattern at its medial and lateral limbs. This incision is continued below the level of the limbs to circumscribe the de-epithelialized pattern, including the nipple–areola, and is beveled in a caudal direction toward the inframammary fold. The limb incisions, both medial and lateral, are made in the standard fashion, developing flaps of thickness similar to those in other techniques. Now the medial and lateral inferior quadrants of skin and breast, as well as the central inferior tissue intervening between the nipple–areola and the inframammary fold, are excised as a single curvilinear, ellipsoid unit that includes the axillary tail (Fig. 59.9). A skin incision at the superior aspect of the keyhole is deepened only enough to allow comfortable transposition of the central mound pedicle with its nipple–areola into the keyhole position. The skin flaps are brought about the pedicle as in other techniques, and closure is performed (Fig. 59.10).

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FIGURE 59.4. McKissock technique. A: Vertical bipedicle folded on itself as key sutures tied. B: Closure.

AUTHOR’S TECHNIQUE The patient is marked in the standing position in the exam room or in the office the day prior to surgery; the markings are made as described above. I often mark the upper border of the breast to give some perspective as to where the breast will lie at the end of the breast reduction procedure. This allows a better appreciation of where the nipple might sit after the breast reduction. The ideal limbs of the keyhole pattern vary between 5 and 8 cm, depending on the size of the breast currently and the size of the planned breast after reduction. The larger the breast and the larger the breast that is to remain after the procedure, the longer these limbs should be. Five centimeters is the minimum length of the vertical limb of the keyhole, and I will often go to 6, 7, or even 8 cm, depending on how big the breasts will be left postoperatively. I am well aware that when the breast is made too large for the skin flaps, the skin flaps will often stretch, and that when the skin flaps are larger than the breast, the skin flaps will often shrink postoperatively. A fairly straight line is then drawn from the lowest-most point of the vertical limb of the keyhole to the medial-most extent of the inframammary fold mark. The same is done laterally to the

FIGURE 59.5. Inferior pedicle technique. A: Preoperative markings with inferior pedicle deepithelialized. B: Medial dermoglandular resection.


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FIGURE 59.6. Inferior pedicle technique. Pedicle developed.

lateral-most extent of the inframammary fold. Having drawn the keyhole and the planned incisions, the pedicle can now be drawn. I am particularly impressed with the versatility and speed of the superomedial pedicle and now use this approach in a large majority of my breast-reduction procedures, regardless of whether they are inverted-T scar patterns or vertical scar patterns. The design for the superomedial pedicle is drawn so that it starts superiorly, along the arch of the previously drawn keyhole, and ends either at or near the bottom of the vertical limb of the keyhole (Fig. 59.11). The planned areola is circumscribed, leaving several centimeters around the areolar margins as the pedicle is drawn. At this point, the patient is observed critically for symmetry of the plan. Particular key points for symmetry include the upper border of the planned areola, as well as the location and length of the vertical limb of the keyhole pattern and the line joining the bottom of the keyhole pattern to the medialmost border of the inframammary fold. As mentioned earlier, because of the preexisting asymmetry that is often found in breast-reduction patients, it is acceptable to have more tissue planned for excision in the larger breast. I like to photograph the patient at this point for reference both intraoperatively and postoperatively. With the advent of digital photography, it is relatively simple to print out these photographs for referencing during the actual surgical procedure.

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I often have the patient lie down at this point and shorten the incisions both medially and laterally by at least 2 cm (Fig. 59.12). This shortening is done in such a way that the medialmost extent of the incision is brought lateral by 2 cm and this new end point is drawn midway between the upper and lower previously planned incisions. The same is done laterally, so that the scars or incisions that will be made will curve somewhat off the inframammary fold as compared to the original plan. Thus, even preoperatively, the planned length of the incision will be 4 cm or more shorter than the preoperative length of the inframammary fold. To be certain that the lines that I have drawn are not lost during the preparation of the patient, I lightly score these lines just prior to surgery using an 18- or 21-gauge needle. One of the most remarkable things with this procedure is the speed of de-epithelializing. Because the pedicle is almost always quite small and substantially smaller than with other techniques, de-epithelialization is brief and is all within the keyhole pattern itself. The incisions are then scored around the margins of the keyhole and from the keyhole to the inframammary fold and along the inframammary fold. I prefer to dissect the lateral flap first, and this is done by incising the dermis along the edge of the skin incision down to a depth of 1 to 2 cm of breast tissue. A lateral-based flap is created that goes out to the axillary tail, leaving sufficient soft tissue to ensure viability of the lateral skin flap (Fig. 59.13). The medial and inferior incisions are made through the dermis down to or near the muscle

FIGURE 59.7. Inferior pedicle technique. A: Nipple–areola positioned. B: Closure.



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fascia. Once all these incisions have been made, the pedicle is held using hooks or atraumatic clamps, and incisions are made straight down along the margins of the pedicle superiorly, laterally, and inferiorly, taking care not to undermine the pedicle (Fig. 59.14). In particular, as the dissection is carried laterally, some beveling is done to leave soft tissue along the chest wall in the anticipated path of the neurovascular supply to the nipple– areolar complex. The breast tissue itself is removed in a C, or inverted-C pattern from either breast (Fig. 59.15). The key elements of this resection are to leave adequate blood supply to the nipple–areola pedicle by not undermining the pedicle and leaving it fully attached to the chest wall. The breast tissue is aggressively removed in the medial wedge area, as well as inferiorly and laterally. The area of greatest risk in this operation is the circulation to the lateral skin flap and, therefore, that flap must not be made too thin or be traumatized in the dissection. I then incise just the dermis of the pedicle itself, where it joins the keyhole medially, to allow for easier rotation of the

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FIGURE 59.8. Central mound technique. A: Preoperative markings. B: Limited central de-epithelialization.

dermoglandular pedicle. After rotation of the nipple–areola, the areola is attached at the meridian of the keyhole aperture. The keyhole pattern is then closed around the pedicle both at the 6 o’clock location of the areolar window and at the 6 o’clock position of the vertical limbs of the keyhole. The pedicle itself may be tacked to the chest wall to prevent malposition. The incisions are approximated with a few staples. Because the flap lengths have been measured preoperatively to approximate one-half of the inframammary fold length, there are rarely any dog-ears to deal with. A small suction drain is usually placed in the inframammary fold and brought out through a stab incision laterally to help facilitate drainage. The final closure is accomplished and the staples removed. The technique is easy to perform and to teach. The same pedicle can also be used as part of a vertical reduction technique. The creation of the pedicle is virtually the same. The only difference is that the skin is tailored to the breast at the end of the operation and excess skin can be removed as

FIGURE 59.9. Central mound technique. Dermoglandular resection.


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FIGURE 59.10. Central mound technique. A: Nipple–areola advanced superiorly. B: Closure.

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necessary either in a vertical or a combined vertical and short T pattern (Fig. 59.16).

BREAST AMPUTATION WITH FREE NIPPLE GRAFT: AUTHOR’S TECHNIQUE An excellent, if often maligned, alternative to reduction mammoplasty with a nipple-bearing pedicle remains breast amputation with free nipple graft. This technique consistently produces well-shaped breasts. In large women, in particular, an attractive breast contour is more easily accomplished with this technique than with conventional approaches. The disadvantage is the relatively unnatural appearance and function of the nipple–areola complex: Specialized sensation is certainly lost,

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as well as some degree of nipple projection, especially erectile nipple projection; lactation is similarly sacrificed; and occasional spotty survival of the grafted areola produces areas of depigmentation that can be troublesome in dark-skinned individuals. This rapid technique is especially indicated for women with gigantomastia, presenting 2,500 g or more of breast tissue per side, as well as for patients with other complicating factors, such as increased age or systemic disease where significant reduction in blood loss and operating time is desired. It remains the preferred alternative for many elderly patients who present for reduction mammoplasty because of increasing symptoms involving a demineralized skeletal system. With respect to the patient with extremely large breasts, I consider this alternative whenever the nipple–areola complex is to be elevated more than 15 cm. This guideline is modified by other factors, especially the age of the patient. I am reluctant to use this alternative in young or unmarried patients, for example. Although concern for ischemic injury to the retained nipple–areola complex in such greatly enlarged breasts remains a major indication for this alternative, it may not be the sole reason to recommend it. Rather, the technical reality of breast reduction for such large breasts may prove unwieldy when a pedicle is maintained.

Preoperative Marking The breast markings remain similar to those for the previously described inverted-T techniques (Fig. 59.17). The wire keyhole pattern is not used for this technique, however. Instead, two diverging arms are drawn from the selected nipple point at an angle approximating 90 degrees. Limb length is measured at 7.5 to 8.5 cm (average 8 cm). The inframammary line is marked, and the medial and lateral extensions from the limbs are indicated as for the standard technique. The areola is marked for reduction with the areolar marker.

Technique FIGURE 59.11. The base of superomedial pedicle should be drawn so that it connects to the keyhole pattern somewhere along the areola window superiorly and along the vertical limb inferiorly. The precise attachment is not critical, but it should be drawn so as to facilitate rotation.

The procedure is begun by removing the nipple–areola complex rapidly with attached subjacent breast tissue and setting it aside in a moist saline sponge, clearly indicating the side of origin, right or left. I do not follow the skin markings as some have suggested when performing the glandular resection,



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because I find it too often results in inadequate central projection of the breast. Far better is Rubin’s alternative of retaining inferior parenchyma at the inframammary line to be covered by the superior skin flaps. I prefer, however, to retain superiorly based parenchyma between the diverging limbs of the pattern, as well as an additional amount dropping below this area if needed. This retained tissue is designated with a single curvilinear line placed below the diverging arms, and the enclosed area is rapidly deskinned. Clearly, the greatest pitfall in this otherwise straightforward procedure is the amputation of excessive breast tissue, leaving only superior flaps with subcutaneous tissue and little breast. If the breast is allowed to hang pendulously, gravity pulls virtually the entire gland below the level of the amputating blade, presenting the surgeon with a regrettable surprise when refashioning an inadequate breast from the remaining superior flaps. On the other hand, when the gland is gathered and presented in a spherical fashion by an assistant, the amputating blade leaves a significant amount of parenchyma superiorly. The dictum that more can always be removed later prevails.

FIGURE 59.13. A laterally based flap of some safe thickness is dissected to allow access to the lateral breast tissue.

The amputating incision is carried perpendicularly to the chest wall musculature. The inframammary incision is similarly carried perpendicularly to the musculature. The large intervening wedge of gland is then dissected progressively from medial to lateral away from the muscle fascia, maintaining exact hemostasis as the resection progresses. The central portion of the remaining superior gland, including the deskinned portion between and below the diverging limbs, is now dissected from the underlying muscle fascia superiorly to the apex of the inverted-V pattern. The dermal edges of the inverted-V are incised to allow infolding of the superiorly bases dermal flap. The most inferior points of the inverted-V are then approximated, thus effectively coning and infolding the breast. Closure is completed in the standard fashion working both vertically and from the extremities centrally.

FIGURE 59.14. The superomedial pedicle is developed by cutting around the previously marked pedicle straight down toward the chest wall, without undermining and with some feathering laterally to protect the neurovascular supply.


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Finally, the site for the nipple–areola complex is determined and measured upward from the inframammary fold on either side. It may or may not fall precisely at the superior extent of the vertical closure. The area is marked with the areolar marker and is de-epithelialized. The defatted nipple–areola complex is sutured in place and secured with a tie-over dressing. It is important not to thin the areolar portion of the graft excessively during the defatting process, so that the resulting areolar graft has a more natural appearance. Similarly, ductal tissue is left within the papilla, to favor nipple projection. A greasy dressing with wet cotton bolus is then tied in place over the complex and is removed at 4 days.

CONCLUSION Despite the many recent advances in breast reduction surgery, the inverted-T scar technique remains a comfortable and predictable technique for the surgeon who performs breast surgery. Although there is appropriate increasing interest in short scar or vertical scar techniques, the inverted-T option has proven reliable and safe, which may be as important to the patient as the length of the scar in the inframammary fold. FIGURE 59.15. The resulting specimen is an inverted-C or C shape, depending on which breast.

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D FIGURE 59.16. A: Frontal view of plan for breast reduction using superomedial pedicle and inverted-T scar pattern. B: Lateral view of plan. C and D: Before and 3 months after 575-g reduction using the author’s technique.



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FIGURE 59.17. Author’s breast amputation with free nipple-areola graft, technique. A: Breast meridian marked. B: Preoperative markings completed. C: Amputation completed. D: Central tissue coned and rotated into retromammary space. E: Free nipple–areolar graft added at closure.

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Suggested Readings Balch C. The central mound technique for reduction mammoplasty. Plast Reconstr Surg. 1981;67:305. Courtiss E, Goldwyn RM. Reduction mammoplasty by the inferior pedicle technique. Plast Reconstr Surg. 1977;59:500. Georgiade NG, et al. Reduction mammoplasty utilizing an inferior pedicle nipple–areola flap. Ann Plast Surg. 1979;3:211. Hall-Findlay EJ. Pedicles in vertical breast reduction and mastopexy. Clin Plast Surg. 2002;29(3):379. Hammond DC. The SPAIR mammaplasty. Clin Plast Surg. 2002;29(3):411. Hammond DC. Short scar periareolar inferior pedicle reduction (SPAIR) mammaplasty. Plast Reconstr Surg. 1999;103(3):890.

Hidalgo DA. Improving safety and aesthetic results in inverted T scar breast reduction. Plast Reconstr Surg. 1999;103(3):874. Marchac D, de Olarte G. Reduction mammoplasty and correction of ptosis with a short inframammary scar. Plast Reconstr Surg. 1982;69:45. McKissock PK. Reduction mammoplasty. Ann Plast Surg. 1979;2:321. McKissock PK. Reduction mammoplasty with a vertical dermal flap. Plast Reconstr Surg. 1972;49:245. Nahabedian MY, McGibbon BM, Manson PN. Medial pedicle reduction mammaplasty for severe mammary hypertrophy. Plast Reconstr Surg. 2000;105(3):896. Nahabeian MY, Mofid MM. Viability and sensation of the nipple–areolar complex after reduction mammaplasty. Ann Plast Surg. 2002;49(1):24. Robbins TH. A reduction mammoplasty with the areola–nipple based on an inferior dermal pedicle. Plast Reconstr Surg. 1977;59:64.


CHAPTER 60 ■ VERTICAL REDUCTION MAMMAPLASTY ELIZABETH J. HALL-FINDLAY

Many options are available to the surgeon for breast reduction. No one technique should be applied to all breasts. Each surgeon must have a few different approaches with which he or she is comfortable. For example, the vertical techniques (1) are ideal for small to medium reductions. The inverted-T techniques (2) may be better for larger reductions or those with considerable skin excess (as occurs in postbariatric patients). Either technique can be used with free nipple grafts (3) for the massive breast. Liposuction only (4) is available as a technique, but is of limited usefulness. Confusion is generated by equating the choice of the skin resection pattern with the choice of pedicle used to transfer the nipple–areola complex. Because the vertical skin resection pattern is often associated with a superior or superomedial pedicle and because the inverted-T tends to be associated with an inferior or central pedicle, the terms are often used without clear distinction. Any pedicle can be used with any skin resection pattern. There are, however, advantages and disadvantages to each.

Anatomy Blood Supply To understand the design choices for breast reduction, one must have a clear understanding of the blood supply to the breast parenchyma and to the nipple–areolar complex (Fig. 60.1A). As described by Ian Taylor (5), the blood supply to the breast is superficial, which is logical because the breast is a structure derived from the ectoderm. There is one large, deep perforator that comes through the pectoralis muscle inferiorly. There are venae comitantes accompanying this artery, but otherwise the veins are very superficial and quite separate from the arteries. Because the arteries are superficial, the design of the pedicle for the nipple–areola complex can be dermal rather than dermoglandular. Because the veins lie just under the dermis, it is important to maintain a dermal connection to most pedicles. The one exception is the inferior or central pedicle, which relies on the artery and vein of the deep perforator. This vessel comes from the internal mammary artery at the level of the fifth or sixth interspace. It usually perforates the pectoralis muscle just medial to the breast meridian, a few centimeters above the inframammary fold. Branching may occur superficial or deep to the muscle. The rest of the arterial input is relatively superficial. There is a large branch of the internal mammary system that emerges from the second or third interspace and runs obliquely toward the breast meridian. This vessel is only about 1 cm deep to the skin as it enters the breast. The fact that this vessel is so superficial and provides such good blood supply allows the superior pedicle to be long and quite thin. Because large breasts are quite ptotic, this vessel seems to be more obliquely oriented than it

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was before puberty—it runs from about the second or third interspace toward the level of the fourth or fifth interspace. There are numerous superficial veins at this level, but they are separate from the arteries. There are additional branches running medially from the internal mammary system at the level of the third to sixth interspace. These vessels supply a medially based pedicle, which can be either dermal or dermoglandular. The lateral thoracic system is also relatively superficial, although deeper than the vessels described above, it is usually found 2 or 3 cm deep to the skin at the level of the inframammary fold. There are also prominent veins in this area. It is these vessels that supply a lateral pedicle.

Nerve Supply Innervation to the nipple–areolar complex is said to be provided by the lateral branch of the fourth intercostal nerve. Although this is true, it does not constitute the only nerve supply (Fig. 60.1B). The Austrians (6) have shown that the lateral branch has both a deep and a superficial branch. The superficial branch supplies a lateral pedicle. The deep branch runs along the surface of the pectoralis fascia and then it turns upwards toward the nipple at the meridian. This is interesting because it means that any full-thickness pedicle designed straight down to the breast meridian (while not exposing pectoralis fascia) should incorporate this deep branch. Clearly, this branch is usually preserved with an inferior or central pedicle as long as the tissue overlying the pectoralis fascia is left intact. There are also medial branches of the intercostal system that run superficially and supply innervation to a medial pedicle. Supraclavicular branches run superficially and supply a superior pedicle.

Ductal Preservation There are approximately 20 to 25 ducts that enter the nipple. Each duct is fed by glandular breast parenchyma. Although dermal pedicles may preserve arterial, venous, and nerve supply, it is unlikely that dermal pedicles will retain much breast-feeding potential. There is some potential for ducts to reconnect, but this is speculative. Dermoglandular pedicles will incorporate more glandular and ductal tissue intact.

Design There has been considerable reluctance to adopt the vertical skin resection patterns in breast reduction surgery (Fig. 60.2). This is based on a lack of understanding that the principles of this technique do not apply to the inverted-T techniques. The inverted-T relies on the skin brassiere to maintain the shape. The pattern was designed to minimize stretching of the skin. To prevent pseudoptosis, the vertical skin length, from nipple to inframammary fold (IMF), was restricted to about


Chapter 60: Vertical Reduction Mammaplasty

A

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B FIGURE 60.1. Anatomy. A: Blood supply. The arterial supply is superficial (A, B, D) except for the deep perforator (C) that comes through the pectoralis muscle. The veins lie just under the dermis and are quite separate from the arteries (except for the venae comitantes which accompany the deep perforator). B: Nerve supply. The main innervation to the nipple and areola is from the lateral fourth intercostal nerve. It should be noted that there is a deep branch that courses just above the pectoralis fascia as well as the more superficial branch. This branch can provide sensation in several full-thickness pedicles. There are also medial intercostal branches that supply innervation.

5 cm. Although some coning of the breast tissue occurs, the nature of the resection of the breast parenchyma plays a minor role in shaping. The skin is removed mainly along a horizontally designed ellipse and the dog-ears are chased medially and laterally. Sometimes this pattern results in a boxy breast with definite limitations on the amount of projection achieved. On the other hand, the vertical skin resection patterns tend to use the breast parenchyma to provide the shape. The skin adapts to the breast shape rather than the other way around. This will vary somewhat with the design of the pedicle chosen. The skin and breast parenchyma are removed mainly along a vertically designed ellipse and the dog-ears are chased up into the new areola and inferiorly toward the inframammary fold. These breasts have a much longer vertical length, which is needed to accommodate the increased projection that results from this design.

The choice of pedicle will also influence the resultant breast shape. The superior, superolateral, and superomedial pedicles will rely less on the skin brassiere to hold the shape. The inferior pedicle may respond more to gravity and the pedicle may need to be sutured up to the chest wall in an attempt to prevent bottoming out. With the inferior pedicle, it is important not to violate the inframammary fold for this reason. Large pedicles of any type may be too heavy and may require suturing to the chest wall, or even amputation and free nipple grafts. There remains some controversy about what method of suturing breast tissue to the chest wall is effective in the long-term. Skin closure will be somewhat determined by the type of pedicle used. A circumvertical skin closure is necessary with an inferior pedicle. Either a straight or circumvertical skin closure can be used with the other pedicles. When there is a considerable amount of loose, inelastic skin, a T or J skin excision

A

B FIGURE 60.2. Pedicles and skin resection patterns. The skin resection pattern and the pedicle used for the nipple–areolar complex need to be assessed separately. Various combinations are available.


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may be needed to remove the excess. This is, however, less frequently necessary than initially thought by those surgeons who have been trained with the inverted-T skin resection patterns. As with most surgical procedures in plastic surgery, there are variations in the technique and variations in the principles used. Marchac (7) uses parenchymal resection for breast shaping, but he removes some of the excess skin by adding a T excision. Lassus (8) does not undermine the skin or remove breast tissue laterally above the inframammary fold. His pattern maintains the original inframammary fold and relies partly on parenchymal resection and partly on the skin brassiere to hold the shape. Lejour (9) relies on liposuction for volume reduction, and breast sutures to hold the shape of the parenchyma. She uses skin undermining and skin gathering to help the skin adapt to the new shape. All of these surgeons prefer a superiorly based pedicle for the nipple areolar complex and inferior parenchymal resection for breast shaping. Hammond (10) uses an inferior pedicle and a circumvertical skin resection pattern. His procedure relies on both parenchymal suturing and the skin brassiere to maintain the shape.

VERTICAL BREAST REDUCTION USING THE MEDIALLY BASED PEDICLE The following describes a vertical skin resection pattern and a medially based pedicle for the nipple–areolar complex (11,12). ■

■

Vertical skin resection pattern: The skin excision is a vertical ellipse, but the parenchymal resection follows the Wise (13) pattern (vertical plus horizontal). The inferior tissue is removed, the inframammary fold can rise if desired, and the remaining breast tissue is superior, superomedial, and superolateral. It is believed that this resection pattern best resists the deforming forces of gravity over time. Medially based pedicle: The pedicle is full thickness and it maintains sensation equivalent to the other pedicles. The nipple–areolar complex rotates easily into position without kinking or compression. The inferior border of the medial pedicle becomes the medial pillar. The fact that the whole base of the pedicle rotates gives an elegant curve to the inferior aspect of the breast. The superior pedicle can also be used, but it can be more difficult to inset. The superior pedicle can be safely thinned to prevent compression, but some depression can occur inferiorly when closing the pillars.

Markings The key to marking the breast for breast reduction is to determine the new nipple position. This should be (with some variation; see below) at the intersection of the inframammary fold and the breast meridian.

Determination of New Nipple Position Inframammary Fold. The IMF varies significantly from person to person. The new nipple needs to be designed according to the patient’s anatomy, not an arbitrary distance from the suprasternal notch. Although a finger in the inframammary fold transposed to contact a finger on the breast skin can be used, the best method to determine the actual fold is to place a measuring tape around the chest under the breasts. The true level of the fold can be marked by drawing a line in the

midline at the upper border of the tape. (It is interesting that this is often significantly lower than the finger method.) There may be some asymmetry in the levels of the breast folds and this needs to be noted. Breast and Chest Wall Meridian. The breast may extend so far laterally that the true chest wall meridian may be much more medial. If lateral breast tissue is to be removed, the true chest wall meridian may be the better marking. Otherwise, the breast meridian should be chosen. The meridian is drawn from the midclavicular line down through the breast. Care must be taken to ignore the existing position of the nipple when marking the true meridian, but it is better to err on the side of placing the new nipple too lateral rather than too medial. The meridian can then be extended on to the chest wall below the inframammary fold. This is usually about 9 to 11 cm from the midline of the body and will obviously vary with different body sizes. New Nipple Position. The new nipple position will be marked approximately at the intersection of the inframammary fold and the breast meridian. Surgeons who are comfortable with the inferior pedicle inverted-T pattern, should place the new nipple position approximately 2 cm lower than what they are used to; this is needed to accommodate the increased projection that results from this approach. This is especially important when a patient has very little existing upper-pole fullness. On the other hand, when a patient has significant upper-pole fullness, more flexibility exists and the new nipple position can be placed higher. If the surgeon is going to attempt to raise the inframammary fold (by clearing out tissue along the Wise pattern above the existing inframammary fold) the new nipple position can be raised slightly. Caution: It is almost impossible to lower a nipple that has been placed too high. It is much easier to raise a nipple that has been placed too low. When there is significant size asymmetry, it is important to mark the new nipple position of the larger breast somewhat lower than the new position on the smaller breast. There are two reasons for this. First, the weight of the breast will stretch the skin and make the new marked position rise when the weight is removed. Second, closure of a vertical ellipse will push the upper end upward and the lower end downward. The inverted-T technique involves closure of a horizontal ellipse and the dog-ears are chased medially and laterally. The vertical technique involves closure of a vertical ellipse and the upper dog-ear is chased into the areola. If the vertical ellipse (of skin and parenchyma) is larger on one side, the upper end will be pushed up higher.

Skin Resection Pattern Areolar Opening. The opening for the areola can be marked preoperatively or intraoperatively. When a surgeon first uses the vertical technique, it is perhaps easier to use the system with which they are familiar. If the areolar opening is made preoperatively, it should be designed so that it becomes a circle when closed. It makes more sense to extend the design vertically than to carry it out laterally in a mosque shape. If a 4.5-cm diameter is used for the new areola, the exact circumference will be 14 cm; if a 5-cm diameter is used for the new areola, the exact circumference will be 16 cm. It is not actually necessary to match the circumferences exactly, but a significant discrepancy will result in widening of the areola, or the scar, or both. A circumvertical type of suture will be required if there is more than a 4-cm circumferential difference. Vertical Resection Pattern. In the vertical techniques, the skin is not important in shaping the breast. Only enough skin needs to be removed to avoid skin redundancy. The skin is not being used as a skin brassiere and it is unnecessary—and detrimental—to make the skin closure tight.



FIGURE 60.3. Design of the skin resection pattern (outlined in red), the medially based pedicle (colored blue) and the parenchymal resection pattern (crosshatched). The parenchymal resection follows a Wise pattern and the skin resection pattern looks like a snowman.

The vertical limbs can be drawn similar to that which would be drawn for a Wise-pattern skin resection. These can also be determined by pushing (and slightly rotating) the breast medially and then laterally to line up the vertical limbs with the previously drawn meridians in the upper and lower chest wall areas. Instead of extending the vertical limbs laterally and medially as would be done in an inverted-T Wise pattern, the vertical limbs are joined to each other well above the inframammary fold. The final shape of the skin resection pattern with both the areolar opening and the vertical skin resection is much like a child’s snowman (Fig. 60.3). The body is round with a smaller round head on top. Some surgeons have made the vertical resection come down as a V in order to limit the skin dog-ear, but, unfortunately, this often does not result in enough redundant lateral skin excision. Instead, the surgeon is forced to add a T or to add further resection and close it as a pursestring. The skin resection pattern should remain well above the existing inframammary fold. There are two reasons for this. First, the parenchyma and skin are excised as a vertical ellipse and closure results in lengthening of the incision. The closure can push the scar below the fold. Second, when the parenchyma is removed along the Wise pattern horizontally (in addition to the resection along the vertical ellipse), the inframammary fold will often rise. If the fold rises, the scar can fall below the new fold. If these two factors are not taken into account, the scar might end up extending below the inframammary fold onto the chest wall. On average, at least 2 cm of skin must be left above the IMF in a small (300-g) reduction. At least 4 cm must be left in a medium (600-g) reduction, and at least 6 cm of skin must be left in a larger reduction (up to 1,000 g). Larger reductions will benefit from an even larger skin bridge.

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To allow easy inset of all medially based pedicles, the base should be designed with half of the base into the areolar opening and half of the base into the vertical skin resection opening. When the original nipple position is quite low, the orientation will definitely be oblique. When the nipple does not have to move much higher, a superior pedicle can be chosen. The medial pedicle, however, does allow easy access to resect the redundant lateral breast tissue. This tissue is often very thick and fibrous and is not amenable to liposuction for volume reduction. The lateral pedicle design was initially chosen because it was presumed to have better sensation (it didn’t) and it was easy to inset, but the lateral breast tissue could not be resected because it formed the base of the pedicle. An unsatisfactory shape (with excess lateral fullness) was the result. Some tissue will be excised above the pedicle superiorly to allow the pedicle to be inset easily. It may be tempting to leave superior tissue and to push it up with the pedicle in order to achieve more upper-pole fullness, but this is usually doomed to fail. The tissue will drop and pseudoptosis will result. Some tissue can be left superiorly to try to incorporate more arterial input and it can also be used to provide a platform for the medially based pedicle. Although the pedicle is full thickness, it will appear to be undermined (much as the inferior pedicle) and providing a small platform can help prevent inversion of the nipple-areolar complex. The base of the pedicle averages about 8 cm. The length of the pedicle to the base width is often about a 1:1 ratio, with the smaller reductions (300 g) having a 6-cm base, the medium-size reductions (600 g) having an 8-cm base, and the larger reductions having a 10-cm base. Wider bases are unlikely to improve circulation for very large reductions. Very long, large pedicles may end up causing pseudoptosis with the excess weight and volume, and free nipple grafts should be considered as an alternative. Suturing up the very large pedicles onto the chest wall may be of benefit, but this is unnecessary with most breast reductions up to 1,000 g.

Parenchymal Resection Design The various types of vertical breast reduction vary. The pedicle chosen will determine to some extent the pattern of the parenchymal resection. For example, using the inferior pedicle means that the breast tissue is removed superiorly. For the other vertical patterns, the breast tissue is removed inferiorly as a vertical ellipse. The principle that the vertical limbs in an inverted-T should measure only 5 cm does not apply to the skin in the vertical techniques, but it is a useful concept for the parenchyma. Keeping the pillar height at about 7 cm gives an ideal breast shape. To keep the pillars relatively short, the remaining parenchyma is removed horizontally below the pillars along a Wise pattern. Once the markings are complete, it helps to draw the inverted-T or Wise pattern on the skin to guide the parenchymal resection. The tissue above is maintained to shape the breast and create the breast pillars. The tissue below is removed.

Pedicle Design The medial pedicle can be either dermoglandular or dermal, but breast-feeding is more likely to be preserved if the pedicle is full thickness. The pedicle is carried down directly to the breast meridian. As with all pedicles, it will be quite mobile and may appear to have been undermined. The medial pedicle is often described as a superomedial pedicle. There is no question that it looks more superior when a patient is standing, but it actually has more of a medial orientation when the patient is lying down. The pedicle can be designed so that it is more superior, but giving the pedicle more of a superior orientation means that it can be sometimes more difficult to inset unless it is thinned.

Operative Technique Figure 60.4 illustrates the operative technique.

Infiltration Some form of vasoconstriction is helpful. Infiltration along the inferior aspect and the base of the breast of about 40 mL per breast of Xylocaine 0.5% with 1:400,000 epinephrine will reduce bleeding during parenchymal resection. Unfortunately, infiltration along the incision lines can result in small hematomas because of the numerous superficial veins just below the dermis.


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A

B

C

D FIGURE 60.4. Operative technique. A: Pedicle and skin resection pattern. B: Rotation of pedicle. Note that the inferior border of the medial pedicle is now the medial pillar. C: Closure of the pillars. The pillar length is only about 5 to 7 cm. The pillar closure starts about half way up the vertical opening because the parenchyma needs to be resected inferiorly as outlined (following the Wise pattern). D: Closure of the areola and skin. Originally it was thought that this vertical incision needed to be gathered to allow the skin to retract. It has become increasingly evident that gathering not only interferes with healing but that it also delays resolution of the puckering.

In obese patients it is advisable to infiltrate about 500 to 1,000 mL of a tumescent-type fluid on each side along the lateral chest wall and the preaxillary areas. This reduces bleeding when these areas are suctioned. Some of the tumescent-type fluid can be infiltrated around the base of the breast as well. If too much is used, the breast will become quite “wet” and cutting cautery will be less effective. Care must be taken to secure accurate hemostasis when using vasoconstrictors for breast reduction. It is especially important to look for and cauterize the perforators that come through the pectoralis fascia. They may remain constricted and not bleed during surgery, but these are usually the vessels that will later open up and cause a postoperative hematoma.

Creation of the Pedicle The skin of the pedicle is de-epithelialized. Putting the skin on tension by using either a commercial device or a lap pad held at the base of the breast with a Kocher clamp, helps the assistant keep the skin taut. Care is taken to preserve the superficial veins that lie just beneath the dermis. The pedicle is full thickness. It is incised directly down to the chest wall. Either a scalpel or cutting cautery can be used. Care is taken not to expose pectoralis fascia to both avoid bleeding and preserve the nerves that run just above the fascia. Some tissue cephalad can be left superiorly to leave a platform for the pedicle, but it is important not to try to push that tissue up in an attempt to increase upper-pole fullness.

As with the inferior pedicle, it will be quite mobile and it is important that the assistant not pull excessively to avoid inadvertent undermining of the pedicle.

Parenchymal Resection Both scalpel and cutting cautery are used to remove breast tissue. The resection is beveled out laterally and medially. The inferior border of the medial pedicle becomes the medial pillar. The whole base of the pedicle rotates as the nipple and areola are inset into position and the pedicle itself gives an elegant curve to the inferior pole of the breast. The lateral resection will be more aggressive, but some tissue (not much) needs to be left to fashion a lateral pillar. There is often a considerable excess of lateral breast tissue and direct excision is necessary because of its thick fibrous nature. Adipose tissue lateral to the breast (which is actually on the lateral chest wall) can be treated later with liposuction. It is important to follow the preoperative plan for the amount of tissue to be resected. Because it can be difficult to resect an adequate amount of breast parenchyma with this technique, it may be tempting to remove tissue superiorly. If the patient has very little upper-pole fullness, it is important not to resect superior tissue for a few centimeters on either side of the breast meridian. On the other hand, tissue can be removed superiorly when the patient has a significant amount of upper-pole fullness. The inferior breast tissue along the Wise pattern is removed by direct excision and then liposuction is used to tailor the



resection inferiorly, both laterally and medially. Liposuction is not used for volume reduction, but it is used to correct asymmetry that remains during closure and it is used for cosmetic refinement. The skin flaps incorporate the breast tissue superiorly and laterally, as well as superiorly and medially. The resection is beveled out laterally and medially and then finished with liposuction. The resection is actually undermined inferiorly so that the inferior breast can now become chest wall (skin and fat) as the inframammary fold rises. The fold will only rise about 1 to 2 cm at the meridian, but it will curve up considerably as it extends laterally and medially. The skin flaps are therefore full thickness superiorly and thinned out (with still a layer of fat to prevent adhesions) inferiorly. Flap thickness is thinnest at the skin margins (about 1 cm) and it gets thicker as one extends laterally and medially. There will be an excess of skin remaining inferiorly compared to breast parenchyma.

Insetting the Pedicle It is easier to inset the pedicle after the base of the areola is closed. A single 3-0 polydioxanone suture (PDS) or Monocryl suture is used. Some dermis is incorporated with the first bite at the base of the pedicle, but the dermis itself does not need to be undermined. Once this suture is tied, the nipple and areola rotate easily into position. The amount of rotation will vary; only enough rotation is needed to allow a comfortable inset with minimal compression. Even though the pedicle is carried full thickness down to the chest meridian, it is very mobile and may appear to have been undermined. The medial and lateral pillars are then closed. Final inset and closure of the areola is performed later.

Closure of the Pillars The inferior border of the medial pedicle now becomes the medial pillar. The pedicle needs to be completely rotated up so that the first pillar suture is placed at the medial end of the inferior border just next to the base of the pedicle. This suture does not need to be deep. Some lateral pillar tissue at the same level on the other side is also incorporated into this first suture. There is no need to take large bites or to include fatty tissue. It is important to place the suture on either side into fibrous tissue. There is some fibrous tissue in even the fattiest breasts. Only a few sutures are needed. If the pedicle is long and heavy, it may be wise to suture some of the pedicle up onto the chest wall to help prevent bottoming-out.

Closure of the Dermis The dermis is closed so that the resultant incision line is vertical. Deep buried 3-0 Monocryl sutures are ideal because they absorb relatively quickly and they are less likely to extrude than are PDS sutures. There is no need to suture the dermis up onto the breast parenchyma (it will delay shape resolution postoperatively). Only enough sutures are used to maintain approximation of the margins.

Liposuction Before final closure of the skin, it is a good idea to stand back and assess asymmetry and shape. Some surgeons prefer to sit the patient up at this stage. Unless the patient has very thick, fibrous breast tissue (which occurs in many normal-weight teenagers) liposuction can be used to correct asymmetry. The area that needs to be carefully checked is the area just above the existing inframammary fold. There should be no excess subcutaneous tissue remaining that will result later in a pucker. The tissue inferiorly at the level of the meridian will

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often need direct excision (there are definite transverse fibers at the level of the fold) especially if the surgeon wishes the fold to rise. Liposuction can be used medially and (especially) laterally to tailor this region. Liposuction is also used to reduce excess fat along the lateral chest wall and in the preaxillary areas. If the patient is obese, then tumescent-type infiltration is recommended for the areas to be suctioned. Patients are warned preoperatively that these areas will bruise and that they are often the source of more discomfort postoperatively than the breasts themselves (Fig. 60.5).

Closure of the Skin The vertical skin closure is best achieved by a running subcuticular 3-0 or 4-0 Monocryl suture. It is important to close this skin relatively loosely. Extra skin does not need to be excised in a lateral or medial direction in order to hold the shape of the breast. Deep bites, tight sutures, and skin tension will only delay wound healing. This suture can be gathered (only at the inferior end) to help the skin to shrink, but this is far less important than originally thought. In fact, excess skin gathering will actually delay resolution of any skin puckering inferiorly. In the past, surgeons were advised to gather this skin to reduce the vertical length by one-half to one-third. The length should actually be reduced only by 1 to 2 cm at most. Good quality skin will adapt very well to the new breast shape. It may be tempting to close the skin as an L, or a J, or even a T, but this is usually unnecessary. When there is a large amount of loose, inelastic skin (such as found in a postbariatric patient), excision may be indicated. On the other hand, this is rarely needed in most breast reductions up to 1,000 g. It is not the amount of the parenchymal resection that is important, but the quality of the redundant skin that will make this determination. The excess skin that remains inferiorly adapts surprisingly well to the new breast shape. It is difficult for surgeons who have been trained to keep the vertical skin length at 5 cm to accept a long (sometimes longer than 12 cm) vertical skin opening. The temptation to excise this extra skin can be difficult to resist.

Closure of the Areola The skin opening for the areola should be round. In the past, when the vertical skin was gathered significantly, a teardrop shape resulted. This could take several months to settle postoperatively. Now that gathering is not recommended, the problem of distortion of the areola is no longer a concern. If there is a considerable discrepancy between the circumference of the skin opening and the circumference of the areola (when it is stretched out properly), then consideration should be given to a permanent type of suture to prevent widening. Usually, however, a 4-cm discrepancy is easily tolerated and closure is best achieved by a few interrupted 3-0 or 4-0 Monocryl sutures followed by a running subcuticular suture.

Drains and Antibiotics The use of both drains and antibiotics is controversial. Drains do not prevent hematoma, but they may reduce the substrate for bacteria. When drains are used postoperatively, they are usually removed on the following day, but some surgeons will leave them in place for several days. Many surgeons do not use drains at all unless there is considerable oozing present (as can occur when patients ignore advice to stop anti-inflammatories for 2 weeks preoperatively). Drains can be brought out through the vertical incision or through a separate stab incision. Cephalosporins are the most commonly used antibiotics. There is controversy over whether they should be used at all,


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A,B

C

D,E

F

G,H

I

J FIGURE 60.5. A 34-year-old, 185-lb, 5’7” patient who wore a 36F brassiere. A: Preoperative frontal view of moderate-size breast reduction. B: Preoperative lateral view. C: Preoperative view with markings (many of these measurements are performed for statistical analysis only). The most important markings note the level of the inframammary fold (and therefore the new nipple position vertically), the breast and chest wall meridian (and therefore the new nipple position horizontally), as well as the areolar opening, the skin resection pattern, and the medial pedicle design. D: Intraoperative view at completion of the vertical approach using the medial pedicle. The patient had 625 g of tissue removed from the right breast and 720 g removed from the left breast. She also had 400 cm3 of fat removed from the lateral chest wall and preaxillary areas with some contouring of the lower portion of the breasts. Surgery time was 90 minutes. I now gather this incision far less than shown in this photograph. E: Frontal view at 10 days postoperatively. F: Lateral view at 10 days postoperatively. G: Arms up view at 10 days. The results do not necessarily take a long time to settle postoperatively. H: Frontal view at 15 months postoperatively. I: Lateral view at 15 months postoperatively. J: Arms up view at 15 months postoperatively.


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A

B

C

D

F

E A 60-year-old patient who was 5 4

FIGURE 60.6. tall, weighed 195 pounds, and wore a 38DD brassiere. She had 680 g of tissue removed from each breast. A: Frontal preoperatively. B: Lateral preoperatively. C: Frontal 10 days postoperatively. D: Lateral 10 days postoperatively. E: Frontal 4.5 years postoperatively. F: Lateral 4.5 years postoperatively.


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whether they should be used only perioperatively, or whether they should be used for several days postoperatively.

Complications

Postoperative Course

Complication rates reported in the literature can be confusing. Care must be taken when comparing complications to determine whether these are “major” or “minor.”

Steri-Strips or Micropore paper tape can be applied to the incisions. If paper tape is used, it can be left in place for about 3 weeks. A couple of horizontal strips can be applied inferiorly to help encourage the redundant inferior skin to settle. Taping of the whole breast is unnecessary. The patient can shower the day after surgery and they wash over the tape and then pat it dry. A brassiere is not used for compression, but can be used to hold gauze bandages (initially) and pantiliners (after a couple of days) in place. Patients are encouraged to gradually increase their activities. Return to desk work may only take 1 to 2 weeks, whereas return to heavy physical activity may take several weeks. The pucker (dog-ear at the inferior end of the vertical incision) may take several weeks to months to settle. A seroma may occur that makes the pucker look more ominous, but seromas will settle relatively quickly without intervention. Patients should be warned about the time it takes for resolution of the shape, any asymmetries, or persistent puckers. They should know that revisions may be necessary in a limited number of patients, but that a full year should pass before considering any corrective surgery. Figures 60.5 to 60.7 show results in three patients.

Hematoma Hematomas may develop postoperatively if transected vessels are not apparent because of the vasoconstrictors used for infiltration. Drains will not prevent hematomas and any significant hematoma will require reoperation.

Nipple–Areolar Necrosis Breast reduction surgery is a blood supply reducing operation. Care must be taken when creating the pedicle to preserve as much blood supply as possible. A clear understanding of anatomy is important, but the actual blood supply in any particular patient is guesswork at best. Although it has been advised to take a nipple and areola that is compromised and convert it to a free nipple graft, this decision is extremely difficult. It is not uncommon for areolas to look dusky and pale at the end of the procedure. Most surgeons are well aware that recovery is the rule. It would be inappropriate to convert these areolae to free grafts, because grafting results in a lack of sensation, a lack of nipple projec-

A

B

C

D FIGURE 60.7. A 24-year-old woman who had 295 g of tissue removed from her right breast and 315 g from her left breast. A: Frontal preoperatively. B: Lateral preoperatively. C: Frontal markings preoperatively. D: Frontal 10 days postoperatively. (Continued)


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F

E

G

H

I FIGURE 60.8. (Continued) E: Lateral 10 days postoperatively. F: Frontal arms elevated 10 days postoperatively. This view is humbling in that it shows any residual puckering or deformity. G: Frontal 18 months postoperatively. H: Lateral 18 months postoperatively. I: Frontal arms elevated 18 months postoperatively.


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tion, and an inability to breast-feed, and grafts can heal with irregular pigmentation. If it is clear that a nipple and areola are suffering from venous congestion postoperatively, then measures such as removing sutures or taking the patient back to the operating room for exploration may help. Many patients are now being discharged as same-day surgery patients and the opportunity for this type of evaluation is not available. It would make sense to keep patients for observation if this evaluation was clearcut. But it isn’t. Necrosis is most likely a lack of arterial input and this cannot be corrected. Necrosis from correctable venous congestion is much less likely. The risk-to-benefit ratio is such that it is probably best to allow almost all questionable cases to resolve without intervention. Blistering and some loss may occur, but this is often preferable to active intervention, which carries its own risks. Rarely, complete loss of the nipple and areola will occur. Intervening on the questionable cases is unlikely to decrease this incidence. Each patient will need to be evaluated over time as to whether the necrotic tissue should be allowed to heal by secondary intention, in-office debridement, or intraoperative debridement. Some form of nipple and areolar reconstruction is then considered.

Infection Infection rates should be no higher with breast-reduction surgery than other clean operations. Many surgeons believe that antibiotics are indicated because the breast ducts are open to the external environment. Some surgeons use no antibiotics, some use perioperative antibiotics, and some use a full course of antibiotics. The most commonly used antibiotics are firstor second-generation cephalosporins.

Wound Healing All types of breast reduction have problems with wound healing. The inverted-T has more problems with necrosis at the T, and the vertical types can have more problems on the vertical incision line. Both of these can be prevented to some degree by avoiding undue tension on the incision lines. Avoiding tension can be harder with the inverted-T because the procedure relies more on the skin to hold the shape. The vertical is more likely to run into problems if the surgeon causes constriction during closure by excising too much skin or by undue skin gathering. Antibiotics may be helpful in reducing wound-healing problems. Extensive flap necrosis is rare. It is more likely to occur when the skin is undermined and when excessive tension is applied to the flaps during closure. Debridement may be necessary. Skin grafting may close the wounds earlier, but the cosmetic result is often better if the open areas are allowed to heal secondarily.

Seromas Seromas can occur with or without the use of drains. Even leaving the drains in for several days does not seem to prevent the development of seromas. Aspiration may be indicated, but the seromas will tend to recur. They can be left to resolve on their own. Although surgeons may be concerned that a pseudobursa may develop, this does not seem to be a problem.

Underresection It is far more difficult to remove enough breast tissue with the vertical techniques than it is with the inverted-T techniques. At the end of the procedure, the breasts actually look smaller than they are. This can be a problem for surgeons who have been accustomed to assessing size with the inverted-T. The extra

projection can be misleading. It is important to determine the amount of breast tissue to be removed preoperatively and to then follow that plan. Usually at least 6 to 12 months should elapse before undertaking any re-reduction. This can be achieved through liposuction-only or by re-reducing tissue in the vertical plane. Most of the re-reduction will involve parenchyma. It is important not to take too much skin in the re-reduction or a torpedotype shape will result. Fortunately, the shape will settle because the skin will inevitably stretch to some degree.

Asymmetry Correction of asymmetry should follow similar guidelines to re-reduction. The problem may be solved by liposuction-only or it may require parenchymal repositioning, scar release, or excision.

Puckers The vertical skin pattern approach usually involves excision of skin and parenchyma in a vertical ellipse. This means that there are two dog-ears—one that is chased into the areolar opening and disappears, and one that is chased inferiorly. The skin excision should remain as a U and not be tapered into a V, especially if this would mean that the scar would extend below the inframammary fold. The excess skin will tuck in under the breast as it settles. It is advisable to wait a full year before performing any revisions. At first glance, the pucker that remains may appear to be a problem of excess skin. But usually the real problem is excess subcutaneous tissue between the original and the new inframammary fold. Very little skin may need excision, and often the skin can be excised by carrying the scar down a bit further vertically, but not below the fold. Adding a T at the initial procedure may obviate the necessity to revise any puckers, but it has been shown that performing a T resection did not alter the revision rate (14). Fortunately, many of these revisions can be performed in the office under local anesthesia. The need for occasional revisions are an integral part of plastic surgery, and breast reduction is no exception. Revisions do tend to be more common with the vertical approaches, especially during the learning curve. Each surgeon will have a different threshold for revision, but a rate of approximately 5% is not unexpected.

CONCLUSION It has been repeatedly documented that both physical and psychological outcomes are excellent after breast-reduction surgery. The challenge is to keep scarring to a minimum while giving the breast a pleasing and long-lasting shape. The vertical approaches are excellent for small- to mediumsize reductions. With experience, surgeons also find that the methods are applicable to larger and larger reductions. There is no question that there is an initial learning curve (as there is with the inverted-T), but surgeons eventually feel rewarded by the improved scarring that results and by the improved shape. The procedures take a shorter time to perform, there is less blood loss, and patient recovery time is faster. The concepts in the vertical techniques involve far more than just a different vector in the skin and parenchymal resection patterns. This vector plus the more superiorly based pedicles give a shape that resists gravity over time. In general, the vertical approaches use the breast to shape the skin,



whereas the inverted-T approaches use the skin to shape the breast.

References 1. Spear SL, Howard MA. Evolution of the vertical reduction mammaplasty. Plast Reconstr Surg. 2003;112:855. 2. Robbins TH. A reduction mammaplasty with the areola-nipple based on an inferior pedicle. Plast Reconstr Surg. 1977;59:64. 3. Gradinger GP. Reduction mammaplasty utilizing nipple–areola transplantation. Clin Plast Surg. 1988;15:641. 4. Gray LN. Update on experience with liposuction breast reduction. Plast Reconstr Surg. 2001;108:1006. 5. Corduff N, Taylor GI. Subglandular breast reduction: the evolution of a minimal scar approach to breast reduction. Plast Reconstr Surg. 2004;113: 175.

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6. Schlenz I, Kuzbari R, Gruber H, et al. The sensitivity of the nipple–areola complex: An anatomic study. Plast Reconstr Surg. 2000;105:905. 7. Lassus C. A 30-year experience with vertical mammaplasty. Plast Reconstr Surg. 1996;97:373. 8. Marchac D, de Olarte G. Reduction mammaplasty and correction of ptosis with a short inframammary scar. Plast Reconstr Surg. 1982;69:45. 9. Lejour M. Vertical Mammaplasty and Liposuction of the Breast. St. Louis, MO: Quality Medical; 1993. 10. Hammond DC. Short scar periareolar inferior pedicle reduction (SPAIR) mammaplasty. Plast Reconstr Surg. 1999;103:890. 11. Asplund O, Davies DM. Vertical scar breast reduction with medial flap or glandular transposition of the nipple–areola. Br J Plast Surg. 1996;49:507. 12. Hall-Findlay EJ. A simplified vertical reduction mammaplasty: shortening the learning curve. Plast Reconstr Surg. 1999;104:748. 13. Wise RJ. A preliminary report on a method of planning the mammaplasty. Plast Reconstr Surg. 1956;17:367. 14. Berthe J-V, Massaut J, Greuse M, et al. The vertical mammaplasty: a reappraisal of the technique and its complications. Plast Reconstr Surg. 2003;111:2192.


CHAPTER 61 ■ GYNECOMASTIA NOLAN S. KARP

Gynecomastia is caused by an increase in ductal tissue, stroma, and/or fat in the male breast. Most frequently, the changes occur at the time of hormonal changes: infancy, adolescence, and old age. The term gynecomastia was introduced by Galen during the second century a.d. and the surgical resection was first described by Paulis of Aegina (1,2) in the seventh century a.d.

ETIOLOGY The most common cause for gynecomastia is idiopathic; Table 61.1 lists the other common causes. Gynecomastia often appears transiently at birth. The process is thought to be related to an increased level of circulating maternal estrogens. After birth, the estrogen level decreases and the gynecomastia usually resolves. Treatment is rarely necessary. Gynecomastia is present in almost 66% of adolescent boys (3). This is thought to be the result of an imbalance of estradiol and testosterone. The adolescent gynecomastia resolves in the vast majority of cases (2). In some cases, a degree of gynecomastia remains, but it is not enough to warrant medical attention. The incidence of gynecomastia rises again in older men (older than age 65 years). This is thought to be the result of a decline in testosterone and a shift in the ratio of testosterone to estrogen. In all three age groups, gynecomastia appears to be related to either an increase in estrogens, a decrease in androgens, or a deficit in androgen receptors (2). Numerous drugs are associated with gynecomastia (Table 61.1). Systemic causes include adrenal diseases, liver diseases, pituitary tumors, thyroid disease, and renal failure. Tumors of adrenal, pituitary, lung, and testis can be associated with a hormonal imbalance that results in gynecomastia. In any male patient with breast enlargement, male breast cancer must be considered because 1% of all breast cancers occur in men. There is no increased risk of breast cancer in patients with gynecomastia when compared to the unaffected male population (4). The exception is patients with Klinefelter syndrome. These patients have an approximately 60 times increased risk of breast cancer.

PATHOLOGY Three types of gynecomastia have been described: florid, fibrous, and intermediate (5). The florid type is characterized by an increase in ductal tissue and vascularity. A variable amount of fat tends to be mixed in with the ductal tissue. The fibrous type has more stromal fibrosis and few ducts. The intermediate type is a mixture of the two. The type of gynecomastia is usually related to the duration of the disorder. Florid gynecomastia is usually seen when the duration is 4 months or less. The fibrous type is usually present after a duration of 1 year. The

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intermediate type is thought to be a progression from florid to fibrous and is usually seen between 4 and 12 months (5).

DIAGNOSIS A careful history and physical examination is the most important part of any work-up for gynecomastia. The history must note the time of onset of the gynecomastia, symptoms associated with the gynecomastia, drug use (both medically prescribed and recreational), and careful review of systems. Organ system changes associated with gynecomastia include liver, renal, adrenal, pulmonary, pituitary, testicular, thyroid, and/or prostate. Physical examination should include assessment of the breast gland. This will include the nature of the tissue, isolated masses, and tenderness. The thyroid should be evaluated for enlargement. The testis should be examined to look for asymmetry, masses, enlargement, or atrophy. Laboratory evaluation is based on the findings of the history and physical examination. Healthy adults with a normal physical examination (other than gynecomastia) and longstanding gynecomastia do not need further work-up. Patients with feminizing characteristics should have endocrine testing. In addition, if marfanoid body habitus is associated with the feminization, Klinefelter syndrome must be ruled out. Any other new positive findings on physical examination should be worked up in an appropriate manner.

CLASSIFICATION Simon et al. (6) divided gynecomastia into four grades as follows: Grade 1 : Grade 2a: Grade 2b: Grade 3 :

Small enlargement, no skin excess Moderate enlargement, no skin excess Moderate enlargement with extra skin Marked enlargement with extra skin.

In their opinion, grades 2b and 3 require some skin resection. The need to excise excess skin depends on the shape of the breast. Large breasts with a wide base may be treated without skin excision. Conversely, smaller, but narrow breasts may need skin excision. Letterman and Schuster (7) created a classification system based on the type of correction as follows: 1: 2: 3:

Intra-areolar incision with no excess skin Intra-areolar incision with mild redundancy corrected with excision of skin through a superior periareolar scar Excision of chest skin with or without shifting the nipple


Chapter 61: Gynecomastia

TA B L E 6 1 . 1 COMMON CAUSES OF GYNECOMASTIA Idiopathic Obesity Physiologic Birth Puberty Old age Endocrine Testis: hypogonadism, Klinefelter syndrome Adrenal: Cushing syndrome, congenital adrenal hyperplasia Thyroid: hypothyroid, hyperthyroid Pituitary: pituitary failure Neoplasms Adrenal Testis Pituitary Bronchogenic Systemic diseases Renal failure Cirrhosis Adrenal Malnutrition Drug-induced Hormones: estrogens, androgens Antiandrogens: spironolactone, cimetidine, ketoconazole, ranitidine, flutamide Cardiovascular drugs: amiodarone, digoxin, nifedipine, reserpine, verapamil Abused drugs: Alcohol, heroin, marijuana

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Rohrich (8), in a paper discussing the usefulness of ultrasound-assisted liposuction in the treatment of gynecomastia, developed the following classification: Grade I : Grade II : Grade III: Grade IV:

Minimal hypertrophy (500 g of breast tissue) with grade I ptosis Severe hypertrophy with grade II or III ptosis

TREATMENT OF GYNECOMASTIA If a patient has gynecomastia for less than 1 year and a normal history and physical examination, observation is probably indicated. If there is a possible etiology noted in the patient’s history, an attempt should be made to either discontinue the drug believed to be causing the gynecomastia or correct the systemic condition. If an abnormality is found on physical examination, work-up is indicated prior to consideration of surgery for the gynecomastia. If the underlying condition is treated and the gynecomastia persists beyond 1 year, surgical correction is indicated (Fig. 61.1). The first surgical procedures used to treat gynecomastia were excisional in nature (9). Suction assisted lipectomy was first reported in the early 1980s (10), and more recently ultrasound-assisted liposuction has been used for certain types of gynecomastia (8). The physical deformity requires evaluation and staging to determine the appropriate treatment. Most fibrous or solid Simon stage 1 or 2a lesions are usually treated with surgical excision or, in some cases, with ultrasonic liposuction. If surgical excision is performed, a periareolar incision is performed as indicated in Figure 61.2A. The

FIGURE 61.1. Algorithm for evaluation and treatment of gynecomastia. (Adapted from Rohrich RJ, Ha RY, Kenkel JM, Adams WP. Classification and management of gynecomastia: defining the role of ultrasound-assisted liposuction. Plast Reconstr Surg. 2003;111:909, with permission.)


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A

B FIGURE 61.2. A: Periareolar incision. Medial and lateral extensions are used only if needed. B: Resection of gynecomastia through periareolar incision. Note the cuff of tissue left under areola.

skin incision is placed at the junction of the areola and skin. If placed within the pigmented area, the scar may appear as a white line. The site of the incision should be marked prior to injection of epinephrine-containing solution. If placed properly, the scar may be nearly invisible. After the incision is made, a cuff of tissue 1 to 1.5 cm in thickness is left directly under the nipple areola complex. This maneuver prevents postoperative nipple areola depression and adherence of the nipple areola to the chest wall (Fig. 61.2B). It is always better to leave more tissue than less under the nipple areola. At the end of the case any excess can be trimmed off. The chest skin flaps are developed in a plane between the subcutaneous fat and the breast tissue. To assure a smooth contour, the edges of the breast are trimmed with either scissors or liposuction. If the patient has a lesion that is glandular, fatty, or mixed in nature and is Simon grade 1 or 2a, the area could be treated with liposuction. Conventional liposuction with sharp-tip cannulas, power-assisted liposuction, or ultrasound-assisted liposuction have all been used in this situation. The patient is marked in the upright position. All areas of tissue excess are marked, as well as the inframammary fold. The patient is either sedated or placed under general anesthesia. The area is infiltrated with a tumescent solution containing lactated Ringer solution, 1 mL of 1:1,000 epinephrine solution, and 20 mL of 2% lidocaine solution. The infiltration is about 1:1 with the expected aspiration volume, and covers a wide area of the chest—from the clavicle to below the inframammary fold. Whichever method of liposuction is performed, special cannulas, specifically designed for gynecomastia surgery, are used. Figure 61.3A shows typical incisions. There is usually a lateral incision at the level of the inframammary fold and a periareolar incision. Liposuction is performed in all directions through both incisions (Fig. 61.3B). The inframammary fold is disrupted when present. The end point is a

flat, smooth contour with an absence of palpable tissue (Fig. 61.4). In cases of pure fatty gynecomastia no further surgery is necessary. When liposuction is unsuccessful at removing all of the tissue required to achieve a good result, the pullthrough (11,12) technique may be used. In this technique, either the lateral or periareolar incision is opened slightly longer (about 1.5 cm) and the residual tissue is grasped. The tissue is pulled out through the wound and removed with scissors or electric cautery. The pullthrough resection is performed until the desired contour is achieved. Again, attention must be maintained not to overresect the subareolar area (Fig. 61.5). Postoperative drainage may be used if the dead space is large. All patients are treated with at least 1 month of a compression garment. In patients with Simon grade 2b gynecomastia, the initial treatment is similar to that given to patients with grade 1 or 2a gynecomastia. If the lesion is fatty, glandular, or mixed in nature and some type of liposuction is the initial treatment modality, no skin resection is performed at the first surgical session. The patients are treated with compression vests and the chest wall tissue is given time to settle and contract. The patient should wait at least 6 to 12 months before considering skin resection. In the majority of cases, no skin resection is required. When skin resection is performed, the amount of skin removed and the length of the incision are much less than if the resection were performed at the time of the initial surgery. If the patient has a Simon grade 2b lesion that is very solid or fibrous in nature and an open approach is selected, skin resection might be incorporated into the initial procedure. If the patient desires to keep the visible scar as short as possible, the tissue could be resected with a minimalist periareolar incision and the patient treated with a compression garment. In many cases, no further skin resection is required. Ultrasonic liposuction with the pullthrough technique (if needed) has also


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Chapter 61: Gynecomastia

A

B FIGURE 61.3. A: Location of incisions for suction-assisted lipectomy of gynecomastia. B: Direction of liposuction through both incisions.

B

A

C

D

FIGURE 61.4. Patient with Simon 2a gynecomastia who underwent suction-assisted lipectomy of the chest. A: and B: Preoperative. C: and D: Postoperative.


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A

B FIGURE 61.5. Demonstration of pullthrough resection of gynecomastia.

been used in Simon 2b cases without skin resection with good results. In patients with Simon grade 3 gynecomastia, skin resection is almost always required. Numerous incisions and techniques to resect the skin and keep the nipple viable have been described, including superior and inferior periareolar incisions, omega incisions, nipple transpositions on a variety of pedicles, concentric circle techniques, and any form of liposuction with skin excision. The choice of technique is based on the preference of the surgeon.

COMPLICATIONS The most common early complication after gynecomastia surgery is hematoma. In an open case, the hematoma should be evacuated if possible. This prevents excessive scarring and distortion of the breast. Postoperative closed suction drainage decreases the incidence of this complication. In liposuction cases, evacuation may not be possible. Underresection of tissue is the most common long-term complication of gynecomastia surgery. This is particularly common in liposuction cases, when a residual mass of tissue is not removed. This can be avoided by using the pullthrough technique. Underresection at the periphery of the breast can result from poor tapering and causes a noticeable deformity. Overresection in the nipple areola can result in a saucer-type deformity that is difficult to correct. Loose skin is usually not considered a complication if it is part of the operative plan. Occasionally, loose skin occurs in an unexpected manner, and surgical excision is required.

Postoperative wound infection is uncommon. The use of prophylactic antibiotics, particularly in liposuction cases, may account for the low incidence of this complication.

References 1. Goldwyn R. Plastic and Reconstructive Surgery of the Breast. Boston: Little Brown; 1976. 2. McGrath MH. Gynecomastia. In: Jurkiewicz MJ, Mathes SJ, Krizek TJ, et al, eds. Plastic Surgery: Principles and Practice. St. Louis: Mosby; 1990. 3. Nydick M, Bustos J, Dale JH, et al. Gynecomastia in adolescent boys. JAMA. 1961;178:449. 4. Cohen IK, Pozez AL, McKeown JE. Gynecomastia. In: Courtiss EH, ed. Male Aesthetic Surgery. St. Louis: Mosby; 1991. 5. Bannayan GA, Hajdu SI. Gynecomastia: clinicopathologic study of 351 cases. 1972;57:431. 6. Simon BE, Hoffman S, Kahn S. Classification and surgical correction of gynecomastia. Plast Reconstr Surg. 1973;51:48. 7. Letterman G, Schuster M. The surgical correction of gynecomastia. A Surg . 1969;35:322. 8. Rohrich RJ, Ha RY, Kenkel JM, et al. Classification and management of gynecomastia: defining the role of ultrasound-assisted liposuction. Plast Reconstr Surg. 2003;111:909. 9. Webster JP. Mastectomy for gynecomastia through a semi-circular incision. Ann Surg. 1946;124:557. 10. Courtiss EH. Gynecomastia: analysis of 159 patients and current recommendations for treatment. Plast Reconstr Surg. 1987;79:740. 11. Hammond DC, Arnold JF, Simon AM, et al. Combined use of ultrasonic liposuction with the pull-through technique for the treatment of gynecomastia. Plast Reconstr Surg. 2003;112:892. 12. Bracaglia R, Fortunato R, Gentileschi S, et al. Our experience with the socalled pull-through technique combined with liposuction for management of gynecomastia. Ann Plast Surg. 2004;53:22.


CHAPTER 62 ■ BREAST CANCER FOR THE PLASTIC SURGEON GRANT W. CARLSON

Cancer of the breast is the second most common cancer in women, skin cancer being the most common. It is the second leading cause of cancer death after lung cancer. There are approximately 180,000 new cases of breast cancer diagnosed each year in the United States, accounting for more than 45,000 deaths a year. The incidence increased dramatically in the 1990s, largely because of increased detection by screening mammography. This is reflected in the fact that noninvasive cancer comprises 30% of new breast cancer cases treated in large medical centers. The treatment of breast cancer has evolved because of the results of large, prospective, randomized clinical trials organized by the National Surgical Adjunctive Breast and Bowel Project (NSABP) in the United States, and the National Cancer Institute in Milan, Italy. The majority of women with breast cancer today are eligible for breast conservation therapy and receive some form of systemic adjuvant chemotherapy.

RISK FACTORS It is estimated that one in nine women in the United States who reaches the age of 85 years will develop breast cancer. The etiology is unknown, but is clearly multifactorial, with many exogenous and endogenous risk factors being identified (Table 62.1). Aside from gender, age is the single most important factor in determining breast cancer risk. The probability that breast cancer will develop increases throughout a woman’s life, with half of all cases occurring in women older than age 65 years. Family history is also important because 20% of breast cancer patients have a relative with the disease. The magnitude of breast cancer risk is influenced by several factors pertaining to family history, including number and proximity of affected relatives, their menstrual status, age at diagnosis, and the presence of bilateral cancer. Hereditary breast cancer accounts for 5% to 10% of breast cancer cases and is caused largely by the presence of BRCA gene mutations. The genes are more common in women of Jewish Ashkenazi ancestry, patients with bilateral breast cancer, cancer diagnosed before age 50 years, and patients with ovarian cancer. The presence of a BRCA gene confers a 60% to 85% risk of developing breast cancer and a 10% to 40% risk of developing ovarian cancer. Many epidemiologic studies have linked early menarche, late menopause, and late age at first full-term pregnancy to breast cancer. The total duration of menstrual cycles and the number of menstrual cycles before full-term pregnancy appear to be proportional to breast cancer risk. Premalignant histology on breast biopsy may increase breast cancer risk, as is discussed in the following section. A woman with unilateral breast cancer is at increased risk of developing cancer in the opposite breast.

Studies have not shown that the development of contralateral breast cancer impacts adversely on survival.

PATHOLOGY Screening mammography, by early detection of breast cancers, has increased our understanding of the malignant transformation process. Most cancers arise from the ductal elements of the breast after passing, presumably, through a sequence of premalignant stages as depicted below. Normal breast → hyperplasia → atypical hyperplasia → ductal carcinoma in situ → invasive cancer This process can occur over a 10- to 20-year period and orderly progression through the various stages is not obligatory. Ductal carcinoma in situ (DCIS), also known as intraductal carcinoma, is cancer confined by the basement membrane of the ducts. It most commonly presents as mammographic microcalcifications and currently comprises 30% of newly diagnosed cancers in populations following screening mammography guidelines. DCIS occurs in several histologic patterns with varying propensity to progress to invasive cancer. Comedo DCIS is characterized by pleomorphic cells, high-grade nuclei, and central areas of necrosis. Noncomedo DCIS occurs in several subtypes that are generally not as cytologically malignant as comedo DCIS. It may be difficult to distinguish noncomedo DCIS from atypical hyperplasia. Invasive ductal carcinoma accounts for the majority of all cases of breast cancer. Grossly, it appears as a gray-white, irregular, speculated mass that is hard and gritty on cut section. It has no specific microscopic features, but can be recognized histologically as an invasive adenocarcinoma involving the ductal elements. A number of histologic variants arise from ductal epithelium. Medullary carcinoma is grossly soft and fleshy and accounts for 6% of invasive cancers. It tends to grow to a large size and is well circumscribed. Histologically, it is characterized by poorly differentiated nuclei and infiltration by lymphocytes. Medullary carcinoma has a favorable prognosis, even in the presence of nodal metastases. Tubular carcinoma is a rare histologic variant in its pure form and accounts for 2% of breast cancer. It is characteristically small and is usually found on mammography. It tends to be highly differentiated and has an excellent prognosis. Mucinous or colloid carcinoma is another well-differentiated variant, which tends to form a well-circumscribed soft, gelatinous mass. Histologically, nests of tumor cells are surrounded by a mucinous matrix. Although most cancers arise from the ductal elements, malignancies may also arise from the epithelium of the breast lobules. Lobular carcinoma in situ (LCIS) has no radiologic or physical manifestations and traditionally has not been


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TA B L E 6 2 . 1

TA B L E 6 2 . 2

BREAST CANCER RISK FACTORS Gender Age Family history Reproductive history Early menarche First birth after age 30 years Late menopause Benign breast disease Atypical hyperplasia Lobular carcinoma in situ Personal history ? Exogenous factors ? Dietary factors

regarded as a malignancy. It is usually an incidental finding after a biopsy of a mass or mammographic abnormality. Current evidence suggests that the histologic diagnosis of LCIS confers a 20% risk of developing cancer in either breast by the 20-year follow-up examination. Five percent to 15% of infiltrating cancers arise from the breast lobules. Once it has become invasive, lobular carcinoma has a similar prognosis to the ductal type. It tends to be extensively infiltrative without a distinct tumor mass. Histologically, the cells demonstrate a characteristic single-file pattern. The tumor does not form microcalcifications and mammographic detection may be difficult.

STAGING The American Joint Committee on Cancer (AJCC) TNM (primary tumor, regional lymph node, remote metastases) staging system is based on clinical and pathologic information. The classification by primary tumor (T), status of axillary lymph nodes (N), and presence of distant metastases (M) places patients in different prognostic groups (Tables 62.2 and 62.3). Stages I and II are considered early breast cancer for which surgery plays a primary role in treatment. Stage III disease is also known as locally advanced breast cancer (LABC). Despite the absence of metastatic disease, this stage has a poor prognosis and is best treated with a combination of chemotherapy, surgery, and radiation therapy. This stage includes inflammatory breast cancer, a clinical entity characterized by breast warmth, erythema, and edema. The orange-peel appearance of the skin, peau de orange, results from dermal lymphatic invasion.

AJCC TNM STAGING SYSTEM OF BREAST CANCER Primary Tumor (T) TX Primary tumor cannot be assessed T0 No evidence of primary tumor Tis Carcinoma in situ, intraductal carcinoma, lobular carcinoma in situ T1 Tumor ≤2 cm in greatest dimension T1mic Microinvasion ≤0.1 cm in greatest dimension T1a Tumor >0.1 cm but ≤0.5 cm in greatest dimension T1b Tumor >0.5 cm but ≤1 cm in greatest dimension T1c Tumor >1 cm but ≤2 cm in greatest dimension T2 Tumor >2 cm but ≤5 cm in greatest dimension T3 Tumor >5 cm in greatest dimension T4 Tumor of any size with direct extension to chest wall or skin only T4a Extension to chest wall T4b Edema (including peau d’orange) or ulceration of the skin of the breast or satellite skin nodules confined to the same breast T4c Both T4a and T4b T4d Inflammatory carcinoma Regional Lymph Nodes (N) NX Regional lymph nodes cannot be assessed (e.g., were previously removed) N0 No regional lymph node metastasis N1 Metastasis to mobile ipsilateral axillary lymph node or nodes N1a Micrometastases only, ≤0.2 cm N1b Metastasis to node or nodes, >0.2 cm N1bi Spread to 1–3 nodes, >0.2 cm, all 0.2 cm, all 5 cm or more than four to five ribs may result in chest wall flail (5,6) with paradoxical respiratory motion and abnormal ventilation. Through proper skeletal reconstruction, chest wall flail may be avoided and respiratory function preserved (5). One option for reconstruction of the chest wall skeleton is autogenous bone grafts, which avoids the use of foreign materials. Donor sites for bone grafts include the ribs, iliac crest, and fibula. For successful reconstruction, the bone graft must be apposed to a large surface area of trabecular bone around the chest wall defect margins so as to enhance graft survival and osteoconduction (5). Autologous fascia lata graft may also provide a semirigid skeletal substitute. The fascia graft can be combined with bone chips or a bone graft. The use of the fascia lata graft is limited by its inherent flaccidity and susceptibility to infection (5). Bone defects of the chest wall skeleton that are 10 cm to allow for 3 cm of overlap between the mesh and the posterior aspect of the abdominal wall, while still having room to place and maneuver the trocars. Other options for treatment of hernias with stable soft tissues include open mesh repairs and closure with sliding myofascial rectus abdominis flaps (modified separation of parts procedure, as is discussed below). Conceptually, mesh repairs are lids attached to the top of an open pot. The quality of the attachment is paramount— when mesh repairs fail, it is typically because of a lack of a durable attachment of the mesh to the abdominal wall. Mesh can be laced on top of the abdominal wall, sewn directly to the edges of the defect, or used as an underlay. The first two methods minimize the amount of bowel in contact with the mesh. Mesh underlays serve to maximize the attachment of the mesh to the abdominal wall, using the pressure of the viscera to push the mesh against the abdominal wall. For mesh underlays, sutures are used to create at least 3 cm of overlap between abdominal wall and the mesh. Enough sutures are needed to prevent the herniation of a bowel loop between stitches, but too many sutures can cause ischemic necrosis of the edge of the abdominal wall, and in turn lead to a poor mesh attachment. Numerous nonabsorbable mesh alternatives exist. Selection of one versus another depends largely on the complication profile associated with each of the meshes. A brief description of the mesh choices currently available and the associated complications for each follows.

Wound Shape and Position

Expanded Polytetrafluoroethylene Mesh

In the infraumbilical area in the obese patient, some wounds are so deep and with so much fat necrosis that local wound care does not suffice to achieve closure. In these selected patients, a panniculectomy encompassing the necrotic tissue is helpful to change the shape of the wound. Even if part of the wound is left open on dressings, a transversely oriented wound closes much more quickly than a vertically oriented wound. Prior to panniculectomy, a CT scan is obtained to confirm the position of the bowel to avoid an iatrogenic enterocutaneous fistula.

Several formulations of this mesh exist (Gore-Tex, W.L. Gore and Assoc., Flagstaff, AZ). The advantage of this material is the smooth, nonporous surface of the mesh to prevent bowel adhesions. The lack of adhesions to the mesh is both its most favorable characteristic and its major drawback. Placed intraperitoneally during laparoscopic repairs, it is “tacked” or “stapled” to the undersurface of the abdominal wall as an underlay patch, and its smooth surface does, indeed, prevent adhesion formation. However, this lack of incorporation means that the mesh is difficult to salvage in the event of an infection. When infection occurs, antibiotics and drainage are provided for local wound control for several weeks, allowing a rind of granulation tissue to occur on the deep side of the mesh. When the mesh is removed, the granulation tissue is generally strong enough to prevent an evisceration. The skin can be closed over the rind (using several drains) to achieve wound closure. The resultant hernia can be repaired when it begins to expand.

ABDOMINAL WALL AND SOFT-TISSUE RECONSTRUCTION (VENTRAL HERNIA REPAIR) As mentioned above, successful hernia repair requires a plan for the abdominal wall and for achieving stable skin coverage. The timing for abdominal wall reconstruction is also important. In the ideal case, the patient has a stable, closed wound with soft, pliable tissues over the hernia sac. An easy rule to remember is that if the hernia is expanding, it is ready to be fixed. An expanding hernia implies that bowel adhesions and scar attaching the bowel to the abdominal wall has significantly softened and will be straightforward to dissect.

Stable Soft Tissues: Midline Abdominal Wall Defects When the skin and subcutaneous tissues are pliable, no wounds are present, and no gastrointestinal surgery is planned, many options exist for this hernia repair. For small hernias less than 3 cm across, a direct repair is often performed, although there is still a surprisingly high recurrence rate (4). For hernias larger than 3 cm, a laparoscopic mesh hernia repair is ideal. These la-

Polypropylene Mesh Polypropylene mesh is porous, allowing for egress of fluid collections and ingrowth of fibrous tissue for improved incorporation into the tissues. Two types of polypropylene mesh are commonly used to replace full-thickness defects of the abdominal wall. Marlex mesh (C.R. Bard Corp., Cranston, RI) and Prolene mesh (U.S. Surgical Corp., Norwalk, CT) are made of the same material, but differ in how they are weaved. Of the two, Prolene mesh has a lower complication rate of such complications as enterocutaneous fistula and the need for removal after infections (6). Several studies advocate intraperitoneal placement of Prolene mesh, stating that bowel adhesions are minimized if the mesh is placed under tension to avoid wrinkles (7). In those cases when Prolene mesh becomes exposed, wound contraction of the soft tissues can often cover the exposure. The strength and good handling characteristics of Marlex were recently paired with Gore-Tex for a bilaminar mesh. The Gore-Tex is presented on its deep surface to the bowel to avoid


Chapter 69: AbdominaL Wall Reconstruction

adhesions and fistulae, whereas the Marlex is on the superficial side to allow for improved incorporation.

Human Acellular Dermis Even though the skin of the hernia sac stretches and deforms as a consequence of underlying abdominal pressure, treated acellular human dermis (AlloDerm, LifeCell Corporation, Branchburg, NJ) has shown interesting characteristics when used to replace full-thickness losses of the abdominal wall (8). In animal models, it has incorporated well and shown resistance to infection. Clinically, the mesh has performed well structurally, but size limitations require that pieces of acellular dermis must be patched together. Placement intraperitoneally is possible because of a low rate of visceral adhesions; thus it may be an excellent adjunct to both direct hernia repairs and to separation of parts repairs. Hernia recurrence rates using this substance are being studied.

Porcine Submucosa Surgisis (Cook Surgical Co., Norwalk, CT), like acellular human dermis, is a biomaterial touted for properties of incorporation and replacement by host tissues. As with AlloDerm, the material is regarded as being more resistant to infection than prosthetic meshes. Surgisis comes in larger sheets than does AlloDerm, and has been used laparoscopically in hernia repairs. No reliable long-term data exists regarding this material.

Fascia Lata Decades of experience and follow-up exist for use of this autogenous biomaterial. The long-term hernia rate is 30% with this graft, although it is used in some of the most difficult and contaminated cases (8). Sheet grafts up to 22 × 12 cm in size can be harvested through long incisions along the posterolateral aspect of the leg. The donor-site complication rate, including seromas and hematomas, approaches 50%.

Stable Soft Tissues: Lateral Abdominal Wall Defects In contrast to midline hernias that tend to be large, lateral abdominal wall defects tend to be smaller and with good softtissue cover. The hernia can typically be repaired using mesh, placed either laparoscopically or by using the open technique. On occasion, for larger nonmidline hernias where there has been a mild loss of domain, a contralateral release of the opposite external oblique (as is described in the next section) is

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performed to give the hernia contents room in the abdominal cavity. More troublesome are the lateral bulges that are associated with some degree of denervation injury to the abdominal musculature. These bulges often occur after flank incisions for exposure of the spine and the retroperitoneum. Informed consent on operative management of these bulges is critical, because surgery generally improves but does not completely resolve the bulge. Exposure of the abdominal bulge with wide elevation of skin flaps, imbrication of the abdominal musculature while flexing the operating table to take tension off the sutures, and a large mesh overlay generally improves the bulge by only 50%.

Unstable Soft Tissues and/or Contaminated Fields: Midline Defects A large number of possible solutions exist for the repair of complex abdominal wall defects, as has been delineated by treatment algorithms published in the literature (9). A simplified approach to the surgical management of these problems is presented below. Again, the solution lies in understanding that abdominal wall reconstruction is the interplay of two competing problems: how to repair the abdominal wall and how to achieve cutaneous coverage. When both skin and abdominal wall are deficient in the midline, the procedure of choice is abdominal wall reconstruction using bilateral myofascial rectus abdominis flaps. Referred to as “components separation” and as the “separation of parts,” the operation described by Ramirez moves the laterally displaced skin and rectus muscles toward the midline (10). The surgical procedure is a radical removal of tissue between the medial aspects of both rectus abdominis muscles. Thin, atrophic hernia skin cover, wounds, infected mesh, draining stitch abscesses, and fistula are removed en bloc, leaving only unscarred tissue for the eventual closure (11). The releases of the external oblique muscle and fascia are performed through bilateral transverse 6-cm incisions located at the inferior border of the rib cage (Fig. 69.2). Tissues over the semilunar line are elevated by blunt dissection. The external oblique muscle and fascia are then divided under direct vision from above the rib cage to the level near the inguinal ligament. The inferior aspect of the release is completed under a small tunnel that joins the lower aspect of the midline laparotomy incision with the lateral dissection. The external oblique is then bluntly dissected off of the internal oblique, allowing the muscles to slide relative to each other. Performed in this manner, the skin over the rectus abdominis muscle has a completely preserved blood supply. After approximation of the fascial edges,

Separation of Parts External oblique

Rectus

1. Weakened sides 2. Augmented center

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FIGURE 69.2. Diagram of forces on the abdominal wall after bilateral releases of the external oblique muscle and fascia along the semilunar lines. (Redrawn from Dumanian GA, Denham W. Comparison of repair techniques for major incisional hernias. Am J Surg. 2003;185:65, with permission.)


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Part VII: Trunk and Lower Extremity

the midline closure appears identical to a standard laparotomy incision. As such, without any undermined skin flaps in the midline, mesh cannot be used in overlay fashion. However, a mesh underlay can be used to augment the midline closure and to distribute tension away from the suture line. The operation done in this manner respects the innervation and vascular anatomy of the tissues. The significantly improved soft-tissue vascularity gives the operative team the confidence to perform simultaneous bowel surgery without an increase in soft-tissue infections (12). Rather than focus on the maximal defect size closeable with releases of the external oblique muscles, an analysis of factors that make hernias easy or difficult to close is helpful. Significant weight loss since the last laparotomy, a hernia centered on the umbilicus, no previous use of retention sutures, and an absence of previous stomas or lateral incisions all make the hernia repair more straightforward. Conversely, an upper abdominal hernia, scarred rectus muscles, stomas, and lateral incisions all make the repair more difficult. Previous mesh repairs cause the dissection to be more difficult, but the repair to be easier, because the mesh typically acts to keep the hernia down to a smaller size. By CT scan measurement, simple releases of the external oblique have allowed each of the rectus muscles to be moved 8 to 9 cm medially. By external measurements, hernias as large as 40 cm across have been closed successfully without any additional releases. Even after external oblique release, there are times when the rectus muscles cannot be closed in the midline without undue tension. The technique, however, still brings well-vascularized skin to the midline, and this good soft-tissue cover allows the use of prosthetic mesh in clean cases, or a biologic mesh in contaminated situations. I have combined the release of the external obliques with a sheet of fascia lata in at least nine instances with no complications. The mesh is a smaller component of the repair after the releases, and the forces on the mesh are decreased because of weakened lateral musculature. Alternatively, releases of additional components of the abdominal wall, including either the transversalis fascia or the internal oblique, can be performed, but this runs the risk of significant weakness along the semilunar line. Consequently, this maneuver is to be avoided. The infraumbilical midline hernia in the obese patient is another example of how the skin problem and the abdominal wall problem are approached separately. For these patients, a panniculectomy addresses the heavy, thick skin while simultaneously exposing the fascial edges of the hernia. Mesh can be used to patch the abdominal wall defect, but I prefer the autogenous closure provided by the separation of parts procedure (Fig. 69.3) (13). Tunnels are elevated over the semilunar lines bluntly, preserving the perforators extending from the rectus muscle to the upper skin flap. The external oblique muscles are released, and the rectus muscles can be brought to the midline in standard fashion. Increased complications, including hernia recurrence and wound complications, have been encountered with increasing body mass index.

FIGURE 69.3. Separation of parts procedure. Transverse incision located at the inferior aspect of the rib cage facilitates the exposure of the semilunar line. Skin vascularity is intact because of preservation of periumbilical perforators. The external oblique muscle is divided off of the rectus fascia at the anterior extent of the muscle fibers.

and biologic mesh for contaminated situations. Pedicled flaps or even free flaps are needed for larger skin replacement situations. Defects in the infraumbilical area can be treated with unilateral or even bilateral tensor fascia lata (TFL) flaps. A delay procedure is helpful to ensure tip viability of the TFL flap. The TFL flap can also be used for simultaneous structural support, but inset of the tissue when used as a flap is difficult in the inguinal area. When used for structural support, tip viability is a critical issue. Large, supraumbilical, nonmidline skin deficits are the most problematic situations, with each case requiring a unique solution for closure. Patients have undergone large adjacent tissue transfers with skin grafts of the donor site, pedicled myocutaneous latissimus flaps, and even free flaps on vein grafts for soft-tissue coverage in this region.

Unstable Soft Tissues and/or Contaminated Fields: Lateral Defects

References

The skin issues are the most important to solve for lateral defects with poor skin, because mesh can often be used for reconstruction of the abdominal wall. For smaller skin defects, such as those that arise from tumor excisions, an assessment is made of local tissues for closure using the pinch test. Incisions along the dermatome lines, wide undermining, flexion of the patient on the operating table, and closure over drains often solves the skin problem. Prosthetic meshes are selected for clean cases,

1. Dumanian GA, Denham W. Comparison of repair techniques for major incisional hernias. Am J Surg. 2003;185:61. 2. Sukkar SM, Dumanian GA, Szczerba SM, et al. Challenging abdominal wall defects. Am J Surg. 2001;181:115.. 3. Dumanian GA, Llull R, Ramasastry SS, et al. Postoperative abdominal wall defects with enterocutaneous fistulae. Am J Surg. 1996;172:332. 4. Luijendijk RW, Hop WCJ, van den Tol MP, et al. A comparison of suture repair with mesh repair for incisional hernia. N Engl J Med. 2000;343:392. 5. Heniford BT, Park A, Ramshaw BJ, et al. Laparoscopic ventral and incisional hernia repair in 407 patients. J Am Coll Surg. 2000;190:645.


Chapter 69: AbdominaL Wall Reconstruction 6. Stone HH, Fabian TC, Turkleson ML, et al. Management of acute fullthickness losses of the abdominal wall. Ann Surg. 1981;193:612. 7. Mathes SJ, Steinwald PM, Foster RD, et al. Complex abdominal wall reconstruction: a comparison of flap and mesh closure. Ann Surg. 2000;232:586. 8. Silverman RP, Singh NK, Li EN, et al. Restoring abdominal wall integrity in contaminated tissue-deficient wounds using autologous fascia grafts. Plast Reconstr Surg. 2004;113:673. 9. Rohrich RJ, Lowe JB, Hackney FL, et al. An algorithm for abdominal wall reconstruction. Plast Reconstr Surg. 2000;105:202. 10. Ramirez OM, Ruas E, Dellon AL. “Components separation” method for

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closure of abdominal wall defects: an anatomic and clinical study. Plast Reconstr Surg. 1990;86:519. 11. Szczerba SR, Dumanian GA. Definitive surgical treatment of infected or exposed ventral hernia mesh. Ann Surg. 2003;237:437. 12. Saulis AS, Dumanian GA. Periumbilical rectus abdominis perforator preservation significantly reduces superficial wound complications in “separation of parts” hernia repairs. Plast Reconstr Surg. 2002;109:2275. 13. Reid RR, Dumanian GA. Panniculectomy and the separation of parts hernia repair: a solution for the large infraumbilical hernia in the obese patient. Plast Reconstr Surg. 2005;116:1006.

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CHAPTER 70 ■ LOWER-EXTREMITY RECONSTRUCTION ARMEN K. KASABIAN AND NOLAN S. KARP

LOWER-EXTREMITY TRAUMA Treatment of high-energy lower-extremity trauma with softtissue and bone injury remains a formidable problem. These injuries often occur in the multiply injured trauma patient, which makes management even more difficult. Current motor vehicle air bag designs have reduced mortality and the incidence of facial fractures, but do not offer adequate protection of the lower extremities in accidents. Pedestrian motor vehicle accidents, falls from heights, and sporting injuries result in open tibial fractures that require the management of complex bone and soft-tissue injuries and may be associated with vascular and nerve injuries. The management of lower-extremity trauma has evolved over the last two decades to the point that many extremities that would have required amputation are now routinely salvaged. Treatment requires a team approach with the orthopedic, vascular, and plastic surgeons as part of the team. Fracture management has improved techniques of external fixation, intermedullary rodding, and internal plating. Bone grafting now includes vascularized bone grafts, Ilizarov bone lengthening, artificial bone matrix and bone growth factors, and nonvascularized bone grafts. Soft-tissue management includes microvascular free tissue transfers, local muscle flaps, and a better understanding of the role of local fasciocutaneous flaps and skin grafts for treatment of defects. Techniques of vascular and nerve repair have been further refined. The goal in treatment of open tibial fractures and lowerextremity salvage is to preserve a limb that will be more functional than if it is amputated. If the extremity cannot be salvaged, the goal is to maintain the maximum functional length. The management of these injuries is a topic of debate in the literature. A severely mangled extremity may take multiple operative procedures and months to years before it can be used for weightbearing and the patient can return to employment. In a review of 72 patients with Gustilo grade IIIB open tibial fractures, Francel et al. found that despite a 93% successful limb salvage rate, a majority of patients had problems with ankle motion or leg edema. Only 28% returned to work after 42 months’ mean follow-up compared to 68% of patients who had a below-knee amputation (1). Similarly, Georgiadis et al. compared 27 patients who had attempted limb salvage with 18 patients who had primary below-knee amputation. They found that patients who had limb salvage took longer to achieve full weightbearing, were less willing to return to work, and had higher hospital charges than those who had primary amputation (2). Laughlin et al. reviewed the functional outcome in eight patients with grade IIIB and six with grade IIIC injuries. He found that despite a long recovery period, eight of nine patients returned to work (3). In a series of 128 patients treated at Bellevue Hospital for open tibial fractures, 66 were available for follow-up for at

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least 5 years. More than 60% of the patients returned to work after extremity salvage. For some patients, the delay to return to work was as long as 10 years after their original injury. A significant cause for the delay to return to work was social factors, such as pending litigation. No patients required further reconstruction more than 5 years after their microvascular free tissue transfer. All but three patients were satisfied with their reconstructions and would do it again if they had the chance. Of the three who were dissatisfied, none were willing to convert the reconstruction to an amputation (4). Extremity salvage is a long, complicated process. Patients must be made aware of the expected course and the anticipated functional outcome. Patient selection is an important variable in evaluating the final outcome. Although normal function is rarely achieved, most patients are grateful for their salvaged limb. In comparing amputees with patients with salvaged limbs, psychological factors must be addressed. A patient with an amputation has a fixed loss and more likely learns to cope with his handicap. A patient with a salvaged limb has a constant reminder of the long, arduous reconstructive process and functional deficits. Long-term studies comparing the functional and psychological difference between patients with amputations and patients with salvage of mangled extremities are needed.

History Amputation was practiced early in the history of humans. One of the earliest writings is that of Hippocrates (460–370 bc), who described amputation as the method of last resort when faced with ischemic gangrene. Celsus (25 bc–50 ad) introduced the rules of wound management, with removal of all foreign bodies and hemostasis. The rules advocated the amputation through viable tissue. Ambroise Pare (1509–1590) described and performed the basic rules of amputation still followed today. He recommended amputation through viable tissue and closure of amputation stumps to fit prostheses. He went on to describe phantom pain and stump revision. Pierre-Joseph Desault (1744–1795) coined the word debridement in the treatment of traumatic wounds. He recommended primary amputation for injuries with extensive vascular, soft tissue, and bone injuries. He recommended secondary amputation only in infected wounds. The concept of immobilization was introduced by Ollier (1825–1900), who introduced the plaster cast. During the U.S. Civil War, numerous lower-extremity injuries were treated. However, the mortality of these injuries was 50%, secondary to sepsis. The advent of antiseptics and antibiotics decreased this mortality rate through World War I. The “closed plaster technique” of management of open tibial fractures was introduced by Orr. It was further advanced


Chapter 70: Lower-Extremity Reconstruction

during the Spanish Civil War by Trueta, who performed surgical debridement prior to placement in plaster. During World War II, no new techniques were employed. However, improvement in aseptic technique and antibiotics decreased the mortality of wound complications from 8% in World War I to 4.5% in World War II. Nonetheless, the increased destructive capacity of military equipment in World War II resulted in a 5.3% amputation rate compared to 2% in World War I. Earlier amputation may have had a role in the reduced mortality. The incidence of postfracture osteomyelitis decreased from 80% in World War I to 25% in World War II. The next major advance in lower extremity salvage came during the Korean conflict. Lower-extremity injuries during this war involved injuries to the major arteries in 59% of the cases. The concept of artery repair as opposed to artery ligation was introduced. This practice decreased the amputation rate from 62% at the beginning of the war to 13% at the end of the war, with wound mortality dropping to 2.5%. In the late 1960s, plastic surgeons discovered the transfer of regional flaps to cover soft-tissue defects of the lower extremity. With the advent of microsurgery in the 1970s, improved techniques of bone coverage with soft tissue and of nerve repair further advanced the ability to salvage traumatic lowerextremity injuries. The free fibular flap also solved the problem of bone gaps in these devastating injuries. The concept of bone lengthening was discovered by Codivilla much earlier and advanced by Ilizarov. It was popularized in the Western world only in the 1980s. This concept provided additional techniques to solve both bone and soft-tissue deficiencies. The concept of negative pressure dressings was introduced in the 1990s by Argenta et al (5). It was found that negative pressure on a wound would decrease edema, decrease bacterial count, promote contraction of the wound, and, with the help of a sponge dressing, promote granulation. Many wounds that were difficult to manage now were easier to manage and enabled simpler reconstructions.

Anatomy The leg has several characteristics that make it susceptible to unique problems. The human is a bipedal animal, thus full weightbearing in the erect position is on the two lower extremities. The full force of the weight of the body is transposed through the legs. The muscles of the leg provide predominantly ankle function with plantar flexion, dorsiflexion, eversion, and inversion. Additional leg muscle functions include toe flexion and knee extension and knee flexion. If the ankle were fused, the functional needs of the leg muscles would be greatly unnecessary and generally tolerated. Therefore, a significant functional muscle loss of the leg can be tolerated and bipedal ambulation will be maintained. Consequently, muscle loss of the leg is not a contraindication to reconstruction and salvage. The hydrostatic pressures imposed on the leg increase the incidence of edema, deep venous thrombosis, and venous stasis problems. These problems are rare in the upper extremity, but common in the lower extremity as a result of its dependent position. The lower extremity is also much more commonly afflicted with atherosclerosis than the upper extremity. These vascular properties of the lower extremity must be considered in the reconstructive procedures of the lower extremity. The anteromedial portion of the tibia is largely covered by skin and subcutaneous fat. This relatively unprotected anatomy leads to many instances of bone exposure, which require specialized soft-tissue coverage in the event of injury. Because the full force of the body is transposed to the feet, sensation of the plantar aspect of the foot is necessary for normal ambulation. The normal sensation is required for tactile sensation, position sensation, and protection of the vulnerable

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pressure-bearing portion of the body. Loss of the posterior tibial nerve, with loss of sensation of the plantar aspect of the foot, is a relative contraindication for lower-extremity salvage. However, many patients with peripheral neuropathy are able to ambulate. They must remain cognizant of the potential problems; motivated patients can enjoy normal ambulation without softtissue breakdown. Thus, in selected patients, loss of sensation of the plantar aspect of the foot may not be a contraindication for lower-extremity salvage.

Bones The bones of the leg are the tibia and the fibula. The tibia provides 85% of the weightbearing capacity of the leg, whereas the fibula serves as a structure for muscle and fascial attachments and as a significant structural portion of the ankle joint. The tibia is the second longest bone in the body. It articulates with the femur at the knee joint on two condyles and joins the fibula to articulate with the talus to form the ankle joint. It articulates with the fibula proximally at the tibiofibular joint and distally at the tibiofibular syndesmosis. The tibia is connected to the fibula in the midportion with the interosseous membrane. It is a classic long bone with a diaphyseal shaft with a thick cortical bone surrounding a marrow cavity. The tibia is wide proximally where it articulates with the femur and narrows to the shaft. The diaphyseal portion is usually described as three surfaces: medial, lateral, and posterior. The medial border is subcutaneous, and thus most prone to exposure during injury. The lateral surface is one of the origins of the tibialis anterior muscle and is protected by the anterior compartment muscles. The posterior surface is well protected by the soleus and gastrocnemius muscles. The fibula is the second, smaller bone of the leg. It originates slightly posterior and distal to the tibia and it articulates with the posterolateral tibia. The shaft of the fibula serves as the origin of many of the muscles of the leg. Distally, it articulates with the talus and forms the lateral malleolus. Because the fibula is not weightbearing and is in a relatively protected position, it is of less concern in trauma, except when the lateral malleolus is involved. Because only the proximal and distal portions are important, and because of an independent blood supply from the peroneal artery, the central portion of fibula is an excellent source of vascularized long bone and can be sacrificed readily.

Compartments The anatomy of the leg is best understood by dividing it into its four muscle compartments. The leg has four muscle groups: anterior, lateral, posterior, and deep posterior. The deep fascia of the leg invests these muscle groups, forming discrete areas or compartments (Table 70.1 and Fig. 70.1). The anterior compartment is comprised of four muscles: the tibialis anterior, the extensor hallucis longus, the extensor digitorum longus, and the peroneus tertius. All four muscles dorsiflex the foot, but the primary dorsiflexor is the tibialis anterior, which also inverts the foot. The extensor hallucis longus primarily extends the great toe; further contraction causes foot dorsiflexion. The extensor digitorum longus extends the phalanges of the lateral four toes and dorsiflexes the foot. The peroneus tertius dorsiflexes and everts the foot. All four muscles are innervated by the deep peroneal nerve, and their blood supply is from muscular branches of the anterior tibial artery. The lateral compartment is comprised of the peroneus longus and peroneus brevis muscles. Both muscles plantarflex and evert the foot. They are both innervated by the superficial peroneal nerve. The vascular supply of the peroneus longus is the muscular branches of the anterior tibial and peroneal arteries. The vascular supply of the peroneus brevis is muscular branches from the peroneal artery.


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TA B L E 7 0 . 1 COMPARTMENTS OF THE LEG Compartment

Muscle function

Nerve

Artery

Anterior tibialis anterior Extensor hallucis longus

Dorsiflex foot, invert foot Extend great toe, dorsiflex foot Extend toes II–V, dorsiflex foot Dorsiflex foot, evert foot Plantarflex and evert foot

Deep peroneal nerve Deep peroneal nerve

Anterior tibial artery Anterior tibial artery

Deep peroneal nerve

Anterior tibial artery

Deep peroneal nerve Superficial peroneal nerve

Peroneus brevis Superficial posterior Gastrocnemius Soleus

Plantarflex and evert foot Plantarflex foot, flex knee

Superficial peroneal nerve Tibial nerve

Plantarflex foot

Tibial nerve

Plantaris Popliteus

Plantarflex foot Flex knee, rotate tibia

Tibial nerve Tibial nerve

Deep posterior Flexor hallucis longus Flexor digitorum profundus Tibialis posterior

Flex great toe, flex foot

Tibial nerve

Anterior tibial artery Anterior tibial and peroneal artery Peroneal artery Popliteal artery, sural branches Posterior tibial, peroneal, sural Sural Popliteal, genicular branches Peroneal artery

Flex toes II–V, flex foot

Tibial nerve

Posterior tibial artery

Plantarflex, invert foot

Tibial nerve

Peroneal artery

Extensor digitorum longus Peroneus tertius Lateral peroneus longus

The superficial posterior compartment is comprised of the gastrocnemius, soleus, plantaris, and popliteus muscles. They are all innervated by the tibial nerve. The gastrocnemius muscle plantarflexes the foot and flexes the knee. Its blood supply is from sural branches of the popliteal artery. The soleus muscle plantarflexes the foot and is supplied by the muscular branches of the posterior tibial, peroneal, and sural branches of the popliteal artery. The plantaris muscle plantarflexes the foot and is supplied by the sural branches of the popliteal. The popliteus flexes the knee and rotates the tibia and is supplied by genicular branches of the popliteal. The deep posterior compartment is comprised of the flexor hallucis longus, flexor digitorum longus, and tibialis posterior muscles. They are all innervated by the tibial nerve. The flexor hallucis longus flexes the great toe and aids in plantarflexion of the foot. It is supplied by muscular branches of the peroneal artery. The flexor digitorum longus flexes the phalanges of the lateral four toes and aids in plantarflexion of the foot. It is sup-

FIGURE 70.1. Cross-sectional anatomy of the leg.

plied by the branches of the posterior tibial artery. The tibialis posterior plantarflexes and inverts the foot. It is supplied by muscular branches from the peroneal artery.

Compartment Syndrome Compartment syndrome is an increase in interstitial fluid pressure within an osseofascial compartment of sufficient magnitude to cause a compromise of the microcirculation, leading to myoneural necrosis. Any crush injury to a closed compartment may lead to compartment syndrome. The literature indicates an incidence of compartment syndrome of 6% to 9% in open tibial fractures. It is important to realize that a laceration with an open fracture may not adequately decompress a compartment. The cardinal signs of compartment syndrome are pain disproportionate to the injury, pain on passive flexion or extension, and palpably swollen or tense compartments. Loss of pulses is usually a late sign and the presence of pulses does not rule out compartment syndrome. The definitive diagnosis is made by measuring the compartment pressure. Various methods have been used to measure the intercompartmental pressure, including slit catheters and saline injection techniques. Although portable, commercially produced units are available, an 18-gauge needle flushed with saline and connected to a transducer is usually adequate. The threshold for fasciotomy is controversial. Some surgeons consider a pressure >30 mm Hg in any compartment an indication for fasciotomy. Allen et al. considered fasciotomy when the compartment pressure was >40 mm Hg for 6 hours or was >50 mm Hg for any length of time (6). Four-compartment fasciotomy should be performed when there is any index of suspicion of compartment syndrome, as the morbidity of a fasciotomy is far less than the morbidity of ischemic necrosis of the lower extremity secondary to compartment syndrome.



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TA B L E 7 0 . 2 GUSTILO CLASSIFICATION OF OPEN FRACTURES OF THE TIBIA Type

Description

I II III IIIA IIIB IIIB

Open fracture with a wound 1 cm without extensive soft-tissue damage Open fracture with extensive soft-tissue damage III with adequate soft-tissue coverage III with soft-tissue loss with periosteal stripping and bone exposure III with arterial injury requiring repair

Fracture Classification Classification of open tibial fractures with relation to fracture pattern and soft-tissue injury is useful in describing injuries and prognosis. The most commonly quoted classification for open fractures is that of Gustilo (Table 70.2). Plastic surgeons are consulted on an open tibial fracture only when the grade is a Gustilo grade IIIB or IIIC. This limits our classification system to two categories. A grade IIIA injury is an open fracture with extensive softtissue damage. However, because it has adequate soft-tissue coverage, it rarely requires plastic surgical consultation. A grade IIIB injury involves an open fracture with periosteal stripping and bone exposure. A grade IIIC injury is an open fracture associated with an arterial injury requiring repair. Although this is the most commonly quoted classification, it remains woefully inadequate to describe the injury or to evaluate the prognosis of an open tibial fracture for which the plastic surgeon is involved. An open tibial fracture with 3 cm of periosteal stripping and exposed bone (Fig. 70.2A) is not the same as an open tibial fracture with an 8-cm bone gap, 12 cm of exposed bone, and necrosis of 16 cm in all four compartment muscles (Fig. 70.2B), though they would be both classified as grade IIIB injuries. Similarly, the phrase “arterial injury requiring repair” in the classification of a grade IIIC injury is ambiguous. Some surgeons may believe it is necessary to repair a second vessel in a one-vessel leg, whereas others may think a single vessel is an adequate blood supply to the foot. In the first case, the injury would be classified as grade IIIC; in the second case, as grade IIIB. The classification also makes no note of nerve injury, which is crucial in the assessment of prognosis.

In an attempt at a better classification, the Mangled Extremity Syndrome Index, Mangled Extremity Severity Score, Predictive Salvage Index, and Limb Salvage Index were created. Even these indices often have proved unhelpful in predicting outcome (7). A more precise classification system needs to be developed to help predict the outcome of salvage efforts for mangled extremities.

MANAGEMENT OF THE MANGLED EXTREMITY Management of the mangled extremity requires the combined expertise of the trauma, vascular, and plastic surgeons. When approaching such a patient, an algorithm must be used to best manage the complicated aspects of this injury. For the management of the mangled extremity, we use the following protocol at Bellevue Hospital (Fig. 70.3).

Initial Evaluation High-energy lower-extremity injuries are usually associated with other life-threatening injuries. The priorities of multisystem injuries are always to salvage the life of the patient, not necessarily the salvage or treatment of the limb. The advanced trauma and life support guidelines must be adhered to prior to fracture management with the priority being the ABCs of trauma: airway, breathing, and circulation. If the patient has other life-threatening injuries, treatment of the extremity injury should be limited to stabilization of the extremity and control of bleeding. Amputation of a mangled extremity in a

A

B FIGURE 70.2. Grade IIIB fractures can vary tremendously in severity. A: Grade IIIB open tibial fracture with periosteal stripping and soft-tissue defect. B: Grade IIIB open tibial fracture with extensive bone and soft-tissue loss.


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FIGURE 70.3. Algorithm for treatment of lowerextremity trauma.

clinically unstable patient may be more prudent than an extensive reconstructive course and should be considered in the initial evaluation of the patient. Assuming that the patient’s other injuries have been addressed, an initial assessment must be made to determine if the extremity is salvageable. The initial evaluation is by visual and manual examination. An assessment of limb viability is made with obvious examination of the wound. A more careful examination of the vascular, bone, soft-tissue, and nerve injuries is then made to determine if the patient is a candidate for limb salvage. Examination of the vascular status of the extremity is made, including examination of the pulses, color, temperature, and turgor of the foot. One must realize that an ischemic limb does not imply a vascular injury. The vessels may be in spasm or may be kinked secondary to the injury. Pulses may return after fracture reduction. Questionable manual exams may require Doppler examination of the vessels. Angiograms are usually necessary to evaluate thoroughly the vascular status of a man-

gled extremity that remains ischemic or requires a microvascular free flap for later reconstruction. Bony evaluation is initially made by visual examination of the open wound. Radiographs are mandatory for evaluation of the fracture. Thorough evaluation of the fracture fragments and accurate assessment of bone loss and devascularization and periosteal stripping of the bone require assessment in the operating room. Soft-tissue evaluation includes examination of the skin subcutaneous tissue, muscle, and periosteum. Avulsion and crush soft tissues can be assessed in the emergency room, but softtissue and muscle viability usually cannot be evaluated except in the operating room on debridement. In complicated cases, even experienced surgeons have difficulty assessing soft-tissue viability and may require serial debridements. Neurologic evaluation includes motor and sensory evaluation of the peroneal and posterior tibial nerves. A complete injury of the neurologic function of the lower extremity may be a relative contraindication for extremity salvage, as nerve



repair in the lower extremity has poor functional results and a below-knee amputation may be preferable to an insensate foot. The initial assessment is to determine if the limb is salvageable. Does the extremity require revascularization and is this technically possible? Is the soft-tissue defect treatable with local or microvascular free tissue transfer? Is there bone loss and is the bone loss reconstructible? Is there nerve injury and is this repairable or does the nerve injury preclude a functional limb? If the extremity is deemed unsalvageable, an amputation is indicated. If the extremity is salvageable, the reconstructive protocol is followed.

Reconstructive Plan After the patient is stabilized and a decision is made to salvage the extremity, the first issue to address is whether or not there is a vascular injury. If there is a vascular injury, a decision must be made as to whether an angiogram should be obtained in the angio suite or in the operating room. If there is quick access to a high-quality angiogram, it is preferable to use it rather than an angiogram in the operating room. If there might be a several-hour delay before an angiogram can be obtained in the angio suite, the patient is taken to the operating room and an on-table angiogram is obtained. The first step in repair is stabilization of the bone injury. If the extremity requires revascularization, the stabilization must be done quickly or consideration be given to the placement of temporary vascular shunts until stabilization is achieved. Once the bone is stabilized, the vascular injury is repaired if indicated. Sometimes posttraumatic ischemia results from spasm, which can be corrected by fracture reduction. If the foot is viable, there may be adequate collateral circulation, or a single intact vessel to the foot may be adequate for extremity viability. If revascularization is performed, fasciotomy to prevent compartment syndrome should be considered. Once bony stability and vascular integrity are established, all nonviable tissue must be debrided. If blood vessels are exposed and an adequate debridement has been performed, immediate soft-tissue coverage is indicated with a microvascular soft-tissue transfer. If there are no vital structures exposed and/or the zone of injury is not clear, the patient should be brought back for a second, or even a third, debridement before definitive soft-tissue coverage is achieved. Most authors agree that early soft-tissue coverage is associated with a lower complication rate. Byrd et al. found that the overall complication rate of wounds closed within the first week of injury was 18% compared to a 50% complication rate for wounds closed in the subacute phase of 1 to 6 weeks (8). In a review of Godina’s work, closure of wounds within the first 72 hours after injury was associated with the lowest complication rate and highest success rate (Table 70.3) (9). Yaremchuk et al. believe that serial, complete debridement is more important than abso-

lute timing of soft-tissue coverage (10). Platelet counts increase nearly fourfold in the subacute phase after injury, which may play a role in the increased complication rate seen during this period (11). Early complete debridement and early soft-tissue coverage improve the results of extremity salvage.

Special Problems Soft-Tissue Avulsion Soft-tissue avulsion must be treated as a special condition. Massive areas of soft tissue may be avulsed that initially appear viable, and it is tempting to suture the avulsed tissue back in place. This avulsed tissue is usually injured much more extensively than is initially appreciated and progressive thrombosis of the subdermal plexus ensues, followed by necrosis of nearly the entire flap of soft tissue. It is usually more prudent to remove the entire avulsed soft tissue, remove the skin as a skin graft, and reapply it to the soft-tissue defect. It may seem radical at the time, especially when the avulsed soft tissue appears viable, but nothing is more disheartening than seeing necrosis of the entire flap with the skin, requiring additional donor defects for later skin grafting.

Vascular Injuries With the advent of repair of vascular injuries instead of ligation, the amputation rate of 50% during World War II was reduced to 15% during the Korean War and to 8% during the war in Croatia. Injury to the popliteal vessels or vessels more proximal represent an emergency that requires immediate repair or reconstruction. Posterior dislocations of the knee are prone to disruption of the popliteal vessels and represent a vascular emergency. The best treatment for injuries to the vessels distal to the trifurcation are somewhat more controversial. Certainly if all three vessels distal to the trifurcation are injured, reconstruction of at least one is indicated. If one vessel is injured, then ligation of one vessel may be more prudent than attempted repair. If two vessels are injured, it is perhaps better to repair at least one; however, there are no studies that demonstrate any difference in outcome whether the leg is a single-vessel leg or a second vessel is reconstructed. Sound surgical judgment is necessary to determine whether the extremity will benefit from a second distal vessel and whether the morbidity of the additional surgery to reconstruct the second vessel is warranted. Vascular injury is initially assessed with physical examination of palpable pulses, color, capillary refill, and turgor of the extremity. Doppler examination may be necessary for equivocal physical examinations. An angiogram is indicated for massive injuries, an ischemic injury that will probably require reconstruction, or an injury that may require microvascular

TA B L E 7 0 . 3 HOW TIMING OF FREE FLAP COVERAGE AFFECTS OUTCOME IN TREATMENT OF OPEN FRACTURES, FROM GODINA Timing 3 weeks

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Failure rate

Infection rate

Bone healing time

Hospital time

1% 12% 10%

2% 18% 6%

68 months 123 months 29 months

27 days 130 days 256 days


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reconstruction. In the ischemic extremity, angiography must be done emergently, with reconstruction to follow. If there is a delay in obtaining an angiogram, an angiogram should be obtained in the operating room. Often, if a vascular bypass is required to revascularize the extremity, an immediate microvascular free flap may be required to cover the bypass graft, further complicating the emergent treatment of the wound. If the extremity is not ischemic, angiography may be delayed after initial treatment of fracture fixation and wound debridement followed by delayed soft-tissue coverage. If pulses are palpable, recent studies show that preoperative angiography may not be necessary prior to microvascular free tissue transfer.

Nerve Injury Injuries to the lower extremity often have associated nerve injuries. Although improved microvascular techniques have allowed for nerve repair and nerve grafting, the results of nerve repair and grafting in the lower extremity have been poor. These poor results are in part a result of the long distance from the spinal cord and the motor endplates, the complex distribution of nerve fascicles, and the long distance required for the nerve to grow to the motor endplate, resulting in endorgan atrophy. Recent experience with nerve grafting shows some promising results. Trumble found an average return of strength of 11% and protective sensation in all of nine patients treated with nerve grafts for repair of the peroneal and sciatic nerves (12). However, most of these patients were in the pediatric age group. Disruption of the peroneal nerve results in foot drop and loss of sensation of the dorsum of the foot. Although not crippling, lifelong foot splinting or tendon transfers are required to offset the foot drop. The loss of sensation of the dorsum of the foot does not cause much morbidity. The loss of the posterior tibial nerve is more devastating. It results in the loss in plantarflexion of the foot, which facilitates the step off in ambulation. The most devastating loss is the loss of sensation of the plantar aspect of the foot. It results in the loss of some position sense and in chronic injury and wounding of the plantar aspect of the foot. Atrophy and vasomotor changes complicate the injury and often result in amputation. Although not an absolute indication for amputation, as it is not much different from the foot of the patient with diabetic neuropathy, it is a relative contraindication. Nerve injuries to the lower extremity should be repaired at the time of injury, if primary repair can be achieved. If nerve grafts are necessary to bridge nerve gaps, they are perhaps best delayed until a healthy soft-tissue bed is established. The prognosis of nerve repair is guarded at best, and most patients require tendon transfers or lifetime splinting.

FRACTURE MANAGEMENT Before vascular or nerve repair can be performed or adequate debridement attempted, a stable framework must be constructed. It is the basis for early fracture management. If a vascular anastomosis is performed prior to fracture fixation, the maneuvering during fracture reduction may disrupt the anastomosis, or the interposition grafts may be found to be too short or redundant after fracture reduction. Consequently, our protocol is to perform fracture fixation first. The techniques available for fracture fixation include traction, casting/splinting, intramedullary nailing, internal fixation, or external fixation. Traction fixation is used only rarely, when the patient is too sick to undergo fracture stabilization. It necessitates immobilization of the entire patient and does not rigidly immobilize the fragments. It is used more commonly in the upper leg; however,

it may be used in the lower leg as a temporary measure for the unstable patient until the patient’s medical condition allows a more stable fixation. Cast immobilization is adequate for closed leg injuries or open tibial fractures once wound management results in a stable wound, but it allows poor fracture immobilization and difficulty in wound care if there is an active wound. Although the “closed plaster technique” was introduced by Orr and popularized by Trueta, it is rarely used for the mangled extremity now that newer techniques are available. Occasionally an open technique is used. In these cases, a window must be made in the cast to allow for dressing changes and wound debridement. This open cast technique can be used until wound control is achieved and definitive wound management approached. Intramedullary nailing is popular because of its many advantages in fracture fixation. There are reamed nails and nonreamed nails. Reamed nails provide rigid fixation by providing a tight fit in the medullary canal after reaming out the canal. There is proximal and distal fixation. With the tight intramedullary fixation, it provides rigid fixation that allows for early ambulation and good fracture reduction and fixation. Intramedullary nails are useful only for minimally comminuted fractures without significant bone loss. The price of the benefits of this technique is the obliteration of the entire endosteal blood supply to the bone by stripping out the medullary canal. In bone that may already have compromised blood supply, devascularization of the injured bone may result, thus the technique may not be indicated for the massively traumatized lower extremity. Nonreamed nails have been advocated by some surgeons for the advantages of reamed nails without their disadvantages. Because they do not take up the entire intramedullary canal, they do not require complete stripping of the endosteal blood supply. They share the advantage of relatively stable fixation and allow early mobilization. They also only can be used in relatively stable fracture patterns; when used for Gustilo grade IIIB or IIIC injuries, immediate coverage of the exposed bone and hardware is required. Exposure of the hardware runs the risk of a progressive, rapid infection up the intramedullary canal; consequently, serial debridements and delayed soft-tissue coverage are contraindicated with this technique. Although it is generally agreed that nonreamed locked nails are effective in open grades I, II, and IIIA tibial fractures, their use in grade IIIB fractures is less clear. In some cases of grade IIIB tibial fractures, however, Trabulsy (13) and Tornetta (14) showed that nonreamed locked nails combined with early soft-tissue coverage and early bone grafting was more effective than external fixation. Internal fixation of diaphyseal tibial long bone injuries with plates and screws provides relatively good alignment and relatively rigid fixation. Application of the fixation devices may require extensive soft tissue and periosteal stripping, and introduces a significant amount of foreign body into the wound. Already compromised tissue may further devascularize. In extensive lower-extremity wounds with soft-tissue injury, already compromised tissue may be further compromised. The introduced foreign body must be covered immediately with soft tissue and local or microvascular free flaps if adequate local softtissue coverage is not available. Again, serial debridement and delayed flap coverage are not indicated in this type of fracture fixation. External fixation is the fixation of choice in a severely traumatized lower extremity with massive soft tissue and bone injury. External fixation allows rigid fixation without additional soft-tissue trauma and minimal bone devascularization. It allows easy access to the wound for additional debridement. It may, however, obstruct surgery when performing microvascular free flaps. Such problems can be avoided with proper planning of placement of the pins and rods. External fixation is more difficult to manage in some patients than internal fixation because pins and rods are bulky. Another potential



complication is pin tract infections. External fixators can be used with the Ilizarov technique for bone lengthening in situations of bone gaps, or they may be left in place after cancellous or vascularized bone grafting until additional stability of the fracture is obtained. Because of the wide zone of injury in grades IIIB and IIIC injuries and contamination at the fracture site, external fixation is usually the fixation of choice.

Management of Bone Gaps There are three ways of managing bone gaps: nonvascularized cancellous bone grafts, Ilizarov bone lengthening, and vascularized bone grafts. The timing of bone grafting remains controversial. One may prophylactically graft bone at the time of soft tissue coverage if a bone gap exists or fill the bone gap with antibiotic beads. Early bone grafting relies on adequate debridement and the confidence that the soft tissue coverage will provide adequate vascularity to support the bone grafting. Many surgeons believe it is better to get wound control prior to bone grafting, avoiding the risk of losing valuable limited bone stock for grafting. We prefer to postpone bone grafting until 6 to 12 weeks after soft-tissue wound coverage has been achieved. Nonvascularized cancellous bone grafts are best used for nonunions or small bone gaps of less than a few centimeters. In well vascularized beds, union rates >90% can be achieved with nonvascularized bone grafts with small gaps. With larger bone gaps, the success of nonvascularized bone grafts decreases and the need for vascularized bone grafts or Ilizarov bone lengthening is indicated. The Ilizarov technique uses the concept of distraction osteogenesis to lengthen bone segments (see Chapter 12). Bone lengthening with the Ilizarov technique theoretically can bridge gaps of large dimensions, but for practical purposes, is best used for gaps of 4 to 8 cm. Two approaches can be used. If a bone gap exists, the gap can be obliterated and the bone can be lengthened subsequently. The other method of treatment is to leave the bones out to length with a bone gap and use distraction osteogenesis to distract one or both segments to meet at the fracture site. Shortening of the bone and later lengthening offer the advantage of easier soft-tissue management. When the bones are left out to length, soft-tissue coverage by microvascular free flaps followed by distraction osteogenesis is also possible. Complications include leg-length discrepancies, axial deformities, refracture, pin track infections, and incomplete “docking” requiring secondary bone grafting. Vascularized fibular grafts can theoretically bridge gaps of ≤24 cm. In harvesting the fibula, it is necessary to preserve the proximal and distal 6 cm of fibula in order not to interfere with knee or ankle function; thus, the limit of fibula harvest is the native fibular length minus 12 cm. The use of the fibula assumes the availability of the contralateral fibula as a donor and of a recipient vessel in the injured leg. The fibula cannot achieve the native strength of the original tibia because of the markedly smaller mass of the fibula compared to the tibia. In fact, the fibula is prone to fracture on stress. However, after healing, the fibula hypertrophies and increases in strength. Weiland had an 87.5% success rate in the use of 32 free fibular grafts, and the average time to full weightbearing was 15 months (15). Fyajima et al. reduced time to weightbearing to 6 months by use of a twin-barreled vascularized fibular graft (16).

Soft-Tissue Management The choice of soft-tissue coverage of open tibial fractures depends on the extent and the location of the injury.

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Split-Thickness Skin Grafts Split-thickness skin grafts are best used to cover exposed muscle or soft tissue, but occasionally they can be used to cover bone with healthy periosteum or tendon with healthy paratenon. In some circumstances, skin graft can also be used to cover small areas of some vessels or nerves, but more substantial soft-tissue coverage with subcutaneous tissue or muscle is recommended to cover vessels, nerves, and—in most situations—bone and tendon, even with healthy periosteum or paratenon. Skin grafts may be adequate to cover Gustilo grade IIIA open tibial fractures, but they are inadequate coverage alone for Gustilo grade IIIB or IIIC injuries.

Local Flaps Local fasciocutaneous or muscle flaps are useful to cover small to moderate defects of bone or to cover exposed vessels or tendons. It is generally accepted that local flaps can cover defects of the proximal or middle third of the leg, but local flaps to cover these defects in the lower third of the leg do not exist. The defects of the lower third of the leg nearly always require free tissue transfer. Fasciocutaneous flaps may be proximally based and cover small defects of bone, exposed vessels, or tendons; however, general principles of rotation flaps must be considered. A small defect will require a rather large flap to be rotated to cover a small defect, and the donor site will always require a splitthickness skin graft. In a series of 67 fasciocutaneous flaps to the lower extremity, Hallock found an 18.5% complication rate. Distally based flaps had a 37.5% complication rate, although wound closure was ultimately achieved in 97% of patients (17). Local fasciocutaneous flaps are usually not available in Gustilo grade IIIB or IIIC injuries in which the local soft tissue is within the zone of injury and unavailable for transfer. Local muscle flaps are quite useful to cover defects of exposed bone, artery, nerve, or tendon in the proximal or middle third of the leg. The lateral or medial gastrocnemius flap is useful for defects of the proximal third of the leg (Fig. 70.4). Defects of the knee can be covered easily. The middle third can be covered by the soleus flap (Fig. 70.5). A hemisoleus muscle can be taken, preserving function of the remaining half of the soleus muscle. Again, it is important to note that large flaps are required to cover even small defects because of the arc of rotation. A considerable donor-site defect that requires skin grafting may be encountered. Functional deficits of muscle harvest are real, but have not been adequately studied. Smaller defects may be covered by the tibialis anterior muscle or other muscles of the anterior and lateral compartments; however, these muscles have a less reliable blood supply and may be less readily expendable for small defects. The tibialis anterior is an important muscle for dorsiflexion of the foot and is not readily expendable. It should be transferred as a bipedicle flap for small defects. The main problem with using local muscle flaps is that they are usually in the zone of injury of high-energy grade IIIB or IIIC injuries. High-energy injuries may result in bone, soft tissue, arterial, nerve, and significant muscle injury. The muscles in these high-energy injuries with significant associated crush injury may not be available for local transfer.

Free Tissue Transfer Microvascular free tissue transfer has revolutionized the treatment of high-energy lower-extremity injuries with associated bone, soft tissue, and muscle loss, and with exposure of bone and vital structures. Once the basic principle of debridement of all devitalized tissue is followed, and if an available recipient artery is available, abundant, healthy muscle and soft-tissue


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A

B

C

FIGURE 70.4. A: An open knee wound with necrotic patella. B: The wound covered with a gastrocnemius rotation flap. C: The healing wound 6 weeks postoperation.

B

A

C

FIGURE 70.5. A: Hemisoleus flap for middle third tibial fracture. B: Insetting of muscle covers a tibial fracture. C: The healing wound 3 weeks postoperation.



A

685

B

FIGURE 70.6. A: A grade IIIB open tibial fracture. B: A large area of soft-tissue loss and exposed bone. C: An area of exposed bone and fracture site covered with latissimus dorsi microvascular free flap.

C

coverage can be supplied to cover the exposed vital structures. The rectus muscle or the latissimus dorsi muscle, or the latissimus dorsi combined with the serratus muscle, can cover large defects (Fig. 70.6). In a review of 304 cases of microvascular free flap reconstruction of the lower extremity, Khouri and Shaw reported a 92% success rate (4). Reported success rates by many authors with early wound coverage with microvascular free flaps has been 85% to 95%.

Negative Pressure Dressings Some wounds may be difficult to manage despite the options of skin grafting, local flaps, or microvascular free tissue transfers. Some patients may not be candidates for these procedures. Chronic wounds may not be amenable to these treatment options because of poor wound beds and inadequate granulation. Argenta et al. described a vacuum-assisted closure using a foam dressing with controlled negative pressure on the dressing sponge and thus the wound. This method of wound care promotes granulation, promotes wound contracture, and decreases bacterial count. The technique has been successful in treating even grade IIIB open tibial fractures that may have required a local muscle flap or a microvascular free tissue transfer (18). Surgical debridements are still necessary as an adjunct to the dressing changes. Though some wounds may be treated with this technique until complete closure has occurred, many wounds require additional surgery, such as a skin graft or flap. The significant improvement in the wound bed, however, makes the reconstructive procedure easier. This technique is ineffective for ischemic wounds.

Chronic Osteomyelitis Chronic osteomyelitis after grade III tibial fractures occurs in approximately 5% of open tibial fractures. Early debridement of open fractures appears to be the key to prevention of osteomyelitis. Once osteomyelitis occurs, the mainstay of treatment is debridement of all devitalized tissue and necrotic bone (Fig. 70.7) and replacement with healthy, well-vascularized tissue, followed by treatment of the bone defect. Anthony et al. treated 34 patients with chronic osteomyelitis with debridement and immediate muscle flap coverage and antibiotics. They had an overall success rate of 96% (19). May reviewed a 13-year experience with treatment of chronic traumatic bone wounds with microvascular free tissue transfer (20). He had a 95% success rate in his series of 96 patients. The treatment of choice for chronic osteomyelitis remains radical debridement of necrotic tissue and coverage with well-vascularized tissue.

Salvage of Below-Knee Amputation Stumps In cases of severe open tibial fractures and lower-extremity traumatic amputations, when limb salvage is not possible, every attempt should be made to preserve as much limb length as possible. This is particularly important with respect to the knee joint. If the knee unit is salvageable, a below-knee amputation should be performed. The work of ambulation is significantly reduced in patients with below-knee amputations as compared to patients with above-knee amputations. Patients with belowknee amputations have a more normal gait and a greater ability to perform more physical activities than patients with


B

A

FIGURE 70.7. A: A chronic wound with exposed bone. B: Radical debridement of all devitalized bone and soft tissue. C: The wound after extensive debridement.

C

Traumatic Below Knee Injury Reconstructable

Unreconstructable

Limb Reconstruction/ Replantation

Amputation

Knee Functional

Knee Irreparable

Below Knee Salvage

Above Knee Amputation

Adequate Soft Tissue

Inadequate Soft Tissue

Primary Reconstruction Dirty Wound Delayed Closure

Below Knee Salvage

Clean Wound

Clean Wound

Primary Closure

Dirty Wound

Immediate Free Flap Foot Available Foot Filet Free Flap

*Delayed Free Flap Foot Not Available

**Parascapular Free Flap

FIGURE 70.8. An algorithm for amputation in lower-extremity injuries.



above-knee amputations. The development of microvascular surgery has allowed salvage of extremities at a more distal level. This is particularly true when the main problem is inadequate soft-tissue coverage.

Advantages of More Distal Amputations A patient with a below-knee amputation has a 25% increased energy and oxygen consumption requirement with ambulation when compared to a person without an amputation. Patients with above-knee amputations have a 65% increase in the oxygen and energy consumption requirement for ambulation when compared to nonamputees. Patients with bilateral below-knee

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amputations have a 45% increased oxygen and energy consumption requirement for ambulation when compared to nonamputees. The amputee will walk more slowly to compensate for the increase in energy required. The higher the level of the amputation, the more energy required, and the slower and less effective the ambulation. Quality of life is also significantly affected by the level of amputation. The daily distance walked is significantly less in above-knee amputation patients as compared to below-knee amputation patients. More above-knee amputation patients walk only in the house or do not walk at all. Above-knee amputation patients have more trouble with stairs and ramps and often require hand controls to drive.

A

B

D

C

FIGURE 70.9. Foot fillet coverage. A: A large zone of injury in proximal tibia area with a long segment of exposed tibia. The foot is relatively uninjured. B: Foot fillet dissection performed. C, D: The final result.


688


Free Flap Salvage of Below-Knee Amputation Stumps If the distal limb is nonsalvageable but the knee joint is functional, every attempt should be made to preserve a below-knee amputation. Although the ideal below-knee amputation stump has >6 cm of tibia below the tubercle, any length of tibia should be preserved as the benefits of a below-knee amputation are great compared to above-knee amputation. If adequate softtissue coverage is present, the stump may either be closed primarily or closed in a delayed fashion, if there is significant contamination. If the soft-tissue coverage is inadequate, a skin graft reconstruction may be possible. If insufficient soft tissue exists to cover the bone, free flap reconstruction is considered. In clean wounds, free flap coverage is accomplished as it is for any open tibial fracture. The flap should be performed in the early postinjury period, depending on the patient’s overall condition. If the foot on the amputated part is uninjured, an immediate foot fillet free flap is considered. If the foot on the amputated part is not usable, then a parascapular free flap or muscle free flap plus skin graft can be performed shortly thereafter. In dirty wounds, the free flap is delayed until wound conditions are optimized. Figure 70.8 summarizes the decision-making tree. In a study by Kasabian (21) patients achieved stable coverage of below-knee amputations with free flap coverage. The most common flap was the parascapular flap, used in 11 patients. The parascapular flap allowed for the most accurate reconstruction of the amputation stump. A foot fillet flap was used in six cases. The other free flaps employed were the latissimus dorsi (4), lateral thigh (1), tensor fascia lata (1), and groin (1). The patients in the study required an average of 4.9 operations related to their injury. There were 1.3 operations after the free flap. Most patients had long hospitalizations as a result of the combination of their injuries and their overall situations. The foot fillet flap offers several advantages over other flaps. It is the only flap available from the amputated part and as such has no donor-site morbidity. In addition, sensory innervation is provided by the tibial nerve, peroneal nerves, and sural nerves. The tibial nerve is used most commonly and provides sensibility to the plantar surface of the foot, which is usually inset at the end of the below-knee amputation stump. Neurorrhaphy may be accomplished to a proximal nerve stump or the nerve may be left in continuity. Finally, the foot fillet has glabrous skin that is durable and not prone to ulceration (Fig. 70.9). Muscle free flaps with skin graft coverage tend to heal slowly. There are often areas of partial graft survival. In addition, as the muscle atrophies and the flap shrinks, revisions are required to both the stump and the prosthesis. The additional surgical procedures lengthen the time to the fitting of the final prosthesis when compared to patients with fasciocutaneous flaps.

References 1. Francel TJ, Vander Kolk CA, Hoopes JE, et al. Microvascular soft-tissue transplantation for reconstruction of acute open tibial fractures: timing of coverage and long-term functional results. Plast Reconstr Surg. 1992;89:478–487. 2. Georgiadis GM, Behrens FF, Joyce MJ, et al. Open tibial fractures with severe soft-tissue loss. Limb salvage compared with below-the-knee amputation. J Bone Joint Surg Am. 1993;75:1431–1441. 3. Laughlin RT, Smith KL, Russell RC, et al. Late functional outcome in patients with tibia fractures covered with free muscle flaps. J Orthop Trauma. 1993;7:123–129. 4. Khouri RK, Shaw WW. Reconstruction of the lower extremity with microvascular free flaps: a 10-year experience with 304 consecutive cases. J Trauma. 1989;29:1086. 5. Argenta LC, Morykwas MJ. Vacuum-assisted closure: a new method for wound control and treatment: clinical experience. Ann Plast Surg. 1997;38(6):563–576. 6. Allen MJ, et al. Intracompartmental pressure monitoring of leg injuries. An aid to management. J Bone Joint Surg. 1985;67B:53. 7. Bonanni F, Rhodes M, Lucke JF. The futility of predictive scoring of mangled lower extremities. J Trauma. 1993;34:99–104. 8. Byrd SH, Spicer ET, Cierny G III. Management of open tibial fractures. Plast Reconstr Surg. 1985;76:719. 9. Godina M. Early microsurgical reconstruction of complex trauma of the extremities. Clin Plast Surg. 1986;13:619. 10. Yaremchuk MJ, Brumback RJ, Manson PN, et al. Acute and definitive management of traumatic osteocutaneous defects of the lower extremity. Plast Reconstr Surg. 1982;80:1–14. 11. Choe IE, Kasabian KA, Kolker RA, et al. Thrombocytosis after major lower extremity trauma: mechanism and possible role in free flap failure. Ann Plast Surg. 1996;36:489–494. 12. Trumble T, Vanderhooft E. Nerve grafting for lower-extremity injuries. J Pediatr Orthop. 1994;14:161–165. 13. Trabulsy PP, Kerley SM, Hoffman WY. A prospective study of early soft tissue coverage of grade IIIB tibial fractures. J Trauma. 1994;36:661– 668. 14. Tornetta P III, Bergman M, Watnik N, et al. Treatment of grade IIIB open tibial fractures. A prospective randomized comparison of external fixation and non-reamed locked nailing. J Bone Joint Surg Br. 1994;76:13– 19. 15. Weiland AJ, Moor JR, Daniel RK. Vascularized bone autografts: experience with 41 cases. Clin Orthop. 1983;174:87. 16. Fyajima H, Tamai S. Twin-barreled vascularized fibular grafting to the pelvis and lower extremity. Clin Orthop. 1994;303:178–184. 17. Hallock GC. Complications of 100 consecutive local fasciocutaneous flaps. Plast Reconstr Surg. 1991;88:264. 18. Greer S, Kasabian A, Thorne C, et al. The use of subatmospheric pressure dressing to salvage a Gustilo grade IIIB open tibial fracture with concomitant osteomyelitis to avert a free flap. Ann Plast Surg. 1998;41(6): 687. 19. Anthony JP, Mathes SJ, Alpert BS. The muscle flap in the treatment of chronic lower extremity osteomyelitis: results in patients over 5 years after treatment. Plast Reconstr Surg. 1991;88:311. 20. May JW, Jupiter JB, Gallico GG, et al. Treatment of chronic traumatic bone wounds. Microvascular free tissue transfer: a 13-year experience in 96 patients. Ann Surg. 1991;214:241. 21. Kasabian AK, Colen SR, Shaw WW, et al. The role of microvascular free flap in salvaging below-knee amputation stumps: a review of 22 cases. J Trauma. 1991;31:495.


CHAPTER 71 ■ FOOT AND ANKLE RECONSTRUCTION CHRISTOPHER E. ATTINGER AND IVICA DUCIC

Ambulation subjects the foot to repetitive trauma. On average, an individual takes more than 10,000 steps each day. The foot possesses specialized plantar tissue that can withstand the effects of such repetitive direct and shear stress forces. Blunt and/or penetrating trauma can also cause immediate breakdown of the soft tissue and/or bone. In addition, infection and changes in blood supply, sensation, immune status, and biomechanics renders the foot susceptible to chronic breakdown. Inability to salvage the injured foot leads to amputation, which mandates a lifetime dependence on prosthetic devices. Some patients never wear the prosthesis and lead a wheelchair existence. Major amputation in diabetics is associated with premature death and high likelihood of subsequent contralateral leg amputation. The foot is a complex body part and salvage requires a team approach, with a team composed of a vascular surgeon skilled in endovascular and distal bypass techniques, a foot and ankle surgeon skilled in bone stabilization techniques including use of the Ilizarov frame, a soft-tissue surgeon familiar with modern wound healing as well as soft-tissue reconstructive techniques, and an infectious disease physician specializing in surgical infections. In addition, a podiatrist skilled in routine foot care and a pedorthotist skilled in orthotics and assistedfoot-orthoses are critical in preventing recurrent breakdown. Medical specialties such as endocrinology, nephrology, hematology, rheumatology, and dermatology are often necessary. Plastic surgeons are called upon to address the wounds that result from trauma and/or infection. The first task is to convert the existing wound into a healing wound by aggressive debridement as well as application of modern wound-healing techniques. Most wounds can then be closed using simple softtissue techniques, such as delayed primary closure, skin grafts, and local flaps. Some wounds, however, require more sophisticated techniques that mandate an intimate knowledge of the local angiosomes, arterial blood supply, and flap anatomy. Finally, all reconstructions have to be biomechanically sound to avoid recurrent breakdown.

ANATOMY Vascular Anatomy The foot and ankle consists of six angiosomes. The following arteries feed the angiosomes of the foot and ankle (1): (a) the distal anterior tibial artery feeds the anterior ankle while its continuation, the dorsalis pedis artery, supplies the dorsum of the foot; (b) the calcaneal branch of the posterior tibial artery feeds the medial and plantar heel; (c) the calcaneal branch of the peroneal artery feeds the lateral and plantar heel, (d) the anterior perforating branch of the peroneal artery feeds the anterolateral ankle; (e) the medial plantar artery feeds the plantar

instep; and (f) the lateral plantar artery feeds the lateral plantar mid- and forefoot (Fig. 71.1). Note that the plantar heel receives dual blood supply from the calcaneal branches of the posterior tibial and peroneal arteries. When the heel develops gangrene, this usually implies severe vascular disease involving both the peroneal and posterior tibial artery. Because the foot is an end organ, there are many arterial– arterial anastomoses that provide a duplication of inflow. These arterial–arterial anastomoses (Fig. 71.2) provide a margin of safety if one of the main arteries becomes occluded. At the ankle, the anterior perforating branch of the peroneal artery is connected to the anterior tibial artery via the lateral malleolar artery. At the Lisfranc joint, the dorsalis pedis artery dives into the first interspace to connect directly with the lateral plantar artery. This vascular loop is critical in determining the direction of flow within the anterior or posterior tibial arteries, which can be antegrade or retrograde or both. In addition, the plantar and dorsal metatarsal arteries are linked to one another at the Lisfranc joint by proximal perforators and at the web space by distal perforators. Finally, the posterior tibial artery and peroneal artery are directly connected deep to the distal Achilles tendon by one to three connecting arteries. Using a Doppler ultrasound probe and selective occlusion, one can determine the patency of these connections as well as the direction of flow. This is critical in designing local flaps, pedicled flaps, and amputations.

Motor and Sensory Anatomy The sciatic nerve divides into the tibial and common peroneal nerves proximal to the popliteal fossa. Within the popliteal fossa, it is lateral to the popliteal vessels, while distally it travels in the deep posterior compartment of the leg. The tibial nerve innervates muscles of the deep and superficial posterior compartments (except gastrocnemius muscle), and ends at the distal inner ankle deep to the flexor retinaculum, trifurcating into the calcaneal and medial plantar and lateral plantar nerves. These nerves supply the motor branches to the intrinsic muscles of the foot (except the extensor digitorum brevis [EDB] muscle). The common peroneal nerve passes around the lateral aspect of the fibular head before splitting into the superficial and deep branches. The deep peroneal nerve innervates the extensor muscles in the anterior compartment before exiting the extensor retinaculum to innervate the extensor digitorum brevis muscle. The superficial peroneal branch innervates the everting peroneal muscles of the lateral compartment before it pierces the fascia to become subcutaneous and provide sensibility to the lateral lower leg and dorsum of the foot. The sensory nerves to the foot and ankle (Fig. 71.3) travel more superficially than the motor nerves, and their degree of function is a useful index to the localization of trauma in the lower extremity. As mentioned above, the superficial peroneal


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C

A,B FIGURE 71.1. Angiosomes of the foot and ankle: Angiosomes include (A) the anterior ankle fed by the anterior tibial artery and the dorsum of the foot fed by the dorsalis pedis artery; (B) the medial and plantar heel fed by the calcaneal branch of the posterior tibial artery, the plantar instep fed by the medial plantar artery, the lateral plantar midfoot and plantar forefoot fed by the lateral plantar artery; and (C) the anterolateral ankle fed by the anterior perforating branch of the peroneal artery and the lateral and plantar heel fed by the calcaneal branch of the peroneal artery.

nerve (L4, L5, S1) supplies the anterolateral calf skin while descending within the anterolateral compartment. It exits approximately 10 to 12 cm above the lateral ankle and travels anterior to extensor retinaculum to supply the dorsum of the foot and skin of all the toes except the lateral side of the fifth toe (sural nerve) and the first web space (deep peroneal nerve). The deep peroneal nerve (L4, L5, S1) exits the anterior compartment deep to the extensor retinaculum to supply ankle and midfoot joints, sinus tarsi, and the first web space. The sural nerve (L5, S1), derived from both the tibial and common peroneal nerves, descends distal to the popliteal fossa in the posterior aspect of the calf along the course of the lesser saphenous vein. It provides sensibility to the posterior and lateral skin of the leg’s distal third, prior to passing between the anterolateral border of the Achilles tendon and lateral malleolus in order to supply skin of the dorsolateral foot and fifth toe. The skin of the medial half of the lower leg and dorsomedial portion of the foot is innervated by saphenous nerve (L5, S1), a cutaneous branch of the femoral nerve. The dorsum of the foot has communicating branches between saphenous, sural, superficial, and deep peroneal nerves, and thus there is often an overlap in their respective terminal areas of innervation. The posterior tibial nerve at the distal portion of the tarsal tunnel divides into three branches that supply the sole of the foot: the calcaneal branch (S1, S2) supplies the medial aspect of the heel pad; the lateral plantar nerve (S1, S2) supplies the lateral twothirds of the sole and the fifth and lateral fourth toes; the medial planter nerve (L4, L5) supplies the medial one-third of the sole and the first, second, third, and medial fourth toes. The medial and lateral plantar nerve can have an overlap in their respective zones with the saphenous and sural nerves, respectively.

Lower Leg, Ankle, and Foot: Muscle and Fasciocutaneous Flaps The following lower leg, ankle, and foot flaps are briefly described, emphasizing their vascular supply and their use in foot

and ankle reconstruction. The details of the individual flap dissection are described in several atlases on flaps (2,3). More importantly, repeated cadaver dissection of these flaps, emphasizing the blood supply, is the most reliable way to become facile in their use.

Lower Leg and Ankle Flaps The lower leg muscles are poor candidates for pedicled flaps because most of them are type 4 muscles with segmental minor arterial pedicles. As a result, only a small portion of the muscle can safely be transferred without applying the delay principle. Even when the minor pedicles are sequentially ligated to delay the muscle flap, the results are disappointing. To successfully transfer a significant portion of the muscle, all the relevant minor perforators have to be preserved with the accompanying major artery. The sacrifice of a major artery should only be considered if all three arteries are open and there is excellent retrograde flow. Although the bulk of these muscles is often disappointing, the distal portion of some of these type 4 muscles (Fig. 71.4) can be used to cover small defects around the ankle medially, anteriorly, laterally. It is important to tenodese the distal end of the severed tendon of the harvested muscle to a muscle with similar function so that the harvested muscle’s function is not lost. For example, if the distal extensor hallucis muscle is harvested, the extensor hallucis longus (EHL) tendon distal to the harvest site should be tenodesed to the extensor digitorum longus so that the hallux maintains its position during gait. Because the loss of the anterior tibial tendon is so debilitating, this muscle should not be harvested unless the ankle has been or is being fused. The extensor hallucis longus muscle can cover small defects that are as distal as 2 cm above the medial malleolus. The extensor digitorum longus muscle and peroneus tertius muscle are used for small defects as distal as 2.1 cm above the medial malleolus. The peroneus brevis muscle can be used for small defects as distal as 4 cm above the medial malleolus. The flexor digitorum longus muscle can be used for small defects as distal as 6 cm above the medial malleolus. The soleus muscle is the


Chapter 71: Foot and Ankle Reconstruction

Ant. tibial a.

Ant. perforating br. of peroneal a. Lateral malleolar a.

Medial malleolar a. Dorsis pedis a.

Lateral tarsal a.

Proximal perforating a.

Vertical descending br. of dorsal pedis a. Dorsal metatarsal a.

Dorsal digital aa.

FIGURE 71.2. Arterial anatomy of the foot and ankle. At the ankle, the anterior tibial artery gives off the lateral malleolar artery at the level of the lateral malleolus. It anastomoses with the anterior perforating branch of the peroneal artery. At the Lisfranc joint, the dorsalis pedis artery dives down in the first interspace to join the lateral plantar artery. At the second, third, and fourth proximal interspaces, the proximal perforators link the dorsal and plantar metatarsal arteries. Not shown is the direct connection between the peroneal and posterior tibial artery underneath the distal Achilles tendon. (From Attinger C. Vascular anatomy of the foot and ankle. Oper Tech Plast Reconstr Surg. 1997;4:183, with permission.)

only type 2 muscle in the distal lower leg where the minor distal pedicles can be detached and the muscle can be rotated with its intact proximal major rotated to cover large (10 × 8 cm) anterior lower-leg defects as distal as 6.6 cm above the medial malleolus. It can be harvested as a hemisoleus for small defects and as an entire soleus for larger defects. These flaps require skin grafting. In addition, the ankle has to be immobilized to avoid dehiscence and ensure adequate skin graft take. External frames are useful for immobilization and vacuum-assisted closure devices (Kinetic Concepts Inc., San Antonio, TX) assist graft take. Fasciocutaneous flaps had their origin in 1981 when Ponten described the medial calf flap. Fasciocutaneous flaps are useful for reconstruction around the foot and ankle, although the donor site usually requires skin grafting (4). The retrograde peroneal flap is useful for ankle, heel, and proximal dorsal foot defects. Its blood flow is retrograde and depends on an intact distal peroneal arterial–arterial anastomosis with either or both the anterior tibial artery and/or posterior tibial artery. The dissection is tedious and it does sacrifice one of the three major arteries of the leg. A similar retrograde anterior tibial artery fasciocutaneous flap has been described for coverage in young

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patients with traumatic wounds over the same areas. Because the anterior compartment is the only compartment of the leg whose muscles depend solely on a single artery, only the lower half of the artery can be safely harvested as a vascular leash. The retrograde sural nerve flap (Fig. 71.5) is a versatile neurofasciocutaneous flap that is useful for ankle and heel defects. The sural artery travels with the sural nerve and receives retrograde flow from a peroneal perforator 5 cm above the lateral malleolus. The artery first courses above the fascia and then penetrates deep to the fascia at midcalf while the accompanying lesser saphenous vein remains above the fascia. The venous congestion often seen with this flap can be minimized if the pedicle is harvested with 3 cm of tissue on either side of the pedicle and with the overlying skin intact. Problems with the venous drainage can be further helped if the flap is delayed, 4 to 10 days earlier, by ligating the proximal lesser saphenous vein and sural artery. The inset of the flap is critical to avoid kinking of the pedicle. Ingenious splinting is necessary to avoid pressure on the pedicle while the flap heals (the Ilizarov external frame can be useful in this regard). The major donor deficit of the flap is the loss of sensibility along the lateral aspect of the foot, while the skin-grafted depression in the posterior calf may pose a problem if the patient subsequently has a belowthe-knee amputation. The supramalleolar flap can be used for lateral malleolar, anterior ankle, and dorsal foot defects. It can be either harvested with the overlying skin or as a fascial layer that can be skin grafted. When harvested as a fascial flap, the donor site can be closed primarily. Small local fasciocutaneous flaps based on individual perforators can also be designed over the row of perforators (Fig. 71.6) originating from the posterior tibial artery medially and the peroneal artery laterally. Although the reach and size of these flaps are limited, these can be expanded by applying the delay principle. These local flaps are extremely useful in the closure of soft-tissue defects around the ankle in patients in an Ilizarov frame because accessibility to pedicled flaps or recipient vessels for free flaps is problematic.

Foot Flaps The muscle flaps in the foot (5) have a type 2 vascular pattern and are useful for coverage of relatively small defects. The abductor digiti minimi muscle (Fig. 71.7A) is very useful for coverage of small mid- and posterior lateral defects of the sole of the foot and lateral distal calcaneus and ankle. The dominant pedicle is medial to the muscle’s origin at the calcaneus and it has a thin distal muscular bulk. The abductor hallucis brevis muscle (Fig. 71.7B) is larger and can be used to cover medial defects of the mid- and hindfoot, as well as the medial distal ankle. Its dominant pedicle is at the takeoff of the medial plantar artery. Both of the above muscles can be used together to cover somewhat larger plantar defects in the midfoot and heel. The flexor digiti minimi brevis muscle is a small muscle that can be used to cover defects over the proximal fifth metatarsal bone. It receives its dominant pedicle at the lateral plantar artery takeoff of the digital artery to the fifth toe. The flexor hallucis brevis muscle has similar vascular anatomy, but can be harvested on a much longer vascular pedicle as an island flap on the medial plantar artery to reach defects as far as the proximal ankle. The extensor digitorum brevis muscle (Fig. 71.8) has disappointingly little bulk but can be used for local defects over the sinus tarsi or lateral calcaneus. The muscle can either be rotated in a limited fashion on its dominant pedicle, the lateral tarsal artery, or in a wider arc if harvested with the dorsalis pedis artery. The flexor digitorum brevis muscle can be used to cover plantar heel defects. Because the muscle bulk is small, it works best if it is used to fill a deep defect that can be covered with plantar tissue.


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FIGURE 71.3. Sensory innervation of the lower leg. Note that the sensory distribution of the deep peroneal nerve is limited to the first web space, whereas the superficial peroneal nerve runs in the lateral compartment and provides sensibility to the dorsum of the foot. The posterior tibial nerve that runs in the deep posterior compartment supplies the sole of the foot and toes.

The most versatile fasciocutaneous flap of the foot is the medial plantar flap, which is the ideal tissue for the coverage of plantar defects. It can also reach medial ankle defects. The flap can be harvested to a size as large as 6 × 10 cm, has sensibility, and has a wide arc of rotation if it is taken with the proximal part of the medial plantar artery whether distally based on the superficial medial plantar artery or on the deep medial plantar artery (Fig. 71.9). Although easier to harvest on the deep medial plantar branch, it is preferable to harvest the flap based on the superficial branch because there is less disturbance of the inflow to the remaining foot. When harvested with retrograde flow, the flap should be based on the deep branch of the medial plantar artery. The lateral calcaneal flap (Fig. 71.10) is useful for posterior calcaneal and distal Achilles defects. Its length can be increased by harvesting it as an L-shape posterior to and below the lateral malleolus. It is harvested with the lesser saphenous vein and sural nerve. Because the calcaneal branch of the peroneal artery lies directly on the periosteum, there is great danger of damaging or cutting it during harvest. The dorsalis pedis flap can be either proximally or distally based for coverage of ankle and dorsal foot defects. A flap wider than 4 cm usually requires skin grafting on top of the extensor tendon paratenon, which deprives the dorsum of the foot of durable coverage. Because the donor site is vulnerable from both a vascular and tissue breakdown perspective, the dorsalis pedis flap is now rarely used. The filet of toe flap is useful for small forefoot web space ulcers and distal forefoot problems, even though the reach of the flap is always less than expected. The technique involves

removal of the nail bed, phalangeal bones, extensor tendons, flexor tendons, and volar plates while leaving the two digital arteries intact. An elegant variation is the toe island flap, where a part of the toe pulp is raised directly over the ipsilateral digital neurovascular bundle and then brought over to close a neighboring defect, while its neurovascular pedicle is buried underneath the intervening tissue.

WOUND CARE The etiology of foot and ankle wounds is usually traumatic, with the underlying pathology complicating the healing process. Significant accompanying disease processes include infection, ischemia, neuropathy, venous hypertension, lymphatic obstruction, immunologic abnormality, hypercoagulability, vasospasm, neoplasm, self-induced wound, or any combination of the preceding. The most frequent systemic comorbidities include diabetes, peripheral vascular disease, venous hypertension, and connective tissue disorders.

Diagnostic Studies Evaluation of the patient with a foot wound or ulcer begins with a complete history and physical examination. Important points in the history include etiology, duration and previous treatment of the wound(s), comorbid conditions (diabetes, peripheral vascular disease, venous insufficiency, atherosclerotic disease, autoimmune disorders, radiation, coagulopathy, etc.),


Chapter 71: Foot and Ankle Reconstruction

FIGURE 71.4. The type 4 muscles of the lower leg. These muscles are thin and can only be harvested for a distance of two to three segmental pedicles. They provide little bulk to cover lower-leg defects. The figure indicates how far proximal to the medial malleolus each muscle is useful for coverage of lower leg defects. For larger defects, a free flap is almost always a better option. (From Attinger C. Plastic surgery techniques for foot and ankle surgery. In: Myerson M, ed. Foot and Ankle Disorders. Philadelphia: WB Saunders; 2000:627, with permission.)

current medications, allergies, and nutritional status. It is also important to assess the patient’s current and anticipated level of activity. If the patient is using the leg in any way, including simple transfers, then salvage, if medically tolerated and technically possible, is usually indicated. However, if the limb is not going to be used, then strong consideration should be given to performing a knee disarticulation or above-knee amputation to cure the problem and minimize the risk of recurrent breakdown. The complete physical examination starts with a careful wound measurement (length, width, and depth), as well as the types of tissue involved (i.e., epithelium, dermis, subcutaneous tissue, fascia, tendon, joint capsule, and/or bone). The most accurate way of assessing if bone is involved is if one can directly feel bone with a metal probe, which correlates 85% of the time with the existence of osteomyelitis (6). Diabetic ulcers with an area >2 cm2 have a 90% chance of underlying osteomyelitis regardless of whether bone is probed at the base of the wound. The levels of tissue necrosis and possible avenues of spread of infection via flexor or extensor tendons are then determined. If cellulitis is present, the border of the cellulitis is delineated with a marker and the date and time are noted.

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This permits the clinician to immediately monitor the progress of the initial treatment despite the lack of bacterial culture results. The vascular supply to the foot is then examined. If pulses are palpable (dorsalis pedis or posterior tibial artery), there is usually adequate blood supply for wound healing. If one cannot palpate pulses, a Doppler should be used. The Doppler ultrasound probe also allows the surgeon to evaluate the nonpalpable anterior perforating branch and the calcaneal branch of the peroneal artery. It also helps determine the direction of flow along the major arteries of the foot to accurately assess local blood flow when designing a flap or amputation. A triphasic Doppler sound indicates excellent blood flow; a biphasic sound indicates adequate blood flow; and a monophasic sound warrants further investigation by the vascular surgeon. A monophasic tone does not necessarily reflect inadequate blood flow as it may reflect of lack of vascular tone and absent distal resistance. If the pulses are nonpalpable or monophasic, then noninvasive arterial Doppler studies are indicated. It is important to obtain PVRs (pulse volume recordings) at each level because arterial brachial indices are unreliable in patients with calcified vessels, that is, in 30% of diabetics. Ischemia may be present if the PVR amplitude is 6 mm static and >3 mm moving 2PD at the fingertips) indicate axonal impairment (3). Two-point discrimination has the advantage of being somewhat quantitative, which allows for comparisons over time and between patients. Even more sensitive than 2PD is vibration sensibility (tuning fork) and pressure thresholds (Semmes-Weinstein monofilament testing). Although some variations and overlap exist in the sensory innervation of the upper limb, there are three autonomous areas on the hand, each of which is innervated by only one of three major nerves. The autonomous zone for the median nerve is the index fingertip, for the ulnar nerve it is the small finger’s tip, and for the radial nerve it is the dorsal side of the first web space. Soft-tissue coverage should be restored before reconstruction of deeper structures is undertaken. Thick scars along the route of tendon transfers or across joints will limit mobility. During open wound examination, any skin deficits or devitalized areas are noted and recorded on a sketch, but deep probing is not performed in the emergency room without appropriate anesthesia, lighting, and instruments.

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Part VIII: Hand

Bone injuries are considered if gentle palpation reveals localized skeletal tenderness. A fracture is suspected when sharp pain is accompanied by deformity, abnormal mobility, progressive swelling, and/or prominent ecchymosis. Radiographs of good quality and a minimum of posteroanterior (PA), lateral, and oblique views are essential. Specialized views may be required to rule out fractures of a specific bone (e.g., scaphoid or hook of the hamate). A fracture should be described according to location, type, and deformity. The location is specified by the name of the bone and the portion involved (base, midshaft, neck, intra-articular, etc.). The type of fracture is described according to the pattern (transverse, oblique, spiral, comminuted, undisplaced) and whether a communicating skin wound (open or closed) is present. Describe the deformity according to the displacement (dorsal, volar, radial, ulnar) and angulation. By tradition, angulation is named for the direction of the apex and rotation for the distal segment in relation to the proximal one. Rotational malalignment in the fingers can best be observed by having the patient slowly bring all the fingers from a fully extended position into flexion. Any scissoring (crossing of fingers) usually indicates a rotational malalignment. For example: “The patient has a right fifth metacarpal neck fracture that is closed and comminuted with 3-mm volar displacement and 45 degrees of dorsal angulation, but no rotational malalignment.” Joints are examined for tenderness, active and passive range of motion, stability, and deformity. Abnormal physical findings necessitate radiographic examination. A “chip” fracture may indicate a ligamentous avulsion injury. Stress radiographs may be required in diagnosing ligamentous injuries, and should be performed after injecting local anesthetic to prevent pain and guarding. Muscle function depends on skeletal stability, functioning joints, and intact motor nerves and muscle–tendon units. Each unit for which there is reason to suspect injury should be tested, first without resistance to assess active range of motion, and then with resistance to assess strength. Pain or weakness against resistance suggests a partial tendon laceration. Dynamometers that measure grip and pinch forces are of little use with acute injuries, but are essential for evaluating and following chronic problems. The absolute numbers are less important than comparison with those of the unaffected side. Some information may be gained by observing the resting posture of the hand. In the supine position, the resting hand should have the fingers in a partially flexed position, falling into a smooth cascade of progressively more flexion from the index to the small finger. A complete tendon laceration will cause the injured digit to fall out of line at rest. The tenodesis effect from passive wrist flexion/extension can also help evaluate suspected tendon injuries, even if the patient is under anesthesia. Wrist flexion increases tension on the digital extensor tendons causing passive digital extension. A digit with a transected extensor tendon will fail to extend when the wrist is passively flexed. This tenodesis effect can also be used to test the flexor tendons, observing the digital cascade, as the wrist is hyperextended. However, a partially severed tendon cannot be diagnosed or excluded by any of these manipulations. Wound exploration is often the only means to establish the presence of partially severed tendons with certainty.

Acute Injury The first priority is to rule out injuries to other parts of the body. To minimize patient discomfort, as much information as possible is obtained from observation rather than manipulation. Proceeding from distal to proximal, every structure in the zone of injury is systematically tested. The entire examination need not be performed in the emergency room. There

are two important questions to be answered in the emergency room. First, are any parts threatened by ischemia? Second, does this injury need to be treated in the operating room? If the answer to either question is yes, extensive exploration of wounds should be deferred to the operating room. Often, the basic information is gained by examining the areas distal to the wound, including circulation, sensibility, and muscle/tendon integrity. The physical findings and appropriate radiographs guide exploration. It is helpful to triage injuries into three categories according to severity and urgency: (a) severe injuries that require immediate treatment; (b) severe injuries that require early treatment; and (c) less-severe injuries. Severe injuries that require immediate treatment include life-threatening situations and injuries that have resulted in ischemia and threaten survival of the parts. There are only two life-threatening upper limb problems: exsanguinating hemorrhage and necrotizing infection (see Chap. 85). Hemorrhage in the absence of a coagulopathy can be controlled by elevation and direct pressure on the bleeding point. Makeshift tourniquets should not be used because they can apply dangerously high pressures, causing permanent damage to underlying muscles and nerves. Clamping of “bleeders” in the emergency room is strongly discouraged because of the risk of injury to adjacent nerves. Tetanus prophylaxis should be considered for every patient with a wound. For clean wounds, tetanus toxoid should be administered if the patient has not been immunized within 10 years or has had fewer than the usual series of immunization doses. For highly contaminated or extensive wounds, tetanus toxoid usually should be administered, and if the patient has not been immunized within 5 years, tetanus immune globulin is recommended. Injuries that result in ischemia include amputations, vascular injuries, crush injuries, and electrical injuries. Muscle is the tissue most vulnerable to hypoxia and must be reperfused within about 6 hours if it is to survive. Hypothermia is our only means of prolonging this time limit, as it lowers the metabolic rate of the tissues. Ischemic parts not amputated should be kept cool with ice, but taking care not to freeze them. One should suspect a compartment syndrome if the patient complains of progressive pain disproportionate to the injury, if a muscle compartment feels tense on palpation, and especially if passive muscle stretching dramatically increases pain. High-pressure injection injuries can cause progressive tissue damage. These injuries vary in severity depending on the toxicity and volume of the injected agent. The history is the key to diagnosis, as the toxic agent may be forced through a tiny, innocuous-appearing wound. Often, injection is at a fingertip with dissection of the material along the tendon sheaths all the way into the forearm. Left untreated, there will be progressive inflammation and destruction of the surrounding tissues and often this is inevitable despite early recognition and immediate operative debridement. Severe injuries that require early surgical repair include those of flexor tendons, open fractures, and joint injuries. If the skin wound is not extensive, it can be irrigated and closed in the emergency room, except for human bites, with delayed primary repair performed within a week. Extensor tendon and nerve injuries can be handled in a similar fashion except that definitive repair can be delayed for a longer period with the exception of independent units such as the extensor pollicis longus (EPL), which will contract and shorten rapidly. Severe injuries that require early treatment, not necessarily surgical, include frostbite, most chemical and thermal burns, and electrical injuries for which specific treatment is discussed in other chapters. The quality of the initial care for injuries is the most important single determinant of the final degree of recovery.


Chapter 77: Principles of Upper Limb Surgery

TA B L E 7 7 . 1 RECONSTRUCTIVE PRIORITIES IN THE UPPER LIMB 1. Restore circulation 2. Obtain good soft-tissue coverage 3. Align and stabilize the skeleton 4. Restore nerve function 5. Mobilize joints 6. Restore tendon function

Reconstructive Cases Planning of surgical reconstruction should begin with the initial treatment, even though the reconstruction may take operations over many months to complete. The first step is to identify all of the injured structures by history, physical examination, and operative exploration. Once the deficits are understood, they should be prioritized if there is no potential for full recovery. Often, mechanical design must be simplified to a lower order of function. It is generally better to have a few things work well than many that work poorly. The following order of reconstructive priorities serves as a general guide based on prerequisites; each step in the sequence depends on successful completion of the preceding steps (Table 77.1). Restoring adequate circulation is the first priority. Inadequate perfusion will impair wound healing, predispose to infection, and result in a cold intolerance. The next priority is good soft-tissue coverage, which might require replacement with skin graft, local flap, or distant tissue transfer. Delayed primary closure is indicated for badly contaminated wounds. Without adequate circulation and softtissue coverage, repair of underlying structures is futile. Even if they heal, it will be with excessive scar and adhesions. The third priority is to align and stabilize the skeleton. Fractures and dislocations should be reduced and stabilized. The fourth priority is to restore nerve function by repair or nerve grafting. The fifth priority is to mobilize joints that may have become stiffened as a result of chronic edema, inflammation, and disuse. Severely stiffened joints may require surgical release. The last priority is to restore tendon function by repair, grafting, tendon transfer, or tenolysis. It is important that passive range of motion of joints crossed by a tendon be maximized before that tendon is reconstructed. The priorities listed above should be incorporated into a master plan, not necessarily separate operations. Replantation is an example of combining all of the steps into one operation. Several staged operations may be needed if the postoperative regimen for one part of the operation is different from that of another part. For example, osteotomy for malunion should not be done at the same time as tenolysis because the first requires immobilization and the second necessitates prompt mobilization. Once the deficits are identified and prioritized, steps with compatible postoperative regimens are combined as far as feasible. Each stage should be deferred until the tissues are soft, edema is resolved, and the joints are supple. This approach of identifying and prioritizing deficits, then grouping them into staged operations, can also be applied to nontraumatic reconstructive problems.

OPERATIVE PRINCIPLES Anesthesia Surgery on the upper limb can be performed with a variety of anesthetic techniques: general, regional, or local infiltra-

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tion. Use of local infiltration anesthesia is limited to small lesions or to supplement a regional nerve block. General anesthesia is usually indicated for children, for uncooperative patients, when multiple operative fields are required, and for long procedures. The upper limb lends itself well to regional block anesthetics, which can be combined with judicious sedation if required for anxiety. The chief disadvantages of regional blocks are the time interval for its full effectiveness, the risk of incomplete anesthesia, and the limited tourniquet time. For a detailed review of local anesthetic agents, see Chapter 11. The most commonly employed regional anesthetic blocks are brachial plexus blocks, intravenous regional (Bier) blocks, median and ulnar wrist blocks, and digital blocks. Either interscalene or supraclavicular brachial plexus blocks can give deep and superb anesthesia of the entire upper limb and allow long tourniquet times but require great skill to administer, are not always complete, and carry a significant risk of pneumothorax or other complication. Blocks of the median or ulnar nerves, or both, at the wrist are safe, easy to perform, hurt less than palmar or digital blocks, and are useful for both emergency and elective operations. Anesthetic injections should be adjacent to and not into the nerves. Intravenous regional anesthesia (Bier block) anesthetizes the whole arm distal to the tourniquet. Thus for some purposes, it fills the gap between brachial plexus blocks and wrist blocks. The Bier block is conceptually simple: exsanguinate the arm and fill the veins with a local anesthetic. The details of administration can be found in all anesthesiology texts. The main advantage of the Bier block is that it is easy to perform and reliable in giving a good anesthetic block. Its main disadvantages are tourniquet pain, which limits operative time; compromised visibility for precision dissections as the anesthetic flows into the line of dissection with every cut; and loss of anesthesia immediately when the tourniquet is deflated. Its risks are essentially that of tourniquet failure, which could allow a toxic dose of the anesthetic to be sent as a bolus into the body. Thus, although simple, this technique should be used only when equipment for resuscitation is readily available. At the wrist, the median nerve is located medial to the flexor carpi radialis (FCR) and directly deep to the palmaris longus (PL) tendon when present. A good block can be expected by simply injecting the anesthetic solution into the carpal tunnel with out eliciting paresthesia (Fig. 77.1). Anesthetic is also injected into the subcutaneous tissues between the PL and the FCR tendons to block the palmar cutaneous branch of the median nerve. At the wrist, the ulnar nerve is situated against the lateral side of the flexor carpi ulnaris (FCU) and directly deep to the ulnar artery. To block it, 5 mL of anesthetic is injected deep to the ulnar artery from the side of the wrist, just deep to the FCU tendon (Fig. 77.2). The dorsal branch of the ulnar nerve can be blocked in the subcutaneous tissues alongside and just distal to the ulnar styloid. The superficial division of the radial nerve emerges from beneath the brachioradials muscle in the midforearm and usually divides into several branches proximal to the radial styloid. Block the branches by injecting 4 to 5 mL of anesthetic solution subcutaneously over the radius or the midforearm, where it often can be felt to roll under a palpating fingertip (Fig. 77.3). Except for the thumb, which has a good dorsal blood supply, digital nerve block should be in the distal palm, where there is good collateral circulation, rather than in the base of the finger. Epinephrine is not recommended for any digital nerve block. A dorsal approach through the interdigital web or a volar injection just distal to the distal palmar crease can be used (Figs. 77.4 and 77.5). To get complete dorsal anesthesia over the proximal and middle phalanges, a subcutaneous injection

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FIGURE 77.1. Median nerve block.

over the base of the proximal phalanx is required. A circumferential “ring block” at the base of a finger is unnecessary and is dangerous.

Tourniquets A bloodless field maintained by a pneumatic tourniquet has become a standard and indispensable instrument for upper limb surgery. The current method of exsanguinating the arm with a flat rubber bandage can be traced back to Esmarch in 1873, and Cushing is credited with introducing the pneumatic tourniquet in 1904, although it was intended for use in craniotomies (1). The main factors of tourniquet safety are pressure and its area of distribution. The pressure must exceed systolic pressure by about 100 mm Hg to maintain a bloodless field, but excessive pressure can cause direct injury to tissues under the tourniquet, especially the nerves. Pneumatic tourniquets should have accurately calibrated pressure gauges. The duration of tourniquet application should be limited to about 1.5 to 2 hours. For a longer operation, the tourniquet should be deflated and the arm reperfused for 12 to 15 minutes per hour of ischemia to clear the acidosis (4). When the tourniquet is no longer needed, maximally elevate the arm and completely remove the cuff and padding to prevent them from acting as a venous tourniquet. In general, it is safer to release the tourniquet before skin closure and to check hemostasis. Exsanguination of the arm with an Esmarch bandage before tourniquet inflation is contraindicated in the presence of infection or malignant tumors. Instead, the limb should be elevated for several minutes for gravity to drain it of blood before the tourniquet is inflated.

FIGURE 77.2. Ulnar nerve block.

FIGURE 77.3. Radial nerve block.

When the operation is limited to a finger, a digital tourniquet can be used but with care that it not be too tight and that its pressure is widely distributed, as with a flat Penrose drain. Rubber bands and cut off pieces of latex glove rolled down on the finger are hazardous because an unknown pressure is applied over a small area.

Magnification Good visualization is essential for atraumatic surgical technique. Loupes with ×2.5 to ×3.5 magnification are ideal for most upper extremity surgery. The binocular operating microscope is preferable for repair of small vessels and for some nerve surgery.

Elective Incisions and Wound Extensions All incisions heal with a scar, and all scars contract. To avoid contracture, incisions must not cross skin flexion creases at joints. Stated another way, they should be along lines that undergo no change in length with movements of the part. There is much more latitude for dorsal skin incisions. The elastic and loosely attached skin can substantially compensate for scar shortening, avoiding restriction of motion. The two most useful incisions in the finger that satisfy the above principles are the midaxial and the Bruner, or zigzag, incisions. The midaxial incision gives access to both volar and dorsal structures but may require very extensive undermining. The Bruner incision is only for the palmar surfaces and crosses

FIGURE 77.4. Digital nerve block.


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tained where essential for the minimal amount of time needed while continued movement of other parts is encouraged.

Protective Position

FIGURE 77.5. Digital nerve block.

the volar skin between flexion creases in a zigzag fashion, which creates a series of short, broadly based, opposing flaps.

Wound Closure Incisions and wounds of the hand can generally be closed with a single layer of interrupted sutures. Vertical mattress sutures are needed if the skin edges tend to invert. Lacerated wounds that cross flexion creases need reorientation by Z-plasties. Wound closure for children with 5-0 or 6-0 plain gut avoids the trauma to patient, family, and surgeon of suture removal. Except in areas of unavoidable tension, such as posterior to the elbow, sutures are removed after 7 to 10 days to minimize suture marks. On the forearm and upper arm, elective incisions can be closed with a continuous intradermal monofilament suture.

POSTOPERATIVE PRINCIPLES Dressing A well-applied dressing is an integral part of the operation in hand surgery and requires the same attention to details as the operation itself. It should conform to the limb to provide support but without compression, which can act as a venous tourniquet to promote edema. The basic hand dressing consists of three layers. The first layer is flat, with slightly moist gauze applied directly to the wounds. The second layer is fluffed gauze placed between the fingers to prevent skin maceration and to cover potential pressure points, such as the ulnar head. The third layer is a 2- or 3-inch roll gauze applied circumferentially to hold the other layers in place but with diminishing pressure from distal to proximal to promote venous return. The original dressing placed in the operating room is left on until suture removal unless there is a specific indication to remove it sooner. Any patient who complains of an unexpected degree of pain after surgery should have the dressing split down to the skin to ensure that the dressing is not too tight. As swelling correlates with pain, this will give great relief to the majority of such patients.

When immobilization is essential, it should be in the “protective” or “safe position.” This keeps ligaments under maximum stretch to prevent their shortening and subsequent restriction of joint mobility. There are just three essential elements of the protective position: interphalangeal (IP) joint extension, metacarpophalangeal (MCP) joint flexion, and palmar abduction of the thumb. Maintaining the interphalangeal joint in extension prevents shortening of the volar plate and flexor tendon sheath. Because of the camlike shape of the metacarpal heads, collateral ligaments of metacarpophalangeal joint are maximally stretched when the joint is in full flexion. Therefore, keeping the MCP joints in flexion prevents shortening of their collateral ligaments and loss of joint mobility during immobilization. Holding the wrist in slight extension takes advantage of the tenodesis effect to make it easier to keep the MCP joints in flexion. Finally, palmar abduction of the thumb simply keeps the soft tissues of the first web space stretched to prevent an adduction contracture. Either a splint or a cast can be used to immobilize the hand. A splint is easier to remove and allows for some expansion to accommodate swelling but a cast can be molded to apply selective pressure to a wound or graft without circumferential constriction. For children, an above-elbow cast is the only reliable dressing. The cast and padding should be split if the patient complains of excessive tightness, progressive pain, or numbness in the digits.

Elevation An accidentally or surgically injured limb should be continuously elevated until effective pumping activity is again functioning to propel venous blood and lymph back to the body. The heart is the point of reference for elevation. While walking, the patient should hold the hand over the contralateral shoulder or even rest it on the head. Slings tend to promote edema by holding the hand at the level of the umbilicus, which is lower than the heart. In the sitting position one should prop the elbow on a table with the hand upright and at night one should rest the hand on pillows or on the chest.

References 1. Green DP. General principles. In: Green DP, ed. Green’s Operative Hand Surgery. 5th ed. New York: Churchill Livingstone; 2005. 2. Levinsohn DG, Gordon L, Sessler DI. The Allen’s test: analysis of four methods. J Hand Surg. 1991;16A:279. 3. Louis DS, Greene TL, Jacobson KE. Evaluation of normal values for stationary and moving two-point discrimination in the hand. J Hand Surg. 1984;9(4):552. 4. Wilgis EF, et al. Observations on the effects of tourniquet ischemia. J Bone Joint Surg AM. 1971;53(7):1343.

Suggested Readings Immobilization Effective immobilization favors wound healing and is essential for the healing of many structures, such as bones and skin grafts. However, because prolonged immobilization can lead to stiffness of the small joints, immobilization should be main-

American Society for Surgery of the Hand. The Hand: Examination and Diagnosis. 3rd ed. New York: Churchill Livingstone; 1990. Beasley RW. Beasley’s Surgery of the Hand. New York: Thieme; 2003. Green DP, ed. Green’s Operative Hand Surgery. 5th ed. New York: Churchill Livingstone; 2005. Smith P. Lister’s The Hand: Diagnosis and Indications. 4th ed. New York: Churchill Livingstone; 2002.

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CHAPTER 78 ■ RADIOLOGIC IMAGING OF THE HAND AND WRIST CORNELIA N. GOLIMBU

The first x-ray image obtained was of a hand. Since then advancements have produced revolutionary changes in the way anatomy and pathology of the human body are imaged: Magnification radiography, arthrography, angiography, nuclear medicine, ultrasound, computed tomography (CT), and magnetic resonance imaging (MRI) all contribute in specific ways to detection and characterization of bone, joint, and softtissue abnormalities.

volved part, such as an intra-articular fracture, to which initiation of the degenerative process can reasonably be attributed. The basic radiographic findings of degenerative arthritis are:

RADIOGRAPHS

Inflammatory Arthritis

With the exception of those cases in which it becomes very obvious that the abnormality is limited to the skin and to the superficial soft-tissue layers (burns, skin disorders, superficial lacerations), almost all patients with hand and wrist problems should have roentgenograms obtained. The most important initial step for radiographic examination of the hand and wrist is to establish where and what is the most likely abnormality. It is obvious that a crush injury to a single distal phalanx can be fully seen simply by obtaining a finger view in frontal and lateral projection. Hand views are necessary when the injury involves the base of fingers or metacarpals, and should include oblique views, as overlapping limits lateral visualization. Acute or chronic trauma to the carpal complex is screened by the three standard radiographic positions of the wrist (posteroanterior, oblique, and lateral). In specific situations additional views can be obtained, such as for the scaphoid, carpal tunnel, or hamate hook. When intermittent abnormal alignment is suspected, special stress views may be needed to diagnose a dynamic instability. Also, stress views may be needed to evaluate digital ligamentous injuries. Studies for suspected foreign bodies may be helpful only when radiopaque materials are retained in the tissues; wood splinters are usually nondetectable by radiographs. Radiologic imaging will aid diagnosis and illustrate the extent of involvement of arthritis. Comparable views of both hands generally are needed to establish the full extent of the disease, for which the symmetry of the lesions is often a strong diagnostic feature, especially with inflammatory types of arthritis.

The most frequent forms of inflammatory arthritis are the common rheumatoid arthritis (RA), the less common psoriatic arthritis, and the rare form associated with lupus erythematosus disorders. The classic radiographic signs of RA are:

1. Narrowing of the joint space normally occupied by articular cartilages 2. Subchondral bone sclerosis 3. Osteophyte formation along articular margins

1. Symmetry of involvement/both hands, progressive from intercarpal joints to metacarpophalangeal (MCP) and proximal interphalangeal (PIP) joints 2. Narrowing of the joint spaces 3. Erosion of articular cortex 4. Malalignment (ulnar deviation of fingers) 5. Soft-tissue swelling centered on the joints 6. Periarticular osteoporosis The classic radiographic findings of psoriatic arthritis are: 1. Distal to proximal progressive involvement of interphalangeal joints 2. Periosteal new bone deposition in paraarticular location 3. Erosions of articular cortex with “pencil-in-cup” deformity 4. Lack of osteoporosis The typical radiographic findings of arthritis associated with lupus erythematosus are: 1. Dominant malalignment deformities 2. Absence of articular cortex erosions 3. Profound, generalized osteoporosis (more than juxtaarticular)

Metabolic Arthritis Degenerative Arthritis The common osteoarthritis usually associated with increasing age and traumatic arthritis are the two types of degenerative arthritis. They are indistinguishable radiographically, and even histologically, and the designation of traumatic arthritis depends entirely on the history of direct trauma to the in-

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Gout and pseudogout are the most frequently encountered forms of metabolic arthritis. Typical radiographic presentations of gout include: 1. Bone erosions with “overhanging margins” in juxta- or intra-articular locations 2. Preservation of joint space 3. Soft-tissue masses representing the tophi


Chapter 78: Radiologic Imaging of the Hand and Wrist

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FIGURE 78.1. Standard radiographic views of the hand. A: Posteroanterior frontal view. B: Posteroanterior oblique view. C: Lateral view.

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FIGURE 78.2. Standard radiographs of the wrist. A: Posteroanterior frontal view. B: Posteroanterior oblique view. C: Lateral view.

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Pseudogout is characterized by: 1. Calcifications in the hyaline cartilage covering the carpal bones or ulnar head 2. Narrowing of the intercarpal and MCP joint spaces 3. Collapse of the lunate 4. Calcium pyrophosphate crystals detected in the synovial fluid analyzed in polarized light microscopy

STANDARD RADIOGRAPHS The complexity of the bone and joint anatomy of the hand and wrist necessitates a multitude of positions for visualization of all the bone surfaces in profile views, in relaxed or stressed position, and in supination or pronation. This chapter succinctly presents the projections most commonly used in

the diagnosis of hand and wrist abnormalities. Detailed textbooks dedicated to this topic can be consulted for additional information.∗

Hand Views Roentgenograms of the hand taken as part of the routine radiologic investigation should consist of frontal and oblique, posteroanterior (PA) views. The frontal view outlines the carpal bones, the carpometacarpal and metacarpophalangeal joints, and the phalanges (Fig. 78.1A). The thumb is seen in oblique or almost lateral view. The oblique view (Fig. 78.1B) is impor∗ A recommended comprehensive text is Gilula LA, Yiu Y. Imaging of the Wrist and Hand. Philadelphia: WB Saunders; 1996.



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distal and middle phalanges of one or more fingers. Such a small field of view is advantageous because it allows tailoring of the exposure factors fit for thin tissue parts, consequently producing films of ideal radiographic density for the small segments in question. Moreover, the hand and wrist are spared the radiation exposure by being purposely omitted.

Wrist Views

FIGURE 78.3. Carpal alignment in frontal view. The contour of the proximal and the distal surfaces of the first carpal row describes two arches that should be parallel to each other. The proximal surface of the capitate and hamate represents the third arch, concentric with the first two.

tant for profile visualization of the metacarpophalangeal joints and for perception of depth localization of any abnormality seen in the frontal views. Occasionally, a lateral view is needed when alignment of the interphalangeal joints is in question. For this purpose the lateral projection of the hand should be obtained with the fingers in a progressive degree of flexion; in such a position, each middle and distal phalanx is projected separately (Fig. 78.1C). In this view, the thumb is projected in a frontal position.

Finger Views Finger radiographs are obtained in lateral and posteroanterior views when the abnormalities are likely to be limited to the

A

The minimum accepted views necessary for roentgenographic study of the wrist include three projections: posteroanterior, lateral, and oblique (1). The normal posteroanterior frontal view outlines the contour of the distal radius and ulna, and the carpal bones and their articulations with the metacarpals. The intercarpal articulations are seen as uniform spaces of 1 to 2 mm; only the scapholunate space may be slightly larger. The ulnar styloid is profiled on the medial side of the ulnar head (Fig. 78.2A). In the frontal projection of the wrist, the joint between trapezium and trapezoid is not well visualized. This anatomic area is better visualized in the posteroanterior oblique projection (Fig. 78.2B). In this view the trapezium is not overlapped by the trapezoid; the articulation of these two carpals with the surrounding bones is projected clearly. The dorsal surface of the triquetrum is seen almost in profile in this position and its dorsal cortex is not overlapped by any other carpal structures. A true lateral projection is essential in determining the position of the lunate in relation to the long axis of the radius and capitate (Fig. 78.2C). The lateral view must be obtained in a neutral position of the forearm (90-degree abduction of the shoulder, 90-degree flexion of the elbow), without pronation or supination, so as to allow exact measurements of the relative length of the radius and ulna (for ulnar variance) or the angle described by the axis of the scaphoid, lunate, and capitate. An easy way to determine the correctness of positioning in the lateral view is to check the overlap of the scaphoid and pisiform. The pisiform’s anterior margin should project halfway between the anterior margin of the scaphoid and the lunate (Fig. 78.2C). The anterior and posterior poles of the lunate should be in symmetric position in a normal wrist; the long axis of the scaphoid describes a 120- to 150-degree angle with the long axis of the wrist. The proximal and distal surfaces of the first carpal row (scaphoid, lunate, triquetrum) and the proximal surface of the

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FIGURE 78.4. Anterior lunate dislocation. A: Posteroanterior view: The lunate is tilted and no longer articulates with the adjacent carpal bones. B: Lateral view: The lunate is dislocated and rotated 90 degrees in a palmar direction. A small fragment of bone represents an avulsion fracture of the intercarpal ligaments insertion site (arrow).


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A FIGURE 78.5. Transcaphoid posterior perilunate dislocation. A: Posteroanterior view: Scaphoid is fractured at the waist (arrowheads). Midcarpal joint space is not seen. B: Lateral view: Distal carpal row is dislocated posteriorly in relation to the lunate (L). The scaphoid (S) fracture is obscured by the slight palmar tilt of the lunate.

capitate and hamate describe the configuration of three parallel arches (Fig. 78.3). Interruption of these arches represents an abnormality such as fracture of carpals, dislocation of lunate, or complex injuries, such as transcaphoid perilunate dislocation (Figs. 78.4 and 78.5). The scaphoid projection (PA with maximum ulnar deviation of the wrist) is necessary for all patients who have pain in the radial side of the wrist following trauma. In this view, the scaphoid appears elongated, allowing visualization of the cortex and trabeculae of its waist (Fig. 78.6). In many instances it is the only view in which a nondisplaced fracture of the scaphoid becomes visible.

FIGURE 78.6. Scaphoid view. The ulnar tilt of the hand allows better visualization of the scaphoid with better detail of the cortical surface and bone trabeculae at its waist.

When the clinical history and localized tenderness indicate possible injury to the hook of the hamate, additional views are indicated in the search for a fracture. The oblique view of the hamate projects the hook in profile, thus often making possible the detection of subtle, nondisplaced fractures (Fig. 78.7). A carpal tunnel view is obtained by directing the central x-ray beam tangential to the floor of the carpal tunnel and, because its bony medial wall is formed by the hook of the hamate, fracture there may be demonstrated. The more proximally situated pisiform also is well visualized in this view. Sagittally oriented fractures of the pisiform may be seen only in this view

FIGURE 78.7. Oblique views for hamate hook. At the base of the hamulus, a lucent line suggests a fracture (arrowhead). A CT scan will consistently identify the fracture if more information is necessary to make the diagnosis. See Fig. 78.17.



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abnormal motion between the carpal bones, which can subsequently lead to degenerative disease of the wrist. For the hand surgeon treating the patient with ligament injuries, it is important to know (a) the precise location of the injury, (b) the character of the lesion (sprain, complete tear, bony avulsion), (c) the significance of this injury to joint stability, and (d) if any instability is present (1). In the search of these answers, the diagnostic test employed is a dynamic study. The motion can be active, performed by the patient (instability series), or passive, performed by an examiner (stress views).

Motion Views (Instability Series) FIGURE 78.8. Carpal tunnel view. Sagittally oriented fracture of the pisiform is seen (arrowheads). Trapezium (Tm) and distal pole of the scaphoid (S) make the lateral wall of the carpal tunnel. The medial wall is made of the pisiform (P) and hook of the hamate (H).

(Fig. 78.8). The carpal tunnel view allows for a profile view of the scaphoid tubercle.

The wrist is positioned in the extremes of its physiologic range of motion. These motion views are posteroanterior views in maximum radial and ulnar deviation, clenched-fist PA and anteroposterior (AP) views, and lateral views with radial and ulnar tilt, as well as maximum flexion and extension. Collectively, these are referred to as an instability series. When abnormal joint openings are demonstrated, a ligamentous tear with dynamic instability is documented. For example, scapholunate dissociation resulting in an abnormally large gap between these two bones may be clearly seen in the clenched-fist AP (supinated) view and not even suggested by routine radiographs (Fig. 78.9).

DYNAMIC STUDY If fractures and dislocations have been excluded by normal radiographs, one must consider that persistent pain and focal swelling of a wrist following acute trauma may be a result of ligament disruption. When untreated, such injuries may allow

Stress Views of the Wrist and Digits Stress views are radiographs obtained while passive stress is applied. The stress applied to the wrist may be physiologic

B

A FIGURE 78.9. Scapholunate dissociation (rotatory subluxation) of the scaphoid. A: Posteroanterior view with ulnar deviation: The scapholunate space is slightly larger than the other intercarpal joints, but not definitely abnormal. B: Anteroposterior (supinated) view with clenched fist: The stress on the carpal bones produced by the tightly clenched fist shows scapholunate dissociation caused by rotatory subluxation of the scaphoid. The ring sign representing projection of the distal pole on the rest of the scaphoid can be seen.

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(radial-ulnar deviation in frontal view or flexion–extension in lateral view) or nonphysiologic (radial and ulnar transposition; passive pronation and supination). The most commonly helpful views are passive ulnar deviation and radial transposition, which may show instability in the scaphotrapezial and scapholunate joints, respectively. In lateral views, dorsally directed stress may unmask subtle midcarpal joint instability, seen as dorsal translation of the capitate in relation to the lunate. Among the most useful stress studies are those of the metacarpophalangeal joint of the thumb. Reliability of observations is enhanced by injection of a local anesthetic into the MCP joint. This not only prevents pain, but also prevents splinting from thenar muscle spasm, which may give a false impression of stability. Frontal views are obtained with ulnar and radial stress with comparison views of the normal thumb. Small tears of the radial or ulnar collateral ligaments are reflected in stress views as 15 to 20 degrees greater angulation of the abnormal joint compared with the normal side. Greater differences in angulation, especially subluxation of the phalanx on the metacarpal head, occur with a complete collateral ligament disruption.

VIDEOFLUOROSCOPY Fluoroscopic observation of motion of the hand and wrist can be recorded on videotape. Because the time of examination is short, irradiation to the hand is minimal, and the opportunity for repeated viewing of the videotapes results in more accurate conclusions about the movement of each carpal bone and degree of opening of individual joint spaces. This is the best method to study the cause of a painful click and intermittent or “dynamic” scapholunate instability in which the abnormality may be only an instantaneous change in position of the carpal bones. Examination begins with a PA view of the wrist while the patient actively moves the hand in maximum ulnar and then radial tilts. This is first done with an open hand and then repeated with a closed fist. The compressive pressure produced by clenching of the wrist may enlarge the space between the scaphoid and the lunate to a degree indicative of scapholunate dissociation. Generally, for comparison, the asymptomatic wrist should also be studied while the same maneuvers are performed as on the abnormal side. Laxity of joints varies considerably from person to person and during the lifetime of each individual. Therefore, the asymptomatic side serves as a “control” of normal joint laxity for each patient. Only very substantial differences of joint opening between the normal and the painful side warrant diagnosis of scapholunate dissociation. The term rotatory subluxation of the scaphoid refers to a scapholunate dissociation characterized by palmar tilt of the scaphoid’s distal pole seen on lateral views and, again, by enlargement of the scapholunate joint space observed on frontal views. In lateral projection, each wrist is studied while the patient performs active flexion, extension, followed by ulnar and radial tilt. The lateral view is most informative for alignment in the central axis of the wrist (radius-lunate-capitate). Subtle instability of the carpal bones (dorsal intercalated segment instability [DISI] or volar intercalated segment instability [VISI]) can be detected during these movements. Subluxation of the distal radioulnar joint is not easily documented by fluoroscopy of wrist motion (see Computed Tomography below).

FIGURE 78.10. Abnormal wrist arthrogram with all three compartments filled from a single injection. Iodinated contrast material introduced in the radiocarpal joint enters through a tear in the triangular fibrocartilage (arrow) into the distal radioulnar joint space (white arrowheads). Also, presence of contrast material in the midcarpal joints (black arrowhead) indicates a tear in the scapholunate ligament.

tilage complex (TFCC), intercarpal ligaments, and/or capsular tears around these joints. Contrast material injected into the radiocarpal joint can traverse torn intercarpal ligaments (scapholunate, lunotriquetral ligaments) and can be seen to accumulate in the midcarpal compartment. Similarly, it can enter the distal radioulnar joint through a gap in the TFCC (Fig. 78.10). When such communications are not seen but are still clinically suspected, separate injections of the midcarpal joint space or distal radioulnar joint may detect unidirectional abnormal flow of contrast medium through tears of ligaments or the triangular fibrocartilage complex (triple-compartment arthrogram) (2). Recent technical advances, such as digital subtraction radiography, have made triple-compartment arthrography more reliable, but its usefulness is diminishing as other means of imaging develop. Arthrography produces a disturbingly high number of false-positive results. The mere flow of contrast from one compartment to the next does not prove that the abnormality of morphology is clinically significant (3,4). For example, a small perforation in the center of the TFCC is present in approximately 50% of all individuals 40 years of age or older (5), most of whom are completely asymptomatic. Arthrography has been replaced by MRI, which is noninvasive and provides much more precise information about synovial cavities, ligaments, and other soft-tissue structures.

BONE SCINTIGRAPHY ARTHROGRAPHY Introduction of iodinated contrast material into the synovial spaces of the wrist and carpometacarpal joints has been devised to aid in diagnosis of injuries to the triangular fibrocar-

Radionuclide imaging is useful, but the scans must be interpreted with careful clinical correlation and in conjunction with radiographs. Bone scintigraphy is based on two basic processes: the physical properties of technetium 99m and the metabolic rate of bone absorption of phosphate compounds. The



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FIGURE 78.11. Three-phase technetium 99m bone scan in reflex sympathetic dystrophy (RSD). A: First phase: Blood flow is diminished on the abnormal side. B: Second phase: Decreased activity in the abnormal hand is consistent with ischemia. C: Delayed phase shows moderate increase in the uptake of multiple joints consistent with RSD. Focal intense activity in the ulnar head (arrow), site of minor bone injury that triggered the disorder.

radioisotope scan is an excellent, sensitive, and relatively inexpensive screening method for many disorders, but is limited by its lack of specificity. Diphosphonate compounds normally cross from the blood to bone, where they are deposited in proportionally larger amount on those segments of the skeleton where metabolic rate of bone turnover is greater or where active deposition represents a repair process (callus, reactive bone sclerosis, etc.). Using diphosphonate compounds bound to a radioisotope such as technetium 99m, we can follow the activity of the radioactive tracer to detect zones of active metabolic turnover. The physical properties of technetium 99m make it an ideal clinical tracer: It is readily available, has a short half-life (6 hours), and emits γ photons with monoenergetic disintegration energy at 140 keV, which can be detected by sodium iodide scintillation crystal. The Anger γ scintillation camera detects these photons, and by usage of collimators and electronic processing, this

information is visually displayed as anatomic structures with diverse levels of isotope activity. For the study, technetium 99m bound to methydiphosphonate is injected intravenously. In a few seconds it reaches the hand through arterial blood flow, diffuses in the capillaries, and returns via the draining veins into the general circulation. In about 5 minutes, it is uniformly mixed in the entire blood pool. Gradually, the technetium bound to diphosphonate is excreted by the kidneys. About 3 to 4 hours after injection, 30% to 40% of the technetium is deposited in the bones, 10% to 15% is diffusely dispersed in other tissues, and 5% is still in the blood, while 35% of the administered dose has been excreted into the urine (1). The study is conducted in three phases. 1. Phase 1: radionuclide angiogram. Following a bolus intravenous injection of tracer, radioactivity is detected

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at its first pass in the ulnar and radial arteries. Venous drainage of the isotope can be seen 10 to 20 seconds later. 2. Phase 2: blood pool phase. At 5 to 8 minutes after injection, an equilibrium is reached in the distribution of the isotope in the entire blood pool. Areas of increased metabolic activity represent hyperemic zones in the tissues. 3. Phase 3: metabolic images or delayed phase. Images obtained at 3 to 4 hours after injection reflect the activity of the technetium bound to diphosphonate deposited in the bone. Foci of abnormally high uptake of isotope seen in the delayed images represent areas of increased absorption of the phosphate compounds bound to the technetium.

FIGURE 78.12. Three-dimensional rendering of CT images. Axial images were reformatted to represent the wrist seen from the dorsal side. Comminuted, impacted fractures are seen in the distal radius and ulna.

The early phases of a bone scan can be used as a crude angiogram, useful to differentiate fast-flowing blood seen in arteriovenous malformations from the slow flow of hemangiomas. In most arteriovenous malformations, a large dominant feeding artery can be detected in the earliest images of radionuclide angiogram. The flow of isotope toward and into the malformations is rapid, and it reaches the hand much faster than the opposite normal side. In hemangioma, the activity of the tracer

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FIGURE 78.13. “Die-punch” fracture of distal radius. A: Posteroanterior view of the wrist shows comminuted intra-articular fracture of the distal radius. B: Sagittal CT image: A fragment of articular cortex is displaced proximally, impacted in the spongy bone of the metaphysis (arrowheads). C: Axial CT image in the distal surface of the radius shows the degree of comminution and the central gap left by the displacement of the articular fragment. D: Axial CT image 6 mm proximal to C shows the missing articular cortex fragment (arrowheads) trapped between the metaphyseal fragments.



is most intense in the second phase of the bone scan, when the entire blood pool is uniformly radioactive (capillary phase). The radionuclide angiogram is useful in assessing the arterial blood flow in patients with acute thrombosis, frostbite, or recent surgery for limb reattachment. Pins, orthopedic hardware, bulky dressings, and skin abnormalities seen in these patients often make MRI or conventional angiography impractical. The first phase of a bone scan can be a practical substitute. The third phase is the most important part of the bone scan for detection of osseous lesions. Delayed images with focally abnormal increased uptake of tracer activity will be seen at fracture sites in their acute phase, during healing when calcified callus is being formed, or even much later as high metabolic activity of the remodeling of the fracture site continues for months after the injury. Technetium bone scan is so sensitive that a negative examination practically excludes any significant osseous abnormality. Thus, the radioisotope bone scan is a good screening modality to exclude bone pathology. The problem with the bone scan is its lack of specificity: Focal uptake may appear the same from fractures, avascular necrosis of bone, erosive arthritis, infection, osteoid osteoma, bone tumors, and so forth. Diffuse, generalized, increased uptake may be a sign of rheumatoid arthritis, septic joint, acute disuse osteoporosis, or other generalized diseases. In reflex sympathetic dystrophy (RSD), a characteristic pattern of abnormalities has been described in the bone scan (1). It consists of diffuse increased activity in all joints of the hand, from radiocarpal to interphalangeal articulations. Less specific for RSD is the asymmetric activity seen in the first and second phase of the bone scan, a manifestation of disturbed blood perfusion to the affected hand (Fig. 78.11). Although these are frequent findings with RSD, as with many other tests, when used alone they are not pathognomonic of the disorder (6).

ULTRASOUND Ultrasound (US) is an imaging modality that is extremely suitable for detection of fluid collections. It can also visualize superficially located tendons of the extremities in different positions. As such it would appear to be the modality of choice for imaging ganglion cysts of the wrist and hand (7). However, two drawbacks diminish significantly the usefulness of ultrasound: US does not visualize the bone structures and it is extremely operator dependent. Only radiologists trained specifically and experienced in the subtle variations of ultrasonography of the musculoskeletal structures can make consistently accurate diagnosis and more specifically so in the hand and wrist where the anatomy is complex. A ganglion cyst appears in ultrasound images as a discrete hypoechoic mass. Cysts located deep between the tendons or those related to pathology of adjacent synovium or intercarpal ligaments are better demonstrated by MRI, which detects all soft-tissue and bone structures and thus gives a more thorough understanding of related pathology. For these reasons ultrasound studies of the hand and wrist are infrequently performed.

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angles (Fig. 78.12). This provides a direct three-dimensional visual representation of the relationship between the bone structures, especially useful in complex fractures or dislocations.

Distal Radial Fractures The vast majority of fractures in the distal radius and ulna are readily detected from plain films. However, details of comminuted fractures that intersect complex articular surfaces can be better visualized by CT images. Specifically, the burst fractures that involve the distal radioulnar joint are seen at best advantage in the axial CT images. Displacement of fragments that can cause permanent incongruity of the distal radioulnar joint can be detected initially by CT scan or the correctness of their reduction verified. Die-punch fractures of the distal radius present difficulty in reduction and stabilization. Planning appropriate treatment requires precise knowledge of the extent of comminution, the size of fragments, and the degree of their displacement into the metaphysis. This information can be readily obtained from CT images (Fig. 78.13). The axial slices evaluate the size and position of the displaced fragment as well as distal radioulnar joint congruency. Sagittal and coronal images show the exact position of the displaced cortical fragment of the radius embedded in the cancellous bone of the metaphysis.

Distal Radioulnar Joint Injuries Distal radioulnar joint (DRUJ) alignment is difficult to assess from plain films or even from videodynamic studies. Axial CT images obtained at the level of the sigmoid notch of the radius directly demonstrate the position of the ulnar head in relation to the radius. Subtle subluxations are more readily diagnosed if these axial images are obtained in three positions: neutral, pronation, and supination, each time simultaneously imaging both wrists. Only three to four sections exactly centered on the distal radioulnar joint are necessary for each position. Such

COMPUTED TOMOGRAPHY CT of the hand and wrist is the modality of choice for imaging the abnormalities of cortical bone. It can obtain primary images in all planes, with sections as thin as 0.5 to 1 mm (8). For example, small avulsion fractures that may be obscured in routine radiographs by complex overlapping of carpal bone are easily detected in CT images. Another advantage of CT is the ability to obtain from multiple axial images a threedimensional rendering of the anatomy viewed from different

FIGURE 78.14. Oblique sagittal CT image in the long axis of the scaphoid. Hairline, nondisplaced fracture of the scaphoid (arrows).

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an examination is expeditious and practical, and provides precise information on the degree of dislocation, subluxation, and the position in which such alignment abnormalities are most pronounced (8).

Scaphoid Fractures Nondisplaced fractures of the scaphoid are notoriously difficult to detect by plain films obtained early after injury. When initial films of patients with clinically suspected scaphoid fractures appear to be normal, the most frequent therapeutic attitude is to immobilize the wrist as if an undisplaced fracture had

been demonstrated and to repeat radiographs in 7 to 10 days. With a fracture, resorption of bone at the fracture margins will generally make it detectable in the follow-up radiographs. For high-performance athletes and others for whom an immediate diagnosis is of practical necessity, CT can be employed for early detection of scaphoid fractures (Fig. 78.14). Computed tomography of the scaphoid should include sagittal views obtained in the long axis of this bone (8). Such images (1- to 2-mm thick slices) will depict the contour of the cortex from the distal to the proximal pole and detect any sagittal angulation between fracture fragments. Displacement of more than 1 mm between fragments and any palmar angulation of the distal pole detected by CT are of great

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FIGURE 78.15. Healing scaphoid fracture. A: Scaphoid view at 4 months follow-up, treated with a cast. Healing of the fracture (arrow) is difficult to assess. Oblique sagittal CT image (B) and coronal CT image (C) both demonstrate that fracture gap is obliterated by callus, an indication of normal healing (arrow).



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such as eburnation of adjacent spongy bone, cystic erosion of bone surface, and marginal osteophytes, develop at the fracture site. Avascular necrosis of bone in the early stage is more readily demonstrated by MRI than by CT; however, subtle changes in density in the trabecular bone can be detected by CT. Care should be exercised in making an early diagnosis of avascular necrosis. During the normal healing of a fracture there is diminished blood supply to the proximal pole of the scaphoid, which consequently is less affected by the natural osteoporosis of disuse seen in all other segments of the carpus. In the first weeks after immobilization, mild, proximal pole high density may be only a transitory phase of the healing process rather than a sign of avascular necrosis of bone. Demonstration of the deposition of calcified callus at the fracture site is a strong indication that normal healing is occurring and supersedes the transitory phase of retained normal density of the proximal fragment of the scaphoid for healing assessment. FIGURE 78.16. Nonunion of scaphoid fracture. Oblique sagittal CT image: Distal fragment is tilted in a horizontal position (arrow); the small comminuted fragment on the dorsal side contributes to the “humpback” deformity of the scaphoid (arrowhead). The fracture surfaces are sclerotic, and the gap between them is irregular. R, radius; Sp, scaphoid proximal fragment.

clinical significance. Also, CT can demonstrate the early healing stage of callous formation, seen in the CT images as blurring or complete obliteration of the fracture line in the bone marrow (Fig. 78.15). Cortical bone healing lags several weeks behind healing of the cancellous bone. Of course, complications of scaphoid fractures, such as nonunion or avascular necrosis of bone (AVN), are also seen in the CT images. Nonunion of a scaphoid fracture is characterized by enlargement of the gap between fragments and sclerosis of the fracture surface (Fig. 78.16). Sagittal CT images obtained in flexion and extension can demonstrate directly motion between the fracture fragments, thus permitting differentiation between fibrous callus and true nonunion. In late stages of nonunion, changes consistent with posttraumatic arthrosis,

Hamate Fractures Hamate hook fractures cannot always be seen on special oblique or carpal tunnel views but are easily detected in axial CT images (Fig. 78.17). Sagittal views can be used to determine any angulation or displacement of the hook fragment in a craniocaudad direction. Computed tomographic images are also useful in evaluation of those fractures of the body of the hamate that intersect and displace part of the carpometacarpal joint surfaces (Fig. 78.18).

Congenital Anomalies Congenital abnormalities of the hand and wrist may have complex involvement of the bones, which necessitates clarification by a multisectional imaging modality such as CT. Especially useful to planning of surgery is the three-dimensional rendering of the deformed bones.

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B FIGURE 78.17. Fracture of hamate hook. A: Axial CT image of both wrists: left hook is normal (arrow); the right one has a fracture through its base (arrowhead). B: Sagittal CT image: nondisplaced fracture through the base of hamate hook (arrowheads). See fig 78.7.

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Tumors Tumors of all the anatomic structures of the hand and wrist are generally best elucidated by MRI. The role of CT is limited to characterization of matrix calcification and cortical bone involvement, giving little more information than routine roentgenograms. The important soft tissue extent of any tumor is the domain of MRI rather than CT. An exception is osteoid osteoma, for which the detection of the nidus, the reactive bone sclerosis around it, and the thickening of the cortex adjacent to the nidus are superbly portrayed in the CT images (Fig. 78.19).

Degenerative Disorders Cystic erosions of carpal bones that communicate with joint spaces are occasionally seen in posttraumatic arthritis or other chronic arthritides of the wrist, including pseudogout. Even though their existence is suspected from the plain films, it is

FIGURE 78.18. Fracture-dislocation of the carpometacarpal joints. A: Axial CT image: fractures (arrowheads) in the dorsal part of the capitate (C) and body of the hamate (H). B: Sagittal image through the hamate: dorsal dislocation of the fifth (5) metacarpal together with a small fragment (arrowhead) detached from the dorsal margin of the hamate (H). C: Sagittal CT image through capitate (C) and lunate (L). The base of fourth metacarpal (4) is displaced dorsally, together with a fragment of capitate (arrowhead).

only in CT images obtained in multiple planes that the exact location of any cortical interruptions can be visualized (Fig. 78.20). Differentiation can be best made between cystic bone marrow abnormalities seen in generalized diseases (sarcoidosis, amyloidosis, etc.) and local diseases related to synovial pathology, leading to erosions or fissures of the cortical bone and cystic lesions in the immediately adjacent spongy bone (posttraumatic arthritis, pseudogout).

Technical Limitations of Computed Tomography Metallic artifacts generated by orthopedic fixation devices such as plates and screws degrade CT images each time the path of the x-ray beam encounters the extreme density of a metal piece. When the metal is large and unavoidable by any change in the orientation of the CT slices, the CT images may be so degraded by artifacts as to become useless. However, by careful inspection of routine radiographs, a compromise can be reached in many cases: The hand and wrist can be placed in the gantry


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FIGURE 78.19. Osteoid osteoma. Coronal CT image: Ring of sclerosis (arrow) surrounds the nidus of an osteoid osteoma in the hamate.

in such a position as to obtain at least several slices that do not pass through the metal pieces. These would not contain artifacts and can be of diagnostic value. An example of such a situation is the CT obtained for follow-up of scaphoid fractures treated with Herbert screw fixation. Care is taken to position the hand so as to align the screw with the exact plane of the oblique sagittal slices. Consequently, only two or three slices will contain artifacts; all the others have the necessary resolution for detection of calcified callus obliterating the fracture gap (Fig. 78.21).

MAGNETIC RESONANCE IMAGING A true revolution of musculoskeletal radiology took place with the advent of MRI. Structures previously invisible by radiologic means became clearly depicted by this new multisectional imag-

FIGURE 78.20. Carpal cystic erosions. Coronal CT image shows a cystic erosion of proximal pole of the hamate with fragmentation of the articular cortex (arrow). A small erosion is also seen in the lunate (arrowhead).

ing modality, which does not deliver any radiation to the patient. Imaging the tendons, ligaments, vessels, and nerves in addition to the bone and joint structures is now possible. Knowledge of nature and exact location of pathology is accomplished better by MRI than by any other imaging modality (9). Magnetic resonance imaging is based on the spinning properties of the hydrogen atom nucleus (a single proton). In the strong magnetic field inside the scanner, these protons line up their spinning vector in a parallel or antiparallel direction. When a radiofrequency (RF) pulse is applied, these protons flip their angle of rotation (are excited); when the RF pulse is interrupted, they return to a resting state (relax) at different rates, depending on their bonding environment (molecules

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A FIGURE 78.21. Scaphoid fracture treated with Herbert screw. A: Sagittal CT image aligned with the screw contains artifacts from the metallic density. B: Adjacent slice carefully planned to reduce the metallic artifact shows some fracture healing, mostly on the palmar side.

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B FIGURE 78.22. Coronal MRI of normal wrist. A: Coronal proton density-weighted image of the wrist shows the carpal bones: scaphoid (S), lunate (L), and triquetrum (T) form the proximal carpal row; trapezium (Tm), capitate (C), trapezoid (Td), and hamate (H) form the distal carpal row. The articular cartilage of distal radius is continuing medially to form the surface of the distal radioulnar joint (arrow). The bone marrow signal is uniformly high, giving a light-gray appearance of the carpal bones. The fibrocartilage of the wrist appears as a triangular low signal structure (black arrowhead). B: Coronal T2*-weighted image obtained at same level as (A) demonstrates the high signal—manifested as a white line—representing summation of the articular fluid and the superficial layer of hyaline cartilage covering the carpal bones. The bone marrow is uniformly low in signal. The triangular fibrocartilage is seen as a low-signal structure against the background of the high signal of the articular fluid (black arrowhead).

of fat, water, etc.). Capturing the radiofrequency generated by these protons returning to their relaxed state of spinning is done by “resonating” their RF with that of a receiving coil, which is extremely sensitive to infinitely small variations of the RF signal intensity. These variations are processed by a com-

puter, which calculates through the Fourier transform formula the intensity of signal in each pixel of the tissue slice in which the protons are relaxing. These pixels are presented in a digital image, with shades of gray proportional to the RF signal intensity of the protons in that volume of tissue. Thus it becomes

FIGURE 78.23. Axial MRI of normal wrist. Axial proton density-weighted image obtained at the level of the hamate hook (H) shows the carpal tunnel and the transverse carpal ligament (arrowheads) underneath which the median nerve is illustrated with a median artery within it (white arrow). On the medial side of the wrist, next to the hook of the hamate, the ulnar artery and ulnar nerve are identified (black arrow). The black oval-shaped structures in the carpal tunnel represent cross-sections of the flexor tendons, separated by a gray layer of synovial sheaths.



FIGURE 78.24. Sagittal MRI of normal wrist. Sagittal T1-weighted image obtained in the center of the wrist demonstrates the longitudinal alignment of the radius (R), lunate (L), capitate (C), and third metacarpal (3). The lunate has no tilt of the palmar or dorsal poles.

possible to differentiate tissues based on the rate of relaxation of the protons they contain.

Technique Satisfactory-quality MRI of the hand and wrist necessitates medium- or high-field scanners (1.0 to 1.5 Tesla units), use

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of dedicated surface coils capable of producing images with a field of view of 100 mm or less, and meticulous attention to the scanning parameters. The most common sequences of RF pulse excitation are spin-echo T1- and T2-weighted images. Each manufacturer of magnetic resonance scanners has devised pulse sequences aimed at showing at best advantage zones of higher water content (tumors, inflammation, cysts, articular fluid). The common denominator of such sequences is T2*weighted; however, each type of magnetic resonance scanner would have a particular name for these images (abbreviated in groups of letters: FLASH, FISP, STIR, etc). In this chapter, illustrations of T2*-weighted images are selected from the FLASH protocol. In all these sequences the bone cortex, ligaments, tendons, and fibrocartilage appear as signal void structures (black in the image). Proton density is a variant of T1-weighted image the sequences with suppression of signal from fat have the advantage of making any zone of edema or intra-articular fluid more conspicuous. In T1-weighted images, the marrow and subcutaneous fat have high signal (white or light-gray shade in the image). The articular fluid, synovial cyst, or any other dominant water zone is showing an intermediate signal (medium-gray in the image). Muscles also are seen as intermediate signal intensity structures and are at times difficult to distinguish from collections of fluid. T2-weighted images show the fat in the bone marrow and subcutaneous layer as a low-intermediate signal tissue (dark gray in the image). Contrary to T1-weighted images, in T2weighted images, the fluid in the joint, cystic structures, and zones of edema exhibit high signal intensity (white in the image). T2*-weighted images (FLASH) and fat-suppressed T2weighted images are characterized by a marked contrast between zones of fluid (white in the image) and bone or fibrocartilage that have low or absent signal (black). This striking difference in signal resembles an arthrographic effect and is especially useful in the evaluation of the TFCC. A complete wrist or hand examination usually consists of coronal T1-weighted coronal FLASH, sagittal T1-, and axial T2-weighted images, but tailoring of the examination to suit ¨ the clinical problem is necessary. For example, in Kienbock

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FIGURE 78.25. Acute traumatic tear of the triangular fibrocartilage of the wrist. A: Coronal T2*-weighted image: gap in the fibrocartilage avulsed from the radius (arrow) and prominent fluid in the distal radioulnar joint (arrowheads). B: Another patient with TFCC avulsed from the ulna with gap marked by arrow.

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Common Pathologic Disorders Detectable by Magnetic Resonance Imaging Triangular Fibrocartilage Tears

FIGURE 78.26. Flap tear of the triangular fibrocartilage. Coronal T2*-weighted image shows a horizontal tear detaching a flap of the TFCC (arrow).

disease, sagittal FLASH images show with better advantage the surrounding synovitis and highlight any fragmentation with displacement of lunate parts. Gadolinium administered intravenously is used to detect small vascular masses (glomus tumor, etc.) and to determine the differential of blood perfusion between normal tissues and tumoral or inflammatory lesions. Gadolinium is also used to enhance the signal in the lumen of the vessels during magnetic resonance angiography (MRA). Magnetic resonance angiography is performed by rapid acquisition of axial slices in a “slab of tissue” configuration, each sequence repeated at 30 seconds. The electronic processed data are displayed as a three-dimensional representation of the vessels seen from different vantage points. The precise timing of the scanning in relation to the bolus of gadolinium injection enables one to visualize separately the arteries or the veins. In cases in which no contrast is used, this is accomplished by modifying the scanning parameters related to the velocity of blood flow.

Lesions of the TFCC are divided in two groups: acute tear secondary to trauma and chronic degeneration. The acute tears are seen in the magnetic resonance images as interruption of the low-signal void representing the TFCC (Fig. 78.25). Fluid from the synovial spaces of the medial side of the wrist enters through the gap of the tear, seen in FLASH images as a white zone in the normally black cartilage band (10). Most acute tears seen in young individuals are from the ulnar attachment. Partial tears may split the TFCC horizontally, leaving a flap of fibrocartilage free to displace toward the ulnar head (Fig. 78.26). Degenerative disease of cartilage, a ubiquitous process histologically demonstrable in the middle-age population, is often observed in the TFCC beginning in the fourth decade. By age 60 years, more than 50% of the population has fissures and perforations in the TFCC (5,10). These abnormalities translate in MRI as thinning of the TFCC, irregular frayed surfaces, fenestration, or large gaps containing fluid. Such appearance of TFCC seen in MRI may be asymptomatic and represent the “normal for age.” This is why images of the magnetic resonance study must be interpreted only with clinical correlation to avoid false-positive interpretations (5).

Thumb Ulnar Collateral Ligament Tears Chronic (gamekeeper’s thumb) or acute disruption of the ulnar collateral ligament (UCL) of the thumb’s metacarpophalangeal joint (ski-pole injury) is easily diagnosed by MRI. Occasionally the distal end of the ruptured UCL will be displaced outside the adductor aponeurosis (Stener lesion). With acute injury, the

Normal Magnetic Resonance Imaging Demonstrated Anatomy Coronal images obtained in the center of the wrist and hand show the distal radius and ulna, the carpals and metacarpals in their longitudinal orientation, and their articulations (Fig. 78.22). The triangular fibrocartilage complex is seen as a signal-void band stretching from the medial margin of the radius across the ulnar head to where it is attached at the base of the ulna styloid. The marrow has characteristic light signal with the bone trabeculae seen as a fine lattice of intersecting thin black lines. Coronal T2-weighted images outline the articular surface of the TFCC and intercarpal ligaments. Axial images are necessary for study of the carpal tunnel. The bone walls, the palmar aponeurosis, the median nerve, and other soft-tissue structures located in the tunnel are clearly visualized (Fig. 78.23). The individual compartments of the extensor tendons will be seen on cross section, on the dorsal side of the wrist. Sagittal T1-weighted images are essential for evaluation of the alignment in the central axis of the wrist and hand: radius–lunate–capitate–third metacarpal (Fig. 78.24).

FIGURE 78.27. Scapholunate ligament tear. Coronal T2*-weighted image shows wide space between scaphoid and the lunate. The scaphoid attachment of the ligament is interrupted (arrow). The normal lunotriquetral ligament is represented by a slender black line on the proximal margin of the joint (arrowhead).


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F,G FIGURE 78.28. Ruptured flexor profundus tendon of the fifth digit. A: Sagittal T1-weighted image of the fourth digit presented as reference demonstrates the longitudinal direction of a continuous flexor tendon from distal phalanx across the metacarpophalangeal joint. B: Sagittal T1-weighted image of the fifth digit: Only the distal portion of flexor digitorum profundus (FDP) is demonstrated with an abrupt discontinuity at the site of rupture (arrow). C: The normal flexor digitorum superficialis (FDS) tendon is visualized as a thin band attaching on the middle phalanx (arrowhead). D to G: Axial images of third, fourth, and fifth digits demonstrate a normal appearance of the FDP at the level of the distal phalangeal base in (D) and the empty sleeve of the flexor tendons at the site of tear (see arrowhead in E). The two black dots on the palmar surface of the middle phalanx represent the two insertion slips of the FDS. The space between them should be occupied by the normal flexor profundus tendon, which is retracted proximally and is therefore absent at this level. Compare with the normal appearance of third and fourth digits. F: The empty sleeve of the flexor digitorum profundus is represented by white zone (fluid in the sleeve) (arrow). G: At the level of the metacarpal head there is normal appearance of both FDS and FDP tendons (arrow). (Courtesy of Dr. E. Lubat.)

T2-weighted images show adjacent edema and hemorrhage as diffuse zones of increased signal surrounding the torn UCL. Bone bruises in the metacarpal head show increased/decreased signal intensity in the T2-/T1-weighted images, respectively.

evident from an abnormally large space between opposing articular surfaces (Fig. 78.27).

Intercarpal Ligament Tears

In most cases, complete tears of finger tendons can be diagnosed by clinical examination. Standard radiographs may show a flake of bone detached from the insertion site of the tendon. Demonstration of the quantity of fibrous tissue in the digital fibro-osseous tunnel and knowledge of the exact location of

Scapholunate and lunotriquetral ligament tears are diagnosed by MRI when the low-signal band of the ligament being evaluated is interrupted. Often the instability of the joint will be

Digital Tendon Lesions

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FIGURE 78.29. Partial extensor tendon tear and tenosynovitis. A: Axial proton density image shows fluid in the second and third extensor compartments. The abductor pollicis longus tendon has abnormal contour and abnormally high signal consistent with a partial tear (arrowhead). B: T2-weighted axial image at the same level with (A) shows with sharper contrast the fluid accumulated in the tendon sheaths of the second and third extensor compartment (arrows).

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the end of the retracted proximal segment of the tendon can be helpful in planning surgery. This information can be obtained precisely from sagittal and axial magnetic resonance images (Fig. 78.28).

Tendonitis and Tenosynovitis Tenosynovitis or chronic partial tears longitudinally oriented in tendons are characterized in the axial T2-weighted images by central zones of high signal within the tendon, distention of sleeve by fluid, and thickening of the synovium, which becomes visible as a cuff around the tendon (Fig. 78.29).

the transverse carpal ligament and edema of the median nerve just proximal to its entrance in the carpal tunnel, seen in axial MRI as increased diameter and higher signal intensity of the nerve. As CTS is a nerve compression caused by tenosynovitis, thickening of the synovium investing the digital flexor tendons may be seen on MRI as intermediate signal layers separating individual tendons. As CTS that is successfully relieved by surgical decompression does not recur, MRI may be strongly indicated for a patient who presents with recurrent symptoms of median nerve compression. Often MRI will reveal discrete masses or other spaceoccupying lesions, such as ganglion cysts in the carpal tunnel, accounting for the recurrence of nerve compression symptoms.

Carpal Tunnel Syndrome Carpal tunnel syndrome (CTS) is essentially a clinical diagnosis from its characteristic signs of nerve compression, and generally can be confirmed by electrodiagnostic studies. Thus, MRI is rarely needed or performed for this condition. The MRI findings of carpal tunnel syndrome include anterior bowing of

Avascular Necrosis of Carpal Bones AVN of the proximal fragment of a fractured scaphoid and ¨ idiopathic osteonecrosis of the lunate (Kienbock disease) are two frequently encountered and serious wrist problems about



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FIGURE 78.32. Avascular necrosis of proximal fragment of fractured scaphoid. Coronal T1-weighted image shows fracture through the waist of the scaphoid and low signal in the bone marrow of the proximal fragment consistent with AVN. ¨ disease. Coronal T1-weighted image shows FIGURE 78.30. Kienbock abnormal low signal in the bone marrow of the lunate consistent with avascular necrosis of bone.

¨ FIGURE 78.31. Advanced Kienbock disease with collapse and fragmentation. Sagittal T1-weighted image shows the fragmentation of the lunate (arrows) through the zone of aseptic necrosis manifested as low signal in the bone marrow.

FIGURE 78.33. Lipoma. Coronal T1-weighted image shows a fatcontaining mass on the ulnar side of the wrist (arrows).

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FIGURE 78.34. Ganglion cyst. A: Coronal T2weighted image shows the multiloculated ganglion cyst located in the palmar surface, near the joints between the capitate, hamate, and metacarpal basis (arrow). B: Axial T2-weighted image shows the deep location of the ganglion cyst (arrow).

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which precise information is needed. A rare similar spontaneous disorder, Preiser disease, occurs to the scaphoid. Magnetic resonance imaging is able to detect the earliest changes in the bone marrow, thus allowing a specific diagnosis even at a time when all radiographs are normal. The most ¨ accepted theory of etiology of Kienbock disease is that initially forces transmitted axially from the forearm converge on the convex surface of the lunate to produce microfractures. A short ulna (negative variance) may be a predisposing factor (see Wrist Views above). This stage can be regarded as the precursor of AVN and is manifested on MRI as lines of low signal traversing the bone marrow horizontally and parallel to the proximal surface of the lunate (9). If the process continues zones of bone marrow become necrotic, appearing in MRI as low-signal areas in T1-weighted images. When most of the bone marrow of the lunate becomes necrotic, subtle increase in the bone density appears in radiographs. At this time, the entire lunate appears low in signal (Fig. 78.30). Fissures of the cortex and collapse of the lunate indicate advanced

¨ and irreversible Kienbock disease (Fig. 78.31). MRI can de¨ disease at a very early stage, hopefully at a time tect Kienbock when treatment can arrest the process. MRI is also helpful in early detection of AVN in the proximal fragment of a fractured scaphoid. Observing zones of abnormal signal in most of the bone marrow and lack of enhancement following intravenous administration of gadolinium are indications of AVN. Such findings at 3 months following injury are a strong indication that healing is not occurring with conservative treatment (Fig. 78.32).

Tumors Tumors of either bone or soft tissues are well visualized in magnetic resonance images. The precise location of the tumor, its extent, and its relationship with adjacent muscles, bones, and neurovascular bundles also can be determined, a significant help in the planning of tumor excision (11). In many instances, the histology of the masses can be reliably concluded: Lipomas


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A

B FIGURE 78.35. Synovial sarcoma of the forearm. A, B: Axial T1-weighted images before (A) and after (B) intravenous administration of gadolinium show an aggressive infiltrating mass in the forearm with high vascularity. The margins are better defined (white arrows) and necrotic parts of the tumor appear more conspicuous after contrast enhancement (black arrows).

have homogeneous fatty content seen in T1-weighted images as a bright signal (Fig. 78.33). Cystic collections of fluid such as those seen in ganglion cysts are characterized in T2-weighted images by a homogeneous bright signal with no internal structure (Fig. 78.34). Malignant soft-tissue tumors often appear in MRI as infiltrative masses with ill-defined margins. Gadolinium administered intravenously enhances the hypervascular parts of these tumors, making more conspicuous the extent of the lesion and any central zone of necrosis (Fig. 78.35). Such information is essential for planning of biopsy and treatment. Hemangiomas or arteriovenous malformations give characteristic magnetic resonance images of a mixture of vascular elements on the background of fat and serpiginous, dilated vascular channels feeding or draining the masses.

In Raynaud disease or other nontraumatic ischemic processes (e.g., Buerger disease), MRA can be used as an objective determination of the response to different therapy protocols: Its being noninvasive and the short time necessary for scanning (1 mm displacement of the fragments, or if more than 20% of the joint surface is involved. As with all intra-articular fractures,

precise fragment reduction to create a congruent MCP joint is essential to achieve optimal results. Computed tomography (CT) evaluation can accurately define fragment alignment and can aid in treatment planning. If operative intervention is required, the modality is dictated by the fracture pattern with unilateral sagittal band division used for exposure. Small

A,B

C FIGURE 81.3. Long spiral oblique fracture of the middle phalanx. A: Preoperation radiograph. B and C: Lateral and posteroanterior views of interfragmentary screw fixation.

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C

A,B

FIGURE 81.4. Intra-articular, comminuted, and impacted fracture of the proximal phalangeal base. A: Preoperation radiograph. B: External fixation device placed to neutralize MCP joint, bony fragments disimpacted and stabilized with bone grafting, and 0.045 Kwires. C: Early removal of external fixation device, allowing digital motion with K-wires still in place. D: Final result after hardware removal and bony contour restored.

D

cortical screws can be used and should be buried and placed outside the MCP joint articular surface. Small joint arthroscopically assisted reduction and fixation is often possible and has the added benefit of limiting surgical trauma. Following reduction, K-wires can be used alone or in combination with interosseous wires. The goals of fixation should be to adequately stabilize the fracture and allow for early mobilization to limit adhesions of not only the extensor tendons, but of the MCP joint as well.

Neck Fractures Neck fractures can occur with any digit but are most common in the little finger. A fracture of the fifth metacarpal neck is known as boxer’s fracture because these injuries are often associated with a blow delivered during an altercation. Prior to appropriate fixation, patients with skin breaks, regardless of size, must be treated as if they have a contaminated joint, and the MCP joint carefully inspected and irrigated. If these frac-

tures are determined to be closed, they can often be treated by closed reduction and carefully fitted cast immobilization. The amount of acceptable angulation for these fractures varies within the literature and between the metacarpals. The index and middle metacarpals can generally tolerate 20 to 30 degrees of angulation; however, in the ring and little fingers, 50 to 70 degrees of angulation can be considered acceptable in some individuals. Increasing fracture angulation may be associated with a prominent metacarpal head in the palm, which is often problematic for laborers and athletes. Treatment, therefore, must be appropriately tailored to each individual patient. Fractures with an unacceptable reduction can be treated with an open procedure and plate fixation using either a lateral or dorsal approach. Simple longitudinal K-wire placement, supplemented with a well-molded plaster cast to control rotation, often suffices, and limits surgically created trauma (Fig. 81.5). Newer percutaneous intramedullary nails introduced into the metaphyseal base of the metacarpal can also be used. K-wire fixation can be effective particularly with border


Chapter 81: Fractures, Dislocations, and Ligamentous Injuries of the Hand

A,B

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C FIGURE 81.5. Displaced metacarpal neck fracture of the small finger and displaced extra-articular oblique metacarpal base fracture of the ring finger. A: Preoperation radiograph. B: Closed reduction and percutaneously placed, longitudinal 0.062 K-wire stabilization. C: Long-term results demonstrating accurate alignment and fracture healing.

metacarpals by the placement of transverse wires proximal and distal to the fracture site supplemented with a single longitudinal wire.

Shaft Fractures The treatment of metacarpal shaft fractures is dictated by fracture pattern, position of the involved metacarpal, and by the number of metacarpals injured. Metacarpal shaft fractures generally have an apex dorsal angulation as a result of the deforming forces of the attached interosseous muscles. Closed reduction can often be achieved with distraction and direct pressure on the fracture apex. The amount of acceptable angulation following reduction varies with the involved digit. The ring and small finger metacarpals can tolerate 40 degrees of angulation because of motion provided by the carpometacarpal (CMC) joint. However, only approximately 15 degrees of angulation is acceptable at the index and middle metacarpals. The length of acceptable shortening is only approximately 5 mm because of the carefully balanced extensor mechanism; however, any degree of rotation that results in finger overlap must be corrected. Although transverse fracture patterns are the most amenable to closed treatment, multiple transverse shaft fractures are an indication for internal fixation to allow for early motion (Fig. 81.6). Stabilization can most often be achieved with percutaneous intramedullary nails or K-wires. Oblique fractures are often unstable even after adequate reduction and thus require operative treatment. Short oblique fractures may be treated with intramedullary nails or crossed K-wires with placement of an additional longitudinal wire after reduction. In addition, perpendicular K-wires traversing the adjacent uninjured metacarpal can also be used to stabilize fractures of the border digits. Short oblique fractures that require open reduction should be approached dorsally with the incision centered along the injured metacarpal or in the intermetacarpal space when multiple adjacent fractures are present; 2.0- or 2.4-mm dorsal plates should be used for fixation (Fig. 81.7). Long oblique fractures are more difficult to reduce and often require open reduction and internal fixation. A dorsal

approach with plate fixation as described for short oblique fractures can be used with the addition of supplementary compression screws. Screw fixation alone can be adequate for long oblique fractures if the length of the fracture line is twice the diameter of the bone. Fractures associated with significant softtissue damage should be treated with external fixation, while coverage is expeditiously established.

Base Fractures Metacarpal base fractures are considered high-energy injuries. These injuries are divided into extra- or intra-articular fractures. If the carpus is involved, CT evaluation is often needed to accurately rule out fractures or dislocations. Extra-articular base fractures can be treated with closed reduction if treated before significant edema develops. A distraction maneuver with force directed over the displaced apex is usually successful in gaining reduction. Degrees of acceptable angulation and shortening vary with the involved digits. The ring and little finger metacarpals can tolerate 10 to 15 degrees of angulation and up to 2-mm of shortening, as there is compensatory motion at their corresponding CMC joints. The index and long fingers, however, are only able to tolerate 5 degrees of angulation. If reduction cannot be maintained in these extra-articular fractures, closed or open reduction with K-wire fixation or dorsal plate application is required (Fig. 81.5). Intra-articular metacarpal base fractures result from highenergy axial loads that cause T- or Y-shaped injuries comparable to the Bennett or Rolando fracture seen in the thumb. These fracture patterns often occur in the fifth metacarpal and are often referred to as either a “baby” or “reverse” Bennett- or Rolando-type fracture. Generally, these fractures require open reduction and internal fixation with K-wires or a mini T or Y plate. Avulsion fractures of the metacarpals are usually associated with forced palmar flexion of the wrist and can be treated closed by placing the wrist in extension as long as less than 20% of the articular surface is involved. Avulsion fractures with more than 20% joint involvement will require open

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A FIGURE 81.6. Multiple transverse metacarpal shaft fractures after gunshot wound with significant softtissue loss. A: Preoperation radiograph. B: Intramedullary rod placement for stabilization.

A

B FIGURE 81.7. Transverse midshaft fractures of fourth and fifth metacarpals with dorsal angulation. A: Preoperation radiograph. B: Reduction and placement of 2-mm plates for rigid fixation, allowing early motion.



reduction and internal fixation, remembering that these patients must be carefully evaluated for associated carpal injuries.

THUMB FRACTURES Distal and Proximal Phalanx Fractures of the thumb phalanges are less common and tend to result from a direct blow. Distal phalanx fractures can be divided into either tuft-, transverse-, or longitudinal-type fractures. Treatment is based on both location and fracture pattern. Tuft fractures, as in the other digits, are treated with appropriate attention to injuries of the nail bed and surrounding soft tissues as described earlier. Transverse fractures, however, differ from those seen in the other fingers because of the strong pull of the flexor pollicis longus (FPL) tendon. The pull from the FPL causes displacement of these fractures, rendering them unstable. Reduction and fixation using percutaneous K-wires that cross the IP joint are required for stabilization. Longitudinal fractures are rare and frequently require open reduction and internal fixation. Nondisplaced transverse and longitudinal fractures can be treated with cast immobilization or protective splinting. Mallet injuries of the thumb, as with other digits, are treated in a similar manner. If no volar subluxation of the distal phalanx is present, these injuries are treated with dorsal extension splinting for 6 to 8 weeks. Volar subluxation or significant (greater than 33%) involvement of the joint surface requires operative treatment with reduction and K-wire fixation, or open reduction with interosseous wiring or screw fixation if fragment size permits.

Thumb Metacarpal Fractures Thumb metacarpal fractures are divided into shaft and base fractures with base fractures further classified into either extraor intra-articular. Shaft fractures are usually the result of direct trauma and are much less common than metacarpal base fractures. These injuries are treated by their radiographic pattern with unstable fractures requiring operative reduction and fixation with percutaneous K-wires. Metacarpal base fractures are much more common than shaft fractures, and the intraarticular types are described as either Bennett- or Rolando-type fractures. Unlike shaft fractures that are usually the result of a direct blow, base fractures occur from an axial load through the metacarpal shaft. Extra-articular (epibasilar) fractures are most commonly transverse or oblique in nature and can be treated with casting if stable. Following closed reduction, these fractures are immobilized for 4 weeks in a thumb spica cast. Mobility of the adjacent CMC joint allows for up to 30 degrees of acceptable angulation at the fracture site. If these fractures prove to be unstable with eventual loss of reduction, operative reduction and percutaneous K-wire fixation is recommended. The pattern of intra-articular base fractures reflects the contributions of the complex and extensive ligamentous structures at the CMC joint, most notably of the volar oblique ligament. In the Bennett-type fracture, which consists of an intra-articular fracture through the volar–ulnar aspect of the metacarpal base, the fracture fragment is held in anatomic position by the volar oblique ligament. The remainder of the metacarpal is displaced dorsally and radially by the strong pull of the abductor pollicis longus. Thus, treatment is aimed to restore articular congruity by reduction of the dorsally displaced metacarpal. If reduction of the metacarpal shaft to the Bennett fragment can be accom-

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plished satisfactorily with a 1-mm or less articular step-off, closed reduction with percutaneous pinning is an acceptable treatment option. With this technique, closed reduction of the metacarpal base to the Bennett fragment is accomplished with longitudinal traction, pressure at the thumb metacarpal base, and pronation. A transarticular K-wire is then passed from the metacarpal to the trapezium or second metacarpal for stabilization (Fig. 81.8). If unacceptable reduction is obtained with the closed technique, open reduction is performed. Open fixation can then be obtained with K-wires, screws, or plate fixation, with stabilization of the metacarpal–trapezial joint if needed. Regardless of the technique used, the thumb is immobilized for 4 weeks in a well-fitted thumb spica cast. The Rolando-type fracture is a high-energy fracture that is made up of at least three fragments, with all comminuted base fractures commonly placed in this category. The classic Rolando fracture, as described in 1910, is a T- or Y-shaped metacarpal base fracture composed of three fragments. These fractures are difficult to treat as they require restoration of both the articular surface as well as the length of the metacarpal. Open reduction with internal fixation using or condylar blade T or Y plate, multiple K-wires, or interosseous wiring is the treatment of choice for these complex fractures (Fig. 81.9). External fixation remains an option with highly comminuted fractures.

JOINT DISLOCATIONS AND LIGAMENTOUS INJURIES Dislocations and injuries to the ligaments of the hand can occur from hyperextension, hyperflexion, lateral deviation, torsion, or impaction. These stress forces lead to subluxation or dislocation that can occur with or without associated fractures. Many of these injuries are primarily from impaction forces that result in fractures that were discussed previously. The following sections focus on the treatment of dislocations and their associated ligamentous and soft-tissue injuries. Various tissues stabilize the joints of the hand, including the collateral ligaments, volar plates, capsular attachments, and numerous tendon insertions. Disruption of any or all of these structures will often require operative repair because of joint instability, or irreducible dislocation secondary to soft-tissue interposition.

Distal Interphalangeal Joint Injuries Commonly encountered dorsal dislocations of the DIP joint are often open and must be treated as a contaminated joint. Patients are treated with antibiotics, copious irrigation of the joint, and accurate reduction and stabilization. Closed dislocations can be reduced using longitudinal traction, with the distal phalanx held in slight flexion. Irreducible dislocations tend to be held by intervening soft tissue, most commonly the volar plate or flexor tendon, which becomes entrapped by the condyle of the middle phalanx. The DIP joint is splinted in slight flexion for 2 to 3 weeks following reduction, but with protected motion begun after 1 week. Although less common, volar dislocations of the DIP joint can occur and are treated with closed reduction and extension block splinting for 6 to 8 weeks. Inability to reduce volar dislocations is usually secondary to partial entrapment of the extensor tendon within the DIP joint and requires open reduction. Hyperextension injuries that do not cause joint dislocation can result in flexor digitorum profundus (FDP) tendon avulsion, commonly referred to as a “jersey” finger, the result of the injured digit being caught in a football “jersey,” resulting in hyperextension and tendon avulsion. These injuries occur

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B

A FIGURE 81.8. Bennett fracture: avulsion of volar–ulnar fragment with displacement of metacarpal shaft. A: Preoperation radiograph. B: Single 0.062 K-wire transfixed to index metacarpal to stabilize thumb metacarpal shaft and maintain reduction to Bennett fragment.

most commonly in the ring finger and can be associated with vincula or bony fragment avulsion. The FDP tendon can retract into the palm with complete rupture of the vincula or can be held at the level of the PIP joint if the vincula remain intact. Both types of avulsions should be treated with anatomic reattachment of the FDP tendon with a heavy, nonabsorbable, pullout suture tied over a dorsally placed button. FDP avulsions with an attached bony fragment tend not to retract beyond the distal extent of the A-4 pulley because of catching of the associated fragment on the distal edge of the pulley system. These injuries can be treated by fixation of the avulsed bony fragment if sufficiently large. FDP avulsions associated with an intact vincula are the most common type of injury and have a better prognosis than those with complete separation of the vincula, as the blood supply to the tendon is not disrupted.

Proximal Interphalangeal Joint Dorsal Dislocations The PIP joint, like the DIP joint, is a bicondylar hinge joint with minimal motion permitted in more than one plane. In addition to strong capsular ligaments, the proper and accessory collateral ligaments are the primary joint and volar plate stabilizers, respectively. Stress forces on the PIP joint can lead to failure of these structures, leading to painful ligamentous injury and joint instability, as well as incomplete or complete dislocation. Dorsal dislocation of the PIP results from hyperextension, which disrupts the volar plate attachment to the base of the middle phalanx. These dislocations are not only the most common type of PIP dislocation, but also represent the most common injury to the joints of the hand (4). Hyperextension

injuries of the PIP can be seen as part of a spectrum of increasing pathology ranging from subluxation to dislocation, and ultimately, fracture dislocation. Subluxation or simple hyperextension results in isolated volar plate injury and can be treated with buddy taping and early range of motion, after 7 to 10 days of immobilization in slight flexion. Failure of the volar plate along with a longitudinal split in the collateral ligaments from hyperextension and torsion can result in dorsal dislocation with or without an associated fracture. Pure dorsal dislocations must be reduced and assessed for stability. Although reduction can usually be achieved by digital block and longitudinal traction, the volar plate occasionally blocks attempts at reduction. If difficulty is encountered with simple traction during reduction, the injury pattern should be reproduced with hyperextension and pressure applied to the base of the middle phalanx in an attempt to achieve reduction. After reduction, joint stability is evaluated and radiographs should be obtained to confirm joint congruity, assess reduction, and search for occult fractures. If stable, dorsal dislocations can be treated with buddy taping and early active motion after a brief period of immobilization. If the joint is found to be unstable, an extension block splint is used, with the PIP blocked at 10 degrees short of instability, but to no more than 20 degrees. Motion is progressively increased by 10 degrees of extension on a weekly basis. Fracture dislocations can be classified as stable or unstable. Fractures that involve less than 30% of the joint surface are considered stable and can be treated with reduction and extension block splinting. The unstable fracture dislocation pattern, those involving greater than 30% of the joint surface, or those exhibiting subluxation, can be difficult to treat and almost always results in residual PIP stiffness. Dynamic traction can allow reduction and fracture stabilization as well as permit



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early motion with an acceptable outcome. Transarticular Kwire fixation of the joint in less than 30 degrees of flexion is an alternative option to achieve and maintain reduction and joint congruity in these unstable fractures. Patients treated by this method should have early pin removal and protected range of motion instituted by 3 weeks. External fixation, either static or dynamic, is another modality for treatment of these complex fracture patterns. This includes the use of the newer “compass hinge” devices that maintain fracture reduction while allowing controlled passive and active motion (Fig. 81.10). Open reduction and internal fixation can be used if the fracture fragments are sufficiently large, but should be reserved for irreducible fractures or dislocations as this is associated with a greater than 50% complication rate, including joint stiffness, infection, instability, and early arthritis. Volar plate arthroplasty has been proposed as an acute treatment option for these fractures (5). However, recurrent dislocation has been reported as the most common complication with this procedure, particularly when more than 50% of the joint surface has been displaced. Osteochondral hamate grafts can be used as a salvage procedure to restore the volar bony restraint of the middle phalangeal base (6).

Proximal Interphalangeal Joint Volar Dislocations

FIGURE 81.9. Reduction and rigid fixation of highly comminuted Rolando fracture using a contoured Y-plate.

Volar dislocations of the PIP joint are much less common than dorsal dislocations and are usually associated with a central slip injury and avulsion fracture. Volar dislocations can also occur in combination with torsion, which can lead to capsular disruption, resulting in the proximal phalangeal condyle becoming trapped between the central slip and the lateral band. Simple volar dislocations can be reduced with longitudinal traction and, although there may be disruption of the central slip,

A

C

B

FIGURE 81.10. Comminuted, impacted “pilon” fracture at base of proximal phalanx. A: Preoperation radiograph. B and C: Reduction and screw fixation with placement of compass hinge dynamic external fixator to maintain reduction and allow early mobilization.

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can be treated nonsurgically with extension splinting of the PIP joint for 6 weeks while allowing DIP motion. However, if joint instability is noted, early operative repair is indicated. Volar dislocations associated with torsional forces often require open reduction, as the proximal phalangeal condyle tears the interval between the central slip and the lateral band, ultimately becoming entrapped. Thus, if closed reduction with traction is unsuccessful, reduction with the PIP and DIP joints flexed can be attempted; however, surgical intervention is necessary if this maneuver fails. At the time of open joint reduction the central tendon can be assessed and, if intact, motion can be instituted after a brief period of 2 to 3 weeks of immobilization. If associated with a minimally displaced (less than 1 mm) avulsion fracture, these volar dislocations can be treated in a similar way to simple dislocation. Avulsion fractures with more than 1 mm of displacement should be treated with precise reduction and internal fixation. K-wire fixation or open reduction with screw fixation can be used for larger fragments.

Proximal Interphalangeal Joint Collateral Ligament Injuries Collateral ligament injuries can occur with or without dislocations. Most of these injuries can be treated with buddy taping the injured digit to an adjacent uninjured digit after a brief 7to 10-day period of immobilization. Complete rupture of the radial collateral ligament of the index finger, however, should be repaired using a midaxial incision and a suture anchor or pullout suture, because of the substantial forces generated during pinch. Collateral ligament injuries in association with volar plate disruption often occur with lateral dislocations. These injuries are treated with closed reduction and a short period of static splinting followed by protected motion and buddy taping. Operative intervention is indicated for irreducible dislocations or those associated with displaced fractures or fractures involving more than 25% of the joint surface. Purely ligamentous injuries can be repaired as above following open reduction, while those associated with fractures are repaired by bony stabilization alone with K-wires, screws, or suture anchors.

Thumb Joint Injuries Ligamentous injuries of the thumb are common and typically involve the ulnar collateral ligament (UCL) of the MCP joint. When forced radial deviation occurs on an outstretched hand while the thumb is adducted, disruption of the ulnar collateral ligament at its distal insertion site occurs. This can occur as a purely ligamentous disruption or include a bony fragment at the proximal phalangeal point of attachment. Diagnosis of UCL injuries is usually by clinical examination. Plain radiographs may demonstrate volar subluxation of the proximal phalanx relative to the metacarpal with complete collateral ligament ruptures. Magnetic resonance imaging (MRI) may occasionally be helpful in identifying a Stener lesion (see below), which is pathognomonic for complete ligamentous disruption. Partial tears can also be differentiated from complete tears by stress testing under local anesthetic block, with or without radiographs, with the finding of an end point in partial tears (Fig. 81.11). Partial tears can be treated with immobilization for 6 weeks. Although there is controversy regarding treatment of complete UCL tears, most clinicians, including the authors, agree that the most favorable outcome is with operative repair. UCL injuries often result in entrapment of the avulsed distal end by the leading proximal edge of the adductor aponeurosis (Stener lesion), which, unless released, will lead to nonhealing of the ligament and instability. Operative repair of UCL injuries is through a sinusoidal incision centered over the ulnar aspect of the MCP joint, with the more distal limb being

Metacarpophalangeal Joint Injuries Ligamentous injury to the MCP joint can occur with either subluxation of the joint or pure dislocation. Lateral subluxation can result in collateral ligament disruption. These injuries are uncommon, but if they result in joint instability, or occur in the index radial position, require operative repair. Stability can be assessed by examining proximal phalanx deviation with the MCP held in 30 degrees of flexion. If stable, the injured digit can be buddy taped to an adjacent digit for 6 weeks. Deviation of greater than 20 degrees, or an avulsion fracture with greater than 2 mm displacement, are indications for operative repair (7). Similar to that described for PIP collateral ligament injuries, a midaxial approach using suture anchors or K-wire fixation can be used for repair. MCP dislocations are usually dorsal or ulnar, and often result in a volar plate injury that can be associated with metacarpal head fractures. Reduction of most dislocations can be achieved with wrist flexion and pressure on the dorsal aspect of the base of the proximal phalanx. Following reduction these injuries are treated with an extension block splint to allow the volar plate to heal. Inability to reduce an MCP dislocation is likely secondary to volar plate entrapment and should be treated with open reduction via a dorsal approach, freeing the entrapped volar plate. Once reduced, MCP dislocations associated with metacarpal head fractures are treated as previously described.

FIGURE 81.11. Stress view of thumb MCP joint after anesthetic block, indicative of complete ulnar collateral ligament tear demonstrating subluxation and >75 degrees of laxity.


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C

A,B FIGURE 81.12. Volar subluxation of proximal phalanx indicative of complete ulnar collateral ligament tear. A: Preoperation radiograph. B and C: Ulnar collateral ligament reinsertion using bone anchor and transarticular MCP joint K-wire fixation for stabilization.

more volar. Repair of the torn UCL can be achieved with direct suture repair, suture anchor, pullout suture, or bony fixation if associated with an avulsion fracture (Fig. 81.12). Delayed repair of UCL injuries more than 3 weeks after injury may require the use of a tendon graft. Injuries to the radial collateral ligament of the thumb are much less common than UCL injuries. A Stener lesion homolog is not present with these injuries because of the broadness of the abductor aponeurosis. However, guidelines for management of these injuries follow those for

the ulnar side, with identification of no end point on stress testing indicative of complete tears. Injuries with >30 degrees of laxity but with an end point relative to the contralateral thumb, are treated as a partial tear with thumb spica immobilization. Complete tears can be treated with immobilization or operative repair, but in patients whom the injury occurs in the dominant hand or who require bilateral manual dexterity, open repair will yield more reliable results, and is the treatment of choice (Fig. 81.13). Fifty percent of radial collateral ligament

A

FIGURE 81.13. Radial collateral ligament injury of thumb MCP joint with bony avulsion. A: Preoperation radiograph. B: Reduction of bone fragment and attached collateral ligament using a single lag screw and MCP stabilization using 0.062 K-wire.

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tears will be midsubstance, as opposed to UCL tears, which, as previously mentioned, usually occur at their distal insertion site. In addition to collateral ligament injuries, dislocations of the joints of the thumb can occur and are often associated with volar plate disruption. IP dislocations of the thumb are relatively uncommon and are usually dorsal in direction. Closed reduction and immobilization with the joint in 20 degrees of flexion is the treatment of choice. Inability to reduce an IP dislocation is likely a result of entrapment of the volar plate and therefore requires open reduction. MCP dislocations usually occur dorsally and are associated with volar plate disruptions as well as collateral ligament and capsular tears. The majority of dorsal dislocations can be reduced by closed reduction and should be treated with 4 to 6 weeks of immobilization in 20 degrees of flexion. Joint stability assessment by stressing the collateral ligaments should be performed, as well as stability testing with hyperextension to assess the continuity of the volar plate. Instability in any direction should be addressed with operative repair. Irreducible dorsal dislocations, as well as most volar dislocations, will require open reduction and appropriate ligamentous or capsular repair. Radiographs that show significant hyperextension of the MCP joint are often associated with irreducible dislocations. Repeated, forceful attempts at reduction of thumb MCP dislocations should be avoided as this indicates entrapment of the volar plate, sesamoids, or flexor pollicis longus tendon. If the sesamoids (and associated volar plate) are noted to be within the MCP joint, open reduction is required. A dorsal or volar approach may be used for open reduction of irreducible MCP joint dislocations, although a dorsal approach is preferred. Following open reduction, the thumb is immobilized for 2 weeks in a thumb spica cast with the MCP joint in 20 degrees of flexion. A removable splint is then fashioned to allow for protected early motion of the MCP and IP joints for an additional 2 to 4 weeks. Purely ligamentous injuries at the base of the thumb in association with first CMC dislocation are extremely rare, as the

Rolando and Bennett fracture patterns are much more common. Disruption of the volar oblique ligament occurs with dorsal dislocation of the first CMC joint. These dislocations tend to easily reduce but are inherently unstable and usually require ligament reconstruction. If stable, immobilization for 6 weeks in a thumb spica cast is required.

CONCLUSION Attention to the soft tissues of the hand is critical if one is to achieve a satisfactory outcome, particularly with more complex injuries and those involving the joint spaces. Generally speaking, the least-invasive form of fixation will serve the patient best and minimize surgical trauma. A careful balance must be reached between achieving stable, rigid fixation, minimizing soft-tissue trauma, and allowing for early, active motion.

References 1. Foucher G, Binhamer P, Cange S, et al. Long-term results of splintage for mallet finger. Int Orthop. 1996;20(3):129–131. 2. Rettig ME, Dassa G, Raskin KB. Volar plate arthroplasty of the distal interphalangeal joint. J Hand Surg [Am]. 2001;23(5):940–944. 3. Hastings H. Unstable metacarpal and phalangeal fracture treatment with screws and plates. Clin Orthop. 1987;214:37–52. 4. Glickel SZ, Barron OA. Proximal interphalangeal joint fracture dislocations. Hand Clin. 2000;16(3):333–344. 5. Eaton RG, Malerich MU. Volar plate arthroplasty of the proximal interphalangeal joint. A review of ten years’ experience. J Hand Surg [Am]. 1980;5(3):260–268. 6. Williams RMM, Kiefhaber TR, Sommerkamp TG, et al. Treatment of unstable dorsal proximal interphalangeal fracture/dislocations using a hemihamate autograft. J Hand Surg [Am]. 2003;28(5):856–865. 7. Delaere OP, Suttor PM, Degolla R, et al. Early surgical treatment for collateral ligament rupture of metacarpophalangeal joints of the fingers. J Hand Surg [Am]. 2003;28(2):309–315.


CHAPTER 82 ■ TENDON HEALING AND FLEXOR TENDON SURGERY PAUL ZIDEL

Successful flexor tendon surgery remains a great surgical challenge. Many biologic factors remain beyond our control. Nevertheless, an accurate diagnosis and knowledge of the biology of wound healing, coupled with meticulous surgical technique and postoperative care, are the controllable factors that optimize results.

HISTORY Kleinert among others reviewed the history of flexor tendon surgery. Galen, who lived in the 2nd century ad and was a surgeon to the gladiators, believed that a tendon was a combination of nerve and ligament, as the nerve entered a muscle and ended in a white cord. Avicenna, a Persian physician who lived 800 years later, was the first to recommend repair of this structure. However, it was not until 1752, when Albrecht von Haller, a Swiss investigator, concluded that this tendinous structure was insensitive to pain, that repair began to be accepted. Poor results led to controversy and experimentation. In 1916, Mayer described the blood supply and avascular zone of tendons. Bunnell used the term “no man’s land” to describe the consistently unfavorable zone of repair in the fingers. Mason developed a clinical guide differentiating between primary and secondary tendon suture repairs and strengthening with stress. In 1959, Verdan described the zones of flexor tendon repairs in the hand. In 1967, Kleinert reported his remarkably high percentage of good results in zone two, the “no man’s land” of Bunnell. Potenza studied tendon healing based on extrinsic fibroblastic invasion and proliferation with adhesion formation. Lundborg, believing tendons had the intrinsic requirements to heal, explored intrinsic tendon healing based on synovial fluid nutrition. Strickland, Manske, Gelberman, and others have studied the delicate balance between healing and motion with regard to such factors as the role of growth factors and fibronectin, the ratio of extrinsic to intrinsic healing, tendon suture techniques and the strength of repairs, and the effects of early active postoperative motion on outcome. Nevertheless, many questions remain unsettled.

TENDON ANATOMY In a complex functional system, muscle fibers extend from their osseous origin and taper into long, narrow, glistening white structures called tendons. Tendons have no inherent contractile properties, but are the important link between muscle and bone, causing motion of the intercalated joint. Tendons are composed of dense, metabolically active connective tissue, the collagen bundles of which are oriented in

regular, spiraling patterns. This arrangement of fibers provides a maximal vector of tissue force parallel to the longitudinal muscle fibers. Tendons are exceptionally strong for transmitting forces, yet are designed to glide easily. Microscopic analysis of the tendon reveals it to be composed of very few tendon cells (tenocytes) and even fewer synovial cells and fibroblasts. There is an abundance of intercellular tissue matrix, mainly type I collagen with small amounts of types III and IV collagen and elastin. The endotenon encloses tendon bundles and is continuous with the perimysium proximally and the periosteum distally. If the tendon is within a synovial sheath, the outer layer of the tendon is called the epitenon, which is vascular and cellular, although the intrasynovial tendon has avascular watershed areas or zones. Early observation of the relative lack of cells and the avascular zones led to the erroneous conclusion that tendons did not have within them the intrinsic capability for repair and needed extrinsic adhesions for healing. Both endotenon and epitenon cells can bridge the tendon gap. If the tendon is outside the sheath (extrasynovial), then the outer, loose, circumferential areolar adventitial layer is called the paratenon, through which blood vessels run longitudinally. Tendons vary both in size and shape from one to another as well as within an individual tendon. The flexor tendons of the wrist, flexor carpi radialis (FCR) and flexor carpi ulnaris (FCU), are strong and thick, while the flexor pollicis longus (FPL) has a distal muscle belly. The flexor tendons of the fingers are arranged into three layers as they approach the carpal tunnel from the distal wrist. The flexor digitorum superficialis (FDS) tendons to the middle and ring fingers are most superficial; deeper are the superficialis tendons of the index and small fingers. The deepest layer is composed of the FPL and the four flexor digitorum profundi (FDP) tendons to the index, middle, ring, and small fingers, which are derived from a common muscle belly. The greatest variability is seen in the FDS to the small finger with deficiency or absence. There is often a tendon slip from the FDP of the index to the FPL, which may require excision to prevent postsurgical complications. At the base of the fingers, the superficialis tendons divide, allowing the deeper profundi tendons to pass through them to become volar or superficial to the FDS (Fig. 82.1). Each of the two slips of the penetrated FDS cross under the FDP, rotate 180 degrees, and rejoin at the Camper chiasm, and insert on the middle phalanx as the prime flexor of the proximal interphalangeal (PIP) joint. The lumbrical muscles originate from the substance of the profundi tendons in the hand, passing palmar to the metacarpophalangeal (MCP) joint and then dorsal to the interphalangeal (IP) joints, inserting into the extensor mechanism at the level of the proximal phalanx. Lumbrical muscle contraction thereby produces flexion at the MCP with simultaneous extension at the IP joints.

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from the A1 pulley to the IP joint. Zone T III is in the thenar eminence. Zones T IV and T V are the same as for fingers.

Digital Fibro-osseous Sheath Zone I

The fibro-osseous sheath is a synovial-lined canal that originates from the periosteum and encloses the flexor tendons in the digits. The sheath is a multilayered double-walled covering. The synovial lubricating fluid is rich in hyaluronate and protein, which contributes to the nutrition of the tendon through imbibition as well as providing lubrication for gliding. It extends from the distal palmar crease to just beyond the distal interphalangeal (DIP) joint. Doyle and Blythe described the pulley system in detail, as there are thickenings of the sheath that act as a biomechanically essential restraining pulley system to keep the tendons tight to the bones regardless of the position of the fingers or wrist. The pulley system maintains a constant moment arm of force and prevents bowstringing. The average excursion is 1.5 mm per 10 degrees of flexion. There are five annular (A) pulleys and three thinner, collapsible crisscross cruciate (C) pulleys (Fig. 82.3). The thumb has two annular pulleys (at the proximal and distal phalanx) and an oblique pulley between them that is important and needs to be preserved. There is also a palmar aponeurosis pulley from the palmar fascia proximal to the A-1 pulley in the palm. The A-1 pulley is the most common site for stenosing tenosynovitis to occur, resulting in a trigger finger. The essential A-2 pulley is found at the proximal portion of the proximal phalanx, and the other essential A-4 pulley is at the middle portion of the middle phalanx. These are the two pulleys that should be preserved to prevent flexor tendon bowstringing.

Zone II Zone T I Zone T II

Zone III

Zone T III Zone IV

Zone T IV

Zone T V

Zone V

FIGURE 82.1. The vincular mesentery system. (Reproduced by permission of The Foundation for Hand Research, Inc.)

Clinical Tendon Zones

TENDON HEALING

Verdan described five flexor tendon zones in the hand based on anatomic factors influencing the prognosis of repairs (Fig. 82.2). Zone I lies distal to the insertion of the FDS and contains only the profundus. Zone II begins at the proximal portion of the flexor tendon sheath A1 pulley and extends to the FDS insertion; it corresponds to Bunnell’s “no man’s land.” Zone III is between the distal palmar crease distally and the distal margin of the carpal tunnel proximally. Zone IV is within the carpal tunnel, where the median nerve and nine flexor tendons are in intimate relation. Injury there almost always includes the median nerve and, being amid fixed fibrous structures, it is in a difficult zone for successful repairs. Zone V is proximal to the carpal tunnel in the distal forearm. In the thumb, Zone T I is distal to the IP joint. Zone T II is over the proximal phalanx

It is now established that tendons have intrinsic healing capability provided that adequate blood supply and nutrition are present. Within the tendon sheath, the blood supply runs through the “mesotenon” to form a vascular mesentery called a vincula (Fig. 82.1). There are two vincula to each FDS and FDP. Their origin is the digital vessels, which join in a four-step ladderlike plexus. Between the vinculum are relative avascular watershed zones. Retraction of a disrupted flexor tendon may avulse its vincular blood supply. Synovial fluid, as well as extracellular tissue fluid, has also been shown to contribute to tendon nutrition. This filtrate of plasma, similar to joint fluid and rich in hyaluronate and protein, bathes the tendons within

A-5 A-4 A-3 A-2

C-3

C-2

C-1

A-1

FIGURE 82.2. Zones of the hand. Note the relationship to underlying structures.


Chapter 82: Tendon Healing and Flexor Tendon Surgery

Vinculum Longum

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FDP

FDS

Vincula Brevis

FIGURE 82.3. Flexor tendon sheath pulley system.

the digital tendon sheath to preserve vitality and contribute to repair. Repair of the tendon sheath when feasible has been advocated to not only aid in healing, but to preserve gliding and prevent catching of the tendon. Extrasynovial tendons receive their blood supply via randomly arranged small vessels from the peritendinous soft tissue and this vascular supply may also be diminished by injury. Severed tendons become united or cemented together by macromolecules of collagen commonly known as scar. The healing process is divided into three overlapping phases. The first is the exudative or inflammatory phase, which is initiated immediately after injury. All cut surfaces, whether tendons or other structures, are flooded with exudate and debriding macrophages. This gives way on about the fifth day to the second phase of fibroplasia, or the proliferative phase, during which macromolecules of collagen are extruded at random into the exudate from fibroblast migration. This “common wound,” described by Littler and Peacock, has the elements of healing distributed over all injured surfaces. The third remodeling phase of wound healing begins 3 to 6 weeks after injury and is one of differentiation and maturation of the common scar and last for months. Adhesions, which are byproducts of fibroplastic proliferation and collagen formation from extrinsic cellular activity, need to be minimized for gliding to occur. As all parts of a wound are initially cemented together equally, tendons that adhere to mobile soft tissue will move with those tissues. When healing firmly unites the repaired tendon to fixed structures, favorable remodeling is precluded. Thus, the functional recovery of a repaired tendon is substantially determined by the mobility or rigidity of those tissues in contact with the site of tendon repair. The strength and size of a tendon repair and its

vascularity can be increased with exercise and motion and diminished with immobilization. Appropriately stressed tendons heal faster, have fewer adhesions, better excursion, and increase tensile strength faster than unstressed tendons. Repair strength decreases (10% to 50%) between days 5 and 21, although it might not decrease significantly in appropriately stressed repairs. Hence, appropriate early active mobilization can improve results. The exact balance between intrinsic and extrinsic healing and subsequent strength and motion is still being studied.

DIAGNOSIS OF FLEXOR TENDON INJURIES A careful history allows an appreciation of the mechanism of injury and guides the subsequent examination. It is assumed that every structure in the area of injury has been damaged and each should be methodically evaluated. The location and size of the wound often define the extent of the injury. Noting the disruption of the normal flexion cascade posture of the resting fingers by a single extended finger, in conjunction with an appropriately located wound, makes the diagnosis of a finger flexor tendon injury virtually certain (Fig. 82.4). Asking the patient if pulsating blood flow occurred following a digital laceration with impaired sensation will aid in the diagnosis of a concomitant neurovascular injury. The flexor tendons move proximally as the finger is flexed. If the finger is examined in extension but was injured while flexed, the cut tendon will be found more distal than the skin wound (Fig. 82.5).

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A,B

C FIGURE 82.4. A: Note the small laceration at the base of the small finger proximal phalanx and the posture of the fingers. B: Note the complete profundus tendon laceration with the proximal tendon edge out of the Camper chiasm. C: The repair is under the A-4 pulley.

Profundus and superficialis tendons are tested individually. Isolated superficialis function is tested by preventing profundus action by holding the distal interphalangeal finger joints fully extended for all fingers except the one being tested. With a common muscle belly supplying all four of the flexor digitorum profundi, blocking DIP joint flexion nullifies FDP flexion of the finger being examined. If strong PIP joint flexion is observed, it can only be the result of an intact, functionally independent FDS. Full, active flexion of the DIP joint can only result from an intact FDP. In the absence of an open wound, failure of digital flexion may be a result of either tendon rupture or nerve palsy. Often the differentiation can be made by placing pressure on the flexor muscle mass in the patient’s forearm and observing for passive digital flexion, which will occur if the tendon is intact or with a tenodesis maneuver. Specific muscle electrical stimulation is also useful in clarifying the differential diagnosis of nerve versus tendon injuries. Partial flexor tendon severance is suspected when there is a corresponding wound with weakness of tendon pull, limited motion, and/or pain produced by the effort. These are often treated conservatively with early mobilization. If rupture occurs, prompt repair is indicated. Tendon ruptures may occur at the insertion on the bone or musculotendinous junction, or occasionally at a diseased ten-

A-2

don’s midsubstance in conditions such as rheumatoid arthritis, fractures, gout, infection, steroid injection, or just “spontaneous” rupture. Tendon avulsion injuries, usually of the FDP and most frequently of the ring finger, result from forced extension while the profundus is being maximally contracted. It may have an associated bony avulsion fracture fragment seen on radiographs and may even retract into the palm. Prompt repair usually has a good prognosis in contrast to secondary repairs.

SURGICAL RECONSTRUCTION OF FLEXOR TENDON CONTINUITY The repair of flexor tendons can be classified as primary, delayed primary, or secondary (early and late). “Primary” indicates repair is performed within 24 hours after injury. Contraindications to primary repair are high-grade contaminations, such as human bites and infection. “Delayed primary” repair is done from 1 to 14 days after injury while the wound can still be pulled open without an incision. A child may have a little more leeway in terms of timing to repair, but presents compliance obstacles. “Early secondary” repairs are performed between 2 and 5 weeks. “Late secondary” repairs are performed

A-4

FIGURE 82.5. Note that the position of the tendon relative to the skin creases is dependent on the posture of the finger. The fingertip moves toward the palm with the tendon force vectors both distal (at DIP) and proximal (at MCP). If the flexor tendons are severed while the finger is fully extended, the level of skin wounding and tendon severance will be the same. If injury occurs with the finger flexed, the tendon division will be distal to the skin wound.


Chapter 82: Tendon Healing and Flexor Tendon Surgery

5 weeks or more after injury and may require tendon substitution procedures rather than a direct repair. This may be a primary tendon graft, a two-stage procedure, a tendon transfer, free vascularized tendon transfer, or a salvage procedure, such as tenodesis (static or dynamic), capsulodesis, or arthrodesis. Repair of flexor tendons should be carried out only under ideal conditions. A failure of primary repair will always compromise the ultimate recovery. Creation of a clean, uncontaminated wound is mandatory. The wound is debrided under adequate anesthesia—regional or general—and with absolute visualization of structures to prevent iatrogenic injuries. A tourniquet is inflated 100 to 150 mm Hg greater than systolic blood pressure after exsanguination with an Esmarch elastic bandage to ensure a bloodless field. Extending the traumatic laceration to allow for adequate exposure requires a thoughtful respect for the lines of skin tension. These extensions may be either proximal or distal or both, in a zigzag or, preferably, a nondominant-side midaxial location, whenever possible. Basic principles include atraumatic technique, which minimizes the handling of the tendon to lessen scar and adhesion formation. Windowing of the intact flexor tendon sheath for tendon retrieval and repair should be performed between the annular pulleys of the sheath. Repair of the sheath, if possible, may help as a barrier against development of fixed adhesions and preserve essential biomechanics. Lister uses an L-shaped funnel incision at the cruciate pulleys for the window from which to retrieve the cut tendon ends. The flexor tendons may require retrieval if they retract away from the initial injury site. Multiple maneuvers using catheters, tendon retrievers, and even endoscopy and other instruments allow for tendon retrieval, preferably under direct vision and as atraumatically as possible. Using a metal probe with eyelet sutured proximally with a slipknot to the cut tendon end and bring it distal, using a thin sheet of silicone background material folded like a funnel to ease the tendon under pulleys. Other techniques include circumferential suturing of the proximal tendon to a cut, beveled small feeding tube or commercially available tendon retrieval kits are frequently used. The tendon ends need to be coapted without undo tension. Tension can be alleviated during the repair with a tendon approximator or by a “blocking technique” whereby a small needle is passed through the sheath and tendon proximal to the repair. Many suture techniques for flexor tendon repairs have been advocated, including the Bunnell, modified Kessler-Kirchmayr and Tajima, Tsuge, augmented Becker, modified Pennington, Pulvertaft, looped repairs of Lee, Lim, and Tsai, locked cruciate, and Sandow’s single cross-grasp fourstrand tenorrhaphy (Fig. 82.6). The significance of the number of sutures crossing the repair site or “core” sutures, the difference between locking, looping, and grasping sutures, and strength versus gap and resistance to gliding have been studied. Present recommendations include a running circumferential or epitenon suture in addition to the core sutures (Fig. 82.7). Strickland advocates four strands of core sutures. A 3-0 or 4-0 synthetic, nonabsorbable braided polyester or polyfilament material is used, placed dorsal. The running circumferential suture of 6-0 Prolene can be simple, locking, or in¨ or verting mattress, or a crisscross locking stitch, Silfverskiold, other variation, depending on the circumstances. The running circumferential suture greatly increases the strength of repair. The tendon should be free of entrapped soft tissue and should be seen to be freely gliding. If other injuries are noted, these are repaired in a logical manner; that is, volar plate first, neurovascular bundles last. The repair of partial tendon lacerations has been controversial. If less than 25% of tendon substance has been injured, repair may not be needed. Usually a single suture repair of laceration

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A

B

C

D FIGURE 82.6. A: Kessler suture, (B) Bunnell suture, (C) modified Kessler suture, and (D) Pulvertaft (weave suture results in a very strong juncture, but is not suitable for use within the flexor tendon sheath because of its bulk).

is performed for a smoother surface. A dorsal extension blocking splint is applied for protection during the initial phases of healing.

Author’s Preferred Method of Tendon Repair If the tendon ends are in close, tension-free approximation, then the back wall is repaired using a 6-0 epitenon suture of ¨ technique. at least 2 mm in a simple locking or Silfverskiold Next, two to four, double-loop, locked, longitudinal core sutures are placed dorsally and as peripheral as possible (Arthrex looped FiberWire when available, otherwise Supramid). If the ends of the tendons are significantly separated, the core sutures are placed in one tendon first without the epitenon and the tendon is retrieved. The running circumferential epitenon suture ¨ Chinese finger-trap manner. The is finished in the Silfverskiold repair is examined so as to be free from trapped tissue and able to glide under the pulleys.

POSTOPERATIVE THERAPY Many factors are involved in postoperative therapy considerations, including age, extent of injury, number of tendons involved, location, concomitant injuries, swelling, motivation and number of core sutures. There has been a steady trend toward early controlled active motion following tendon repair. This appears to facilitate strengthening of the repair, provided it does not exceed the critical rupture force. Many factors are involved in the calculation of bursting strength such as edema formation and bulk of repair, making the friction coefficient difficult to calculate. The

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A

B

C

D FIGURE 82.7. Author’s preferred method for tendon repair: A: The back wall is sutured first with ¨ or cross-locking 6-0. B: 3-0 or 4-0, Silfverskiold looped if available. Arthrex or supramid, is first placed from the inside and then brought back along the periphery. C: 4-core sutures (or 8 if looped) lock¨ ing are placed and tied in the center. D: Silfverskiold finishes repair.

presently estimated average tensile strength needed for passive motion without resistance on a normal flexor tendon is 500 g; light grip is 1,500 g; and strong grip is 5,000 g. There are several postoperative therapy splinting protocols, including the Duran and the Kleinert rubber-band traction, the Brooke Army palmar-bar modification, the Mayo Clinic synergistic wrist splint, Evan’s short arc motion, and the Strickland hinged wrist splint and active tenodesis. The relationship of tendon excursion with respect to tendon and joint motion and finger position helped determine aspects of these protocols. Wehbe and Hunter et al. showed the three finger positions for maximal differential gliding of FDP to FDS to minimize adhesions. Increasing wrist motion with tenodesis is also considered. However, standard protocols employ a dorsal shell with the wrist, MCPs, and IPs flexed. Active extension (to prevent PIP contracture) and passive flexion are encouraged after the first postoperative day, when bleeding should not be provoked. After 2 to 3 weeks, “place and hold no power” can be initiated along with protected passive motion to maintain joint mobility and avoid contractures especially the PIP joint. Differential gliding of the uninjured tendons can also start at that time with wrist tenodesis and “suitcase” power fist. Isolated active tendon differential gliding of the injured tendon begins by at least 4 to 6 weeks and active, assisted, complete fist and passive range of motion. Protective splinting may continue with progressive resistance exercises for up to 8 weeks total, with gradually increased active resistance-strengthening exercises up to 12 weeks. To evaluate results, Boyes’ method of “fingertip to distal palmar crease” can be used. To standardize and compare results, the Strickland classification based on total active motion (TAM) can be used. The formula is Strickland’s Adjusted System: (PIP + DIP) flexion − extension deficit × 100/175 degrees = %normal Excellent 75−100% Good 50−74 Fair 25−49 Poor 20% reduction in CMAP amplitude. Treatment in the early stages may involve changing the patient’s sleeping posture. An acutely flexed elbow can cause symptoms. A simple static elbow extension splint usually breaks such a habit. Direct trauma activities such as resting the arm on the elbow while taking telephone calls may also produce symptoms. However, chronic cases and those with documented axonal damage and muscle atrophy are helped only by appropriate surgery, which includes transposition of the nerve anterior to the axis of rotation of the elbow so that elbow flexion relaxes rather than stretches the nerve. Simple unroofing of the cubital tunnel does not deal with the problem of nerve adhesions. Subcutaneous transpositions leave the nerve superficial and subject to trauma and painful subluxation across the medial epicondyle. Efforts to prevent the latter by suturing a strip of fascia from the PT muscles across the transposed ulnar nerve should be avoided because of an unacceptably high rate of complications. By far, the best operation for cubital tunnel syndrome is a submuscular anterior transposition, carefully dissecting along physiologic planes and avoiding injury to the medial antebrachial cutaneous nerve to the forearm. The most common failure of this operation is a result of kinking of the ulnar nerve as it enters the forearm distal to the medial epicondyle because of inadequate distal mobilization. Although it is undesirable to inject nerves already in trouble, the procedure can be performed with local infiltration anesthetics, if general anesthesia is medically contraindicated. For all cases, the rate and the degree of recovery of liberated ulnar nerves are substantially less predictable than for the median or radial nerves.

Radial Compression Neuropathies The radial nerve, unlike both median and ulnar nerves, has no anatomic arrangement at the wrist level that predisposes to its entrapment. It has three areas where it is vulnerable to inflammatory or compression pathology: (a) the entire radial nerve in the proximal forearm, (b) the posterior interosseous division at the proximal margin of the supinator muscle, and


Chapter 86: Compression Neuropathies in the Upper Limb and Electrophysiologic Studies

(c) the superficial sensory branch as it emerges from beneath the brachioradialis muscle to become subcutaneous in the midforearm.

Proximal Radial Nerve Compressions Radial nerve compressions at the elbow have been reported, purportedly caused by a fibrous band from the shaft of the humerus that crosses the nerve to the lateral epicondyle. If this entity exists, it is exceedingly rare. Radial neuropathies at the elbow or distally will have no disturbance of the radial wrist extensor muscles (extensor carpi radialis brevis [ECRB] and extensor carpi radialis longus [ECRL]) as their motor nerves separate from the radial nerve proximal to the elbow. However, thickening of the radial nerve epineurium as a result of inflammation will be encountered and will disturb function of the superficial sensory branch of the nerve, the posterior interosseous (PI) motor division to the digital extensor muscles, or both. Radial nerve pathology in this area has been referred to as “radial tunnel syndrome,” but this is a misnomer as there are no structures resembling walls of a tunnel, only soft muscle tissues adjacent to the nerves. Just distal to the elbow the radial nerve is regularly crossed by several large veins, the “leash of Henry,” but these do not appear to compress the nerve. Symptoms typically have an insidious onset with soreness of proximal–lateral forearm muscles. If only the superficial sensory division of the nerve is involved, symptoms are mild with some paresthesia or numbness on the dorsal–lateral aspects of the hand. If pain radiating to the neck and shoulder is severe and there is a profound sense of “heaviness” of the arm, the PI division of the nerve is involved, as is discussed subsequently. With only moderate symptoms limited to the superficial (sensory) division of the nerve, a trial of systemic steroids and rest of the arm usually is considered. Spontaneous remission has been reported. Only rarely will symptoms, limited to the sensory branch of the radial nerve alone, be progressive, severe, or recalcitrant enough to indicate surgical decompression.

Posterior Interosseous Nerve Compressions Two varieties of pathology of the PI nerve are encountered. The rare one is a spontaneous onset of weakness of the digital extensor muscles innervated by the nerve. Unlike the anterior interosseous nerve, rarely is there a documented history of trauma to the proximal forearm. Resisted passive flexion of the middle finger usually aggravates discomfort and, because the nerve is primarily motor, an EDS usually documents the diagnosis. Because spontaneous recovery for mild cases of PI neuritis are not infrequent, a few weeks of observation is warranted, but severely symptomatic or protracted cases need surgical decompression. Unfortunately the rate or degree of recovery is relatively unpredictable and subsequent tendon transfers often are needed. The more common variety of PI compression also occurs spontaneously but is characterized by persistent and severe pain from the forearm radiating into the neck and shoulder, despite our being taught that this is a “motor” nerve. Profound heaviness of the arm is so frequent a complaint that one author (RWB) once wrote about it under the title “The Heavy Arm Syndrome.” If the patient turns in sleep to the involved side, the patient will awaken. Maximum tenderness is in the proximal forearm, about 5 to 6 cm distal to the elbow skin crease where the PI nerve passes beneath the fibrous proximal margin of the supinator muscle. Digital pressure intensifies the radiating pain dramatically. The same is true for active supination of the forearm while it is being passively held in pronation. The majority of cases have no sensory disturbance in the distribution of the superficial branch of the radial nerve, but occasion-

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ally inflammation will “spill over” causing mild disturbance. The diagnosis is basically from careful, and often serial, evaluations. EDS are of little help although occasionally increased polyphasic patterns are found in the extensor indicis proprius (EIP) muscle to which terminal branches of the PI nerve distribute. Spontaneous remission may occur when symptoms are minor but usually only after many months of misery. In the majority of cases, there has been an extended failure of diagnosis. These cases need surgical decompression, which has little risk, very low morbidity, and is typically followed by prompt relief from the pain. The incision is made directly over the radial nerve starting 2 cm distal to the elbow crease. It is carried through the subcutaneous tissues with as little damage to cutaneous nerves as possible. After opening the fascia of the “extensor mobile wad” muscles (ECRB, ECRL, and brachioradialis [BR]), passive extension and flexion of the wrist will enable one to identify the physiologic plane between the BR and the radial wrist extensor muscles. In this plane, the tissues can be atraumatically separated and the superficial branch of the radial nerve readily visualized. A careful external neurolysis is performed. Proximally a careful microneurolysis is done along the branches of the PI nerve, which pass deep to the proximal margin of the supinator muscle. No gross pathology will be seen, although the tissues being separated have a “tacky” resistance. Because the pathology is under the fibrous proximal margin of the supinator muscle, it is not seen until that sling is severed longitudinally. Even then the pathology is usually only a subtle reduction in nerve size, but generally the operation is followed by immediate and dramatic relief of even chronic pain.

Wartenberg Syndrome The superficial (sensory) branch of the radial nerve passes distally in the forearm beneath the BR muscle to the midforearm where it turns laterally into the subcutaneous tissues along the distal radius. At the point of exit from beneath the muscle, a compression of the nerve can develop, causing local pain and sensory disturbance to the dorsal–lateral skin of the hand. This condition is referred to as Wartenberg syndrome and does not develop spontaneously, but is an infrequent complication of trauma to the midforearm. The diagnosis is made by history, the finding of a strong Tinel sign at the point of exit of the nerve from beneath the BR muscle, and sensory disturbance in the nerve’s distribution. As the BR is a supinator muscle, pain is accentuated by attempting this motion while the forearm is passively pronated. Treatment is through a short incision at the site of entrapment indicated by the Tinel sign. The nerve is carefully protected and the fibrous margin of the BR muscle is transected several times at 1-cm intervals to relieve all tension. The prognosis is excellent.

Thoracic Outlet Syndrome Thoracic outlet syndrome (TOS) refers to neurologic or vascular disorders that occur where divisions of the brachial plexus and the subclavian artery pass from the neck into the arms through the interscalene triangle. The sides of the triangle are anterior and medial scalene muscles and the first rib. Many respected authorities question even the existence of this syndrome, and if it is a reality, it is so extremely rare as to dictate extreme caution in entertaining the diagnosis. The typical suspect for the condition is an obese, lethargic woman with heavy pendulous breasts, poor posture, and emotional or psychiatric issues. The neurologic symptoms are ill-defined and inconsistent, except they tend to be of the lower roots (ulnar nerve) of the brachial plexus. Patients will complain of having the greatest distress with activities in which the arms are overhead. Some will have a cervical rib, but this is


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not pathognomonic of the alleged syndrome. Nor is an abnormal arteriogram pathognomonic. EDS data from most cases fall within the average ranges. The diagnosis of TOS so precarious that a conservative attitude about treatment should be maintained. Efforts should be directed toward weight reduction, general fitness, and posture

correction. Reduction mammoplasty should also be considered. In the rare case for which surgical treatment is warranted, transaxillary first rib resection is the method of choice. Unfortunately, far too many patients are seen who have undergone multiple procedures for a diagnosis of TOS only to be progressively more symptomatic after each procedure.


CHAPTER 87 ■ THUMB RECONSTRUCTION CHARLES J. EATON

Efforts to restore the structure, function, and appearance of the thumb span the history of hand surgery (1). Staged, pedicled toe-to-thumb transfer without microvascular anastomosis, now only of historical interest, was performed by Nicoladoni in 1898. Forms of phalangization, osteoplastic reconstruction, pollicization, and pedicled digital transfers date back 100 years. Digital neurovascular island flaps and free toe transfers, developed 50 and 40 years ago, respectively, are established techniques now in common use.

INDICATIONS Loss of thumb function impairs the entire upper limb, and carries a high priority for reconstruction. Despite this, some patients accommodate well to thumb amputation, and therefore reconstruction is indicated for selected cases. Even a replanted thumb, which would appear to be the best possible reconstruction, is not always more functional than an amputation properly revised at the same level (2). Thumb reconstruction is technically demanding, and patient motivation and accommodation are critical factors for good outcome. Strong contraindications to elective thumb reconstruction include significant vascular disease, short life expectancy, chronic pain with disuse of the limb, unreconstructable sensory loss, unrealistic patient expectations, and other contraindications dictated by the common sense of the surgeon.

EVALUATION Because the key functions of the thumb are always in relation to the rest of the hand, thumb reconstruction is considered in the context of the entire hand. As with any digital injury, initial evaluation includes an assessment of soft tissue deficits, bone loss, condition of joints, the nail bed, zone of tendon injuries, and neurologic status. In addition, the following points relevant to thumb reconstruction are considered: 1. What is the status of the basal joint? The thumb carpometacarpal joint is evaluated clinically and radiographically. An injured, stiff, or painful basal joint is a poor foundation for a new thumb, but salvage by arthroplasty may be a possibility (Fig. 87.1). 2. Is there a first web space contracture or skin deficit? Web space contracture may be a result of unappreciated skin loss, scar contractures, abductor muscle destruction or paralysis, basal joint pathology, adductor/flexor muscle contracture, or a combination of the above. Preliminary correction of such contractures should be considered (Fig. 87.2), recognizing that first web space contractures often cannot be fully corrected, even with determined surgical efforts.

3. Are there problems with the remaining digits? Optimum length, mobility, and position of the thumb are all judged in relation to the remaining fingers. A stiff reconstructed thumb may not make useful contact with stiff, short, or insensate fingers. On the other hand, a damaged and otherwise useless finger may be suitable for transfer either as a free transfer (Fig. 87.3), pollicization (Fig. 87.4), or an on-top plasty thumb lengthening (Fig. 87.5). 4. Has the patient developed maladaptive patterns of use? Heroic efforts at thumb reconstruction will be unrewarding if the patient has developed a fixed pattern of not using remaining parts of the mutilated hand. This tendency to become functionally “one-handed” is particularly frequent if the situation is long standing or has been complicated by chronic pain. 5. Do the patient’s complaints match the apparent deficit? Patients with thumb amputation may have less obvious impairments contributing to the restricted use of the hand. Crush/avulsion injuries may result in a wide zone of deep scarring, with prolonged stiffness, swelling, intrinsic tightness and swelling, and compression neuropathies. 6. What are the patient’s expectations? Although thumb function is the primary reconstructive goal, concerns about social presentation and aesthetics may be equally important. A technical triumph to the surgeon may be seen as a grotesque deformity by the patient. Photographs of other reconstructed thumbs may help some patients understand what is being recommended, but even this must be done carefully to avoid creating false expectations. If it appears that a patient is likely to be disappointed with the result and especially the appearance of a reconstructed thumb, a lifelike prosthesis, which involves no irreversible procedures, may be the best recommendation if technically feasible (see Chapter 93).

TYPES OF DEFICIENCIES Thumb deficiencies are considered as either amputation or component loss (Fig. 87.6). Component loss includes soft tissue coverage or segmental loss of neurovascular, tendon, or skeletal components. Reconstruction may be either emergency (possible replantation), urgent (fresh open wound), subacute (unhealed wounds), or elective (healed wounds). Timing of reconstruction is important. The likelihood of septic or flap-threatening complications are greatest when surgery is performed in the subacute healing period (3). As with any extremity injury, reconstructive priorities are first healing (blood supply, stable skeleton, mobile soft-tissue cover) and then function (nerve function, passive range of motion, active range of motion).


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A

B

FIGURE 87.1. The most common salvage procedures for unreconstructable joint injuries are arthrodeses. A: Interphalangeal arthrodesis. B: Metacarpophalangeal arthrodesis. C: Soft-tissue arthroplasty of the carpometacarpal joint.

C

Component Losses Skeletal injuries are managed by anatomic reduction and fixation. Nonreconstructible injuries of the interphalangeal or metacarpophalangeal joints are treated with arthrodesis, but carpometacarpal injuries are best salvaged with soft-tissue arthroplasty (Fig. 87.1). Soft-tissue loss of the thumb is managed as for other digits, with skin grafts or flaps as indicated by the particular defect. Composite loss of soft tissue and skeletal

A

B FIGURE 87.2. First web space contracture release with reverse pedicled posterior interosseous artery island flap. A: Defect and flap design. B: After flap insert.

elements requires urgent soft-tissue cover with skeletal stabilization and possible bone grafting. As with any mangling limb injury, the best time to proceed with completion of amputation is at the first operation. Reconstructing component loss requires an appropriate flap. Because sensory perception is key to effective use of the thumb, innervated flaps are much preferred for contact area resurfacing, but their availability is limited. Innervated flaps appropriate for the thumb include the Moberg palmar advancement flap, the Holevich first dorsal metacarpal flap from the index finger, heterodigital neurovascular sensory “island” flaps, and free finger or toe pulp flaps (Figs. 87.3, 87.7, and 87.8). Standard local digital flaps may be used as well, including V-Y advancements, dorsal transposition, and dorsal or volar cross-finger flaps. Noninnervated regional flaps, such as posterior interosseous (Fig. 87.2), radial forearm (Fig. 87.9), and intrinsic muscle flaps (Fig. 87.10), are appropriate for complex proximal and web space defects. Choice of the specific flap depends on the size, location, and orientation of the defect, condition of donor sites, and the surgeon’s experience. Table 87.1 lists my preferences for flap coverage of thumb defects. Unique pitfalls in the management of degloving or circumferential soft-tissue loss deserve special mention. If circumferential soft-tissue loss extends proximal to the base of the proximal phalanx, the distal phalanx will eventually be lost to avascular necrosis despite flap cover, and primary interphalangeal disarticulation should be considered. Denuded skeleton should be covered in a tubed or closed flap (Fig. 87.9), not buried in a pocket. Planning the flap with a thin template may be misleading: The flap must be designed wide enough to allow for the thickness of the flap itself, and also to allow for flap swelling.

Amputation Whenever possible, replantation should be considered for thumb amputation.


Chapter 87: Thumb Reconstruction

A

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B

FIGURE 87.3. Emergency thumb pulp resurfacing with free pulp flap harvested from a ring finger amputated in the same accident. A: Initial injury with amputated ring finger and loss of thumb soft tissue. B: Tissue harvested from amputated part. C: Thumb after flap transfer.

C

Amputation Distal to the Metacarpophalangeal Joint If there is a functional remnant of the proximal phalanx (Fig. 87.6), primary reconstructive goals are length, stability, and adequate web space (Fig. 87.11). Choices include bone graft with a local flap, osteoplastic reconstruction, phalangization, distraction lengthening, pedicled transfer of a damaged finger remnant to the thumb, or toe-to-thumb transfer (Figs. 87.4 and 87.12 to 87.15).

ESTABLISHED THUMB RECONSTRUCTION PROCEDURES Many procedures for thumb reconstruction have been described. Table 87.2 summarizes the preferred procedure in various circumstances.

Osteoplastic Thumb Reconstruction Amputation Proximal to the Metacarpophalangeal Joint When the level of amputation is at or proximal to the metacarpophalangeal joint, the thumb ray does not project beyond the web space skin. Functionally, this is a complete thumb amputation, but there is the potential for functional reconstruction pivoting (literally) on having a good basal joint with sufficient metacarpal length and thenar muscle to control it (Fig. 87.6). Options when loss is through the distal metacarpal include osteoplastic reconstruction, pedicled finger remnant transfer, pollicization, and free toe transfer. A proximal metacarpal amputation retains the basal joint but has no intrinsic muscles. With this or an amputation including the basal joint, there are two options: (a) if the fingers are functioning well, provide a stable, static post to oppose the fingers, or (b) full-finger pollicization.

Best Indication/Unique Advantages Partial or distal subtotal amputation may necessitate this procedure. No digit is sacrificed.

Disadvantages and Special Requirements Multiple staged procedures may be required. Results may be unaesthetic: can be bulky, floppy, and without a thumb nail. Additional neurovascular flap is required for sensibility.

Technique Osteoplastic reconstruction involves the combination of a bone graft and flap to lengthen the thumb remnant (Fig. 87.14). It typically involves three procedures: lengthening the skeleton with an iliac crest bone graft covered in a tubed distant flap; flap


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Amputation

Component Loss

Partial Complete Distal Subtotal

Proximal Subtotal Total FIGURE 87.6. Level of thumb loss. Thumb defects are classified as either component loss or amputation. Amputations are grouped as partial or complete, and complete amputations can be identified as distal subtotal (retaining the entire metacarpal), proximal subtotal (retaining basal joint but not thenar muscles), and total, with loss of the basal joint.

FIGURE 87.4. Pedicled digital transfer to the thumb position. A: Total reconstruction of the thumb may be achieved with pollicization of the index finger, which provides the thenar muscle replacements in addition to the entire thumb skeletal ray. B: Pedicled transfer of a previously damaged or amputated digit (on-top plasty) may be used to lengthen a partial or distal subtotal thumb amputation.

pedicle division; and transfer of a neurovascular sensory island flap from the ulnar side of the middle finger to the thumb’s pinch contact surface. Additional debulking flap revisions are usually required. There are many donor-site variations, including reversed pedicled forearm flaps (radial or posterior interosseous), primary neurovascular island transfer, and combinations with dorsal hand flaps. A variety of free tissue transfers may be used, including the excellent “wraparound” toe transfer, which is discussed below (see Wraparound Toe Transfer) (4).

C

A,B FIGURE 87.5. On-top plasty damaged middle finger remnant is transferred to the thumb, combined with a ray resection. A: Initial appearance of the hand. B: Mobilization of remaining middle finger. C: Final result with long thenal thumb and middle finger ray resection.



Cross Finger A

B

First Dorsal Metacarpal

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C

Neurovascular Island

Free Toe Pulp Palmar Advancement D

E

FIGURE 87.7. Sensory flaps for thumb reconstruction. Innervated flaps applicable to the thumb include (A and B) dorsal flaps from the index finger, including branches of the superficial radial nerve, (C) digital neurovascular island transfer, (D) Moberg palmar advancement, and (E) free neurovascular toe pulp flaps.

A

B

C

D FIGURE 87.8. Holevich flap. The dorsal index finger skin may be mobilized on a narrow skin or subcutaneous pedicle for transfer to the thumb. This flap has been used to resurface the distal half of the palmar skin, including the entire pulp surface. A: Defect of thumb pulp. B: Transfer of flap from index finger. C: Palmar view of result. D: Dorsal lateral view of result.


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ticularly if the web is converted to a cleft by an aggressive Z-plasty.

Technique

FIGURE 87.9. Circumferential thumb resurfacing with contralateral free radial forearm flap.

This is a web-deepening procedure, results of which are so often disappointing that it is rarely a good recommendation in view of today’s alternatives (Fig. 87.12). To allow creation of the cleft, the adductor muscle insertion is detached and repositioned proximally, and the first web space is deepened with a Z-plasty. Correction of an associated first web space contracture may require stripping of the entire ulnar border of the first metacarpal and capsulotomy of the basal joint. The mechanical advantage of the adductor is progressively lessened with more proximal reattachment. If the index finger has been partially amputated or is too damaged to transfer for thumb lengthening, it should be resected to increase the web space.

Phalangization

Metacarpal Distraction Lengthening

Best Indication/Unique Advantages


Thumb lengthening by finger transfer is a possible consideration (rare) if the thumb is nearly long enough, such as base of proximal phalanx. Usually this is a single-stage operation.

Distal subtotal amputation (region of metacarpophalangeal [MCP] joint) is an indication for this procedure and there is little or no donor defect except scar.

Disadvantages and Special Requirements

Disadvantages and Special Requirements

Phalangization may not provide much functional improvement, and may result in a very unnatural appearance, par-

Only limited lengthening is possible, and absolute cooperation is required.

A B

D

C FIGURE 87.10. Thumb metacarpal resurfacing with a muscle flap. This complex wound was a complication of dialysis access surgery. After debridement and proximal row carpectomy, the abductor pollicis brevis muscle was disinserted and transposed dorsally to cover the exposed metacarpal and remaining carpus. A: Defect. B: Abductor pollicis brevis coverage of exposed bone. C: Radiograph showing proximal row carpectomy. D: Final result.


841


TA B L E 8 7 . 1 FLAP SELECTION FOR SOFT-TISSUE DEFECTS OF THE THUMB Site of defect requiring flap cover Location Dorsal or radial Palmar Ulnar Circumferential

Distal phalanx

Proximal phalanx

Both phalanges

Cross-finger from index Local thumb, First dorsal or middle cross-finger metacarpal Moberg palmar advancement, Local thumb, first Distant volar cross-finger from middle dorsal metacarpal Cross-finger from Local thumb Distant ring or small Regional or distant: radial forearm, pedicled groin, posterior interosseous, toe flap

Technique After osteotomy, the thumb’s metacarpal is slowly lengthened using progressive adjustments of an external fixator in the manner introduced by Ilizarov for the lower limbs (Fig. 87.15). The metacarpal is exposed through a longitudinal incision, and the fixator placed, a corticotomy made circumferentially and subperiosteally through the metacarpal shaft. Efforts are made to minimize medullary bone disruption. After 1 week, distraction is begun at a rate of 1 mm per day. If any proximal phalanx exists, the MCP joint will be progressively flexed unless stabilized with a strong Kirschner pin. In small children, new bone growth from the periosteum and medullary bone may adequately fill in the distraction gap, but interposition bone grafting is usually required for adults once maximum lengthening is achieved. Generally, this should incorporate MCP joint arthrodesis and removal of sesamoid bones. Once healed, more bone and soft-

tissue removal can result in a much more pleasing part, which also lends itself to prosthetic fitting if desired.

On-Top Plasty Best Indication/Unique Advantages Amputation in the area of the MCP joint is an indication for this procedure, which will enhance the value of a damaged finger.

Disadvantages and Special Requirements The appropriate finger is infrequently available, and this procedure narrows the palm. Transferred injured parts carry a higher risk of a complication.

C

A,B FIGURE 87.11. Thumb amputation through the interphalangeal joint treated with replantation and interphalangeal joint fusion. A: Amputated part. B: Replanted part. C: Functional result.


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A

B

Phalanglzation

Osteoplastic C

Distraction FIGURE 87.12. Thumb lengthening. Options for lengthening a partial or distal subtotal thumb amputation with the least donor-site morbidity include (A) osteoplastic reconstruction, (B) phalangization, and (C) metacarpal distraction lengthening.

Technique

Pollicization

On-top plasty refers to the neurovascular pedicle transfer of the distal segment of a damaged or partially amputated finger to lengthen the thumb (Figs. 87.4 and 87.5). If the metacarpal of the transformed finger is not needed, usually it is removed by ray resection. Preoperative arteriography may be helpful in planning for some patients.

The best indication is proximal subtotal or total amputation. This procedure is the only satisfactory means of basal joint reconstruction and results in extensive physiologic sensory restoration.


TA B L E 8 7 . 2 CHOICES OF TECHNIQUE FOR THUMB RECONSTRUCTION Partial

Distal subtotal

Isolated, acquired

Distraction Wraparound osteoplastic

Single mutilated finger Multiple mutilated fingers

Congenital—child

On-top plasty Distraction Osteoplastic Toe transfer Prosthesis Osteoplastic Distraction Distraction

Osteoplastic Distraction wraparound Great toe (adult) Second toe (child) On-top plasty Osteoplastic Toe transfer

Congenital—adult No transferrable digit

Prosthesis Osteoplastic

Cosmetic concerns Manual labor

Prosthesis Toe transfer Distraction Second toe transfer Prosthesis Osteoplastic

Proximal subtotal or complete Pollicization Skin flap, then second toe + metacarpal Pollicization Pollicization Skin flap, then second toe + metacarpal Prosthesis Pollicization Pollicization Second toe transfer Prosthesis Osteoplastic



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FIGURE 87.13. Toe transfer for thumb reconstruction. Many variations of toe transfer exist, but the most commonly used are the great toe, second toe, and wraparound toe transfers. a, Artery; e, extensor tendon; f, flexor tendon; n, nerve; v, vein.

Disadvantages and Special Requirements This procedure narrows the palm.

Technique Pollicization refers to the neurovascular pedicle movement of a finger, often with its metacarpal, for thumb reconstruction (Fig. 87.6). For congenital absence of the thumb, a simplified modification is recommended (4). The index finger is basically recessed by resection of a segment of the second metacarpal base, then pronated about 130 degrees and projected in palmar abduction at its fixed base. Incisions are planned to convert dorsal or palmar skin into a web between middle finger and the new thumb. The extensor tendons must always be shortened as part of the primary procedure. Flexor tendons, in contrast, follow a circuitous route, and length adjustments are performed secondarily if necessary. Structures receive new identities: The extensor digitorum communis becomes the abductor pollicis longus; the extensor indicis becomes the extensor pollicis longus; the first dorsal interosseous becomes the abductor pollicis brevis; the first palmar interosseous becomes the adductor pollicis; the metacarpal head and the proximal and middle phalanges become the trapezium and the metacarpal and proximal phalanges, respectively. For a proximal thumb amputation, with an intact basal joint, the proximal phalanx of a transferred index finger may be fused to the base of the remaining first metacarpal (5). Obviously, there are an infinite number of variations required for

individual circumstances, but common to all is preservation of intact nerves for critical sensibility, although in adults it has cortical mislocation. Secondary surgery will be needed for approximately 50% of patients undergoing pollicization, yet in the right circumstances and for the right indication, results will be superior to that of all other available alternatives.

Toe-to-Thumb Transfers Best Indication/Unique Advantages A toe-to-thumb transfer is performed when most of a wellcontrolled first metacarpal is present but length is needed. Advantages include (a) a good level of sensory recovery, (b) bone growth continues, and (c) that it is a single-stage operation.

Disadvantages and Special Requirements Foot disability may occur, and the thumb always looks like a toe.

Technique With the majority of toe-to-thumb transfers, a skin deficit on the hand is encountered. If the recipient site has skin grafts or tight scars, plans should be made for adequate soft tissue prior to the transfer operation (Figs. 87.13 and 87.16).


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A

B

C

D FIGURE 87.14. Osteoplastic thumb reconstruction. Partial amputation, lengthened with an iliac crest bone graft wrapped in a tubed pedicled inferior epigastric flap. After flap division, innervation is provided with a neurovascular sensory island flap transferred from the ring finger. A: Initial appearance. B: Tubed inferior epigastric flap. C: Sensory island flap D: Final result. (Case of R. W. Beasley.)

Preoperative arteriography of the hand and foot are generally recommended. Skeletal reconstruction for correct length is tailored to match the defect. Second toe transfers generally are favored for children, and great toe transfers are favored for adults (6), although there is no universal agreement about this, and there are individual considerations for each case. Toe-to-thumb operations can be performed by one or two teams. The level of toe osteotomy is a convenient reference point from which lengths of skin, tendons, nerves, and vessels may be measured. Recipient vessels in the hand are exposed first to verify their adequacy and to define the necessary donor pedicle length. The radial artery is preferred. Once satisfactory recipient vessels are isolated, foot dissection commences. A racquet-shaped incision is made, which gives more dorsal than plantar skin. Veins are dissected first, elevating thin skin flaps proximally and carefully freeing the venous pedicle up to the skin margin of the toe. Branches of the deep venous system are followed to the deep and variable arterial system. The dorsalis pedis and first dorsal metatarsal artery are dissected to the flap. The plantar digital nerves are small and short compared to those of the thumb, and intraneural dissection of the common digital nerve may be needed. Tendons are severed proximally to allow tendon repairs at a distance from vascular and skele-

tal work. Normal metatrarsophalangeal joint range of motion is hyperextended relative to the thumb metacarpophalangeal joint. If the metatarsophalangeal joint is included in the reconstruction, an oblique metatarsal osteotomy should be used to increase flexion for more natural thumb function. Although the reconstructed thumb is usually pronated, the degree is determined for each case to function best with remaining fingers. If opponensplasty is needed, it can be performed as a primary or secondary procedure. If the vascular pedicle crosses the wrist, a midlateral path is preferred to avoid tension from wrist motion, and end-to-side arterial anastomoses are preferred. Second toe donor sites can usually be closed primarily, and this is facilitated by resection of the second metatarsal. Great toe donor-site closure often requires a skin graft. Donor-site morbidity is small, but cannot be dismissed entirely (7).

Wraparound Toe Transfer Best Indication/Unique Advantages For amputation near the MCP joint or distal to it, this is the procedure of choice. It results in the most normal-appearing reconstruction from the foot.


845


A

B

FIGURE 87.15. Distraction lengthening. This patient had undergone a traumatic metacarpophalangeal level thumb amputation, covered in a groin flap, in addition to multilevel injuries of the wrist and all fingers. After metacarpal corticotomy, a distraction fixator was used to lengthen the metacarpal, followed by interpositional bone grafting. A: Distractor applied. B: After lengthening. C: Bone graft placement.

C

A

B FIGURE 87.16. Toe-to-thumb transfer. Modified wraparound great toe transfer for a degloving injury. A: Toe flap isolated. B: Final result.


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Part VIII: Hand

Disadvantages and Special Requirements This technically complex and demanding procedure results in limited functional improvement when used without an MCP joint. It requires an iliac bone graft.

narrow and thumblike reconstruction than is achieved with a great toe transfer, and the great toe length is almost fully preserved.

Technique

References

Wraparound toe transfer is a hybrid of great toe transfer and osteoplastic reconstruction (8) (Fig. 87.13). During harvest, the great toe is filleted, leaving on the foot the medial toe skin out to the tip and its skeleton to the base of the toenail. The isolated free flap for transfer to the hand includes the distal half of the distal phalanx with the plantar, lateral, and dorsal tissues, including the toenail. This complex is wrapped around a bone graft, which spans the gap between the remaining thumb skeleton and the distal phalanx of the transferred toe. The donor-site defect is closed with the medial toe flap, a cross-toe flap from the second toe, and a dorsal skin graft. The ultimate fingernail is narrowed by resection of the germinal matrix from each side. There are no tendon repairs. The typical end result is a more

1. Littler JW. On making a thumb: one hundred years of surgical effort. J Hand Surg. 1976;1:35. 2. Goldner RD, Howson MP, Nunley JA, et al. One hundred eleven thumb amputations: replantation vs. revision. Microsurgery. 1990;11:243. 3. Godina M. Early microsurgical reconstruction of complex trauma of the extremities. Plast Reconstr Surg. 1986;78:285. 4. Morrison WA, O’Brien BM, MacLeod AM. Thumb reconstruction with a free neurovascular wrap-around flap from the big toe. J Hand Surg. 1980;5:575. 5. Buck-Gramcko D. Thumb reconstruction by digital transposition. Orthop Clin North Am. 1977;8:329. 6. Stern PJ, Lister GD. Pollicization after traumatic amputation of the thumb. Clin Orthop. 1981;155:85. 7. May JW, Bartlett SP. Great toe-to-hand free tissue transfer for thumb reconstruction. Hand Clin. 1985;1:271. 8. Lipton HA, May JW, Simon SR. Preoperative and postoperative gait analyses of patients undergoing great toe-to-thumb transfer. J Hand Surg. 1987;12:66.


CHAPTER 88 ■ TENDON TRANSFERS ROBERT W. BEASLEY

Tendon or muscle transfers follow a basic concept of reconstructive surgery: Nothing new is created but functional parts, or those that can be made functional, are rearranged into the best possible working combination. Tendon transfers involve detachment of the tendon distally, mobilization without damage to the neurovascular pedicle, and rerouting it to a new distal attachment. In no area is a thorough knowledge of functional anatomy more essential. The procedures are among the most interesting, diversified, challenging, and rewarding of upper limb surgery. Littler (1) has given a brief but historic summary of the development of tendon transfer surgery and pointed out that the partially paralyzed limb offers a unique opportunity to gain a working knowledge of hand dynamics. In 1867, Duchenne used faradic current to study the physiology of motion, but it was only with World War I that real progress in clinical application was made. Classic contributions were made by Jones in England (1912), Meyer in Berlin (1916), and Steindler (1918) in America (5). Bunnell and others made refinements with the surge of interest attending World War II (1939–1945), but the landmark publication that set the standard was in 1949 by Littler (5), and it is still applicable today. Occasionally, a muscle proper rather than just the tendon may be transferred. An example is transfer of the abductor digiti minimi on an intact neurovascular pedicle for thumb opponensplasty (7). More recently this has been performed as free composite tissue transfers by microvascular technique.

BASIC TENETS The basic principles for all successful tendon transfers can be summarized as follows: 1. Tendon transfers involve the redistribution, not the creation, of new power units. Muscle power is transferred from less important to more important functions so as to improve the system overall. 2. Simplicity in mechanical design predisposes to good results, whereas complexity mitigates against them. More than one change of direction cannot be introduced into the system. 3. Even simple-appearing actions are the results of complex interaction of prime movers, antagonists, and numerous stabilizers (prime movers and antagonists in balanced opposition). Every joint between the muscle’s origin and new insertion must be stabilized, or with contraction, the system will buckle. When inadequate muscle is available for stabilization, joints of lesser importance require arthrodesis. 4. If any one of the three major nerves to the hand and forearm are lost, the potential for good reconstruction exists, but if two of the three nerves are lost, a major functional impairment is inevitable. Any worthwhile reconstruction will entail a major simplification of mechanical design.

5. Normal skin sensibility is always desirable, so long as it is above a protective level, but decreased sensibility does not preclude the usefulness of tendon transfers. 6. With interruption of motor nerves, muscle imbalance is immediate, but not deformity. Deformity develops from persistent imbalance and can usually be prevented by appropriate splinting, etc.

INDICATIONS FOR TENDON TRANSFERS Neurologic Deficits Poliomyelitis is no longer the most frequent indication for tendon transfers. Rather, paralysis of healthy muscle, usually from nerve injury, is the most frequent indication. Prompt consideration of tendon transfers is indicated if (a) the prognosis for neurologic recovery is poor even with nerve repair, (b) muscles have been destroyed, or (c) nerve grafts have been required to restore nerve continuity. Tendon transfers do not prevent recovered function of a paralyzed muscle if an unanticipated degree of neurologic recovery occurs.

Loss of Muscle–Tendon Unit or as an Alternative to Tendon Repair Muscles can be directly destroyed or their tendons hopelessly damaged, as with rheumatoid arthritis. For these cases, restoration of an important function may best be accomplished by tendon transfer (Fig. 88.1).

Other Indications Treating spastic disorders may rarely incorporate tendon transfers. Results are unpredictable because the transferred unit does not have normal neurologic control. It is difficult to treat peripherally an essentially central nervous system problem. Arthrodesis is far more frequently used to improve balance of spastic patients.

EVALUATION AND ESTABLISHMENT OF GOALS As with most areas of medicine, evaluation and accurate diagnosis begins with taking a detailed and accurate history. Not only does this provide information about the mechanism of injury, but much is learned about the patient, such as intellectual capacity, expectations, and motivation. The patient generally will interpret these efforts as expression of concern, so it goes far toward establishing good rapport.


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A

B

FIGURE 88.1. Tendon transfer for rheumatoid arthritis. A: Rupture of extensor digiti minimi and extensor digitorum communis to ring and small fingers as a result of rheumatoid synovitis/arthritis. B: Surgical exposure of the rheumatoid-ravaged wrist with ruptured tendons seen toward top of picture. C: Restoration of ring- and smallfinger extensor by transfer of the distal segments of their ruptured tendon into the side of the intact extensor tendons to middle and index fingers.

C

Task Analysis and Establishment of Goals

Soft-Tissue Coverage

Obviously every patient wants the affected hand to return to its normal status, but most often this is outside the realm of reality. Consequently, it is important that the basis for judgment of care be the crippled hand as presented rather than the normal hand. For elective cases, it is important to sort out the complaints and arrange them in order of priority. With subsequent reference to this list, progress will be appreciated that otherwise would be unrecognized.

Transferred tendons will glide only if transplanted through mobile, unscarred, healthy tissues. The transfer usually entails subcutaneous rerouting or flap-tissue replacement to provide such coverage. Wounds should be thoroughly healed before consideration is given to tendon transfer.

Motivation Motivation is no less a factor for obtaining good results from tendon transfers than it is in any other surgical hand procedure. The patient who shows little interest and/or unrealistic expectations is a poor candidate for surgical repairs. In general, never do an elective operation that you “had to sell.”

Precede Transfers with Maximum Joint Mobilization One rarely gains more active range of motion from tendon transfers than the preoperative passive range of motion.

Skeletal Stabilization Usually skeletal stabilization requiring arthrodesis should be performed prior to tendon transfers. The exception is a wrist fusion, because observations of the tenodesis effects from wrist flexion–extension is essential to judging tension of the tendon transfer.

PREREQUISITES TO SURGERY Open Wounds In general, a patient is not a candidate for tendon transfers if there are open wounds that could predispose to infection.

Restore Sensibility When possible restoration of at least protective sensibility should precede tendon transfers. Skin sensibility is not absolutely necessary for tendon transfers to be useful, but it is desirable.


Chapter 88: Tendon Transfers

SELECTION OF MUSCLES FOR TRANSFER Availability Having established the functional needs and goals and that the patient is emotionally a suitable candidate, the next step is to develop the plan that will best meet those needs (1). A detailed inventory of the existing assets is generated by grading the power of each muscle in the limb on a 0 to 5 scale, 0 being no active movement, 1 being ability to move against gravity, 2 being movement but too weak for any basic tasks, 3 being weak but useful power, 4 being near-normal power, and 5 being fully normal power. Essentially, only muscles of 4 and 5 power ratings are suitable for tendon transfers.

Control A muscle for transfer should be nonspastic, have good volitional control, and be an independently functional unit, such as the finger superficial flexor muscles or the extensor indicis proprius.

Amplitude of Excursion The muscle to be transferred must have an adequate amplitude of excursion for its new job or be situated so that it can be enhanced by tenodesis as it crosses an actively controlled joint. Most often this joint will be the wrist.

Anatomic Location To be considered for tendon transfer a muscle must be so located that its transfer is anatomically and mechanically feasible. The rerouting should be as direct as possible between the muscle’s origin and its new insertion. Otherwise, as it begins to function, it will work into a straight line of pull and become too slack. Never is more than one change of direction workable, and simplicity of mechanical design predisposes good results.

Synergism Muscles that automatically contract simultaneously are referred to as synergistic. One of the many examples of this is wrist extension with finger flexion to grasp. Because of the way our muscle control system works, synergism does not have the importance once ascribed to it. From a control point of view, any muscle can function well at a new task and the ease with which it adapts to it is determined basically by how useful is the new function, not the muscle original function.

Expendability If a muscle is given a new duty, we must be certain that it will be of more benefit to the patient than keeping the muscle in its normal situation.

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RELATION OF MUSCLE LENGTH TO POWER OUTPUT A muscle’s power output is greatest at its resting length and diminishes with either stretching or redundancy as illustrated by the Blix curve. A muscle can shorten approximately 40% by contraction and at that point, power output ceases. It can be stretched approximately 40% before it ruptures, and measurements are deceptive as the energy required for stretching can be substantially recovered, making muscle output appear to be artificially increased (5). For example, when grasping, the wrist positions itself for tenodesis of the finger flexor muscles to maintain a range of optimal muscle power output depending on the size of the object being grasped or pinched.

TENDON TRANSFERS FOR DESTROYED MUSCLE–TENDON UNITS In many circumstances, a tendon transfer to restore function may be more feasible than trying to restore the normal system (Fig. 88.2). An example illustrating a frequent application of this fact is tendon transfer of an extensor pollicis longus tendon following a fracture of the distal radius (Fig. 88.3).

TENDON TRANSFERS FOR SPECIFIC PALSIES Radial Nerve Palsies Radial nerve losses are divided into high and low nerve disruptions. Low lesions are essentially posterior interosseous palsies, without loss of wrist extension. They demonstrate loss of thumb extension–abduction and finger extension at their metacarpophalangeal (MCP) joints, the intrinsic muscles providing interphalangeal extension. The favored scheme of transfers for low radial nerve lesions is the flexor carpi ulnaris (FCU) to extensor digitorum communis (EDC), the extensor indicis longus (EIP), and the extensor pollicis longus (EPL) as a common unit. With normal median- and ulnar-controlled antagonist muscles, independent action of each of these muscles’ function is observed. The extensor digiti minimi is not included, unless there is no EDC slip to the small finger, as it results in excessive small finger abduction. Tension for each of the transfers is adjusted according to observation with wrist passive extension and flexion. An option is to repower the abductor pollicis longus (APL) with the palmaris, but I have yet to have a patient complain about APL loss. Remember that simplicity generates good results. If the FCU is unavailable for transfer, two finger superficial flexor muscles, not their tendons, can be brought through the interosseous membrane, using one for the thumb and the other for the combined fingers.

Extensors High radial nerve palsies demonstrate the losses of low nerve lesions with the addition of total loss of active wrist extension as a result of paralysis of the extensor carpi radialis longus (ECRL) and brevis (ECRB). The ECRB is both the most central and the prime wrist extensor, so the transferred tendon is sutured into the ECRB. Transfer of the median innervated pronator teres (PT) into the ECRB works so reliably that it is essentially a classic transfer for restoring active wrist extension (Fig. 88.4). With the PT’s insertion into the ECRB over the


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A

B

C

D

FIGURE 88.2. A: Spontaneous rupture of the extensor pollicis longus (EPL) at Lister’s tubercle, with loss of interphalangeal extension. B: Extensor indicis proprius (EIP) tendon detached distally and withdrawn at the muscle level in the forearm for transfer to the EPL. C: EIP rerouted subcutaneously, avoiding friction against the Lister’s tubercle. The tendons are joined in the soft subcutaneous tissue over the first metacarpal. D, E: Functional recovery of thumb extension.

E

radius superficial to its normal insertion, there is no loss of active forearm pronation as a result of this transfer.

Ulnar Nerve Palsies Ulnar nerve lesions may be high or low, with the low lesions being of tremendous importance as there is interruption of innervation of all interosseous muscles and of the lumbricals of the ring and small fingers, as well as all intrinsic muscles of thumb adduction. Approximately 35% of patients have sufficient overlap in the thenar eminence from the median nerve so as not to be significantly troubled by weakened thumb adduction power. A “claw deformity” of hyperextension of MCP joints with flexion of the proximal interphalangeal (PIP) joints does not occur with the middle and index fingers, as their lumbrical muscles are median innervated. With weakened thumb

adduction, MCP hyperextension with a compensatory hyperflexion of the thumb’s interphalangeal (IP) joint may be observed; that is, the Froment sign. The difference between a high and a low ulnar palsy is that the high lesion has weakness of flexion of the distal joint of the small finger from denervation of its flexor digitorum profundus muscle. With median and radial innervated muscles functioning, loss of the FCU is not missed. The vast majority of ulnar nerve palsies occur at the elbow (cubital tunnel). Low lesions at the Guyon tunnel adjacent to the pisiform bone are not only rare, but almost unknown unless there has been direct trauma to that area. With ulnar palsies there is paralysis of all interosseous muscles, lumbricals of the ring and small fingers, and muscles of thumb adduction. The clinical manifestation of thumb weakness of adduction varies greatly, depending on the amount of median nerve overlap into adductor muscle group.



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A

B

D

C

FIGURE 88.3. Tendon transfers for radial nerve palsy. A: High radial nerve palsy with paralysis of both wrist and digital extensor muscles. The pronator teres was transferred to the extensor carpi radialis brevis to restore wrist extension, and the flexor carpi ulnaris (FCU) was transferred to the combined extensor digitorum communis, extensor indicis proprius, and EPL. B: Motion is a result of the prime mover, the antagonist, and the stabilizers. After transfer of the FCU to the combined digital extensor, the index finger can point alone, as the antagonist (intact flexors) of the middle, ring, and small fingers prevent their extension. C: Restored wrist and digital extension. Note the long incision required to mobilize the FCU for dorsal transfer. D, E: Postoperative full, active extension and unimpaired digital flexion.

E

Approximately 35% of patients with complete ulnar palsy have sufficient median innervation to the superficial head of the flexor pollicis brevis for clinically satisfactory thumb adduction. Tendon transfer for ulnar palsy to the fingers can be only incomplete, with restoration of MCP flexion and correction of “clawing,” whereas the normal independent function of each interosseous muscle cannot be restored. The best transfer to restore active MCP finger flexion is with the two slips of a superficial flexor being divided to provide four slips, one for each finger, passed anterior to the intercapsular (intermetacarpal) ligaments and inserted into the flexor tendon sheath’s A-2 pulley. Inserting them into the interosseous tendons (lateral bands) alongside the proximal phalangeals risks excessive PIP exten-

sion and “swan neck” deformities, and putting them into bone is excessively traumatic (Fig. 88.5). If thumb adduction power requires augmentation, this generally is done with transfer of a finger superficial flexor tendon. Ideally, the line of pull should be across the palm tangential to the thumb. The problem is that no functioning muscle lies sufficiently distal for this line of pull, so a tendon transfer has to be taken around a “pulley” for a 90-degree change of direction. The best of the available compromises is to leave a finger superficial flexor in the carpal tunnel, using the distal edge of the transverse carpal ligament as a pulley. This is not distal enough to be mechanically correct, but the power of those muscles is so great that a functional level of thumb adduction is restored.


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A

B

C

D FIGURE 88.4. A: Thenar muscle opponens group atrophy from median nerve injury, without ulnar nerve thenar overlapping innervation. B: Opponens palsy seen on right prevents flat pulp-to-pulp opposition to finger pulp. C: Classic opponens transfer rerouting the superficial flexor tendon from the ring finger around the FCU (but not around the ulnar artery and nerve) to change its direction of pull to that of the paralyzed abductor pollicis brevis muscle. D: Postoperation illustration of restored thumb opposition and good pulp-to-pulp pinch.

Among other schemes advocated for thumb adduction is to carry a tendon graft dorsally, down between the metacarpals, into the palm, and across to the thumb. This is too complex, subject to tendon adhesion fixation, and rarely satisfactory.

Median Nerve Palsies As with radial and ulnar nerve lesions, two types of lesions will be encountered, that of high and low levels.

Low Median Nerve Palsies Functional impairment from a low median nerve lesion is predominantly loss of skin sensibility on the working surfaces of the thumb, index, middle, and adjacent side of the ring fingers. These are the areas needed for refined manipulations. The muscle loss of the thumb is that of positioning or opposition and there is a 35% probability of this not being a problem because of ulnar nerve overlap into the superficial head of the flexor pollicis brevis. If augmentation of thumb opposition is needed, there are several satisfactory options available. The vector force for the three paralyzed muscles is along the abductor pollicis brevis (4). The method most often used to restore thumb opposition is transfer of a ring or middle finger superficial flexor, rerouting it around the FCU at the pisiform for its change of direction, and

carrying it subcutaneously over the paralyzed abductor pollicis brevis (APB) for a line of pull directly toward the pisiform (Fig. 88.4). The tendon must be passed around the FCU superficial to the ulnar artery and nerve to avoid compression. An alternative is to bring a finger superficial flexor from the carpal tunnel through a window cut in the transverse carpal ligament and then to the thumb. This procedure has a substantially greater risk of restrictive adhesions. The major problem common to all schemes for restoration of thumb opposition is adequate pronation and rotation needed for a flat pulp-to-pulp pinch between the thumb and finger pads. Thumb pronation requires great power because the powerful ulnar innervated adductor pollicis is a thumb supinator. In an effort to resolve this problem many distal transfer insertions have been proposed, such as carrying the tendon transfer dorsally across thumb’s proximal phalangeal base and inserting into the collateral ligament on the medial side of the MCP joint. Most often a flexor digitorum superficialis (FDS) tendon is used for these transfers, but others have been reported. The functionally independent EIP is excellent. Usually it is routed around the ulnar side of the wrist, but it can be brought through a large opening cut in the interosseous membrane. The abductor digiti quinti (ADQ) muscle can be mobilized on its intact neurovascular pellicle and transferred into the thenar eminence over the paralyzed APB, but the downside of this complex procedure is an unattractive mass across the base of the palm.



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sally. Another option is to transfer the biceps insertion from the medial to the lateral side of the radius.

Tendon Transfers for Combined Nerve Palsies Remember this basic principle: If function of any two of the hand’s major nerves is lost, reconstruction approaching normal is absolutely precluded and any useful reconstruction requires a great simplification of mechanical design (8). Loss of critical skin sensibility with median nerve losses precludes ability for fine manipulations even if functional muscle rebalancing can be achieved. Although only combined median ulnar palsies are discussed here, the principles are applicable to other combinations.

Split FPL Sheath

Low Combined Median Ulnar Palsies

ECRL

FPL

FIGURE 88.5. Scheme for maximum use of the four muscles functioning distal to the elbow with C5–C6 tetraplegia. Less important joints are stabilized by arthrodesis. Available muscle power is transferred through normal routes. The scheme provides MCP flexion to initiate the finger flexion arc for small-object pinch, as well as independent PIP flexion to accommodate larger objects. Full active finger extension is independent of wrist motion—not an inefficient tenodesis system.

Restoring thumb opposition should be considered only if a good flexion–extension arc can be restored to the fingers. Such restoration requires active finger MCP flexion as a minimum, otherwise finger flexion will start at the distal interphalangeal (DIP) joints, with the fingers rolling up and their pads never facing that of the thumb in opposition. If these requirements cannot be met, it is far better to accept the simple scheme of the thumb adducting against the side of the fully flexed index finger, the “key pinch.” However, with low lesions the valuable finger superficial flexors usually are available for tendon transfers. Having them available is a strong indication for their repair if severed in a classic anterior wrist laceration. Usually the FDS of the middle finger is large enough to be split into four slips, one restoring active MCP flexion to a finger for initiation on its flexion there. With combined median ulnar palsies the thumb has lost function of the median innervated muscle for its positioning and the ulnar innervated group for adduction power. In theory, a single tendon transfer along the vector line between these two groups should be useful, but in practice, it provides grossly inadequate power for usefulness. It is trying to do too much with too little. Many schemes to cope with this situation are possible but, generally, arthrodesis of the first MCP joint with carefully considered thumb projection is best and certainly the most reliable.

High Combined Median Ulnar Palsies Perhaps the best solution to this problem of restoring good thumb pronation is to transfer the insertion of the deep head of the flexor pollicis brevis from the medial to the lateral side of the first MCP joint. Technically this is difficult, as it is conducted in a small and deep space and great care must be exercised not to injure one of the neurovascular bundles beneath which it is carried.

High Median Nerve Palsies In addition to the losses of a low nerve lesion, high median nerve palsies involve paralysis of both superficial and deep interphalangeal flexors of the index and middle fingers and the IP joint of the thumb. Interphalangeal flexion of the index and middle fingers can be restored by suturing their profundus tendons into that of the ring and small fingers, which are ulnar innervated. If much greater power is needed, it can be provided by transfer of the ECRL to the group. Excellent restoration of thumb IP flexion can be provided by transfer of the functionally independent EIP into the flexor pollicis longus (FPL). The tendon junction should be in the forearm amid soft, mobile tissues. High median nerve palsy also results in very weak forearm pronation. If this needs augmentation, the extensor carpi ulnaris (ECU) can be withdrawn from its sheath and rerouted anteriorly across the forearm and attached into the radius dor-

In addition to the losses of low lesions, those at a high level have loss of all finger and thumb flexion and sensibility to the critical working surfaced of the palmar skin. Tendon transfers results are very poor functionally, assisting at best. Having only radially innervated muscles with which to work, it is best to fuse the base of the thumb in a carefully selected projection from the palm and to concentrate available functioning muscles to restore finger motion. Several possibilities exist according to the exact situation, but MCP finger flexion usually can be restored by tendon grafts powered by the brachioradialis and interphalangeal finger flexion by transfer of the ECRL to the four-finger flexor digitorum profundus (FDP) tendons as a single unit. The thumb can be provided with independent IP flexion by the EIP. If forearm pronation needs augmentation, it can be provided by ECU transfer or by change of the biceps insertion from the medial to the lateral side of the radius.

HAND RECONSTRUCTION FOR PARALYSIS CAUSED BY SPINAL CORD INJURIES C5–C6 is the highest level of spinal cord injury for which impressive reconstructions are possible (3). The important thing is the level of cord injury, which may vary considerably from


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the level of vertebral fractures. Patients with C5–C6 cord injuries have good shoulder control and strong elbow flexion by the biceps but no active elbow extension. Distal to the elbow they typically have only four functioning muscles. If only one muscle is functioning, it is the brachioradialis, followed by the pronator teres, then by the ECRL, and, finally, by the ECRB. If wrist extension is weak, the important ECRB will be weak, and to take the ECRL for a tendon transfer would be disastrous. Skin sensibility in both radial and median nerve distributions is usually not disturbed, but that of the ulnar nerve area is almost anesthetic. If only the brachioradialis is functioning, it can be useful if transferred to the ECRB to provide active wrist extension. Wrist arthrodesis is the last thing to consider for these patients. When the cord lesion is lower than C5–C6, the digital extensors will be functioning and the situation is essentially that of combined median ulnar paralysis. There are two basic types of reconstruction for C5–C6 cord-injured patients: simple lateral pinch with the thumb and the more complex tripod-type reconstructions.

Key Pinch Reconstructions Simple adduction of the thumb against the side of the fully flexed, and thus stable, index finger was championed by Moberg (9). It has the advantages of simplicity and predictability, and requires only a single operation. Yet pinch is weak; thumb extension–abduction is not active, but is by wrist tenodesis and it does not use the available functioning units to near their potential. The thumb IP joint is stabilized, either by arthrodesis or by putting a screw across it, and thumb adduction is provided by transfer of the ECRL into the paralyzed FPL. The proximal FPL sheath is opened so that the FPL “bowstrings” to increase its moment arm or force for thumb MCP joint flexion (Fig. 88.6).

Tripod-Type Reconstruction The other basic type of reconstruction restores some precisiontype pinch with thumb-finger pad approximations and generally some type of active finger grasping capability. Obviously there must be good median nerve skin sensibility for this type of reconstruction even to be considered. With four muscles functioning, it is possible to restore active finger extension without relying on wrist tenodesis. PT

BR

ECRL ECRB

Several designs are feasible, but space restraints here are such that I shall present the one I developed, which optimally uses the few available functioning units (3). It provides finger extension and flexion at both the MCP and PIP joint levels, independent of each other and without a requirement of wrist tenodesis. In addition, it creates the capability for smallobject manipulations between the pads of the thumb and indexmiddle fingers. The downsides of the design are that it is complex, with little margin for error, and that it usually is done in three surgical stages: skeletal stabilization, restoration of flexor systems, and, finally, the extensor mechanisms (3). However, it should be feasible to combine the skeletal stabilization and extensor restoration stages together. In this design, the thumb is fixed by arthrodesis in a carefully planned projection from the palm so that its pad can be met by the pads of the remobilized index and middle fingers. The scheme is unique in that power is transferred through the tendons of paralyzed muscles free of adhesions as they are in their normal beds, and the MCP and PIP joint can be flexed independently to accommodate varioussize objects. Full finger extension is independent of wrist movement. A composite illustration of the whole system is shown in Figure 89.5.

RESTORATION OF ACTIVE ELBOW EXTENSION With paralysis of the triceps, the elbow is unstable and incapable of active extension. Restoration of these capabilities is helpful and generally feasible by extending the posterior deltoid muscle, using strong tendon grafts as substitutes for the triceps. The chief objection to this operation is that the elbow must be immobilized in full extension for 6 weeks, after which permissible flexion can be increased by only about 5 degrees per week.

POSTOPERATIVE MANAGEMENT FOR TENDON TRANSFERS Transferred tendons must be protected carefully from disruption by rigid cast or splinting for at least 4 to 6 weeks, with the length of time being determined by the amount of stress to which they will be subject. This requires special efforts with children, as they promptly become uninhibited as soon as pain ceases. Flexor tendons require protective immobilization for

EDC

FDP FDS FIGURE 88.6. Scheme of the simple lateral “key pinch” (Moberg) for C5–C6 tetraplegia. Restored thumb adduction is against the side of the immobile index finger, which has sufficient lateral stability to serve as an anvil. Opening is by wristdrop tenodesis of the EPL attached to the radius proximal to the wrist joint.



3 to 4 weeks, after which active but unresisted movement is encouraged. In general, extensor systems require longer protection not because they heal differently, but because their antagonists are the powerful flexors. No transfer should be submitted to full stress for at least 8 weeks after the transfer.

RE-EDUCATION OF TRANSFERRED MUSCLES The difficulty of “re-educating” into use of a tendon transfer is inversely related to the usefulness of the new arrangement. Most tendon transfers that have been well-considered and skillfully done almost immediately and automatically function at their new task with no “re-education.” This is readily understandable if one considers that the normal control system is basically an extremely rapid “trial-and-error” operation that is guided by constant monitoring of progress toward desired goals. If progress is unsatisfactory, the cortex will recruit other muscle combinations until the desired results occur. A patient with loss of sensory feedback who is blindfolded to block visual

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input will have illegible handwriting because of their loss of a critical link in the muscle control system.

References 1. Beasley RW. Principles of tendon transfers. Orthop Clin North Am. 1970; 1:433. 2. Beasley RW. Tendon transfers for radial nerve palsy. Orthop Clin North Am. 1970;1–439. 3. Beasley RW. Surgical treatment of hands for C5-6 tetraplegia. Orthop Clin North Am. 1983;14893. 4. Brand P. Tendon transfers for median and ulnar paralysis. Orthop Clin North Am. 1970;1–447. 5. Brand P. Tendon transfer reconstruction for radial, ulnar, median and combined paralysis. Principles and techniques. In: McCarthy J, ed. Plastic Surgery. Philadelphia: WB Saunders; 1990 . 6. Litter JW. Tendon transfers and arthrodesis is combined median and ulnar nerve paralysis. J Bone Joint Surg. 1949;31A:225. 7. Littler JW, Cooley S. Opposition of the thumb and its restoration by abductor digiti quinti transfer. J Bone Joint Surg. 1963;45A:1389. 8. Littler JW. Restoration of power and stability to the partially paralyzed hand. In: Converse JM, ed. Reconstructive Plastic Surgery. Philadelphia: WB Saunders; 1979. 9. Moberg E. The current state of surgical rehabilitation of the upper limb in tetraplegia. Paraplegia. 1987;25:351.


CHAPTER 89 ■ CONGENITAL HAND ABNORMALITIES MIHYE CHOI, SHEEL SHARMA, AND OTWAY LOUIE

Congenital hand anomalies vary over a spectrum from scarcely noticeable to an absent upper extremity. It is incumbent on the surgeon to decide if further work-up is required for associated anomalies, if surgical intervention is necessary, and what the timing of surgery should be. This chapter presents an overview of the relevant embryology, classification, and treatment of the most common congenital hand abnormalities.

EMBRYOLOGY The upper limb buds form on the lateral wall of the embryo 4 weeks after fertilization. These buds consist of mesodermal cells covered by ectoderm, and develop into a complete limb under the guidance of three signaling centers: (a) the apical ectodermal ridge (AER); (b) the zone of polarizing activity (ZPA); and (c) the nonridge ectoderm. Each controls growth and patterning along a specific orthogonal axis. The apical ectodermal ridge is located at the distal aspect of the developing limb and is required for growth in a proximalto-distal direction. Removal of the AER results in growth arrest and a truncated limb. Moreover, the earlier the AER is removed, the more proximal the defect. The zone of polarizing activity is a group of mesodermal cells at the posterior limb bud, which functions in anterior-toposterior limb development. Transplantation of posterior cells to the anterior border of the normal limb results in a mirror duplication of the limb. The ZPA cells act through the Sonic hedgehog (Shh) gene (1). The nonridge ectoderm, also known as the Wingless-type (Wnt) signaling center, controls patterning in the dorsal–ventral axis. It is required for alignment of the limb in a dorsal orientation (dorsalization).

CLASSIFICATION Although multiple classification schemes of upper limb abnormalities exist, the most widely accepted is that of Swanson (Table 89.1), which categorizes congenital hand abnormalities based on their embryologic origin as well as their clinical manifestation. It has been accepted by the American Society for Surgery of the Hand, as well as the International Federation of Societies for Surgery of the Hand.

Failure of Formation of Parts (Developmental Arrest) Failure of formation can be transverse or longitudinal. Transverse arrests result in truncated limbs at various levels, most commonly at the midforearm. Generally, there is no role for surgical intervention and, with unilateral involvement, these

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children seldom require prostheses. Rarely, distraction lengthening and phalangeal transfer may be indicated. More recently, toe-to-hand transfers have been performed. There are four kinds of longitudinal arrest: preaxial, postaxial, central, and intercalary. Preaxial and postaxial arrest leads to the radial and ulnar club hand, respectively. Central arrest leads to a cleft hand. Intercalary arrest leads to phocomelia, where an intervening segment of limb is absent.

Preaxial Deficiency: Radial Club Hand Radial dysplasias occur in 1 in 55,000 births. They are typically sporadic and unilateral, more common in males, and more common on the right side. Radial dysplasias are commonly associated with syndromes including Fanconi anemia, thrombocytopenia absent radius (TAR) syndrome, Holt-Oram syndrome (associated with cardiac septal defects), and VATER (vertebral abnormality, anal imperforation, tracheoesophageal fistula, radial, ray, or renal anomalies vertebral, anus, tracheoesophageal, radial, and renal abnormalities) syndrome (2,3). The presence of these syndromes must be evaluated prior to any surgical reconstruction. The clinical manifestation of radial club hand is a shortened forearm with radial deviation at the wrist. The pathology affects all structures on the preaxial side of the limb: skeleton, musculotendinous units, joints, neurovascular structures, and soft tissues. Based on the severity of the deformity, Bayne and Klug classified radial dysplasia into four categories (4) (Table 89.2). Functional Considerations. In radial aplasia, the carpus lacks support from the distal radius, and the ulna is inadequate to provide stability. This causes the wrist to deviate radially. The forearm flexors worsen the radial deviation and the unopposed action of the wrist and finger flexors cause palmar displacement. The flexor muscles are short, stiff, and often fibrotic. The radial nerve and vessels are deficient and the median nerve is often subluxed toward the concave side. The ulna is also always deficient. Prehension is abnormal, caused by the deficiency of the thumb. Management. Early manipulation emphasizing elbow flexion and ulnar deviation of the wrist is taught to the parents. Mild type I dysplasia may only require splinting. After evaluation for associated anomalies, surgical options are considered. In types I and II dysplasia with an unstable wrist, distraction lengthening of the radius is recommended. Centralization or radialization are the treatments of choice in severe type II, and in types III and IV; repair should be performed at 6 to 12 months of age. Preoperative splinting to achieve passive flexion of the elbow should be performed. In centralization, the angulation in the forearm is corrected by freeing the distal ulna, cutting a corresponding slot in the carpus, and stabilizing the wrist by passing a pin from the third metacarpal


Chapter 89: Congenital Hand Abnormalities

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Postaxial Deficiency: Ulnar Club Hand

TA B L E 8 9 . 1 SWANSON CLASSIFICATION OF CONGENITAL UPPER LIMB ABNORMALITIES

I. Failure of Formation of Parts Transverse Longitudinal Radial club hand Cleft hand Ulnar club hand Phocomelia II. Failure of Differentiation or Separation of Parts Synostosis Radial head dislocation Symphalangism Syndactyly Contracture Arthrogryposis Trigger finger Clasped thumb Camptodactyly Clinodactyly Windblown hand Kirner deformity III. Duplication Polydactyly IV. Overgrowth Macrodactyly V. Undergrowth Thumb hypoplasia Madelung deformity VI. Congenital Constriction Ring Syndrome VII. Generalized Skeletal Abnormalities and Syndromes

to the ulna. A complementary tendon transfer of the radial flexor-extensor mass to the extensor carpi ulnaris is performed (Fig. 89.1). In radialization, the distal ulna is aligned with the second metacarpal and a dynamic transfer of the flexor– extensor mass from its insertion to the radial side of the carpus is performed (5). The key to the success of the operation lies in the rebalancing of forces by tendon transfers. For associated severe thumb hypoplasia or aplasia, pollicization is considered, usually 6 months after centralization or radialization.

Compared to radial deficiency, the incidence of ulnar ray deficiency is quite rare, with the incidence varying between 1 per 100,000 and 7.4 per 100,000 live births (6). Typically, the defect is more common in males, unilateral, and left-sided. Unlike radial club hand, it is rarely associated with defects in other organs. Although the cause of ulnar ray deficiency is unknown, it is hypothesized by Cole and Manske to be a defect in the zone of polarizing activity. The anatomic findings in ulnar ray deficiency include a short, bowed radius with a hypoplastic or absent ulna. The Bayne classification is the most commonly used (Table 89.3). Because of the small number of patients with ulnar ray deficiency, a consensus on the ideal treatment has not been reached. Hand deformities should be treated, as improvement in function may result. Excision of the ulna anlage, which theoretically could remove an ulnar deviating force, has been promoted by some, and discouraged by others. Creation of a one-bone forearm for types I and II can stabilize and improve function in those with a hypoplastic ulna. Humeral osteotomy remains an option for those with radiohumeral synostosis (7).

Central Deficiency: Cleft Hand A longitudinal deficiency of the central rays results in cleft hand. Cleft hands are classified as typical or atypical. The typical cleft hand contains a deep V-shaped central defect secondary to hypoplasia of the long ray. The defect is typically bilateral and inherited. Association with foot clefts is common. In contrast, atypical clefts present as a U-shaped defect secondary to absence of the index, long, and ring fingers. They are unilateral and inheritance sporadic. Association with foot clefts are relatively rare; however, atypical clefts have been documented in Poland syndrome. Atypical clefts are now known to be a form of symbrachydactyly. Snow and Littler described the original technique for correcting typical clefts. The index ray is transposed into the central defect, deepening the first web space. A palmar-based skin flap is then used to recreate the first web space. More recently, Upton modified this technique to avoid problems with necrosis of the narrow-based palmar flap. He described a circumferential incision around the base of the index finger, with extensions radially and ulnarly at the level of the new digitopalmar flexion crease. After wide exposure, the first dorsal interosseus muscle is released, the index finger transposed, and the transverse intermetacarpal ligament recreated.

Intercalary Deficiency: Phocomelia Intercalary arrest results in phocomelia, where an intervening segment of the limb is absent. The arm or forearm may be missing, with a normal hand. The use of thalidomide in the first trimester of pregnancy resulted in a marked increase in this deformity. Surgery is usually not indicated.

TA B L E 8 9 . 2 CLASSIFICATION OF RADIAL DYSPLASIA Type

Failure of Separation or Differentiation of Parts

Characteristics

Radius has a normal appearance but is shorter than the ulna II Hypoplastic radius Distal and proximal epiphyses present but defective hypoplastic radius III Partial absence of The proximal, middle, or distal radius portion of the radius is absent IV Total absence of The most severe and common type radius

Syndactyly

I Short radius

Syndactyly is one of the most common congenital hand deficiencies, with an incidence of 1 per 2,000 to 2,500 live births. There is a strong familial tendency: 10% to 40% cases are inherited as a result of a dominant gene with variable penetrance. Males are affected twice as frequently as females. The third web is the most commonly involved, followed by the fourth and second webs. Association with Poland or Apert syndrome is common. The embryologic etiology of syndactyly is thought


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B

A

C

FIGURE 89.1. Radial Club Hand. A: Preoperative photograph. B: Preoperative radiograph. C: Radialization. The second metacarpal was placed in alignment with the ulna, with a retrograde Kirschner wire holding fixation. A corrective osteotomy of the ulna shaft was performed.

to be related to (a) failure of digital patterning, (b) failure of apoptosis, or (c) failure of AER regression. Fusion can be limited to skin and soft tissue (simple), or include bone (complex). It may involve either the entire digit (complete), or a portion of the finger (incomplete). Complicated syndactyly refers to complex cases that involve some degree of synostosis. Finally, acrosyndactyly refers to fusion of the distal tips of the digits. Timing of Surgery. Separation as early as 6 months is indicated when syndactyly involves digits of unequal length (i.e., the ring and little fingers). Early separation is also required in complex syndactyly and cases of acrosyndactyly. The timing of all other cases of syndactyly remains somewhat controversial; most advocate surgical correction before age 18 months, whereas others prefer to wait until after this age. The principles of correction include (a) separation of the digits, (b) creation of a web space, (c) skin coverage, and (d) immobilization.

Separation is carried out via dorsal and volar zigzag incisions creating interdigitating flaps (Fig. 89.2). The nail fusion can be corrected by opposing Z-flaps as described by Buck-Gramcko. After making the incisions, the neurovascular bundles are identified prior to completing the separation. The web can be created using either a large dorsal flap or double opposing triangular flaps from dorsal and volar aspects. The flaps are then interdigitated. There will always be residual raw areas both proximally and on the sides of digits; these should be grafted with skin obtained from the groin crease. To avoid vascular compromise to a single digit, it is critical that separation should not be performed simultaneously on adjacent webs. The authors recommend immobilizing the child’s arm in an above-elbow cast until the grafts heal. Complex syndactyly is a feature of Apert syndrome (see Chapter 25). The Apert hand can be classified into three categories as shown in Table 89.4.



TA B L E 8 9 . 3 CLASSIFICATION OF ULNAR DEFICIENCY Type

Characteristics

I Hypoplasia of the ulna

Presence of distal and proximal ulnar epiphysis Absence of the distal or middle one third of the ulna Complete absence of the ulna Synostosis of radius to humerus

II Partial aplasia of the ulna III Total aplasia of the ulna IV Radiohumeral synostosis

Types I and II Apert hands should be corrected in two stages: in the first stage, the position of the thumb is corrected with an osteotomy and a three-finger hand is created by separating the second and fourth webs. The second stage involves separation of the remaining digits. The timing of correction of the synostosis between the fourth and fifth metacarpal is disputable. Type 3 deformities may be accompanied with recurrent nail infections, and thus may require separation of the nail prior to formal syndactyly correction.

Symphalangism Symphalangism is failure of differentiation of the interphalangeal joint. Although the distal interphalangeal joint can be involved, symphalangism of the proximal interphalangeal joint is more common. Inheritance is autosomal dominant. Anatomically, there is no joint capsule. On radiographs, a clear joint space is seen, although ankylosis can appear after adolescence.

The most commonly affected digit is the little finger, followed by the ring, long, and index fingers, respectively. Treatment is usually not required as the hand with isolated symphalangism functions quite well; surgical options include arthrodesis to obtain a more functional position. Arthroplasty and free vascularized joint transfers have also been performed.

Congenital Trigger Thumb In trigger thumb, there is an inability to extend the interphalangeal joint. A nodule is palpable over the flexor aspect of the metacarpophalangeal joint (Notta node). This differs from a clasped thumb in which the metacarpophalangeal joint is also affected. Spontaneous resolution of the triggering can occur in a third of the affected children by 1 year of age. However, surgical correction is recommended before the age of 3 years so as to avoid any deformity. Treatment involves division of the A-1 pulley, confirming full mobility of the interphalangeal joint at the operation. The digital nerves should be carefully identified.

Clinodactyly Clinodactyly is defined as curvature of a digit in a radioulnar plane. The most common form is radial deviation of the little finger at the distal interphalangeal (DIP) joint. It occurs as a result of the presence of a delta phalanx, a trapezoidshaped middle phalanx resulting from an abnormal epiphysis. Clinodactyly rarely interferes with function, and treatment is not indicated for aesthetic reasons. In cases of severe angulation with functional problems, a wedge osteotomy can be performed to correct the deformity, but not before 5 to 6 years of age, when the bones are reasonable in size.

B

A

C

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FIGURE 89.2. Syndactyly. A: Preoperative markings for Brunner incisions in a case of syndactyly. B: Radiograph showing complex complete syndactyly. C: Postoperative result after release.


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Camptodactyly

TA B L E 8 9 . 4

Camptodactyly is congenital flexion deformity of the proximal interphalangeal joint. The little finger is most commonly involved. There are two types: one that appears in infancy with an equal sex incidence and a second that presents in adolescent girls. Function is rarely impaired, and patients mostly seek consultation regarding its appearance. Skin shortening, tight retinaculum cutis, short sublimis, abnormal lumbricals, lateral band adhesions, central slip anomalies, and bony defects can all be present in these cases. The extensor deficit should be measured with the metacarpophalangeal joint in extension and flexion to rule out intrinsic tightness. Splinting may be attempted to correct the deformity. Surgical correction is only indicated in a rapidly progressing deformity. Skin shortage is treated with Z-plasties. The abnormal retinaculum and lateral bands are freed from the phalanx. A short sublimis is lengthened and any abnormal lumbrical insertion is released. An extensor tendon transfer has also been suggested for extensor deficits.

Polydactyly can occur either as an isolated malformation or as part of a syndrome. There are at least 119 disorders that contain polydactyly: 97 are syndromic, and 22 are nonsyndromic.

II Duplicated distal phalanx

V Bifid metacarpal

Type

Characteristics

I

Thumb and little fingers are free; other digits form a central mass Only the thumb is free; there is a central digital mass with a common nail and fourth web syndactyly, the so-called spade deformity The rosebud hand, in which the thumb and the digital mass are fused together and share a common nail

II III

For simplification, these subgroups of congenital hand anomalies can be divided into (a) radial (preaxial), (b) central, and (c) ulnar (postaxial). Mixed polydactyly refers to simultaneous radial and ulnar polydactyly, whereas crossed polydactyly occurs with involvement of both hands and feet.

Radial Polydactyly

Duplications

I Bifid distal phalanx

APERT HAND ABNORMALITIES

The incidence of radial polydactyly is approximately 0.08 per 1,000 live births, and is exemplified by thumb duplication. The Wassel classification scheme is the most commonly used (Fig. 89.3).

III Bifid proximal phalanx

VI Duplicated metacarpal

IV Duplicated proximal phalanx

VII Triphalangia

FIGURE 89.3. Thumb duplication: Wassel classification.


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Types I and II Wassel thumbs can be treated by removal of one of the duplicate thumbs or the Bilhaut-Cloquet procedure, which consists of excision of the central wedge of the duplicated thumb segment and bringing the remaining segments together (8). Type IV is the most common (43%). Treatment involves ablation of the radial thumb, followed by reconstruction of the radial collateral ligament and intrinsic thenar tendons (Fig. 89.4). Type VII triphalangeal thumbs are treated with the goal of retaining the most functional thumb, regardless of whether it is tri- or biphalangeal.

Central Polydactyly Included within the term central polydactyly are duplications of the index, long, and ring fingers. Inheritance is autosomal dominant. The supernumerary digit is often fused to its adjacent digit. Odd transverse phalanges bridging two adjacent digits have been described. Surgical treatment of central polydactyly can be difficult and the results often suboptimal. The goal is to ablate the duplicated digit with augmentation of the retained digit. Given the complex nature of these deformities, multiple operations are often required.

Ulnar Polydactyly Temtamy and McKusick divided ulnar polydactyly into welldeveloped (type A) and rudimentary (type B). Type A is a well-formed supernumerary digit, whereas type B is typically a small and pedunculated skin tag. There is a male predominance and a higher prevalence in African Americans (9). True type A digits require operative amputation, with reconstruction of key structures (i.e., ulnar collateral ligament and ab-

ductor digiti minimi). Type B skin tags can be ligated in the nursery.

Overgrowth or Gigantism Macrodactyly, or digital gigantism, refers to the enlargement of all elements of an involved digit. Lipofibromatous hamartomas, with excessive fat in all tissues, are characteristic. Single or multiple digits can be involved; the index finger is most frequently affected. The defect is more common in males and the majority of cases are unilateral. Two forms exist: (a) static, where there is enlargement at birth with subsequent proportionate growth, and (b) progressive, where there is increasingly disproportionate enlargement with age. Children presenting early with mild enlargement are candidates for debulking and epiphysiodesis to arrest skeletal growth. Untreated patients who present later in childhood are more difficult to manage, often requiring shortening and debulking. Distal amputation may be required for severe cases.

Undergrowth or Hypoplasia (Hypoplastic thumb) The hypoplastic thumb fails to extend to the midaspect of the proximal phalanx of the index finger. It can occur as an isolated deformity, or as part of a broader radial deficiency. Functional limitations in pinch and grasp can result, depending on the severity of the defect. The classification system of Blauth is most commonly used (Table 89.5). The critical determinant in choosing between reconstruction and ablation is the presence of a carpometacarpal joint. A

A

B

C

FIGURE 89.4. Thumb duplication. A: Duplicated thumb. B: Type IV duplicated proximal phalanx. C: Postoperative result after excision of the more hypoplastic digit and reconstruction of the remaining digit.


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Part VIII: Hand

TA B L E 8 9 . 5 BLAUTH CLASSIFICATION OF HYPOPLASTIC THUMB Type

Characteristics

I II III

Mild hypoplasia, all structures present Absence of thenar muscles Absence of thenar muscles, abnormal extrinsic tendons, and skeletal hypoplasia: subdivided into presence of (a) stable carpometacarpal joint and (b) unstable carpometacarpal joint Pouce flottant; the floating thumb Total aplasia of the thumb

IV V

stable basal joint allows reconstruction, whereas an unstable or absent carpometacarpal joint requires ablation. Type I defects rarely require operative intervention. Type II defects can be treated with opponensplasty, release of the first web space, and ulnar collateral ligament reconstruction. Type IIIA defects can be managed similarly, with the addition of extensor tendon transfers. Types IIIB, IV, and V defects are treated with pollicization (10). Pollicization repositions the index finger to act as a thumb. The ulnar neurovascular bundle to the index finger is freed by ligating the radial artery to the long finger. The A-1 and A-2 pulleys are divided, releasing the flexor tendons, and the extensor tendons are mobilized by dividing any junctura. The metacarpal is divided, and the index finger rotated 150 degrees into pronation and 40 degrees into abduction. The metacarpal head is rotated 70 degrees, and fixed to its base using ab-

sorbable sutures. The interosseous muscles are attached to the lateral bands of the extensor mechanism.

Congenital Constriction Band Syndrome The incidence of congenital constriction band syndrome is 1 per 15,000. Inheritance is sporadic, although association with other anomalies, such as club feet or cleft lip and palate, has been described. The etiology remains unknown; both extrinsic (i.e., constricting amniotic band) and intrinsic causes have been proposed. The clinical presentation varies greatly. Anything from shallow grooves in the skin to complete amputations can be found. Patterson classified constriction bands into four types: (a) simple constrictions only; (b) constrictions with distal deformity; (c) constrictions with fusion of distal parts (acrosyndactyly); and (d) intrauterine amputation (11). Treatment varies depending on the extent of the deformity. Mild simple constrictions may not require any treatment. More severe simple constrictions, as well as those with distal deformity, can be treated with Z-plasty (Fig. 89.5). The procedure is staged, with only half the circumference corrected at the first operation to prevent vascular compromise. The remaining constriction is corrected at a second operation. Those with acrosyndactyly are treated early; separation of the fused digits allows unimpeded growth. Management of intrauterine amputations is tailored to the deformity. A functional amputation may not require surgical intervention. Distraction lengthening with bone grafts and toe-to-hand transfers have been performed for severe defects. Fetoscopic lysis of amniotic bands has been performed in utero (12).

A

B

C

FIGURE 89.5. Constriction band syndrome. A: Simple constriction ring. B: Preoperative markings for release. C: Postoperative result after release.



References 1. Riddle RD, Johnson RL, Laufer E, et al. Sonic hedgehog mediates the polarizing activity of the ZPA. Cell. 1993;75:1401–1416. 2. Smith PJ.In: Lister’s The Hand: Diagnosis and Indications. 4th ed. Churchill Livingstone; 2002: 457. 3. Flatt AE.In: The Care of Congenital Hand Anomalies. 2nd ed. St. Louis: Quality Medical Publishing: 1994. 4. Bayne LG, Klug MS. Long-term review of the surgical treatment of radial deficiencies. J Hand Surg. 1987;12A(2):169–179. 5. Buck-Gramcko D. Radialization as a new treatment for radial club hand. J Hand Surg [Am]. 1985;10:964–968.

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6. Froster UG, Baird PA. Upper limb deficiencies and associated malformations: a population based study. Am J Med Genet. 1985;1:499–510. 7. Miller JK, Wenner SM, Kruger LM. Ulnar deficiency. J Hand Surg [Am]. 1986;11:822–829. 8. Bilhaut M. Guerison d’un pounce bifide par un nouveau procede operatoire. Congres Francais de Chir. 1890;4:576. 9. Rayan GM, Frey B. Ulnar polydactyly. Plast Reconstr Surg. 2001;107:1449. 10. Kozin SH. Upper-extremity congenital anomalies. J Bone Joint Surg Am. 2003;85:1564–1576. 11. Patterson TS. Congenital ring constrictions. Br J Plast Surg. 1961;14: 1. 12. Quintero RA, Morales WJ, Philips J, et al. In utero lysis of amniotic bands. Ultrasound Obstet Gynecol. 1997;10:316–320.


CHAPTER 90 ■ DUPUYTREN’S DISEASE M. FELIX FRESHWATER

Unlike the patient seeking cosmetic surgery, a patient rarely arrives in a plastic surgeon’s office stating, “I have Dupuytren’s disease and want surgery as soon as possible.” More commonly, the patient is concerned about the malignant potential of a palmar thickening or mass, or about the inexorable contracture of one or more digits that is interfering with function. The initial consultation provides the plastic surgeon with the opportunity to educate the patient about his disease and treatment choices. This chapter discusses Dupuytren’s disease and includes current theories about the etiology, pathologic anatomy, available surgical treatment, expected results, and attendant complications.

NORMAL ANATOMY In the past three decades, we have learned much about the normal anatomy of the palmar fascia. This is primarily a result of the anatomic work of Stack and McGrouther. Stack studied cross-sectional anatomy in fetuses. McGrouther dissected a series of fresh and preserved cadavers with Dupuytren’s disease using an operating microscope with magnification up to 10× power. He discovered that the palmar fascia was composed of a three-dimensional matrix of transverse, longitudinal, and vertical skin ligaments. McGrouther hypothesized that this matrix enables the skin on the working surface of the hand to better withstand compressive and shear forces while still allowing the digits to move (Fig. 90.1).

PATHOLOGIC ANATOMY McGrouther was able to correlate the nodules, pits, cords, and joint contractures that extended from the palm into the phalanges.

Dupuytren’s Disease versus Dupuytren’s Contracture Dupuytren’s disease is the development of scar tissue in the palm and digits. This scar tissue is different from ordinary scar tissue because it contains proportionally more immature type 3 collagen than normally occurring type 1 collagen, which is found in the palmar fascia. Initially, pits or nodules of scar tissue develop in the palm, but most progress to form cords of scar tissue that involve digits as well as the first web space. The cords result in contraction of the metacarpophalangeal joint. As they progress, the proximal interphalangeal joints contract with hyperextension of the distal interphalangeal joints, resulting in a pseudoboutonnière deformity. McFarlane described three types of pathologic cords: the pretendinous cord that develops from the pretendinous band; the lateral cord that develops from the lateral sheet; and the spiral cord that is caused by the confluence of the pretendinous band with the spiral band and lateral

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digital sheet. The spinal cord wraps around the neurovascular bundle, placing it at greater risk during surgery. The first web space cord can cause an adduction contracture of the thumb. When the cords of scar tissue result in joint stiffness, the process is called Dupuytren’s contracture. We know that pits or nodules form in the palm and can rest peacefully for years or, over the course of time, they can progress to the formation of cords that extend into the digits. Myofibroblasts are found in all stages of Dupuytren’s disease. Chiu and McFarlane believe that contractile elements in the myofibroblasts that contain α smooth muscle actin adhere to each other via desmosomal attachments on each cell wall. However, myofibroblasts alone cannot explain the degree of contracture that develops in Dupuytren’s disease let alone in Dupuytren’s contracture. The effect of mechanical compression of scar tissue has been hypothesized to result in its hypertrophy. This theory has been supported by recent tissue culture research suggesting that Dupuytren’s disease fibroblasts have a delayed response to achieving tensional homeostasis. Regression of Dupuytren’s contracture via the release of tension in the cords has been described and is part of the rationale for various treatment modalities.

WHO IS AT RISK FOR DEVELOPING DUPUYTREN’S DISEASE? Dupuytren’s disease has a genetic predisposition. The population at greatest risk for Dupuytren’s disease is of northern European descent. It is extremely rare in black patients. A landmark epidemiologic study was performed by Mikkelsen in 1969, in a small, isolated, Norwegian coastal town. Almost 16,000 of the town’s 27,000 inhabitants older than age 16 years were examined. The prevalence of Dupuytren’s disease was 10.5% for men and 3.1% for women. However, the ratio of men to women uniformly decreased from 8:1 in the 40- to 44-yearold age group to 1:1 in the 85- to 89-year-old age group. The International Federation of Societies for Surgery of the Hand (IFSSH) undertook an epidemiologic study of 1,150 patients who consulted hand surgeons worldwide. Among the conclusions of this study were the following: ■ ■ ■ ■ ■ ■ ■

The typical patient was a 57-year-old male with a 10-year history of Dupuytren’s disease. The disease was bilateral with one hand being more severe, and severity being unrelated to hand dominance. The patient is unlikely to admit any diathesis factors. In females, the disease had a later onset and was less severe. Japanese had later onset, fewer diathesis factors, and lesssevere disease. Unilateral disease was less severe. Alcoholism and epilepsy were associated with more severe disease, trauma was associated with less severe disease.


Chapter 90: Dupuytren’s Disease

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1 Graysons Ligament 2 Clelands Ligament 3 Lateral Digital Sheet 4 Natatory Ligament 5 Transverse Fibers

2

6 Pretendinous Bands 6a Skin Insertion of Pretendinous Bands

1

7 Bands of Legeu & Juvara

3

8 Spiral Band 4

1 4 8

6a

3

5

7 6

FIGURE 90.1. Anatomy of the palmar and digital fascia. A thorough knowledge of the anatomy of the palmar and digital fascia in the normal palm and finger is essential for an understanding of the patterns of anatomic distortion in the hand with Dupuytren’s contracture.

Other factors have been implicated in the development of Dupuytren’s disease, including alcoholism, drug therapy for epilepsy, diabetes, and smoking. It is thought that these factors are related to their respective metabolic effects. Repetitive trauma, however, has not been implicated as a cause. A single traumatic event can cause traumatic palmar fascitis (TPF) in some patients with a genetic predisposition (Fig. 90.2). TPF is histologically indistinguishable from Dupuytren’s disease. Factors that distinguish traumatic palmar fascitis from Dupuytren’s disease include the following: ■ ■ ■ ■

■

TPF can result from a relatively trivial palmar wound or blunt trauma. TPF occurs in young patients. TPF progresses unpredictably, but can occur within days of the event. The lesion from TPF is often painful, sometimes burning, and fails to respond to either systemic or locally injected steroids. TPF has a high incidence of postsurgical recurrence.

Recently research has focused on the exact genetic mechanism for the development of the disease with involvement of the Zf9 transcription factor gene that increases transforming growth factor-beta 1 (TGF-β 1 ), a cytokine that stimulates fibroblast proliferation and extracellular matrix deposition.

THE INITIAL CONSULTATION A pertinent history is mandatory. As previously noted, the patient usually presents with one of two chief complaints caused by Dupuytren’s disease. Either the patient has a nodule or cord and is concerned about its malignant potential, or has a contracture and is concerned about loss of hand function. The history should include a determination of family history of Dupuytren’s disease. Merely asking about Dupuytren’s disease is insufficient because the disease is frequently misdiagnosed. An older relative with “arthritis” may have had Dupuytren’s contracture. It is important to ascertain the duration of the

FIGURE 90.2. Case report of traumatic palmar fasciitis. This now 54-year-old female court reporter fell while jogging 17 years prior to this photograph. She developed a hematoma at the intersection of her fourth ray with the proximal palmar crease. The hematoma was replaced by a painful palmar mass that was diagnosed by an orthopedic surgeon as a “ganglion.” Eventually the pain resolved; however, 10 years later the patient developed the bands that are visible in the photograph. They are asymptomatic and do not interfere with her ability to consistently report verbatim more than 250 words per minute.

patient’s nodules or cords. If the patient has developed a contracture, the examiner should assess the rate the contracture is progressing. A thorough hand examination should be performed with particular attention to palpating the hand and digits for any asymptomatic nodules or cords. Frequently, the patient is unaware of pathology in the first web space, which may not be apparent until the examiner palpates it and compares radial abduction in both hands. One must accurately measure the sensory status of the digits because a patient with Dupuytren’s disease may have underlying median neuropathy that can present postoperatively as an unrecognized cause of complex regional pain syndrome. Furthermore, if a patient develops a postoperative neuropathy, it is important to know the baseline preoperative sensibility. This enables the surgeon to advise the patient of the potential for recovery from a postoperative neurapraxia that can develop if there has been a longstanding joint contracture. Accurate measurement of joint range of motion is mandatory. These measurements allow the surgeon to follow the patient’s condition should surgery be deferred. Postoperatively, joint measurements are useful for measuring the rate of recovery. If the surgeon notes contracture of a proximal interphalangeal joint, the surgeon should test that joint for attenuation of its extensor mechanism. This is accomplished by having the patient fully flex his or her wrist. The examiner uses his or her digit on the dorsum of the proximal phalanx to flex the metacarpophalangeal joint of the digit being examined. This creates a tenodesis effect on the central slip and, if it is not intact, an extensor lag will develop. If the patient cannot extend the joint in this manner, postoperative splinting of the joint will be necessary.


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WHAT DO YOU COUNSEL THE PATIENT? Patients are informed that the rate of progression cannot be predicted. For example, decades may pass before a nodule progresses to a cord and then to a contracture. A useful means of empowering the patient and allowing the patient to be involved in the patient’s own treatment planning is the “tabletop test,” which was developed by Hueston. In this form of self-examination, the patient is advised to return for treatment when the patient can no longer place his or her hand flat on a table. A discussion of surgical risks and complications should include the following points: 1. Surgery for Dupuytren’s contracture is akin to an antibiotic rather than a vaccine. In other words, just as an antibiotic may cure a bacterial infection, surgery may cure the immediate problem of joint contracture. However, unlike a vaccine that prevents the contraction of a disease, surgery does not prevent either its recurrence in the operative site or the extension of Dupuytren’s disease to elsewhere in the hand. 2. Surgery has inherent risks beyond the anesthetic risks, including the following: a. Wound infection; b. Bleeding or hematoma formation; c. Numbness from either direct injury to or stretching of digital nerves; d. Tissue necrosis, including flap necrosis; e. Vascular problems ranging from cold intolerance to gangrene from either direct injury to or stretching of digital arteries; f. Stiffness from either regression of released joints or stiffness of uninvolved joints; g. Pain ranging from postoperative incisional pain to the dreaded complication of complex regional pain syndrome. The surgeon should discuss these risks with the patient, be sure that all of the patient’s questions are answered, and not rely on the patient’s completing a consent form as being the sole basis for these risks having been understood by the patient.

WHAT DO YOU DO IN THE OPERATING ROOM? A complete description of the types of surgery available to treat Dupuytren’s contracture is beyond the scope of this chapter and there are excellent descriptions of worthwhile techniques by other authors. There are five types of surgical treatment for the diseased fascia. 1. Fasciotomy, which was the procedure performed by Dupuytren’s in the early 19th century without anesthesia or aseptic technique. This is typically reserved for the frail, elderly patient who is not a candidate for major surgery and postoperative rehabilitation. It is the simple division of any cords in the palm and can even be performed percutaneously. Typically, fasciotomy is performed in these patients to improve skin hygiene and make custodial care more facile. The rationale for performing fasciotomy is that it relieves longitudinal traction, albeit temporarily. 2. Radical fasciectomy, which was popularized in England after World War II. It was based on the premise that Dupuytren’s disease was like a tumor and complete

excision of the palmar fascia would improve function while lessening recurrence or extension. Sadly, this procedure produced many surgical cripples. Fortunately, it has been abandoned. 3. Limited fasciectomy, which is the most common form of treating Dupuytren’s contracture today. Only the diseased tissue in the palm and digits is excised and local flaps are fashioned as needed in order to minimize unfavorable scar formation. The technique is predicated on the fact that there is no skin deficiency in Dupuytren’s contracture so that rearrangement of the skin by Zplasties, Y–V plasties, and combinations thereof, is sufficient to relieve the tension that incites the progression of the Dupuytren’s disease. The open palm technique of McCash is a modification of the limited fasciectomy technique in which the palm is allowed to heal by secondary intention. It was developed to lessen the dreaded consequences of hematoma formation and flap necrosis. 4. Dermofasciectomy with skin grafting, which is the removal of the diseased fascia and its overlying skin. It is reserved for three specific circumstances—when treating patients with recurrent disease; when replacing flaps of uncertain viability; and when treating younger patients with a very strong diathesis. 5. Segmental aponeurectomy, which is the removal of approximately 1-cm segments of the diseased cords and nodules without skin undermining.

TREATING THE CONTRACTURES Metacarpophalangeal Joints Because these joints are cam shaped, their collateral ligaments are stretched in flexion. Thus when the pretendinous cords are released, the metacarpophalangeal joints readily return to extension.

Proximal Interphalangeal Joints These joints are less forgiving than the metacarpophalangeal joints. Despite careful release of the cords that are causing the contracture, the proximal interphalangeal joints may have intrinsic structural tightness that limits their satisfactory release. Furthermore, if these joints have been severely flexed for years, attempts to completely correct the contracture may result in stretching of the neurovascular structures, resulting in further damage to or even loss of the digit.

WHAT ARE THE EXPECTED RESULTS? Although there are many retrospective studies by different authors describing their clinical experiences, there is a dearth of useful studies discussing the results of surgical treatment. A recent prospective trial supports the theory that longitudinal tension incites the development of Dupuytren’s disease. Half the patients were treated by fasciotomy through a transverse incision and the other half had a Z-plasty performed after the fasciotomy. The patients were followed for 2 years, but the trial had to be stopped because the recurrence rate was statistically significantly greater in the first group. The most comprehensive epidemiologic study was described by McFarlane using the IFSSH data. He concluded that no


Chapter 90: Dupuytren’s Disease

matter which procedure was performed, the results of metacarpophalangeal joint release were satisfactory, but the degree of proximal interphalangeal joint correction was less if the open palm technique had been performed. He also found that no matter which technique had been employed, the recurrence rate was between 50% and 60%. The variables that contributed to the worse results were alcoholism, extensive involvement, and the open palm technique. Many authors have dealt with the problem of proximal interphalangeal joint correction. Techniques ranging from gentle manipulation to arthroplasty have been advocated. A prospective study of patients with proximal interphalangeal joints with contractures of 60 degrees or more divided them into two groups. The first group had fasciectomy performed and the second group had additional surgery to release the joints. Both groups had identical postoperative therapy. At 6-month followup examination there was no statistical difference in the results.

WHAT DOES THE FUTURE HOLD FOR ALTERNATIVE TREATMENT? Various forms of nonsurgical treatment of Dupuytren’s disease have been tried. The most promising modality is an enzymatic fasciotomy via the injection of clostridial collagenase. Clinical trials have been conducted suggesting that improvement will occur within 1 month of a single injection, that metacarpophalangeal joints respond better than interphalangeal joints, and that there were fewer recurrences during a 4-year follow-up period.

Suggested Readings Badalamente MA, Hurst LC, Hentz VR: Collagen as a clinical target: nonoperative treatment of Dupuytren’s’s disease. J Hand Surg. 2002;27A:788–798. Bayat A, Watson JS, Stanley JK, et al. Genetic susceptibility to Dupuytren’s disease: association of Zf9 transcription factor gene. Plast Reconstr Surg. 2003;111:2133–2139.

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Beasley RW. Dupuytren’s’s disease. In: Beasley RW, ed. Beasley’s Surgery of the Hand. New York: Thieme; 2003:468–487. Beyermann K, Prommersberger KJ, Jacobs C, et al. Severe contracture of the proximal interphalangeal joint in Dupuytren’s’s disease: does capsuloligamentous release improve outcome? J Hand Surg. 2004;29(B):240– 243. Bisson MA, Mudera V, McGrouther DA, et al. The contractile properties and responses to tensional-loading of Dupuytren’s’s disease-derived fibroblasts are altered: a cause of contracture? Plast Reconstr Surg. 2004;113:611– 621. Brickley-Parsons D, Glimcher MJ, Smith RJ, et al. Biochemical changes in the collagen of the palmar fascia in patients with Dupuytren’s’s disease. J Bone Joint Surg Am. 1981;63:787–797. Brody GS, Peng STJ, Landel RF. The Etiology of Hypertrophic Scar Contracture: Another View. Plast Reconstr Surg 1981;67:673–684. Burge P, Hoy G, Regan P, et al. Smoking, alcohol and the risk of Dupuytren’s’s contracture. J Bone Joint Surg Br. 1997;79:206–210. Chiu HF, MacFarlane RM. Pathogenesis of Dupuytren’s contracture: a correlative clinical-pathological study. J Hand Surg. 1978;3A:1–10. Citron N, Hearnden A. Skin tension in the aetiology of Dupuytren’s disease: a prospective trial. J Hand Surg. 2003;28B:528–530. Furnas DW. Dupuytren’s contracture in a black patient in East Africa. Plast Reconstr Surg. 1979;64:250–251. Gabbiani G, Majno G. Dupuytren’s’s contracture: fibroblast contraction? An ultrastructural study. Am J Pathol. 1972;66:131–146. Hueston JT. Regression of Dupuytren’s contracture. J Hand Surg. 1992;17B:453– 457. Hueston JT. The table top test. Med J Aust. 1976;2:189–190. Hurst LC and Badalamente MA. Associated Diseases in McFarlane RM, McGrouther DH, and Flint MH eds. Dupuytren’s Disease: Biology and Teatment. Edinburgh: Churchill Livingstone, 1990:253–260. McFarlane RM. Patterns of diseased fascia in the fingers in Dupuytren’s contracture. Displacement of the neurovascular bundle. Plast Reconstr Surg. 1974;54:31–44. McFarlane RM. The results of treatment. In: McFarlane RM, McGrouther DH, Flint MH, eds. Dupuytren’s Disease: Biology and Treatment. Edinburgh: Churchill Livingstone; 1990:387–412. McFarlane RM, Botz JS, Cheung H. Epidemiology of surgical patients. In: McFarlane RM, McGrouther DH, Flint MH, eds. Dupuytren’s Disease: Biology and Treatment. Edinburgh: Churchill Livingstone; 1990:201– 238. McGrouther DA. Dupuytren’s contracture. In: Green DP, Hotchkiss RN, Pederson WC, eds. Green’s Operative Hand Surgery. 5th ed. New York: Churchill Livingstone; 2005:159–186. McGrouther DA. The Hand. 1984;14:215–236. Moermans JP. Long-term results after segmental aponeurectomy for Dupuytren’s disease. J Hand Surg. 1996;21B:797–800. Stack HG. The Palmar Fascia. London: Churchill Livingstone; 1973. Smith P, Breed C. Central slip attenuation in Dupuytren’s contracture: a cause of persistent flexion of the proximal interphalangeal joint. J Hand Surg. 1994;19(A):840–843 .


CHAPTER 91 ■ REPLANTATION IN THE UPPER EXTREMITY NEIL F. JONES

Replantation describes the re-attachment of a completely amputated part by restoration of arterial inflow and venous outflow, whereas revascularization describes restoration of arterial inflow or venous outflow, or both, to an incompletely amputated part, no matter how small the point of attachment. Following the first successful replantation of an upper arm amputation by Malt and McKhann in 1962, the first successful replantation of an amputated thumb was performed in 1968 by Komatsu and Tamai. Since then replantation teams have been organized in most major hospitals, and microsurgical techniques have become an integral part of the training of plastic surgeons and hand surgeons, leading directly to the evolution of elective microsurgical free tissue transfer.

INDICATIONS In general, any patient with an amputation involving the upper extremity is a candidate for replantation, but ideal candidates have sharp, guillotine-type amputations of the thumb, multiple digits, hand, wrist, and forearm that are minimally contaminated (Table 91.1). The decision to proceed with replantation of an amputated part can only be made by an experienced microsurgeon or hand surgeon. Because the patient and family naturally expect a miraculous result, it is important that the referring physician explain that the patient is being transferred for evaluation by an experienced microsurgeon to determine whether replantation is possible, rather than raising their hopes unrealistically. When faced with a difficult decision regarding replantation, the surgeon should consider whether the function of the hand can be improved by replantation when compared to closing the amputation stump and future fitting of a prosthesis.

CONTRAINDICATIONS Contraindications to replantation may be either absolute or relative (Tables 91.2 and 91.3).

ABSOLUTE CONTRAINDICATIONS

Multiple Injuries within the Amputated Part If there are segmental amputations at multiple levels in the amputated extremity (Fig. 91.1A), or if there is extensive crushing or degloving of the amputated part (Fig. 91.1B), replantation is contraindicated. Clinical inspection of the amputated part is correlated with radiographs that may reveal fractures at multiple levels. In the digits, a red line along the lateral aspect of the finger—the “Chinese red streak sign”—is indicative of an avulsion of the digital artery and usually precludes successful replantation. Similarly, coiling or tortuosity of the digital arteries when the digit is inspected under loupe magnification is also evidence of an avulsion mechanism and indicates extensive damage along the digital artery.

Systemic Illness Finally, elderly patients with previous history of a myocardial infarct, heart failure, chronic obstructive pulmonary disease, or insulin-dependent diabetes may not be candidates for prolonged surgery and anesthesia.

RELATIVE CONTRAINDICATIONS Age Elderly patients may have significant systemic disease, but more importantly, the recovery of tendon and nerve function in the replanted digit is poorer than in a younger patient and there is the added risk of producing stiffness in the interphalangeal joints of adjacent uninjured fingers. Arteriosclerosis is relatively rare in the arteries of the upper extremity but can occasionally complicate the anastomoses of the radial and ulnar arteries during replantation at the wrist level in an elderly patient. Replantation in young children may be more technically demanding because of the small caliber of the vessels and the propensity for vasospasm, but every effort should be made to replant a digit in a child, as the digit will continue to grow and the results of the tendon and nerve repairs are so much better than in an adult (1,2).

Significant Associated Injuries

Avulsion Injuries

Digital amputations are rarely associated with other major injuries, but major amputations of the arm are frequently associated with head, chest, and abdominal injuries. These may be life-threatening and may preclude replantation of the upper extremity amputation.

With avulsion injuries, there is usually extensive damage to the digital arteries and digital nerves both proximal and distal to the level of amputation (Fig. 91.2). Experimentally, actual injury to the digital artery has been shown to extend as far as 4 cm from the site of transection when examined by

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AMPUTATIONS SUITABLE FOR REPLANTATION Thumb Multiple digits Transmetacarpal Wrist Forearm Single digit in children

RELATIVE CONTRAINDICATIONS TO REPLANTATION Patient’s advanced age Avulsion injuries Prolonged warm ischemia time Massive contamination Patient’s psychological problems Single-digit amputation

electron microscopy compared with 0.8 cm under the operating microscope. Injuries resulting from rodeo or waterskiing demonstrate obvious avulsions of nerves and tendons, with long segments of these structures hanging from the amputated digit (Fig. 91.2C). In contrast, the digital arteries are usually avulsed distally from within the digit, sometimes all the way to the trifurcation of the digital artery at the level of the distal interphalangeal joint. Replantation will only be successful if a normal lumen of digital artery can be found before the artery trifurcates. In addition, replantation requires the use of interposition vein grafts or transposition of a neurovascular bundle from an adjacent digit (3). The most extreme example of an avulsion injury is the socalled ring avulsion injury. These injuries range from circumferential lacerations at the level of the proximal phalanx with thrombosis or transection of the dorsal veins and both digital arteries (Fig. 91.3) to complete degloving of the soft-tissue envelope of the digit or amputation of the digit through the distal interphalangeal joint (Fig. 91.4). The Urbaniak classification of ring avulsion injuries has been expanded by Kay et al. (4) into four categories (Table 91.4). Arterial revascularization usually requiring interposition vein grafts is necessary for class IIa and class IIIa injuries whereas class IIv and class IIIv injuries require venous anastomoses. Class IV complete degloving or complete amputations require a full replantation procedure. Approximately 75% of classes II, III, and IV ring avulsion injuries can be successfully salvaged by revascularization or replantation.

Prolonged Warm Ischemia Time Muscle is the tissue most susceptible to ischemia and undergoes irreversible changes after 6 hours at room temperature. Because a proximal forearm or upper arm amputation contains significant muscle mass, it is vitally important that such amputations be cooled as quickly as possible, and if necessary, reperfused through arterial shunts to reduce the warm and cold ischemia times. Because digits do not contain muscle, they have a much longer ischemic tolerance. With multiple digital amputations, cases have been reported of successful replantation after 33 hours of warm ischemia, and after 94 hours of cold ischemia. A hand amputation has been successfully replanted after 54 hours of cold ischemia.

Massive Contamination Surgical debridement precedes any major upper extremity replantation, but occasionally, massive contamination in farm injuries or tissue impregnation by oil or grease in machine injuries preclude replantation because of the risk of infection and overwhelming sepsis. In rare situations in which the distal part is devascularized and the zone of injury is extensive, massively contaminated, or ill defined, temporary ectopic implantation of the distal part with anastomoses to the thoracodorsal artery and vein is a reasonable option. The proximal stump can then be treated with conservative debridement and after healing has been achieved, the distal part can be electively replanted onto the healed stump several months later.

Psychological Problems Self-inflicted amputations, usually of the hand or wrist, may foreshadow a later successful suicide attempt. These patients require an emergency psychiatric evaluation prior to any decision regarding replantation.

Single-Digit Amputations Although a single-digit amputation should always be replanted in children (Fig. 91.5), replantation of a single digit in an adult remains controversial. Even though viability can be restored after amputation proximal to the proximal interphalangeal (PIP) joint, digital motion is compromised because of the adhesions associated with flexor tendon repairs in zone II, resulting in less than satisfactory flexion at the PIP and distal interphalangeal (DIP) joints. Replantation of an index finger amputation proximal to the PIP joint in an adult is almost universally unrewarding, because the brain excludes the index finger and substitutes the middle finger for thumb–middle finger pinch. Similarly, replantation of a single middle, ring, or small finger may interfere with the motion of the other two fingers because of the common origin of the flexor digitorum profundus tendons. However, replantation of a single-digit amputation through the middle phalanx distal to the insertion of the flexor digitorum sublimis tendon, or through the distal phalanx, may provide excellent sensory return, with maintenance of full flexion at the PIP joint.

TA B L E 9 1 . 2 ABSOLUTE CONTRAINDICATIONS TO REPLANTATION Significant associated injuries Multiple injuries within the amputated part Systemic illness

TRANSFER TO A REPLANTATION SERVICE Once the surgeon has decided, usually by telephone, that the patient and the amputated part are suitable for potential replantation, the referring physician should ensure that hemorrhage from the amputation stump has been stopped by

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B FIGURE 91.1. Contraindication to replantation. A: A multisegmental amputation through the distal forearm, palm, and within the thumb and index finger sustained in an agricultural injury is an absolute contraindication to replantation. B: Extensive lacerations and crushing of these three digits precludes replantation.

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FIGURE 91.2. Avulsion injuries. A and B: Avulsion of the right upper extremity through the proximal third of the humerus in a snowmobile accident resulted in avulsion of the median, ulnar, and radial nerves. Replantation is contraindicated. C: Typical avulsion amputation of the thumb at the level of the metacarpophalangeal (MCP) joint with avulsion of the flexor pollicis longus from the musculotendinous junction in the forearm. Contrary to other avulsion amputations, every attempt should be made to replant a thumb avulsion.


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B FIGURE 91.3. Class II ring avulsion injury of the right long finger with partial degloving of the soft-tissue envelope and transection of all dorsal veins and both digital arteries, but without an associated phalangeal fracture.

application of a pressure dressing and elevation, and that fluid resuscitation has been instituted if necessary. Tetanus prophylaxis may be required and broad-spectrum intravenous antibiotics are begun. The amputated part is wrapped in sterile gauze moistened with lactated Ringer solution, sealed in a plastic bag,

and placed in a container of water and ice at a temperature of 39.2◦ F (4◦ C). The surgeon should also advise the referring physician of the urgency of transfer of the patient and amputated part either by ambulance or, occasionally for major replantations, by helicopter.

B

A FIGURE 91.4. Class III ring avulsion injury of the dominant right small finger in an 11-year-old girl. The digital nerves and arteries were avulsed at the level of the distal interphalangeal joint and replantation could not be completed.

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TA B L E 9 1 . 4 CLASSIFICATION OF RING AVULSION INJURIES (4) Class I Class IIa Class IIv Class IIIa Class IIIv Class IV

Circulation adequate, with or without skeletal injury Arterial circulation inadequate, no skeletal injury Venous circulation inadequate, no skeletal injury Arterial circulation inadequate with fracture or joint injury Venous circulation inadequate with fracture or joint injury Complete amputation

PREPARATION OF THE AMPUTATED PART If the surgeon decides that the patient and the amputated part fulfill the criteria for replantation, the amputated part and radiographs are taken to the operating room so that the amputated part can be prepared while the patient is being made ready for anesthesia and surgery. The amputated part is cleaned with routine bacteriocidal solution and placed on a small operating table. If there is gross contamination, the part can be irrigated with pulsatile jet lavage. All of the structures in the amputated part are then identified and tagged, initially under loupe magnification and later under the operating microscope.

Skin Incisions

EVALUATION FOR REPLANTATION SURGERY A member of the replantation team should obtain a history from the patient, including the patient’s age, hand dominance, occupation, and pre-existing systemic illness. A description of the mechanism of injury usually allows the surgeon to determine whether the amputation was caused by a sharp transection or a crushing or avulsion mechanism. Physical examination is performed to exclude other injuries. Radiographs of the amputated part and the proximal extremity should be obtained if they have not already been sent with the patient. It is important to exclude any associated fractures in the limb proximal to the level of amputation. Routine investigations include a chest radiograph, electrocardiogram, complete blood count, and electrolytes. Blood typing and cross-matching are necessary for all major replantation procedures.

In an amputated digit, two midlateral incisions are made so that anterior and posterior skin flaps can be mobilized to provide access to the radial and ulnar neurovascular bundles. For ring avulsion injuries, a single dorsal midline incision may be used. For arm and forearm amputations, the incisions are not placed directly over the nerves and arteries, because it is likely that primary closure will not be possible and it is better not to place skin grafts directly over the repaired arteries and nerves. The incisions in the amputated part and in the amputation stump can be staggered so that the flaps can be transposed in a Z-plasty fashion during final closure. Contused skin margins and contaminated subcutaneous tissue are sharply debrided.

Debridement In major forearm and upper arm amputations, it is difficult to determine how much of the muscle will eventually remain

A

FIGURE 91.5. Replantation of a single-digit amputation in a child should always be attempted and is usually associated with very satisfactory flexor tendon function, sensory return, and relatively normal growth. In this 2-year-old child, a steel door severed all structures from the dorsum of the left index finger through the proximal interphalangeal (PIP) joint, leaving only a small pedicle of palmar skin.


B


viable. Contused, lacerated, or contaminated muscle is sharply debrided. Irrigation with heparinized lactated Ringer solution through a catheter inserted into one of the inflow arteries can be used to determine which portions of the muscles will remain viable once arterial inflow is restored. Any muscle that does not “weep” the lactated Ringer solution should be aggressively excised as it will not be perfused after the arterial and venous anastomoses are completed. Fasciotomies are usually required in upper arm and forearm amputations, and are designed over the anterior and posterior forearm muscle compartments and over the second and fourth metacarpals to decompress the intrinsic muscle compartments.

Tagging of Neurovascular Structures Under loupe magnification or the operating microscope, the two digital arteries and the radial and ulnar digital nerves are identified through the midlateral incisions and traced in a distal-to-proximal direction to identify the digital nerves and arteries at the level of the amputation. With avulsion amputations, there may be tortuosity of the digital arteries, which should be traced, until the arterial lumen appears normal under the operating microscope. In some avulsion injuries, the digital artery is not present at the level of the amputation and has been avulsed from within the digit. The surgeon must find the distal end of the digital artery, and replantation will require interposition vein grafts. The two digital arteries and two digital nerves are identified with an 8-0 nylon marking suture or small metallic clips to allow easier identification later in the surgery. To distinguish between the digital artery and the digital nerve, either both ends of the suture or a single end of the suture can be left long. The digital nerves are cut 1 to 2 mm distal to the level of the amputation until a normal-appearing fascicular pattern is seen. Similarly the digital arteries are cut with the microdissecting scissors and the vessel lumen dilated with a vessel dilator. Serial sectioning is continued distally until a normal-appearing lumen of the digital artery is seen under the operating microscope. The dorsal skin flap is elevated distally in the plane between the subcutaneous tissues and the underlying extensor tendons to visualize the dorsal veins within the subcutaneous tissues. The dorsal skin is then elevated 1 to 2 mm from the level of the amputation to identify two or three veins, which are again tagged with 8-0 nylon sutures as small clips. In upper arm and forearm amputations, the brachial, radial, and ulnar arteries, together with the median, ulnar, and radial nerves and several large subcutaneous veins, are identified and tagged.

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Bony Shortening and Fixation Bony shortening is an integral component of replantation surgery in all upper extremity amputations, as it potentially allows primary nerve repair and end-to-end vessel anastomoses. Depending on the level of amputation, the surgeon decides whether bony shortening should be performed on the amputated part only, on the amputation stump only, or in both places. However, it is important to maintain the mobility of the metacarpophalangeal (MCP), PIP, and DIP joints, and the insertion of the flexor and extensor tendons. The periosteum on the amputated bone is elevated. A small hole is made in a piece of Esmarch bandage or surgical glove, and the bone end is placed through this hole to protect the soft tissues during bony resection. The bone is then cut transversely, using a power saw. In forearm amputations, the radius and ulna may require 2.5 to 5 cm of shortening, and in upper arm amputations, the humerus may require 4 to 8 cm of shortening to allow primary nerve and muscle repair. Rigid internal fixation is the technique of choice in replantation surgery, primarily to allow early protected motion of the adjacent joints. Type A intraosseous wiring or 90-90 intraosseous wiring is used for replantations through the phalanges. Longitudinal K-wires or minicompression plates are best for transmetacarpal amputations. Rigid fixation of the radius and ulna requires 3.5-mm dynamic compression plates, and fixation of the humerus requires 4.5-mm plates (5). These plates or intraosseous wires may be applied to the bone within the amputated part prior to fixation of the part to the amputation stump. If the amputation passes through a joint, primary arthrodesis accomplishes both bony shortening and bony fixation. This is especially indicated in amputations of the thumb at the level of the MCP joint (Fig. 91.6) and amputations of the hand at the level of the radio-carpal joint. However, for amputations of the digit through the metacarpophalangeal joints, an alternative option is immediate placement of a silastic implant arthroplasty to preserve motion at this joint.

Hemostasis Finally, hemostasis is achieved in the amputated part by bipolar coagulation as this can be difficult once revascularization is performed. Hemostasis is particularly important in transmetacarpal amputations where branches of the deep metacarpal arteries may bleed profusely, as well as in forearm amputations. The amputated part is now ready for replantation and is wrapped in gauze moistened with ice-cold lactated Ringer solution.

Preparation of Flexor and Extensor Tendons The extensor tendon in the amputated digit does not usually retract and can be gently elevated from the underlying periosteum for a distance of 5 mm. The flexor digitorum profundus and flexor digitorum sublimis tendons may be apparent at the level of the amputation or may be found more distally in the digit, depending on the position of the hand at the time of amputation. The flexor tendon sheath is incised to identify the two flexor tendons, but care should be taken to preserve at least 50% of the A-2 and A-4 pulleys. The ends of the two flexor tendons are cut sharply with a scalpel to debride any ragged or contaminated tendon. A core suture of 4-0 braided nylon may be placed into the flexor digitorum profundus tendon prior to bony fixation of the amputated part, as it may become more difficult to place this core suture later in the replantation sequence.

PREPARATION OF THE AMPUTATION STUMP The patient is usually placed under continuous axillary block anesthesia using 0.5% bupivacaine (Marcaine) or under general anesthesia. A urinary catheter is inserted because of the length of the procedure. A padded tourniquet is applied around the upper arm for all amputations other than those through the humerus itself. Debridement, identification, and tagging of all structures is performed exactly as described for the amputated part. The flexor tendons may have retracted proximally and after retrieval can be held out to a suitable length by transfixion with a 23-gauge needle. A similar core suture of 4-0 braided nylon can be placed into the proximal stump of the

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TECHNIQUE OF REPLANTATION Once the surgeon has established that there is good proximal arterial inflow and sufficient time (20 minutes) has elapsed since the previous tourniquet deflation, the tourniquet is re-inflated as this will facilitate bony fixation and repair of the flexor and extensor tendons and digital nerves. Although the following sequence of repair during digital replantation has been advocated: 1. 2. 3. 4. 5. 6. 7. 8.

Bony fixation Repair of periosteum Extensor tendon repair Flexor tendon repairs Arterial anastomoses Nerve repairs Venous anastomoses Skin closure

the sequence can vary, depending on the surgeon’s preference. It is probably more logical to perform the bony fixation, flexor and extensor tendon repairs, and the digital nerve repairs under the tourniquet, and then complete the replantation with the venous anastomoses and digital artery anastomoses.

Bone Fixation The distal amputated part is aligned with the proximal stump and fixation completed using compression plates for the humerus, radius, and ulna; longitudinal K-wires or minicompression plates for the metacarpals; and Lister type A intraosseous wiring or 90-90 intraosseous wiring for the phalanges. For amputations through the metacarpophalangeal joint of the thumb or through the radiocarpal joint at the wrist, primary arthrodesis is performed using similar techniques (Fig. 91.6).

FIGURE 91.6. Postoperative radiograph following thumb replantation showing primary arthrodesis of the MCP joint using 90-90 intraosseous wiring.

flexor digitorum profundus tendon prior to replantation. After identification of the digital arteries, they can be mobilized more proximally into the palm. The ends of the digital arteries are then sharply cut with microdissecting scissors and the vessel lumen is dilated with vessel dilators. The arteries are serially sectioned until a normal-appearing intima is seen under the operating microscope. After debridement, identification, and tagging of all structures, the tourniquet is deflated to assess the force of arterial inflow. Distal traction is applied to each proper or common digital artery using jeweller’s forceps, and if there is a good “spurt” test, each digital artery is occluded with a single vessel clamp. If there is poor inflow through the proximal arteries, this may be a result of vasospasm or because of more proximal compression of the ulnar artery in Guyon’s canal. The digital arteries can be bathed with 2% lidocaine (Xylocaine) or papaverine to relieve vasospasm. In transmetacarpal amputations, it is better to release the ulnar artery through the Guyon’s canal and expose the entire superficial palmar arch. Finally, hemostasis is achieved in the proximal stump, especially in transmetacarpal, forearm, and upper arm amputations.

Periosteum If possible, the dorsal periosteum is repaired using 5-0 absorbable suture. This probably enhances bony union, but more importantly may prevent extensor tendon adhesions at the site of bony fixation.

Extensor Tendon The extensor tendon is then repaired using 4-0 nonabsorbable, interrupted mattress or figure-of-eight sutures.

Flexor Tendons The hand is then turned over and the palmar periosteum repaired with 5-0 absorbable sutures. If possible, both flexor digitorum profundus and flexor digitorum sublimis tendons are repaired. The flat flexor digitorum sublimis tendon is repaired with interrupted mattress or modified Kessler sutures of 4-0 braided nylon. The two core sutures previously placed into the proximal and distal stumps of the flexor digitorum profundus tendon are then tied and the tendon repair completed with a circumferential epitendinous running suture using 6-0 nylon. The same meticulous technique should be used for repair of the flexor tendons for a replant as in an isolated zone II flexor tendon repair so as to provide the best possible circumstances for independent gliding of the flexor tendons following replantation.



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compared with conventional sutured anastomoses, especially when multiple anastomoses have to be performed.

Nerve Repair Under the microscope, the proximal and distal digital nerves are coapted by an epineurial repair using 9-0 or 10-0 nylon sutures. In more proximal amputations at the wrist, forearm, or upper arm level, group fascicular repair of the median, ulnar, and radial nerves is performed using 9-0 nylon sutures. Obviously, the median, ulnar, and radial nerve repairs are performed without tension, and this is usually possible because of the previous bony shortening.

Venous Anastomoses If the usual tourniquet time of 120 minutes has not been exceeded during bony fixation, extensor and flexor tendon repairs, and the nerve repairs, the venous anastomoses can be started under the tourniquet. Otherwise the tourniquet is deflated and the venous and arterial anastomoses performed with the tourniquet down. Two or three dorsal veins in each digit are anastomosed end-to-end using standard microsurgical techniques, usually using 10-0 nylon sutures. If there is any tension whatsoever on the venous anastomoses when the proximal and distal stumps of the vein are introduced into the approximator clamp, interposition vein grafts should be considered. For transmetacarpal amputations and amputations at the level of the wrist, at least three or four dorsal veins should be anastomosed, approximately two veins for each artery. Performing the venous anastomoses before the arterial anastomoses reduces blood loss and avoids performing the venous anastomoses in a pool of blood once arterial inflow has been restored. However, the arterial anastomoses must be performed before the venous anastomoses 1. if there has been a long ischemic interval; 2. in distal amputations in which restoration of arterial inflow allows easier identification of the distal veins; 3. in upper arm and proximal forearm replantations where there is a significant mass of devascularized muscle, in which event, the arterial anastomoses must always be performed first and the patient allowed to bleed from the open veins in the distal part before completing the venous anastomoses. Otherwise, if the venous anastomoses were completed first, the acidotic, hyperkalemic venous blood returning to the systemic circulation from the reperfused ischemic muscle could (occasionally) result in cardiac arrest.

Arterial Anastomoses

Interposition Grafts Interposition vein grafts may be required in the following three circumstances (6): 1. To preserve a functional joint when bony shortening cannot be performed. 2. In avulsion or crush injuries where there is an extensive zone of injury along the artery. 3. To facilitate positioning of the hand in order to perform the microsurgical anastomoses. In thumb amputations where the ulnar digital artery is usually the dominant arterial blood supply to the thumb, it is necessary to hypersupinate the hand in order to perform an endto-end anastomosis of the ulnar digital artery. It is much easier to anastomose an interposition vein graft to the ulnar digital artery while the amputated thumb is on the back table. The interposition vein graft then can be anastomosed to the princeps pollicis artery on the dorsum of the first web space, which is a much more convenient position both for the surgeons and the operating microscope.

Harvesting of Vein Grafts Vein grafts can be harvested from the anterior aspect of the distal forearm for digital replantations, or from the dorsum of the foot and lower leg for forearm vessels. Vein grafts should be harvested under tourniquet control with bipolar coagulation or fine suture ligation of small branches. A suture is placed on the distal end of the vein graft to orientate the direction of flow and further sutures may be placed along the length of the vein graft to prevent torsion. Y-shaped vein grafts may be harvested to facilitate the anastomosis of a single common digital artery to the digital arteries of two adjacent digits (Fig. 91.7).

Arterial Grafts An inherent disadvantage of vein grafts is that the proximal (outflow) end of a vein graft is usually of larger caliber than the distal (inflow) end; consequently, there may be a discrepancy between the proximal (outflow) end of a vein graft and the distal digital artery. For this reason, Godina advocated the use of interposition arterial grafts harvested from the subscapularthoracodorsal-circumflex scapular and serratus arterial system. This branching system also provides a mechanism to graft a single inflow common digital artery to two distal digital arteries. Lister also recommended using the posterior interosseous artery as an interposition arterial graft.

Composite Venous Grafts

The adventitia is removed from the ends of the digital arteries and the lumen dilated with vessel dilators. If the digital arteries can be approximated under minimal tension using a double approximator clamp, direct end-to-end anastomoses are performed using interrupted 9-0 or 10-0 nylon sutures. If there is excessive tension, or if there is a definite segmental gap between the proximal and distal ends of the artery, then interposition vein grafts are necessary. Most digits can be successfully replanted by anastomosis of only one digital artery, but it is preferable to repair both arteries. In the forearm, both the radial and ulnar arteries should be repaired. Instead of conventional end-to-end sutured anastomoses, the Precise Anastomotic Coupler (3M Company, Minneapolis-Saint Paul, MN) may be used for anastomosis of the radial and ulnar arteries at the wrist, the common digital arteries in the hand, and the veins over the dorsum of the hand. Couplers may save time

Finally, a composite venous flap, consisting of a small skin flap and a subcutaneous vein, can be harvested from an adjacent finger or from the dorsum of the foot to provide an interposition vein graft for a segmental defect in the venous outflow of a digital replant, especially if there is also an associated skin defect.

Vein Graft Anastomoses Many interposition vein grafts or arterial grafts can be anastomosed to the distal digital artery in the amputated part on a back table prior to bony fixation. Alternatively, the interposition graft is anastomosed end-to-end to the proximal digital artery, or end-to-side to the superficial palmar arch or to the radial or ulnar artery at the wrist. After completion of this proximal anastomosis, the microsurgical clamps are released

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to allow flow into the interposition vein graft or arterial graft. This sequence has the advantage of confirming the patency of the proximal anastomosis and in addition avoids torsion of the graft and allows accurate estimation of the length of graft required to reach the distal vessel. The distal anastomosis can then be performed end-to-end with arterial blood remaining within the graft, or, alternatively, a single microvascular clamp can be applied proximal to the proximal anastomosis and the blood irrigated out of the graft with heparinized saline. Finally, if the vein graft is too long, it may kink, which could result in eventual occlusion of the vein graft and an unsuccessful replant, especially in the fingers. Consequently, if there is any kinking, either the proximal or distal anastomosis should be revised with a shorter length of graft.

FIGURE 91.7. A Y-shaped vein graft harvested from the dorsum of the foot can be anastomosed on a back table to the digital arteries of two adjacent digits to facilitate multiple digit replantation.

may indicate vasospasm that can be relieved pharmacologically or may mandate placement of a vein graft from a larger, more proximal, inflow artery such as the superficial palmar arch or the radial or ulnar arteries at the wrist. Alternatively, if the digit becomes swollen and cyanotic with rapid capillary refill, the surgeon should examine the venous anastomoses under the operating microscope. Although vasospasm is a potential cause, it is much more likely that venous outflow is occluded because of a technical problem at one of the anastomoses, and this requires either revision of the anastomosis or insertion of a small vein graft to relieve any tension at the anastomosis.

Closure Reperfusion of the Amputated Part Once the arterial anastomoses or interposition vein grafts are complete, the microsurgical clamps are released. All anastomoses are bathed with a solution of 2% lidocaine (Xylocaine) and papaverine, and the extremity is irrigated with warm saline. Successful restoration of perfusion to the amputated digit or extremity is then assessed by return of turgor and color to the distal pulp and capillary refill in the distal phalanx. In addition, bright red bleeding should be seen at the edges of the amputated part. The patency of each arterial and venous anastomosis is tested using the Acland test, stripping a segment of vessel with two vessel dilators distal to the anastomosis followed by release of the proximal vessel dilator. If the digit or hand does not “pink-up,” there are three possibilities: 1. Vasospasm 2. Technical problems at the arterial anastomoses 3. Inadequate proximal arterial inflow. Vasospasm can be relieved by lidocaine (Xylocaine) or papaverine and by warming the extremity. If the Acland patency test reveals poor flow distal to an anastomosis, then the anastomosis is explored and redone, or a vein graft interposed. If there is poor inflow proximal to the anastomosis, this either

Once the surgeon is satisfied with perfusion of the extremity, the skin is closed. Tight closure is avoided because this will compress the venous outflow and lead to secondary venous thrombosis. Skin flaps can be transposed as Z-plasties, or small, split-thickness skin grafts can be applied, even directly over arterial or venous anastomoses or vein grafts. If at any time during skin closure the fingertip loses its pinkish color or becomes dusky, then excessive tension is compromising either arterial inflow or venous outflow. Sutures must be removed and a split-thickness skin graft applied or the wound allowed to granulate. It is vitally important that dressings remain loose and not be applied circumferentially. Finally, the extremity is immobilized in a plaster-of-Paris splint and elevated.

POSTOPERATIVE CARE AND MONITORING Smoking The patient should not be allowed to smoke because of the potentially detrimental effect of the vasoconstrictive mechanism of nicotine (7).



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Antithrombotic Medications

RE-EXPLORATION

On release of the microsurgical clamps a bolus of 40 mL of dextran 40 is given intravenously followed by a continuous infusion of dextran 40 at 25 mL per hour for 5 days (based on a 70-kg adult). Aspirin 80 mg is given daily and antibiotics are continued for several days at the discretion of the surgeon. Heparin anticoagulation is not used in most replantations except in special circumstances where there has been an extensive crushing injury or where there have been prolonged difficulties restoring arterial inflow or venous outflow. The dose of continuous intravenous heparin is adjusted based on the activated partial thromboplastin time. However, heparin may cause hemorrhage within the replant itself, producing edema and swelling that inevitably results in compression of the arterial or venous anastomoses and eventually secondary thrombosis.

If clinical examination or a more objective monitoring technique suggests that perfusion is compromised, the surgeon should initially check that congealed blood within the dressings has not become constricting. All dressings are removed and if any sutures appear tight, they are cut immediately. If there is no improvement in color and capillary refill of the fingertip, the patient should be returned immediately to the operating room for re-exploration of the arterial and venous anastomoses. Thrombosis of one or more of the anastomoses may be obvious, but otherwise a patency test should be performed distal to each anastomosis. If there is either thrombosis or lack of flow, the anastomosis is taken down and revised, which almost always necessitates the use of an interposition vein graft. Providing that compromised perfusion is detected in a timely manner, revision of the anastomoses is often successful. In cases of venous congestion where no further venous anastomoses can be performed, the nail plate is removed, the nail bed roughened, and heparin-soaked pledgets applied to promote venous bleeding. Alternatively, serial application of leeches can occasionally salvage replants compromised by venous congestion.

Clinical Observation Experienced nursing staff should monitor the perfusion of the replant hourly for 48 hours by inspection of the color of the fingertip and capillary refill. If the fingertip becomes pale with slow capillary refill, arterial thrombosis or vasospasm of the arterial inflow is suspected. A swollen and blue fingertip with increased capillary return indicates venous congestion caused by constrictive dressings or thrombosis of the venous anastomoses.

Monitoring Techniques More objective techniques of postoperative monitoring of perfusion following replantation include temperature monitoring, laser Doppler flowmetry, transcutaneous partial pressure of oxygen (Po2 ), and pulse oximetry. Differential temperature monitoring by comparison of the temperature of the replanted digit with an adjacent normal digit or the contralateral hand is the most popular method. A temperature drop of 3.6◦ F (2◦ C) or an absolute temperature of less than 86◦ F (30◦ C) mandates immediate re-exploration of the arterial and venous anastomoses. A pulse oximeter probe secured to the distal phalanx is the simplest technique for postoperative monitoring and provides continuous recordings of the pulse rate and the oxygen saturation within the digit. Loss of the pulse rate indicates arterial occlusion whereas a fall in the oxygen saturation below 90% usually indicates venous occlusion.

REPLANTATION FOR SPECIFIC LEVELS OF AMPUTATION Distal Phalanx With sharp amputations through the distal phalanx, replantation may be a superior option to other forms of fingertip coverage (8). Although it can be technically demanding because of the small size of the distal arteries, successful replantation restores a virtually normal appearance and satisfactory sensibility if the digital nerves can be approximated (Fig. 91.8). A 0.028 or 0.035 K-wire is passed retrograde through the distal fragment of the distal phalanx and the amputated distal phalanx is partially sutured with one or two sutures along its palmar surface to temporarily stabilize the distal fragment. One digital artery and the two digital nerves are repaired under the operating microscope. The distal phalanx is then reduced and the K-wire drilled antegrade to just beneath the articular surface of the distal phalanx, or, if necessary, across the distal interphalangeal joint into the middle phalanx. Finding a suitable vein in the replanted distal phalanx may be a problem. Occasionally after release of the tourniquet, a small vein can be identified dorsally just proximal to the nail fold and a single venous anastomosis performed. Alternative solutions to prevent venous congestion include removal of the

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FIGURE 91.8. Successful replantation of an amputation through the distal phalanx of the left thumb.


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nail plate and application of heparin-soaked pledgets, temporary application of leeches, or the creation of an arteriovenous anastomosis between the other distal digital artery and a proximal vein. Finally, the dorsal skin and nail bed are loosely repaired.

Middle Phalanx Good functional results can be achieved after replantation of digital amputations through the middle phalanges distal to the

insertion of the flexor digitorum sublimis tendon, because PIP joint flexion can be maintained and the return of sensation is relatively good after repair of the digital nerves (9).

Proximal Phalanx The results of replantation of amputations through the proximal phalanges are compromised by tendon adhesions in zone II. Consequently, it is vitally important to use the same

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FIGURE 91.9. Amputation of the thumb, which is usually in the region of the MCP joint, is an absolute indication for replantation and is associated with excellent functional results. A: Amputated part. B: Radiograph of amputated part. C: Amputation stump. D: Radiograph of amputation stump.



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free skin flaps or free joint transfers can be salvaged from a nonreplantable digit to reconstruct an adjacent digit.

Thumb Because the thumb contributes 40% to the overall function of the hand, all thumb amputations should be considered candidates for replantation (Fig. 91.9) (11). The majority of thumb amputations occur at or distal to the MCP joint and because the thumb is relatively unprotected by the other digits, avulsion amputations are relatively common, such as in waterskiing and rodeo injuries (Fig. 91.2C). Specific considerations for replantation of the thumb include the following: E

FIGURE 91.9. (Continued ) E: Postoperative result.

meticulous technique to repair the flexor digitorum profundus and flexor digitorum sublimis tendons in a replanted finger as in an isolated zone II flexor tendon repair. If K-wires are used for bony fixation, they should not transfix the MCP or PIP joints so that early gentle passive and active range-of-motion exercises can be instituted. Destruction of the articular cartilage at the PIP joint mandates arthrodesis of the PIP joint in a functional position. PIP joint arthrodesis can be accomplished by the same techniques of bony fixation—either 90-90 intraosseous wiring or Lister type A intraosseous wiring. The PIP joint of the index finger is usually arthrodesed in a position of 20 degrees of flexion, and the PIP joints of the middle, ring, and small fingers at angles of 30, 40, and 50 degrees, respectively.

Multiple Digits With multidigit amputations through the proximal or middle phalanges, the surgeon can either perform the replantation in a digit-by-digit sequence or in a structure-by-structure sequence. In the first technique, all the structures in a single finger are repaired before proceeding to replant the subsequent digits. In the structure-by-structure technique, the same structure is repaired in all the replanted digits sequentially. For example, bony fixation of all the digits is performed followed by repair of all the flexor tendons and so on. Which technique is used depends on the surgeon’s preference, but a structure-by-structure sequence may be faster and associated with a slightly improved survival rate (10). If a structure-by-structure approach is selected, the digital arteries in each digit are repaired last so that repair of other structures is not obscured by bleeding and there is less swelling. Replantation should always be attempted when more than two digits are amputated, even though the circumstances may be less than ideal. Such “salvage” replantations may involve transposition of an amputated digit to replace a more important digit that cannot be replanted. For example, if in a multiple-digit amputation the thumb is so badly damaged that it cannot be replanted, one of the other digits (occasionally) can be replanted in the thumb position to provide a better functional reconstruction of the hand. Similarly, transposition of a longer amputated digit from the ulnar side of the hand may preserve a more appropriate length of a digit on the more important radial side of the hand, or may allow PIP joint motion to be maintained in the transposed replanted digit. Most importantly, vein grafts, nerve grafts, skin grafts, and even small

1. Bony fixation of amputations through the MCP and IP joints; 2. Use of interposition vein grafts to facilitate positioning of the thumb for completion of the arterial anastomoses; and 3. Use of immediate tendon transfers for avulsion injuries. If the thumb amputation involves disarticulation through the MCP or interphalangeal (IP) joint, bony shortening is performed on either side of the joint and primary arthrodesis of the joint is performed using either crossed K-wires, tension band wiring, or intraosseous wiring in a position of slight flexion (Fig. 91.6). The ulnar digital artery of the thumb is usually the dominant arterial blood supply to the thumb and it is usually much easier to anastomose an interposition vein graft end-to-end to the ulnar digital artery during preparation of the thumb on the back table. The vein graft can then be anastomosed to the radial artery on the dorsal aspect of the thumb–index finger web space in a much more convenient position for completing the arterial anastomosis than having to hypersupinate the hand. If the radial digital artery to the thumb is of satisfactory caliber, it can also be repaired end-to-side to the same vein graft “upstream” to the anastomosis of the vein graft to the ulnar digital artery. In avulsion injuries of the thumb, if the extensor pollicis longus and flexor pollicis longus tendons have been avulsed from their musculotendinous junction, immediate tendon transfers can be performed using the extensor indicis proprius to the extensor pollicis longus and the flexor digitorum sublimis from the ring finger to the flexor pollicis longus. Obviously, these tendon transfers are only performed if the avulsion amputation does not involve the interphalangeal joint.

Transmetacarpal Excellent functional results can be achieved following replantation of transmetacarpal amputations. Care must be taken during bony fixation to prevent malrotation of an individual digit because rotation at the metacarpal level translates into a greater functional deficit than a similar degree of malrotation further distally in the digit. Bony fixation can be achieved very simply by longitudinal K-wires in children (Fig. 91.10) or with rigid internal fixation using plates and screws in adults. At least 1 cm of bony shortening should be performed to prevent secondary intrinsic tightness in the fingers. In addition, because the distal portions of the interosseous muscles have lost both their nerve and blood supply, they should be completely debrided, which may lead to some degree of clawing of the fingers. The carpal tunnel and Guyon’s canal should be released prophylactically during the initial preparation of the

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FIGURE 91.10. An 11-month-old child with a transmetacarpal devascularization of his right hand in an exercise bicycle. The four metacarpal fractures were fixed with longitudinal K-wires and the entire superficial palmar arch reconstructed with an interposition vein graft from the distal ulnar artery with end-to-side anastomoses of the three common digital arteries into this “new” palmar arch. He regained virtually normal flexion and extension of the fingers. Five years after the operation, despite good sensation, he still had cold intolerance.


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Regardless of the time required to revascularize the hand, fasciotomies of the thenar, hypothenar, and interosseous muscle compartments must be performed. Primary epineurial or group fascicular repair of the median, ulnar, and superficial radial nerves is optimal if bony shortening allows this option. Otherwise, the nerve ends should be tagged and group fascicular nerve grafting performed as a secondary procedure a few weeks later.

The amount of bony shortening should be sufficient to allow primary repair of the median, ulnar, and radial nerves, but may also facilitate skin closure over the vital structures. Rigid internal fixation is achieved with 4.5-mm dynamic compression plates for the humerus and 3.5-mm dynamic compression plates for the radius and ulna. The arterial anastomosis is performed immediately after bony fixation and before the venous anastomoses are performed. After arterial inflow has been re-established, the veins in the distal part are allowed to bleed to prevent this venous blood, which contains high concentrations of potassium and lactic acid, from reaching the systemic circulation and potentially triggering a cardiac arrest. Three to four venous anastomoses are then performed, but prior to release of the microsurgical clamps on the venous anastomoses, the patient is given intravenous sodium bicarbonate, again to neutralize the potential acidosis. The obvious disadvantage of re-establishing arterial inflow before venous outflow is that blood loss may be considerable and is usually underestimated. The flexor and extensor muscles or tendons are then repaired, followed by epineurial or group fascicular repair of the median, ulnar, and radial nerves. If bony shortening was insufficient to allow primary nerve repair, the nerve ends should be tagged and sural nerve grafts performed as a secondary procedure (Fig. 91.11). The skin should be loosely approximated to cover the anastomoses and nerve repairs. If necessary, meshed split-thickness skin grafts can be harvested to provide complete coverage. Occasionally, an emergency free skin or muscle flap may be required to provide coverage of vital structures in those amputations in which there has been extensive skin loss. Unlike replantations in the hand, successful replantations through the forearm and upper arm usually require a “secondlook” operation 48 to 72 hours later to check for infection and to ensure that no further debridement of the wound is necessary. The best functional results are achieved with replantations through the distal forearm and wrist, because the extrinsic flexor and extensor muscles remain innervated and satisfactory sensory return can be expected in young individuals.

Forearm and Upper Arm

COMPLICATIONS

Because more proximal amputations through the forearm and upper arm are rarely caused by a sharp guillotine-type mechanism, there is usually extensive damage to the adjacent muscles. Radical debridement of the muscles in the amputated part and in the stump is essential to prevent secondary infection and overwhelming sepsis. Debridement of forearm and elbow amputations should be performed under a sterile tourniquet, but a tourniquet cannot really be used for amputations above the elbow. Fasciotomies of the anterior and posterior forearm compartments are an absolute necessity, and release of the transverse carpal ligament and fasciotomies of the intrinsic muscles in the hand may also be necessary, if there is excessive swelling of the hand, or if increased compartmental pressures are measured after reperfusion of the hand. It is vital to re-establish arterial inflow as quickly as possible in amputations of the upper arm and forearm. If the ischemia time has been prolonged, it is probably beneficial to re-establish arterial inflow using a temporary vascular shunt from the proximal brachial artery into the distal brachial artery or radial artery. This temporary arterial shunt will allow reperfusion of the extremity while debridement, identification of tendons and nerves, and bony fixation are completed. Alternatively, if the ischemic time is relatively short, rigid bony fixation can be performed after radical debridement followed immediately by arterial repair.

Replantation in the upper extremity may be associated with a relatively high rate of complications (Table 91.5).

amputation stump so that postoperative swelling does not result in compression of the median nerve or, more importantly, the ulnar artery. Finally, branches of the deep metacarpal arteries should be identified both in the distal amputated part and in the amputation stump, and ligated to prevent postoperative hemorrhage causing a hematoma after revascularization is completed.

Wrist Obviously, replantation at the transcarpal level is technically much easier than replantation of amputations across the palm or out in the digits because the radial and ulnar arteries and dorsal veins are much larger than the common digital and proper digital arteries and veins. Specific considerations for amputations at the level of the wrist include the technique of bony shortening, the need for fasciotomies of the intrinsic muscles, and whether primary nerve repair or delayed secondary nerve grafting is required. There are three choices for bony shortening of amputations around the level of the wrist: 1. Partial or total carpectomy and primary arthrodesis of the wrist. This is especially indicated if the radiocarpal joint is destroyed or in a young, working man. 2. Proximal row carpectomy if the distal articular surface of the radius is preserved. 3. Shortening osteotomy of the radius and Darrach resection of the distal ulna if the level of amputation is just proximal to the distal articular surface of the radius.

Malunion and Nonunion Whitney et al. (12) reported an overall 50% incidence of bony problems and a 16% rate of nonunion in digital replantations fixed with tetrahedral wiring or K-wires, but this high complication rate might be reduced by improved techniques of rigid internal fixation using 90-90 intraosseous wiring or miniplate fixation.

Joint Stiffness Stiffness of the MCP, PIP, and DIP joints remains a problem because of edema and swelling in the replanted digit. The surgeon should avoid using longitudinal K-wires to transfix joints, and the hand therapist should begin gentle passive range-ofmotion exercises when the dressings are changed 5 to 7 days postoperatively. It is important to encourage active and passive range-of-motion exercises of the joints of adjacent noninjured digits, otherwise these, too, can become stiff.

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Tendon Adhesions

Muscle Contractures

Replantations, especially at the level of the proximal phalanges and at the wrist, are associated with restricted range of motion as a result of adhesions around the flexor tendon repairs. Meticulous repair of the flexor tendons and early protected active flexion protocols for tendon rehabilitation may reduce the restriction. Secondary tenolyses or two-stage flexor tendon grafting may significantly increase the total active range of motion of a replanted digit.

Intrinsic muscle contracture may develop after replantation proximal to the wrist, and ischemic contracture of either the forearm flexor or extensor muscles may compromise successful replantation at the forearm or elbow level. Intrinsic muscle contractures can be treated by release of a portion of the intrinsic tendon or by an intrinsic muscle slide. Loss of intrinsic muscle function might be restored by conventional tendon transfers.

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F FIGURE 91.11. A 21-year-old man with an amputation of his right forearm just below the elbow by a triple-bladed saw in a lumber mill. He underwent creation of a one-bone forearm with osteosynthesis of the distal radius to the proximal ulna. Excellent wrist flexion and extension and finger flexion and extension were regained. After secondary sural nerve grafting of the median nerve and a tendon transfer for abduction of the thumb he recovered protective sensibility and returned to work driving heavy plant machinery.



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FIGURE 91.11. (Continued )

Sensory Return and Cold Intolerance Sensory return (13) after upper extremity replantation is dependent on the level of amputation and whether bony shortening has allowed primary nerve repair. Replantation at the level of the middle phalanx is obviously associated with a better return of sensation than is replantation at the level of the upper arm. Gelberman et al. showed that return of digital sensibility is related primarily to the level of blood flow in the replanted finger and then to the level of amputation, the mechanism of injury, and the patient’s age. In their study, 46% of digital replantations regained two-point discrimination better than 10 mm, but this was not as good as the two-point discrimination achieved after digital nerve repair alone. A pulse pressure below 70% of the contralateral digit was associated with poor two-point discrimination of 15 mm or greater and severe cold intolerance. Pain on exposure to cold (cold intolerance) after replantation is a significant problem, but does not appear to be any more disabling than after simple closure of the amputation stump. Functional outcome, especially after major upper extremity amputations, is crucially dependent on bony shortening to allow primary nerve repair and, hopefully, return of

TA B L E 9 1 . 5 COMPLICATIONS OF REPLANTATION Malunion and nonunion Joint stiffness Tendon adhesions Muscle contractures Poor sensation Cold intolerance

sensation in the hand and digits (14,15). Chen stated that “a viable upper extremity replantation without return of sensation is not a functional success.”

References 1. Cheng GL, Pan DD, Yang ZX, et al. Digital replantation in children. Ann Plast Surg. 1985;15:325. 2. Daigle JP, Kleinert JM. Major limb replantation in children. Microsurgery. 1991;12:221. 3. Alpert BS, Buncke HJ, Brownstein M. Replacement of damaged arteries and veins with vein grafts when replanting crushed, amputated fingers. Plast Reconstr Surg. 1978;61:17. 4. Kay S, Werntz, J, Wolff TW. Ring avulsion injuries: Classification and prognosis. J Hand Surg. 1989;14A:204. 5. Meuli H, Meyer V, Segmuller G. Stabilization of bone in replantation surgery of the upper limb. Clin Orthop. 1978;133:179. 6. Greenberg BM, Cuadros CL, Jupiter JB. Interpositional vein grafts to restore the superficial palmar arch in severe devascularizing injuries of the hand. J Hand Surg. 1988;13A:753. 7. Wilson GR, Jones BM. The damaging effect of smoking on digital revascularisation. Two further case reports. Br J Plast Surg. 1984;37:613. 8. Foucher G, Norris RW. Distal and very distal digital replantations. Br J Plast Surg. 1992;45:199. 9. May JW, Toth BA, Gardner M. Digital replantation distal to the proximal interphalangeal joint. J Hand Surg. 1982;7:161. 10. Camacho FJ, Wood MB. Polydigit replantation. Hand Clin. 1992;8:3, 409. 11. Schlenker JD, Kleinert HE, Tsai T. Methods and results of replantation following traumatic amputation of the thumb in sixty-four patients. J Hand Surg. 1980;5:63. 12. Whitney TM, Lineaweaver WC, Buncke HJ, et al. Clinical results of bony fixation methods in digital replantation. J Hand Surg. 1990;15A: 328. 13. Yamauchi S, Nomura S, Yoshimura M, et al. A clinical study of the order and speed of sensory recovery after distal replantation. J Hand Surg. 1983;8: 545. 14. Kleinert HE, Jablon M, Tsai T. An overview of replantation and results of 347 replants in 245 patients. J Trauma. 1980;20:390. 15. Tamai S. Twenty years’ experience of limb replantation-review of 293 upper extremity replants. J Hand Surg. 1982;7:549.

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CHAPTER 92 ■ UPPER LIMB ARTHRITIS ALAMGIR ISANI

Arthritis falls into two general categories. By far the most common is the degenerative group, (e.g., osteoarthritis) characterized by primary articular destruction. The second major group has inflammation as the primary feature, with bone/cartilage destruction being secondary. Rheumatoid arthritis is a typical example of the latter.

DEGENERATIVE JOINT DISEASE Degenerative arthritis is a general term incorporating common idiopathic osteoarthritis (Fig. 92.1), aggressive erosive osteoarthritis (Fig. 92.2), and traumatic arthritis, development of which is attributed to injury. All are chronic, progressive arthropathies characterized by degeneration of cartilaginous joint surfaces and by hypertrophy of bone at the articular margins. A strong family history of similar problems, especially among females is typical. Inflammation may be surprisingly minimal, in contrast to rheumatoid arthritis, which is characterized primarily by painful inflammation of the synovial membranes of joints and tendon sheaths, with joint destruction being secondary. Furthermore, osteoarthritis occurs in an older age group than does rheumatoid disease. Degenerative arthritis is by far the most frequently encountered arthropathy in the hands, and most commonly begins in the basal joint of the thumb or distal interphalangeal joints. An uncommon but dramatic variant of primary osteoarthritis is erosive osteoarthritis. Exhibiting clinical and pathologic manifestations similar to those of rheumatoid disease, with violent inflammatory episodes, this variant mysteriously causes total destruction of individual joints without any pathology in adjacent joints (Fig. 92.2).

Traumatic Arthritis Traumatic arthritis is considered a separate entity, even though the clinical, radiographic, and histologic characteristics are indistinguishable from spontaneously occurring osteoarthritis. By definition, there must be a clear history of specific injury to the joint. Degenerative osteoarthritis, in contrast, is spontaneous and is attributable to the “wear and tear” associated with daily use and for which genetic factors are apparent. The distinction is not clear-cut, and the term traumatic arthritis is applied in some cases in the sense that trauma may have accelerated a normally occurring degenerative process. Often, the issue of delineation between traumatic and degenerative arthritis is of more legal than clinical concern.

Incidence and Clinical Presentation of Degenerative Arthritis All types of degenerative arthritis are characterized by joint deformity, both clinically and radiographically, localized tender-

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ness, variable pain, and eventual restriction of joint motion. Pathologically, there is destruction of cartilage on opposing surfaces of normal joints. Anti-inflammatory medications may give transient improvement in symptoms, but once the articular surfaces are destroyed, there is no possibility of spontaneous recovery or permanent relief of symptoms by conservative or nonsurgical treatment. The basic indication for treatment is pain, and the individual tolerance to pain is highly variable. The symptoms are evaluated on an individual basis in the context of age, health, and occupation. Although radiographs are diagnostic, there is essentially no correlation between the degree of disease they illustrate and the pain each individual experiences. Osteoarthritis is common. Approximately 10% of adults older than age 50 years have significant symptomatic osteoarthritis. An even greater percentage of them have radiographically demonstrable but asymptomatic disease. The prevalence increases with age and in postmenopausal women, and there is clearly a familial predisposition. Occupational influences are controversial, but in the legal arena have been linked to repetitive mechanical use, at least to the extent that such activity aggravates a naturally developing disorder. The initial manifestation of primary osteoarthritis occurs in weight-bearing joints of the legs or back, or in joints of the hands, where it characteristically involves the carpometacarpal joint at the base of the thumb and the distal interphalangeal joints of the fingers.

Pathogenesis Although the pathogenesis remains unresolved, primary osteoarthritis is considered a wear-and-tear phenomenon with the progressive loss of cartilage and exposure and later destruction of underlying bone. The synovial tissue is minimally affected. The progressive destruction of articular cartilage is the sine qua non of osteoarthritis.

Degenerative Arthritis of Basal Joints of the Thumb The term basal joint of the thumb is used imprecisely to refer to either the metacarpal–trapezial, the scaphotrapezial, or both of these joints (pantrapezial). The first metacarpal– trapezial joint has opposing, reciprocally concave articular surfaces. The double-saddle configuration of this special joint allows a tremendous range of motion in flexion–extension and abduction–adduction planes, and also permits some axial rotation. The joint is stabilized by capsular structures and the strong volar carpometacarpal ligament, which securely tethers the base of the metacarpal to the carpus. Additionally, dynamic stability is provided by muscle and tendon units disposed circumferentially around the first metacarpal.


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A FIGURE 92.1. A: Typical metacarpal-trapezial deformity of advanced thumb basal joint idiopathic osteoarthritis with subluxed and flexed first metacarpal-trapezial joint and reciprocal metacarpophalangeal (MCP) hyperextension. B: Radiographs demonstrating the advanced pathology of this case.

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B FIGURE 92.2. A and B: Clinical and radiographic findings of erosive osteoarthritis showing marked destruction of the proximal interphalangeal joints.


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Pathogenesis The thumb is the key unit for opposition, pinch, and precision manipulation. These functions impose special demands at each joint. Motion at the interphalangeal and the metacarpophalangeal (MCP) joints occurs primarily in the flexion–extension axis. In contrast, the metacarpocarpal joint has to be widely adaptive in order to position the thumb effectively for its range of activity. With thumb motion, the distribution of force vectors is uneven, being concentrated disproportionately along the dorsal facet of the trapezium, where capsular support is weakest. The abductor pollicis longus tendon, which inserts at the base of the first metacarpal, reinforces this weak capsule, but it also is a powerful force for subluxation of the base of the metacarpal. Although these anatomic and mechanical alterations contribute to basal joint arthrosis, poorly understood biologic and genetic factors also influence the predisposition of certain individuals to the disease process. The preponderance of postmenopausal women with this disease is a paradox as most older women impose relatively low stress demands on their hands.

Clinical Presentation The chief symptoms of degenerative arthritis of either joint at the base of the thumb are pain and swelling, aggravated by use and relieved by rest. Pain is typically of a piercing type, provoked especially by twisting motions and lasting only moments until the late stages of the disease when deep and constant aches are typical. A frequent early complaint is the “loss of strength” and inability to perform simple tasks such as turning a key or opening a jar top. The natural history is generally one of gradual, but progressive, deterioration, with variable periods of pain remission. In general, this common disorder is not an indication of generalized, disabling arthritis, although there is often asymptomatic evidence of osteoarthritic damage to other joints, especially in distal finger joints. Physical examination reveals swelling, tenderness, and variable crepitation directly over the first metacarpal (MC) and/or scaphotrapezial joints. Subluxation is common, and passive reduction reproduces the typical piercing pain. With advanced destruction, the joints may become fixed in adduction/flexion with reciprocal MCP joint hyperextension (Fig. 92.1). With loss of motion, pain frequently diminishes. Axial compression and rotation of the thumb metacarpal may elicit a painful grinding.

Radiographic Findings Radiographic evidence of degenerative arthritis may precede clinical manifestations by several years, often with an episode of trauma apparently initiating symptoms. In other cases, radiographic changes are not detected in patients with early symptoms. As noted earlier, radiographically demonstrated joint destruction correlates poorly with the severity of clinical symptoms, and it is the latter that determines treatment. Classic radiographic findings include narrowing of the joint space as cartilage deteriorates, marginal bone erosions, subchondral sclerosis or condensation of bone, reactive cystic changes, and marginal bone hypertrophy with osteophyte or spur formation (Fig. 92.1B).

Collapse Deformity A multiarticulate system, such as the thumb, is prone to a mathematically predictable pattern of collapse, according to the principle elaborated by Landsmeer (1). In short, each joint in a multiarticulate system (such as a finger), when subjected to longitudinal compression, will buckle in a sequentially opposite direction, forming a zigzag collapse pattern. With pro-

gressive thumb basal joint flexion/adduction and subluxation, a compensatory hyperextension of the MCP joint develops (Fig. 92.1B).

Stages of Thumb Basal Joint Degenerative Disease Clinical staging, as suggested by Burton et al. (2), is a helpful guide to management and is briefly reviewed. Stage I is associated with a lax joint and is characterized by pain. Stress radiography often documents pathologic joint subluxation whereas standard radiographs often reveal minimal, if any, pathology. Intolerable pain associated with long periods of writing is the most typical chief complaint, and the patients often are young. Tenderness over the joint and pain as its subluxation is passively reduced may be the only abnormal physical finding. Stage II is characterized by more intense and more constant symptoms, chronic joint subluxation, and radiographic changes of joint space narrowing, subchondral bone sclerosis, and/or cystic changes with minor osteophyte formation. Stage III of pantrapezial arthrosis is characterized by pain and weakness at a level that impedes many activities and frequent extension of the process into neighboring joints. Often pain is felt deep in the thenar eminence and radiates up the forearm. Although there is little correlation between radiographic findings and of symptoms, films at this stage will demonstrate joint destruction. Stage IV is characterized by pantrapezial arthritic destruction, joint subluxation, and a zigzag deformity of MC joint flexion and MCP hyperextension (Fig. 92.1B). Functional impairment is severe with impaired range of motion, but the loss of motion may be accompanied by a reduction in pain.

Treatment of Thumb Basal Joint Arthritis Treatment is determined by the severity of symptoms and disability for each individual patient. Conservative Treatment. A trial of nonsurgical therapy helps to establish rapport and confidence, but pain reduction is only transient. Such measures include immobilization with a splint, direct steroid injections into the involved joints, and altered work activity to reduce forceful and strenuous use of the thumb. Oral nonsteroidal anti-inflammatory medications during periods of acute exacerbations are occasionally helpful. Surgical Treatment. Once the cartilaginous articular surfaces are destroyed, relief can only be provided by surgical separation of the denuded bones. Persistent intractable pain and progressive handicap that is not responsive to conservative measures constitute the primary indications for surgical treatment. The basic types of operation for this are briefly described in the following material. Ligament reconstruction. When symptoms warrant repair for stage I disease, extra-articular ligament reconstruction, using a portion of the flexor carpi radialis tendon, is the preferred treatment. Ligamentous stabilization of the subluxating joint halts the otherwise inexorable progression of the degenerative process. Arthrodesis. Arthrodesis of an arthritic first MC joint is a reasonable option only if one can be certain that the pathology is confined to that specific joint, such as a late complication of a Bennett fracture. Currently, arthrodesis (fusion) (Fig. 92.3A) is infrequently employed, being recommended occasionally for traumatic arthritis of the trapezial–metacarpal joint of young patients engaged in heavy labor. If the diagnosis of localized disease is correct, relief of pain is predictable, but the arthrodesis significantly restricts motion, requires a prolonged period of immobilization, and the nonunion rate is substantial. Treatment of Stages II to IV Arthritis. Resection of the trapezium relieves pain but does not prevent thumb shortening, instability at its base, and weakness. Consequently, some



A

B

type of trapezial resection arthroplasty with ligament reconstruction (Fig. 92.3B) is the most frequently employed surgical treatment of thumb basal joint arthritis today. It predictably relieves pain and preserves most mobility; in addition, recovery is relatively rapid. Implant arthroplasty is the term used when some kind of material is placed in the space created by trapezial resection in an effort to prevent shortening. Such materials have included fascia, tendon, silicone, and Vitallium. Until recently, silicone rubber spacers were most often used (3). Clinical results were generally good, but development of synovitis and local cystic bone degeneration from silicone particles, along with concern about the long-term effects of silicone implants, resulted in abandonment of their use. Despite this, if an old implant has to be removed after thorough encapsulation and healing, its removal has not proved to compromise significantly the good functional recovery. The most accepted operation today is trapezial resection with a tendon suspension of the thumb’s metacarpal to the base of the index metacarpal, which gives stability and prevents excessive shortening (2,4). Stuffing tendon or fascia into the space created by trapezial removal alone will not prevent thumb shortening. After about 4 weeks of immobilization, progressive remobilization and muscle rehabilitation exercises are started. These are among the most rewarding and satisfying of reconstructive operations.

Interphalangeal Joint Arthritis Osteoarthritis tends to develop insidiously and affects multiple distal interphalangeal (DIP) finger joints. In contrast, erosive osteoarthritis tends to single out and rapidly destroy one of the proximal interphalangeal joints in a violent manner (Fig. 92.2). Because of the common occurrence of osteoarthritis of DIP joints, even patients with severe deformity may have surprisingly little pain or impairment of use. The chief concern is frequently the disturbing appearance, a fact that patients may not readily acknowledge. The knobby appearance of the distal joints is caused by osteophytes and hard connective-tissue nodules called Heberden nodes. Infrequently, similar subcutaneous

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FIGURE 92.3. A: Schematic of fusion of the trapeziometacarpal joint. B. Schematic of trapezial excisional arthroplasty with ligament suspension using a split portion of the flexor carpi radialis tendon.

nodules develop at the proximal interphalangeal (PIP) joints, where they are called Bouchard nodes. Treatment of typical distal interphalangeal joint osteoarthritis is dictated by the degree of symptoms. Rest provided by restriction of activities and splinting is the mainstay of initial treatment. Oral anti-inflammatory medications should be tried, but response is unpredictable and often poor. Intra-articular steroid injections are transiently helpful for the majority of cases. With supportive measures for symptomatic relief, acute episodes often go into spontaneous remission. Surgery is indicated for intractable pain or deformation of alignment severe enough to interfere with effective function. The presence of Heberden or Bouchard nodes, although aesthetically displeasing, are infrequently, in themselves, an indication for excision. Because implant arthroplasties for distal joints have limited success, arthrodesis in a functional position is the treatment of choice. This provides relief of pain, improved alignment, and better appearance. The treatment of mild degenerative arthritis of PIP joints is intra-articular injection of steroids and splinting for rest. Surgery is the only option for advanced or recalcitrant cases, but a truly good solution does not exist. Joint fusion offers the most reliable means of relieving pain but results in total loss of motion at the joint. PIP joint fusion is least disturbing for the index finger. The index works against the thumb in order to pinch, for which PIP mobility is not required. The lack of pain and good stability are more important than flexion for the index and middle fingers. For the ring and small fingers, which are principally involved in power grasp, loss of PIP mobility from arthrodesis is much more debilitating and has to be considered carefully and individually. The success of implant arthroplasty at the PIP joints is determined chiefly by the condition of the adjacent tendons, ligaments, and supporting soft-tissue structures. When these are in good condition, an implant arthroplasty is clearly more desirable than arthrodesis for a destroyed PIP joint of the middle, ring, or small finger. Because these joints have little axial loading, silicone spacers in the shape of a hinge continue to be used. When supporting soft-tissue structures are in good condition, a stable joint with an extension/flexion arc of 60 to 80 degrees frequently is achieved.


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A

FIGURE 92.4. A: Radiographic demonstration of osteoarthritic changes in the DIP joint giving rise to synovitis, the cyst, and its pressure damages to the skin and fingernail germinal matrix. B: Typical synovial (mucous) cyst with fingernail deformity, which developed in response to irritation of osteoarthritic osteophyte at the interphalangeal joint.

B

Associated Disorders A common complication of osteoarthritis at the DIP is a dorsal synovial cyst, commonly referred to as a “mucous cyst,” with or without fingernail deformity (Fig. 92.4). These cysts develop in response to irritation of arthritic osteophytes at the margins of the arthritic joint. The pressure of the expanding cyst thins the overlying skin and damages the germinal matrix of the fingernail, resulting in its progressive deformity. Recurrent inflammation is common. The risk, aside from fingernail deformity, is infection communicating directly into the arthritic joint and troublesome chondritis. Surgical correction requires synovectomy with excision of the cyst, debridement of osteophyte from the arthritic joint margins, and repair of the skin defect, usually with local flaps and occasionally supplemented with a skin graft. The technical challenge is removal of the osteophytes from the dorsal margin of the base of the distal

phalanx without detaching the insertion of the attenuated extensor tendon.

Metacarpal Boss A metacarpal boss results from degenerative arthritis of the second and/or third metacarpocarpal joints, and is often mistaken for a dorsal ganglion cyst. Symptoms include deep aching and variable tenderness, accentuated by compression or torsion with activities such as golf. Localized tenderness, with pressure aggravating the symptoms, is the key to diagnosis. Usually, a boss can be illustrated with lateral-oblique wrist radiographs showing subtle dorsal joint lipping and/or narrowing of space in the tender joint.



In the majority of cases, no treatment is required. Direct steroid injections into the joint and rest are employed. When symptoms persist but are not severe, surgical excision of only the dorsal lipping of joint margins down to healthy articular cartilages will generally give relief, provided these joints are stable. When there is joint instability or if symptoms are severe, arthrodesis is required for predictable pain relief.

RHEUMATOID ARTHRITIS Rheumatoid arthritis (RA) is a systemic autoimmune disease of uncertain etiology, which is characterized primarily by synovial inflammation with secondary skeletal destruction (Fig. 92.5). Polyarticular involvement is the rule, with an age prevalence between 20 and 40 years and a female preponderance. Although synovial and articular tissues are focal target structures, the immunologic disorder frequently affects disparate visceral organs such as the heart, pericardium, and lungs. Juvenile rheumatoid arthritis is a particularly aggressive variant that affects teenage children. The clinical course of rheumatoid arthritis (also known as polyarthritis) is extremely varied in terms of distribution, severity, rapidity of progression, and ultimate damage. In most cases, the diagnosis will have been established and medical treatment initiated before the surgeon is consulted. However, RA must be considered in any patient with ill-defined and persistent joint inflammation and pain. Variation in early symptoms is the rule rather than the exception, with onset occasionally being heralded by unexplained, painful swelling of a single joint. At this stage, minimal if any derangement of laboratory tests, except perhaps an elevated erythrocyte sedimentation rate, is common. The course of rheumatoid arthritis is as unpredictable as its onset, but when progressive, the diseased synovium causes both enzymatic and mechanical destruction of tendons, laxity and attenuation of ligamentous support systems of joints, and eventual enzymatic degradation of articular cartilage and subchondral bone. The ultimate deformities are as varied as the presentation of the disease.

Rheumatoid Synovitis Rheumatoid synovitis damages extensor and flexor tendons. Joint destruction and shifts in alignment result in abnormal frictions and vector forces on the tendons traversing them. The extensor tendons are usually most involved over the dorsal aspect of the wrist, where a boggy swelling of diseased synovium

FIGURE 92.5. Hand ravaged by severe rheumatoid arthritis.

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may be visible with an hourglass configuration, proximal and distal to the extensor retinaculum. As the tendons are attenuated, even a simple act, such as snapping fingers together or lifting a cup, may result in tendon ruptures and loss of extension of one or more fingers, most often those on the ulnar aspect of the hand. The risk of tendon rupture is so high that prophylactic tenosynovectomy to minimize probability of tendon ruptures should be considered if the tenosynovitis has not responded to medical treatment over a period of 4 to 6 months. While not absolute, synovectomy reduces substantially the chance of tendon rupture, especially at the wrist level (5). Synovectomy is usually performed in conjunction with other needed repairs, such as realignment of a subluxed wrist. A painless, and thus deceptive, variant of rheumatoid synovitis that occurs along extensor tendons at the wrist and dorsal hand is termed villonodular synovitis. It presents insidiously as a soft, ill-defined, but prominent mass about the digital extensor tendons at the wrist level. Typically painless, without the usual inflammatory signs of soreness, redness, or increased temperature, this entity causes spontaneous tendon rupture in some cases but is unpredictable, and spontaneous remissions can occur. Synovectomy is considered if the mass persists for more than 6 months. Flexor tenosynovitis usually presents with pain, swelling, decreased wrist motion, and impaired finger flexion. Classic carpal tunnel syndrome very rarely indicates rheumatoid involvement. Synovectomy is not indicated for the classic carpal tunnel syndrome, which demonstrates a dry, tenacious type of flexor synovitis. Occasionally with symptoms of carpal tunnel syndrome, a wet, proliferative, and invasive synovitis (rheumatoid type) is unexpectedly encountered. For such cases a thorough flexor synovectomy is indicated to minimize risk of tendon ruptures. The proliferative synovitis may extend distally into the fibro-osseous flexor tendon sheaths of the fingers, causing a “trigger finger” (see Chapter 82) to be the presenting symptoms of the disease.

Wrist Synovitis Dorsal tenosynovitis is usually visible, but radiocarpal and intracarpal rheumatoid synovitis leading to progressive and serious cartilage and bone destruction is less readily apparent. Pain with diffuse swelling and diminishing range of motion are typical, and progressive destruction with loss of ligament integrity leads to anterior wrist subluxation, loss of carpal height, and collapse. The malalignment of the wrist greatly increases the chance tendons rupture. Prominent ulnar side wrist pain is frequently encountered owing to synovitis and destruction of the distal radioulnar joint (DRUJ). Typically, the loss of soft-tissue support results in painful dorsal DRUJ instability and subluxation. Attritional ruptures of the extensor tendons to the ulnar digits from the sharp end of the distal ulna are common. Prophylactic synovectomy with distal ulna resection offers the best probability of prevention, while also relieving pain at the DRUJ. Flexor tendon ruptures at the proximal wrist are relatively infrequent. Although synovectomy does not always prevent tendon ruptures, in conjunction with DRUJ resection, it is consistently effective in alleviating wrist pain. Wrist arthrodesis may be required for advanced wrist destruction and collapse. However, the alternative of thorough synovectomy followed by 4 to 6 weeks of wrist immobilization often results in a fibrous union that has some resiliency, remains aligned, and is stable, as the forces on it are of such low magnitude. Wrist collapse and deviation profoundly affect function at the metacarpophalangeal finger joints, shifting forces of both extensor and flexor tendons ulnarward, to become a factor in the typical ulnar finger drift of advanced rheumatoid arthritis.


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Rheumatoid Disease of Fingers Metacarpophalangeal joint problems frequently herald the onset of rheumatoid arthritis and may begin as an unexplained and single painful and swollen joint without radiographic changes. Less often it may be “triggering” a finger or early ulnar finger deviation. With progressive disease, the hypertrophic synovitis attenuates and weakens the joint-supporting structures. With weakened joint capsule and ligaments accompanied by intrinsic muscle tightness, a volar subluxation of the proximal phalanges occurs. Deforming forces, including an ulnar shift of the flexor tendons traversing the MCP joints, cause progressive ulnar finger drift. As deformity increases, the extensor tendons sublux from their central and dorsal position over the MCP joints and migrate eventually to the respective ulnar intermetacarpal gullies. This results in further ulnar drift, loss of MCP joint extension, and eventually volar dislocation of the proximal phalanges. Synovectomy of diseased MCP joints usually relieves pain, but is often of short-term benefit, as it does not address the imbalance of intrinsic muscle tightness. Treatment is by MCP joint resection, which shortens the skeleton and provides relative lengthening of the intrinsic muscle system. MCP joint resection is combined with a thorough synovectomy and dorsal repositioning of the extensor tendons over the joints to restore active extension. Like the PIP joints, the MCP joints have low axial loading, and so silicone spacers are used as interposition arthroplasties. These combined procedures offer the best possibility for lasting improvement. Proximal interphalangeal joint complications of the rheumatoid process are common and disabling. Complications include central slip disruption, leading to boutonnière deformity or intrinsic muscle tightness, and progressive disruption of joint support tissues, causing swan-neck deformities. Treatment is difficult because direct repairs cannot satisfactorily be accomplished with the diseased, disrupted tissues. Interposition arthroplasty for the PIP joints is rarely feasible in rheumatoid arthritis because success depends on good connective tissue support. As a result, arthrodesis of a badly diseased PIP joint in a more functional position is the only realistic option. In practice, simple pinning of the joint in the selected position for 4 to 6 weeks is usually sufficient without a formal arthrodesis.

Rheumatoid Disease of the Thumb The thumb is a separate functional unit. Although RA destruction at the basal joint can be severe, unlike osteoarthritis, RA rarely causes pain in that site. Fixed flexion deformity from intrinsic muscle contractures or gross instability of the thumb MCP and/or interphalangeal (IP) joints generally is the greatest problem. In most cases, arthrodesis is the only option, but provides impressive functional improvement. As the MCP joint develops a flexion contracture, a reciprocal hyperextension of the thumb IP joint follows. If symptomatic, arthrodesis offers the only worthwhile treatment.

PSORIATIC ARTHRITIS Psoriatic arthritis (6) is a seronegative arthropathy associated with psoriatic skin changes, although initially the latter may be difficult to locate. Rheumatoid factor and antinuclear antibodies are usually absent. Joint involvement may be monoarticular but more commonly is polyarticular. Fortunately, the vast majority of patients with characteristic dermal psoriasis never develop associated arthropathies. Any joint in the body

may be affected, but hand involvement is common and often is associated with onychodystrophy. The clinical presentation is characterized by moderately painful joint stiffness, weakness, and insidious but progressive flexion contractures. Pain is usually not as severe as with rheumatoid arthritis. Radiographic articular destruction is evident with chronic joint involvement although bone stock and density remain normal. Treatment of psoriatic arthritis is essentially medical and supportive, with splinting and functional adaptions of prime importance in the early stages to retard the progression of joint contractures and destruction, for which occasional arthrodesis in a better position is worthwhile. Most patients with psoriatic arthritis requiring surgical treatment are managed in a manner similar to that required for rheumatoid disease.

ARTHRITIS OF SYSTEMIC LUPUS ERYTHEMATOSUS As the name implies, disseminated lupus erythematosus (systemic LE) is a seropositive systemic autoimmune disorder with multiorgan involvement and a characteristic photosensitive cutaneous facial rash. Musculoskeletal involvement is common and frequently severe and progressive. The periarticular soft tissues are primarily involved, with resulting generalized ligamentous laxity and joint incompetence leading to progressive deformity. Unlike rheumatoid disease, articular and skeletal structures are basically spared, with little radiographic change, even when deformity is severe. Raynaud phenomenon, with pain and cold intolerance, is a common accompaniment, and may be among a patient’s early symptoms. As the disease progresses with development of deformities, appearance of the hands has much in common with that of rheumatoid arthritis, except that generally there is much less gross synovitis even as deformities become severe. The biomechanical needs for treatment are also similar to those for rheumatoid disease, but the response to surgical repair is different. Appropriate repair of rheumatoid-deformed hands always incorporates soft-tissue reconstructions, which generally are predictable and followed by imperfect, but at least rewarding, long-term improvement. In contrast, soft-tissue repair of the hand affected with lupus deformities does not provide longterm improvement, and results are consistently disappointing. Thus, one must be extremely conservative with regard to surgical indications, undertaking only an absolute minimum of soft-tissue repairs. This makes selective arthrodesis the mainstay of treatment.

GOUTY ARTHRITIS Gout is a metabolic disorder characterized by hyperuricemia and clinically manifests as an acute monoarticular inflammatory condition. Approximately 90% of patients with gout are men, and the metatarsophalangeal joint of the big toe is involved in approximately 50% of cases. Diagnosis is usually based on clinical grounds, aided by elevated uric acid blood levels and identification of the urate crystals in joint fluid or tophi. The therapeutic response to colchicine is dramatic. The characteristic histologic lesion is the tophus, which is a nodular deposit of monosodium urate crystals with an associated foreign body reaction. The clinical signs of an acute attack are a painful, swollen, exquisitely tender and hot joint. Surgical intervention is restricted to removing larger tophi that are unsightly or a mechanical hindrance to joint motion. Occasionally, joint destruction of the interphalangeal joints is so great that an arthrodesis in a functional position is warranted.



Pseudogout affects older people and is characterized by acute recurrent arthritis involving larger joints. It is always accompanied by chondrocalcinosis of the affected joint. Identification of calcium pyrophosphate crystals in the joint aspirate is diagnostic of pseudogout.

References 1. Landsmeer JM. Anatomical and functional investigation of the articulations of the fingers. Acta Anat. 1955;24(Suppl):1.

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2. Burton RI, Pellegrini VD. Surgical management of basal joint arthritis of the thumb: II. Ligament reconstruction with tendon interposition arthroplasty. J Hand Surg. 1986;11:324. 3. Swanson A. Disabling arthritis at the base of the thumb: treatment by resection of the trapezium and flexible (silicone) implant arthroplasty. J Bone Joint Surg. 1972;54A:456. 4. Eaton RO, Glickel SZ, Littler IW. Tendon interposition arthroplasty for degenerative arthritis of the trapezius in metacarpal joint of the thumb. J Hand Surg. 1985;IOA:645. 5. Millender LH, Nalebuff B. A. Preventive surgery—Tenosynovectomy and synovectomy. Orthop Clin North Am. 1969;6:765. 6. Belsky MR, Feldon PF, Millender LH, et al. Hand involvement in psoriatic arthritis. J Hand Surg. 1982;7:203.


CHAPTER 93 ■ UPPER LIMB AMPUTATIONS AND PROSTHESES ROBERT W. BEASLEY AND GENEVIEVE DE BESE

Despite the impressive advances in reparative surgery, management of amputations remains an important part of upper limb surgery. The negative aura that surrounds amputations favors rapid disposition of the problem, but it should be looked upon as a rehabilitative operation, leaving the parts in the best possible condition for prosthetic development, if that is contemplated. Initial treatment substantially determines long-term outcome, so the surgeon assuming responsibility for initial care should be knowledgeable about prosthetic requirements. The goal for the remaining limb is that it heal painfree and be left in as useful a condition as possible (Fig. 93.1). The treating surgeon should not “go as far as he can” and then refer the patient for prosthetic development. Thoughtful consideration of the total impact of amputations is as important as the physical impairment on which attention tends to be centered. Survival of the part is not always in the patient’s best interest, even if technically possible. Although each case needs individual consideration, some basic guidelines are useful. The greater the number of injured parts, the less likely one is to amputate damaged parts to which vascularity can possibly be restored. In general if any four of the six basic parts (skin, vessels, skeleton, nerves, and extensor and flexor tendons) are irreparably damaged, amputation is considered. The concept of elective levels of amputation has given way to saving all length feasible, at least initially. If amputation is just distal to a normal or minimally damaged joint, a flap for wound closure to preserve length may be indicated. This is especially true for the elbow, through the base of the proximal phalanx of the thumb or base of the middle phalanx of fingers. Severed nerves are cut short while under tension so the ends retract into healthy tissues. It is not a question of preventing neuromas, as they are inevitable, but of preventing neuroma symptoms. Chronic pain problems are rare among patients who enjoyed primary wound healing and early active motion. Sharp spicules of severed bone are smoothed and, if joint condyles are present, they are tapered to avoid a bulbous end of the finger, which is unsightly and may prevent top-quality prosthetic development (Fig. 93.1).

PATIENT RESPONSE TO AMPUTATIONS Function is considered in the global sense of how well the individual achieves an independent, adjusted, and productive life, not simply the ability for pinch or grasping. The tendency is to overestimate physical impairment while neglecting the total impact on an individual. Regardless of whether persistent disability is a result of physical or emotional factors, the economic consequences are the same. Also note that the patient’s total response to loss bears almost no relation to the actual amount of physical loss. It cannot be assumed that a patient with only a finger tip amputation will make a rapid recovery and adjustment. Response to amputations can be considered in three basic phases. The first phase is one of denial and disbelief. This is a short phase during which the patient gets lots of attention, and most patients handle it well. The second phase is recognition of reality and is usually characterized by anxiety about the future and sometimes anger with a sense of being “victimized.” It is a period of many consultations, with emotional turmoil and seeking “miracle” solutions. It also is the phase in which enlightened guidance can be most helpful. The third phase of emotional responses goes in one of two directions. The majority of patients make appropriate accommodation to their losses and fully use their remaining assets, whereas a few find “a new friend” on whom they can blame failures or who can act as a vehicle for secondary gains. Successful help in the latter case is generally very discouraging.

CLASSIFICATION OF HAND AMPUTATIONS The variety of hand amputations is infinite, but organizing them into four major categories is useful for discussion of the subject. There is overlapping of the groups, but the majority of amputations fall primarily into one of the categories.

Lateral (Radial) Amputations

AESTHETIC CONSIDERATIONS The hands, like the face, are constantly exposed to scrutiny, portray personality, and are major communicators. Amputation is not a cosmetic issue, but one of disfigurement. To ignore or deny that disfigurement is of real socioeconomic importance is unrealistic, as confirmed by the United States Supreme Court.

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Radial amputations involve primarily the thumb and/or index finger, the “fine manipulations” unit of the hand. If there is a functional thumb, but substantial loss of the index finger, the patient will subconsciously shift to a thumb-middle finger small-object-handling unit. There was a time when “ray” index resection (through the base of the second metacarpal) was strongly advocated for index finger amputations proximal to the neck of the proximal phalanx, but it is infrequently performed now. If about 12 mm or more of proximal phalanx


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Chapter 93: Upper Limb Amputations and Prostheses

B

A FIGURE 93.1. A: Bulbous finger amputation is unsightly and precludes prosthetic fitting. B: Amputation closure with taper and good soft-tissue coverage, which is socially presentable.

A

B

C

D FIGURE 93.2. A: Distal thumb amputation healed with unstable and painful scar. B: Volar cross-finger flap from middle finger attached. C: Repair with tissue of perfect match, good pulp, and good recovery of sensibility. D: Middle finger flap donor-site repair with skin grafts from wrist.


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A

B

C

FIGURE 93.3. A: Ring avulsion injury. B: Essential amputation too short to be useful. C: Fourth ray resection. Balance restored and gap in palm eliminated by transposition of small finger onto the base of the metacarpal.

distal to the interdigital web is present, a finger prosthesis with passively changeable contour can be developed for most patients. With this development, ray index resection as part of primary treatment is rarely, if ever, indicated. The proximal interphalangeal (PIP) joint of the fingers is most important and in general should be saved, even if a flap for wound closure is required. Preservation of length for thumb amputations is almost always indicated and very often requires a flap to accomplish. Traditionally this was by a dorsal flap from the adjacent index finger, but the donor-site mutilation. Beasley (1981) developed an alternative, the volar cross-finger flap (Fig. 93.2). Thumb amputations proximal to the metacarpophalangeal (MCP) joint are usually best treated by one of the numerous reconstructive procedures (see Chapter 88).

Medial (Ulnar) Amputations The ring and small fingers, with some contribution from the middle finger, constitute the power grasping unit of our hands. To be effective they need length and a good flexion–extension arc. This functional unit is of much more value than that generally accorded to it. If the ring finger is lost, balance is improved by transposition of the small finger on to the fourth metacarpal with advancement to reduce gross shortness compared to the adjacent middle finger (Fig. 93.3).

While both pinch and grasping capability is preserved, these losses are troublesome because of small objects rolling from the palm and, of course, they are aesthetically disturbing. Surgical help is limited to the provision of soft-tissue coverage and displacement of sensitive neuromas. Some may be candidates for prosthetic development, especially for the deformity, but for technical reasons this is usually short of satisfactory. If any finger has a length of 12 to 15 mm distal to the interdigital web, preservation of length is important and often requires flap closure. With middle finger ray resection (through its metacarpal), index finger transposition onto the base of the third metacarpal gives excellent restoration of balance to the hand (Fig. 93.4).

Transverse Amputations Physical impairment increases geometrically as the level of amputation becomes more proximal. Commonly encountered is transverse amputation of all fingers through their metacarpals, but with an uninjured thumb. There should be a conservative attitude about constructing a unit to oppose the thumb by flapbone-grafts or by toe transfers. These procedures for the unilateral amputee badly accentuate the disfigurement, rarely improve needed capability significantly, and often preclude prosthetic development, which most patient’s will choose if aware of what is available today.

Central Unit Amputations

UPPER LIMB PROSTHESES

Machines such as punch presses can cause central amputations, limited to the ring and/or middle fingers and their metacarpals.

The most basic axiom concerning prostheses is that more of them replace missing parts. The purpose is to minimize the



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A

B

C

FIGURE 93.4. A: Middle finger ray resection leaves central gap in hand. B and C: Index finger transposition to base of third metacarpal restores balance and good function to hand.

physical, emotional, social, and economic consequences of the loss. Despite impressive surgical advances, there are situations for which a prosthesis, alone or in combination with surgical repair, offers the best option. A realistic master plan should be agreed upon, surgery done with the same care and skill used in any reconstructive procedure, and a prosthesis fabricated to the highest standards (Fig. 93.5). Except in wartime, major bilateral upper limb amputations are rare. Even unilateral total hand amputations are infrequent. The big numbers are in digital and partial hand amputations and there is increasing awareness that to be acceptable in most circumstances today, each must have a socially acceptable presentation. With the constant shifting of the workers into service industries, deformity is recognized as a real socioeconomic handicap, not a cosmetic issue (Fig. 93.6). This has been confirmed by the United States Supreme Court (Arlene vs. Nassau County, 1987).

Unilateral versus Bilateral Fortunately, bilateral total hand amputations are rare. Although bilateral amputees suffer socioeconomically as do unilateral amputees, for the bilateral cases the physical impairment is so extreme as to overshadow other considerations. Their management is beyond the scope of this overview, but in gen-

eral there is still a tendency to overestimate physical impairment to the neglect of emotional and total impact of losses.

Specificity of Prostheses It is essential to recognize that any prosthesis can meet only specific and limited needs. The term “artificial hand” should be discarded as it implies unrealistic expectations. Also, the same patient may need different types of prostheses for different occasions. For example, one might need a rugged and ugly clamping device for the factory, but a mechanically simpler, passively adjustable prosthesis of near-normal appearance for business and social occasions. The prime needs of each patient should be determined accurately and prostheses targeted to these needs. This minimizes unrealistic expectations, disappointments, and failures.

Congenital versus Acquired Losses A child born without a hand (agenesis) does not experience the sense of physical impairment of one with an acquired amputation that disrupts learned functional patterns. With agenesis, techniques may be different, but to that individual they seem normal. The basic problem of almost all those with congenital defects is not physical, but development of a strong


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A

B

C

D

E

FIGURE 93.5. A: Severely burned hand with distal amputations of all digits. B: Master plan was to separate out remaining parts in one operation, using a combination of local flaps and skin grafts, followed by prosthetic development. C: Healed hand with “liberated” parts. D and E: Custom-developed partial hand prosthesis is moved by the “liberated” short digits and also restores near-normal social presentation. (Courtesy of American Hand Prostheses, Inc., New York, NY.)

A

B FIGURE 93.6. A: Unilateral hand agenesis. Having grown up this way, the patient has no sense of physical impairment, so the essential problems are emotional and social adjustment. B: A first-class, precisely adjustable prosthesis is the only means of giving a normal social presentation. (Courtesy of American Hand Prostheses, Inc., New York, NY.)



A

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B FIGURE 93.7. A: Distal finger amputations of professional musician. B: Precise-fitting digital prostheses restores their tips to where the brain, through learned patterns, expects them to be, resulting in unconscious or automatic control. (Courtesy of American Hand Prostheses, Inc., New York, NY.)

and secure personality in face of being “different.” The family is the prime influencing factor on early personality development and if their manner reflects the child’s being inferior, the child will firmly adopt this attitude. Appropriate prostheses may eventually be helpful in dealing with a sense of inferiority (Fig. 93.6), but is not applicable in the early formative years when it is the family and not the child who need guidance. Prostheses should be considered when the child, not the parents, demands it. With infrequent exceptions, this is rarely before age 10 to 12 years, when social awareness is heightened.

Levels of Amputation Generally the more distal the level of amputation, the more useful will be prosthetic fitting. This is because the more distal the amputation, the more sensory feedback systems will be functioning to give automatic control. Traditional teaching is that finger prostheses are “cosmetic” and only impair capability. In fact, a digital prosthesis of high quality, as available today, fits so perfectly that both position and pressure feedback is provided. Combined with the prosthetic finger tip being where the brain expects it to be, this results in a remarkable degree of subconscious control and can be among the most helpful of prostheses (Fig. 93.7).

FIGURE 93.8. Split-hook active prosthetic terminal device is rugged and easily positioned, but for many is not socially acceptable.

Aesthetic Considerations The issue is whether the disfigurement is so great as to disturb the purpose of encounters, break the line of thought, or is genuinely grotesque. It is unrealistic to deny that disfigurement is of real socioeconomic importance. It has nothing to do with “cosmesis,” which is changing something normal to have better appearance in one’s opinion. There are two areas of consideration. One is the area of artistic factors (size, shape, color, etc.), which the artist can duplicate remarkably. The other area, and of equal or greater importance, is the ability to do ordinary tasks in the expected manner. Improving physical capability should be an important design concern for all hand prostheses to reduce the conspicuousness of the disfigurement.

Types of Prostheses There are only two basic types of hand prostheses, active (mechanical) or passive (purposely without internal mechanical

FIGURE 93.9. The most commonly used externally powered active prosthesis is a myoelectrically controlled, opening and closing electric clamp, but it has none of the manipulating capabilities of our hands. No currently available externally powered active prosthesis has a good, socially acceptable appearance.


898

Part VIII: Hand

A

B FIGURE 93.10. A: Wrist disarticulation. B: The light, stain-resistant silicone prosthesis with passively adjustable digital armatures can be pressed around light objects while simultaneously restoring social presentation. (Courtesy of American Hand Prostheses, Inc., New York, NY.)

A

B FIGURE 93.11. A: Blast injury leaving only the small finger. B: The single remaining finger placed in the middle finger position of a fine partial prosthesis has its usefulness vastly enhanced. (Courtesy of American Hand Prostheses, Inc., New York, NY.)

B

A FIGURE 93.12. A: Thumb and index finger amputations. B: Manipulating capability and social presentation improved by precise-fitting digital prostheses. (Courtesy of American Hand Prostheses, Inc., New York, NY.)



899

B

A FIGURE 93.13. A: A mutilated distal phalanx and fingernail. B: The unique sub-mini digital prosthesis covers only the distal phalanx, is thin like a surgeon’s glove to transmit sensibility, and provides for the first time a practical and secure methods of attaching a prosthetic fingernail to an intact distal phalanx. (Courtesy of American Hand Prostheses, Inc., New York, NY.)

units, although changing of their configuration with the other hand is often desirable). Active prostheses are no more than simple clamping devices that have none of the manipulating capability characteristic of our hands. They may be body powered (Fig. 93.8) or externally powered. Of the latter, only electric motors have proven to be practical because of ready availability of recharging facilities, but they deliver energy slowly, make noise, and have no subconscious control because there is no sensory feedback The control system that is almost exclusively used is the myoelectric system, which is velocity based rather than position and force directed, so activities are essentially visually guided. Their greatest virtue for unilateral hand amputees is that great clamping forces can be generated and suspension straps for below-elbow amputees are eliminated. Aesthetically, myoelectric hands are poor because of their shape, the thumb moving straight away from the index and middle finger pads rather than in an arc laterally, and their slow, abnormal, and noisy motion of parts (Fig. 93.9). Considerable improvement in the artistic aspects can result from covering with a high-quality, custom-made silicone glove. During the phase of emotional turmoil, looking for miracle devices, most unilateral above-elbow amputees try myoelectric hand prostheses, but the majority eventually opt for the lightweight, lifelike passive prosthesis constructed with a passively positionable elbow joint, which makes the prosthetic forearm useful for many activities. Passive prostheses purposefully have no internal mechanical units, but best meet the needs of the vast majority of hand amputees today as the big numbers are in partial hand and digital amputations. While not containing motors, the digits of passive prostheses can be constructed with armatures that permit change in their configuration by the normal hand. The introduction of microhinged rather than wire armatures was a major advance, as the problem of breakage from metal

fatigue and the necessity for firm anchorage of their proximal ends was eliminated (Fig. 93.10). Partial hand prostheses provide prosthetic parts against which remaining normal one can work (Fig. 93.11). The variety of losses encountered is innumerable, but the principles are the same. Digital prostheses are among the most rewarding, not only for restoring excellent social presentation, but for enhancing capability as a result of their substantial subconscious control. With the loss of both interphalangeal joints, the digital prosthesis can be fabricated with a passively adjustable, multihinged armature (Fig. 93.12). Until recently all finger prostheses were made to cover the whole finger, even if a good proximal interphalangeal joint were present. The technological breakthrough of the Bio-Chromatic (American Hand Prosthetics, New York, NY) coloring system led to development of the superb “mini” prosthesis for fingers with intact PIP joints (Fig. 93.7). In turn, this led to the subminidigital prosthesis for loss of part of the distal phalanx or even damaged or lost fingernails (Fig. 93.13).

Suggested Readings Baumgartner R. Active and carrier-tool prostheses for upper limb amputations. Orthop Clin North Am. 1981;12:955. Beasley R. Hand Injuries. Philadelphia: WB Saunders; 1981. Beasley R. Reconstructive surgery in the management of congenital anomalies of the upper extremities. In: Swinyard C, ed. Limb Development and Deformity. St. Louis: Charles Thomas; 1969. Beasley R, de Bese G. Upper limb amputations and prostheses. Orthop Clin North Am. 1986;17:395. Brown P. The rational selection of treatment for upper extremity amputations. Orthop Clin North Am. 1981;12:893. Simpson D. Extended physiologic proprioception. In: Symposium on Upper Extremity Prostheses and Orthoses. Goteborg, Sweden: 1971.



INDEX

Page numbers followed by f indicate figures; t indicate tabular material. A-1 pulley, digital flexor tenosynovitis, 824–825, 826f A frame deformity, blepharoplasty, 491f ABA. See American Burn Association Abbe flap dip defect and, 366, 368f tight upper lip and, 221 upper lip defects, 368–369, 368f ABCDE criteria, malignant melanoma and, 124 Abdominal flap elevation mini-abdominoplasty, 543f traditional abdominoplasty, 544f Abdominal laxity, divers test for, 543f Abdominal surgery, open wounds after, 669 Abdominal viscera, 668 Abdominal wall forces on, 668, 669f reconstruction closing wound, 668–670 management criteria, 668 Abdominoplasty body contouring of lower trunk and, 540–548 complications, 547–548, 547t technique, 543–544 traditional, 545f Abductor hallucis brevis (AHB), muscle flaps, 689, 693f Abductor pollicis brevis paralysis (APB), median nerve palsies, 850 Ablative lasers, 170, 462 Abscess cavity felon and, 818 paronychia and, 816 Absorption, lasers and, 462 Accessory parotid tumors, 342 ACD. See Anastomotic coupling device Achilles tendon foot and ankle wound care, 691 lengthening, 697f ulceration of metatarsal head, 697f, 698 Acid burns, 145 strength, local anesthetic agent and, 91 Acinic cell carcinoma, 340 Acland test, microsurgery and, 70, 71f Acne Galderma for, 113 isotretinoin, 113 light-activated drugs and, 171 scars, laser treatments and, 175 Acne rosacea, 111 Acne vulgaris, 110–111 Acquired amputation, hand agenesis v., 893, 895 Acquired cheek defects, reconstructive technique summary, 386f Acquired defects of female perineum, 707–708 of vagina, 709 Acquired deformity, auricular reconstruction of, congenital microtia v., 308 Acquired perineal fistulas, 713, 714f

Acrocephalosyndactyly type I. See Apert syndrome Acrocephalosyndactyly type II. See Crouzon syndrome Acrocephalosyndactyly type III. See Saethre-Chotzen syndrome Acrocephalosyndactyly type V. See Pfeiffer syndrome Acticoat donor site, burn injury and, 143 Actinic cheilitis, 107–108, 108f Actinic keratosis (AKs), 107–108, 108f laser treatments for, 174 Levulan photodynamic therapy, 171 Actinic skin damage, 457 Action potential, local anesthetics, 91 Activation period, 96 Active elbow extension restoration, 852 Active extension, flexor tendon continuity, 806 Active prostheses, hand, 895–896, 895f Acute auricular burns, 309 Acute auricular trauma, 308, 308f Acute burn injury, transition, 151 Acute injury, upper limb surgery and, 740 Acute othematoma, 308, 308f Acute scaphoid fractures, operative fixation of open technique, 784 percutaneous and arthroscopic techniques, 784, 786f Acute scaphoid trauma, imaging algorithm for, 767f, 768 Acute tendon injuries, 809–811 Zone 1 injuries, treatment, 809–810 Zone II injuries, treatment, 809–810 Zone III injuries, treatment, 810 Zone IV injuries, treatment, 810 Zone IX injuries, treatment, 811 Zone VI injuries, treatment, 811 Zone VII injuries, treatment, 811 Zone VIII injuries, treatment, 811 Acute wound, 16 Acute wrist injuries, imaging algorithm for, 766f, 768 Acyclovir herpes virus, TCA peel and, 459 herpetic whitlow and, 818, 820f laser abrasion, 464 Adaptive instability, 782 AdatoSil-5000, filler materials and, 471 Adenocarcinoma of parotid gland, 340 Adenoid cystic carcinoma, 340 Adenoma sebaceum, laser treatments for, 174 Adenomatous polyp, colon and, 21 Adhesive-retained silicone prosthesis, 352f Adjuvant chemotherapy, breast cancer, 622 Adnexal tumors, 108–109 Adult respiratory distress syndrome (ARDS) high-frequency oscillatory ventilators, 149 inhalation injury, 139 Advanced glycosylated end products (AGEs), wounds and, 702 Advanced melanoma, treatment of, 130–131 Advanced Trauma Life Support (ATLS), burn patient, 132

medwedi.ru

Advancement skin flaps, 10, 12, 13f cheek reconstruction and, 374–375, 376f Aesthetic appearance complications in, breast implants and, 580–581, 580f–581f facial skeletal augmentation and, 549, 550f fat grafting and, 482–483 osseous genioplasty and, 557 TRAM techniques and, 640, 641f, 642, 642f–643f, 644 Afferent pupillary defect (APD), orbital fractures and, 318 Age replantation in upper extremity and, 866 wound healing and, 23–24 AGEs. See Advanced glycosylated end products Aging blepharoplasty and, 495 face, forehead lift and, 508f facelifting and, 496 RARs and, 113 skin, effects of, 457 surface orbital anatomy, 488 AHAs. See Alpha-hydroxy acids AHB. See Abductor hallucis brevis AIDS-related lymphoepithelioma, 341 Air embolus, craniosynostosis, 233 Airway burn patient and, 132, 133t facial injuries and, 313 AJCC staging (American Joint Committee on Cancer staging) head and neck cancer, 331, 341f stage grouping with, 620, 621t AJCC-TNM staging system, breast cancer, 620, 620t AK. See Actinic keratosis Alar base, 519, 519f unilateral cleft lip repair, 208 Alar-columellar relationship, 522, 522f Alar rims, 519, 519f, 520f Albumin, fluid resuscitation and, 138 Alcoholism, Dupuytren disease and, 862–863 Aldara. See Imiquimod Alginates, wound healing and, 30 Alkaline burns, 145 Alkaline phosphatase, malignant melanoma and, 124 Allergenicity, local anesthetics, 91 Allergy, silver sulfadiazine, 136–137 AlloDerm, 467 burn wound and, 147, 148, 148f implants, 63 midline abdominal wall defects and, 671 parotid gland tumors, 344 Allogeneic limb tissues, 57 Allogeneic transplantation, 53 Allografts, 9, 52 cyclosporine and, 53 Alloplastic augmentation, osseous genioplasty v., chin implants, 555 Alloplastic implants, facial skeletal augmentation, 549–554


901

902

Index

Alloplastic materials facial skeletal augmentation and, 549 mandibular ramus augmentation, operative technique, 553 Alopecia, hair transplantation and, 569f Alpha-hydroxy acids (AHAs), 457, 458 laser abrasion, 464 skin and, 113 Alpha-tocopherol, 114 ALS. See Antilymphocyte sera Alveolar cleft, treatment approaches, 219 Alveolar ridge malignancies, 333 American Burn Association (ABA), burn center criteria, 132, 133t American College of Mohs Micrographic Surgery and Cutaneous Oncology, 119 American Joint Committee on Cancer staging. See AJCC staging American Society for Surgery of Hand System, flexor tendon continuity and, 807 Amides, local anesthetics and, 91 AMPLE acronym, trauma history and, 314 Amputated body part, 876f preparation of, replantation and, 870–871 Amputated ear, 309 Amputated penis replantation, 713 Amputation, 674, 675. See also Prostheses; Replantation; specific body part amputation i.e. Thumb combined vascular malformation syndromes, 198 of digits, 894f levels of, 895 lower-extremity traumatic, algorithm for, 683, 684f MCP joint, 835, 839f osteomyelitis, 822 subungual melanoma and, level of, 127f suitable for replantation, 867t thumb deficiencies as, 833–835 Amputation stump, 876f preparation of, replantation surgery, 871–872 Anaerobes, necrotizing fasciitis, 821 Anastomoses. See also specific type anastomoses i.e. Arterial anastomoses end-to-end, history of, 66 end-to-side anastomosis, 68, 69, 69f magnification equipment and, 67 Anastomotic coupling device (ACD), 71f Anatomic concepts, skin blood supply, 35–41 Anesthesia blepharoplasty, 490 facelifting and, 498 facial skeletal augmentation, 551 fat grafting and, 481 foreheadplasty and, 510 hair transplantation, 561 liposuction and, 532 preoperative preparation, rhinoplasty, 523 soft tissue injuries, 315–316 upper limb reconstruction, 741–742 Anesthetic reversal, microsurgery and, 70 Angel kiss, 194 Angiofibroma, 110 Angiogenesis, distraction zone and, 97 Angiomas, 189 Angiosarcoma, MMS and, 117 Angiosomes concept, 35–36, 36f–37f foot and ankle, 687, 688f Animal bites, 820 Animal experiments. See also Clinical studies distraction zone, 97 ePTFE, 468 Anitia-Buch helical advancement, otoplasty and, 299f Ankle

defect, reconstruction, 701–702 flaps, 688–689, 691f reconstruction, 687–705 vascular supply, 688 Anterior compartment of leg, 675 Anterior cranial fossa. See Anterior skull base Anterior graft, mandible reconstruction, 427f, 433 Anterior incisors, number 1 Tessier craniofacial clefts and, 267, 269f Anterior interosseous neuropathies, 830 Anterior lamella, eyelid and, 395 Anterior lateral thigh flap, 449–450 Anterior lunate dislocation, 747f Anterior skull base (Anterior cranial fossa) lesions, 345 reconstruction, flap selection for, 441f, 443 Anterior skull base (Anterior cranial fossa) tumors, endoscopic approach, 346f Anterolateral thigh flap, 383, 385f Antibiotics acne vulgaris and, 111 animal bites, 820 burn eschar and, 136 hand infection and, 817t hydradenitis suppurativa and, 111, 111f intravenous, necrotizing fasciitis, 821 long-term therapy, osteomyelitis, 822 lymphangitis and, 816 mandibular fracture, 326 pressure sores, 727 prosthetic breast reconstruction and, postoperative care, 630 Pyoderma gangrenosum and, 111 pyogenic flexor tenosynovitis and, 819–820, 822f vertical breast reduction, 607, 610 wounds and complications, 675 healing and, 25 Antigen-presenting cells (APCs) allogeneic transplantation and, 53 transplantation antigens and, 52 Antihelical fold manipulation, 296–297 Antilymphocyte sera (ALS), immunosuppression and, 54 Antimicrobial dressings, wound healing and, 30 Antimicrobial therapy, hand infection and, 816 Antispasmodic agents, microsurgery and, 70 Antithrombotic medications, replantation in upper extremity and, 875 Antiviral prophylaxis, laser abrasion, 464 APB. See Abductor pollicis brevis paralysis APCs. See Antigen-presenting cells APD. See Afferent pupillary defect Apert syndrome (Acrocephalosyndactyly type I), 235–236, 236f classification, 855–857, 858t preoperative v. postoperative views, 244f syndactyly of digits, 237f Apertognathia, 254, 258–259 Apocrine cystadenoma, 109 Apocrine tumors, 109 Appliances, PSIO and, 203 Aquamid injectable, filler materials and, 467 ARC of rotation, myocutaneous flap and, 44, 45f ARDS. See Adult respiratory distress syndrome Areola closure, vertical breast reduction, 607 opening, skin resection patterns, 604 tattooing cartilage graft nipple reconstruction, 658f penny flaps and, nipple reconstruction and, 658–659, 658f

Argiform, filler materials and, 467 Argon laser, 171 Arsenic basal cell carcinomas, 111 Bowen disease and, 108 Artecoll/Artefill, filler materials and, 467 Arteplast, filler materials and, 467 Arterial anastomoses, replantation in upper extremity and, 873 Arterial-arterial anastomoses, of foot and ankle, 687, 689f Arterial blood gas, inhalation injury, 139 Arterial grafts, replantation in upper extremity and, 873 Arteries, of foot and ankle, 687 Arteriography, vascular malformations, 194 Arteriovenous malformations (AVMs), 193, 197 MRI and, 765 natural history of, 197 Artery ligation, lower-extremity trauma, 675 Artesia, 303 Arthritis stages II to IV, treatment of, 884 of systemic lupus erythematosus, 888 Arthrodesis, thumb basal joint arthritis and, 884 Arthrography, hand and wrist, 750 Articulator, 254 Aseptic technique, wound complications, 675 Aspiration of fat, liposuction and, 534 Asymmetry eyelid ptosis correction, 408 prosthetic breast reconstruction with, 630 vertical breast reduction, 612 ATG. See Polyclonal antithyroglobulin Atherosclerotic disease, foot ulcers, 703 Ativan, burn patient, 141 ATLS. See Advanced Trauma Life Support Atypical microtia, 303 Atypical moles, 105–106, 106f Augmentation mammoplasty anatomic considerations in, 573–574 breast cancer detection/survival, 578–579 complications, 573–582 overview, 576 endoscopic applications, 574, 575f government regulations and, 573 history, 573 surgical technique, 574, 574f Augmentation mastopexy, 586–590 Augmentation of thumb opposition, 850 Auricle, craniofacial microsomia and, 249 Auricular prostheses, 348–350, 349f Auricular reconstruction, authors thoughts, 306, 308 Autogenous auricular reconstruction, microtia, 304–305 Autogenous material, skull base defects reconstruction, 443 Autogenous reconstruction, maxillary defect restoration and, osseointegration in, 354 Autogenous tissues, maxillary defect reconstruction, 436 Autograft, 52 scalp and, 143 Autoimmune disorders, augmentation mammoplasty and, 578 Autologen filler materials and, 467 wrinkles and, 466 Autologous augmentation, augmentation mammoplasty and, 576 Autologous fat transplantation, filler materials and, 469 Autologous nerve grafts, 56 Autonomic neuropathy, wounds and, 702


Index Avascular necrosis of carpal bones, MRI and, 762, 763f, 764 of fracture scaphoid, MRI and, 763f, 764 AVFs. See Macroarteriovenous fistulas AVM. See Arteriovenous malformations Avulsion injuries classification of, 870t replantation in upper extremity, 866–867, 868f, 869f Axial-based flaps, hand and, 737 Axial flaps, 39, 774–777, 775f Axial images, MRI and, 758f, 760 Axial-pattern flaps, blood supply of, 42–43 Axilla, breast cancer and, 621 Axillary incision, 574, 574f Axillary scarring, 158 Axonal injury, upper limb compression and, 829 Axonotmesis, 73, 75f Axons, nerve grafts and, 78 Azathioprine graft rejection and, 53 peripheral nerve allotransplantation, 82 Bacitracin ointments, 30 post burn period and, 137 Background pain, burn patient, 141 Baclofen, spasm, 723 Bacteria, wound healing and, 25 Bacteroides, animal bites, 820 Baker classification of capsular contracture, after augmentation mammoplasty, 577t Baker-Gordon formula, phenol and, 460, 460t, 461 Bands of Bungner, 73 Bands of Fontana, 76 Banked cartilage, nipple reconstruction, 656–658, 657f Banked fork flap repair, 213 Bannayan-Riley-Ruvalcaba syndrome, 198 Banner flaps, cheek reconstruction and, 375, 377f Barbed sutures, facelifting, 505 Barrel stave osteotomies bilateral coronal synostosis and, 231 lambdoid synostosis, 232f Basal cell carcinomas (BBC), 105, 111–112, 112f, 116 cervicofacial flaps, 381f Sebaceus nevus of Jadassohn, 109 Basal energy expenditure (BEE), burn injuries and, 140 Base of phalanx factures, 790, 792f Bay 43-9006, melanoma and, 130 Bazex syndrome, basal cell carcinomas, 111 BCC. See Basal cell carcinomas Becaplermin (Regranex), wound healing and, 28 BEE. See Basal energy expenditure Below-knee amputation advantages of, 685 free flap salvage, 686 stumps, limb salvage and, 683–685 Benign lesions, malignant lesions v., 105 Benign pigmented lesions green light lasers, 175–176 pigmented lesion lasers and, 171 Benign salivary neoplasms, 344 Bennett fracture, 795, 796f, 884, 886f Benzodiazepines, burn patient, 141 Benzoyl peroxide, acne vulgaris and, 111 Bevacizumab, head and neck cancer and, 338 Biggs-Graf mastopexy, 587f patient before, 588f Bilateral cleft lip, 221 NAM and, 205, 206f

and nose repair, cartilage paradigm, 213–214 premaxillary setback and, 221 repair, skin paradigm of, 212–213 Bilateral cleft nose repair, skin paradigm of, 212–213 Bilobed flap, 11, 11f cheek reconstruction and, 378f nasal reconstruction, 389 Bilobed flaps, cheek reconstruction and, 375, 378f Bio-Alcamid, filler materials and, 468 Bio-Chromatic coloring system, prostheses and, 897 Bioactive glass, bone grafts substitutes and, 59 Bioburden, wound healing and, 25 Biocell Ultravital, filler materials and, 468 Biochemotherapy, melanoma and, 130 Biodegradable polyesters, 61, 61f Biologic debriding agents, wound reconstruction, foot and ankle, 694 Biologic dressings, skin grafts and, 9 Biologic implant materials, 63 Biomedical implants, 58 Bioplastique, filler materials and, 468 Biopsy basal cell carcinomas and, 112 CMN and, 120 lesions and, 105 malignant melanoma and, 124 nevus sebaceous of Jadassohn and, 109, 109f Birth defects, isotretinoin, 113 Birthmarks, 189 Bite wounds, 820 Blast injury, partial finger prosthesis, 896f Blauth classification, of hypoplastic thumb, 859, 860t Bleaching agents, 457 skin and, 114 Bleeding dermabrasion, 461 hair transplantation, 560 infantile hemangioma and, 192 lower truncal contouring and, 548 oral cavity reconstruction and, 448 Bleomycin, warts and, 822 Blepharochalasis, blepharoplasty and, 490 Blepharoplasty, 484–495 complications, 493 operative technique, 490–493 outcomes, 494–495, 494f, 495f postoperative care, 493 preoperative evaluation, 488–490 Blood-brain barrier, toxicity anesthetic agents and, 94 Blood flow TRAM flap procedure, 653–654 wound reconstruction of foot and ankle, 696 Blood glucose levels, burn injuries and, 140 Blood loss burn-wound excision, 142 craniosynostosis, 233 Blood perfusion, problems, microsurgery and, 70 Blood pool phase, bone scintigraphy and, 752 Blood pressure, facelifting and, 498 Blood supply breast, 602, 603f muscle flaps and, 42–43 of nose, 515 scalp, 356–357 scalp and forehead, 356–357, 357f of skin, 33–41 overview of, 33–35, 34f, 35f Blue nevus, 105, 107f Blue rubber bleb nevus, 196

medwedi.ru

903

Body contouring of lower trunk. See Lower truncal contouring Bone growth factors, calcium phosphate ceramics, 59–60 Bone remodeling distraction zone and, 97 sagittal synostosis and, 229 Bone scan, osteomyelitis, 822 Bone scintigraphy, processes of, 750–753 Bone(s) allograft, 55 architecture, foot and ankle wound care, 691 autograft, 55 craniofacial distraction and, 96 current transplantation and, 55 debridement, osteomyelitis and, 49, 50f fixation, replantation in upper extremity and, 872, 872f gaps, management of, 681 grafts facial trauma, 326–327 substitutes, calcium ceramics as, 59–60 survival, 55 healing, craniosynostosis, 233 injuries, upper limb surgery and, 740 of leg, 675 reconstruction polymers and, 60–63 skull base defects reconstruction, 443 replacement, PMMA and, 60 Bony fixation, mandible reconstruction, 430, 432f Bony shortening, amputated body part and, replantation surgery, 871 Botox, 92, 466 Botulinum toxins brow lift and, 475 crow’s feet and, 475 depressor anguli oris, 477 dosage, 474 forehead and, 474 functional facial anatomy and, 474 glabella and, 474 hyperhidrosis and, 477 lower eyelid, 475 mechanism of action, 473 mentalis muscles, 476–477 nasolabial fold and, 476 neck and, 475–476 perioral lines and, 476 preparation, 474 surgery complications of, 477 Boutonniere deformity, 812–813, 813f Bowen disease, 108 MMS and, 117 Bowstring canthal advancement technique, 228f Boyes method, flexor tendon continuity, 806 Brachial arches, hypoplasia and, 246, 247t Brachial plexus block, 92 Brain multiple sutures and, 224 size, craniosynostosis syndromes and, 238 Brain metastasis, systemic melanoma, 130 Branchial apparatus, head and neck embryology and, 177–178, 181 Branchial arches components of, head and neck embryology and, 177–178, 178f derivatives, head and neck embryology and, 179t, 181 external ear and, 186, 186f facial development and, 181 head and neck embryology and, 177, 178f Branchial grooves, head and neck embryology and, 178, 178f


904

Index

Breast anatomy, 573–574, 602 and physiology, 591 shaping, LTTF and, 653 silicone elastomer implants and, 60 vessels and, 39, 40f Breast amputation, with free nipple graft, Spear technique, 598–600, 601f Breast cancer AJCC-TNM staging system, 620, 620t augmentation mammoplasty and, 578–579 early, 620 locoregional treatment, 620–622 pathology, 619–620 plastic surgery and, 619–622 risk factors, 619 staging, 620, 620t Breast conservation surgery, 620–621 contraindications to, 621, 621t Breast-fed children, silicone, 578 Breast implants. See also Saline breast implants; Silicone breast cancer detection/survival, 578–579 imaging, 579, 580f polyurethane and, 63 Breast meridian, vertical breast reduction, 604 Breast ptosis, 586 classification, 583, 584f Breast reconstruction free flap techniques, 646–654 immediate implant placement and, 628–629 prosthetic techniques for, 623–631 radiation and, 165–166 TRAM flap surgical delay and, 645 techniques, 639–645 Breast reduction. See Reduction mammoplasty Brent technique, 306 complications, 305 microtia, 304, 304f, 305f, 306f stages of, 304, 304f Broad-spectrum antimicrobial coverage, burn patient, infection and, 141 Bronchoscopy chest wall irradiation, 167 inhalation injury, 139 Brook and Evans formulas, fluid resuscitation and, 138 Brow, preoperative evaluation of, 488–489 Browlift procedure blepharoplasty, 494f, 495, 495f botulinum toxins and, 475 facial paralysis and, 418 Buccal cavity, 254 reconstruction, 446 Buccal fat pad, facelift anatomy and, 500 Buccal mucosa, 445 malignancy, 333 Bunnell, S., hand specialization and, 736, 736f Bupivacaine (Marcaine), 91 cardiovascular compromise and, 94 Buried devices, 100f, 101 Burn care, organization of, 132 Burn Center facility, referral criteria, ABA and, 132, 133t Burn shock physiology, fluid resuscitation and, 138 Burn wound. See also Thermal injuries excision, 141 techniques of, 141–142 management, advances, 149 sepsis, 141 Burn(s). See also specific type burn i.e. Scald burn

broad-spectrum antimicrobial coverage, 141 depth categories, 136t determination, 134 extent, determination of, 133 full-thickness, immersion time for, 133t injuries depth of, 133–134, 136f etiology of, 132 fluid resuscitation and, 138–139 future horizons, 149 gastrointestinal prophylaxis and, 140–141 infection and, 141 late effects of, 148–149 management initial, 134–137 outpatient, 145 overview of, 132–139 patient evaluation of, 132–134 management, 140–141 reconstruction surgery evaluation and treatment, 158–159, 161 general concepts, 150 plan, 153 principles of, 150–161 timing of, 151, 153 scar, 153 size calculation, age-based diagram, 133, 135f C5a. See Complement cascade Cafe-au-lait spots CMN v., 120 pigmented lesion lasers and, 171 Calcaneal defects, 701 Calcification augmentation mammoplasty, 576 distraction zone and, 97 Calcium ceramics, bone grafts substitutes and, 59–60 Calcium gluconate gel, chemical injury and, 146 Calcium phosphate bone cements, 59, 59f Caloric requirement formulas, burn injuries and, 140 Calvaria, development of, 187–188 Calvarial bone grafts, 363 Calvarial reconstruction, 363–364 CAM Walker, ulceration of metatarsal head, 698–699 Camptodactyly, 858 Canaloplasty, middle ear reconstruction, 303 Cancer. See specific type cancer or cancer location i.e. Head and neck CancerVax vaccine, melanoma and, 130 Candida albicans chronic paronychia, 821 onychomycosis, 822 Canthi, eyelid and, 395 Canthopexy, 410 blepharoplasty and, 492f Canthoplasty, 408–413, 410 blepharoplasty and, 492f lower eyelid, facial paralysis and, 419–420 Capillary blood pressure, ulceration v., 720–721, 721f Capillary malformation-arteriovenous malformation (AM-AVM), 193 Capillary malformation (CM), 193, 194–195 laser treatments for, 171–172 Capitate fractures, 787 Capsular contracture. See also Baker classification of capsular contracture augmentation mammoplasty, 576 breast and, 576–577, 577f

delayed-primary breast reconstruction, 87 prosthetic breast reconstruction with, 630 treatment, 577–578 Capsule, silicone elastomer implants and, 60 Capsulotomy, capsular contracture, 577 Carcinogenesis, augmentation mammoplasty and, 578 Carcinoma, pressure sores, 727 Carcinoma ex pleomorphic adenoma, 340 Cardiac arrest, topical cocaine and, 95 Cardiac monitoring, phenol and, 460 Cardiac pacemakers, MRI and, 765 Cardiovascular system (CVS), toxicity anesthetic agents and, 93 Carol-Gerard screw, orbitozygomatic fractures, 320, 320f Carpal alignment, standard radiographs, 747f, 748 Carpal fractures, 782, 785–787 Carpal instability, classification of, 779–780 Carpal instability dissociation (CID), 779–780 Carpal instability nondissociative (CIND), 779 Carpal theories of wrist, 779–780, 781f Carpal tunnel syndrome (CTS), 829 MRI and, 762 Carpal tunnel view, standard radiographs, 749, 749f Carpenter syndromes, 235, 237–238 Cartilage current transplantation and, 55–56 head and neck embryology and, 177 paradigm, bilateral cleft lip and nose repair, 213–214 Cartilage allograft, 56 Cartilage autograft, 56 Cartilage grafts harvest, septal reconstruction and, 525 middle-third auricle defects, 300–301, 301f nipple reconstruction, areolar tattooing and, 658f Cartilage xenograft, 56 Cast, 254 Cast immobilization, fractures and, 680 Cat bites, 820 Cat-scratch fever, cat bites, 820 Catecholamines, topical cocaine and, 94 Catheter irrigation technique, pyogenic flexor tenosynovitis and, 819, 822f Cauliflower ear, 308 Cavernous nerve grafting, prostatectomy and, 714 CBC. See Complete blood count Cell proliferation, tissue expansion and, 84 Cellular differentiation, squamous cell carcinomas and, 113 Cellulitis hand and, 816 hand infection, 816 Central defects, forehead reconstruction, 363 Central lip vermilion, construction methods for, primary bilateral cleft lip repair and, 211–212 Central mound technique, reduction mammoplasty, 597f, 598f Central nervous system (CNS) melanoma, 122 toxicity, anesthetic agents and, 93, 94 Central nervous system (CNS) injury electrical, 147 facial, 313 regeneration, 21 Central polydactyly, 859 Central unit amputations, 892, 893f Centric occlusion, 254 Centric relation, 254 Cephalexin, rhinoplasty and, 530


Index Cephalic mesoderm cellular origin of, 186–187 development interruption, 187 Cephalic trim, indications for, 525 Cephalometric radiograph, 254 orthognathic surgery and, 255–256 Cephalometric tracing orthognathic surgery and, 256, 256f preoperation, 259–260 Cephalosporins, vertical breast reduction, 607, 610 Cerebellopontine angle tumors, endoscopic approach, 347f Cerebrospinal fluid leak, skull base defects and, 442 Cervical contracture, burn reconstruction surgery and, 156f Cervical esophagus anatomy and T staging, 331, 336f cancer, 334–335 ablative surgery for, 453–454 functional anatomy of, 451 reconstruction, 451–454 methods for, 452 principles of, 451–452 site locations, 331, 335t Cervical flaps, cervical esophagus reconstruction, 452 Cervical sinus, head and neck embryology and, 178, 178f Cervical spine injury, facial injuries and, 314 Cervical vertebrae malformations, craniofacial microsomia and, 246–247 C5-C6 spinal cord injury, hand reconstruction and, 851–852 Cervicoaxillary LM, 196 Cervicofacial flaps basal cell cancer and, 381f cheek reconstruction and, 376–377, 379f lower eyelid reconstruction, 401 Cervicopectoral flaps, 383f cheek reconstruction and, 377–378 Champy’s lines of osteosynthesis, 325, 325f Charcot foot, 32, 691, 701 wounds and, 702 Cheek anatomy, 373 defect analysis, 373 reconstruction, 373–386 facial paralysis and, 420 options, 373–386 resection, 431f Chemical carcinogens, basal cell carcinomas, 111 Chemical injuries, 132–149, 145–146 Chemical peels, 457–461 AK and, 107 CMN and, 122 complications of, 461 Chemically toxic agents, ingestion, 146 Chemotherapy head and neck cancer and, 338 infantile hemangioma, 192 melanoma and, 130 Chest radiography inhalation injury, 139 malignant melanoma and, 124 Chest wall defects etiology of, 663–664, 664t reconstructive choices, 667 irradiation, complications, 166–167 reconstructions GoreTex and, 63, 64f metastatic breast cancer and, 666f soft-tissue reconstruction and, 665–667 Chest wall meridian, vertical breast reduction, 604

Chest wall skeleton, anatomy and physiology of, 663 Childhood congenital mishaps of hands, 738 early AVM in, 197 infantile hemangioma in, 193 late, infantile hemangioma in, 193 Children acinic cell carcinoma, 340 IFN and, 192 indications for, auricular reconstruction, 306 infantile hemangioma and, 191 mandible distraction, 99 maxillary Le Fort I distraction, 101 midface distraction, 101 prosthetic auricular reconstruction, microtia and, 305–306 replantation surgery, 866, 870, 870f Romberg disease and, 285 scar and, 3 vascular malformations and, 339–340 warts and, 822 Chin augmentation, 552–553 implant design, 553 preferred technique, 551f implants, alloplastic augmentation and, osseous genioplasty v., 555 mandibular rotation, 261f Chloroprocaine, 91 Choke anastomoses, 33, 35f Chondroid syringoma, 109 Chondromas, 663 Chronic infections, of hand, 821–823 Chronic osteomyelitis, tibial fractures and, 683 Chronic paronychia, 821 Chronic scapholunate instability, 780 Chronic wounds, 16 debridement of, 684f Chronic wrist pain, imaging algorithm for, 767f, 768 CID. See Carpal instability dissociation Cigarette smoking facelifting and, 497 hair transplantation, 560 prosthetic breast reconstruction with, 630 replantation in upper extremity and, 874 TRAM techniques and, 644, 645 CIND. See Carpal instability nondissociative Circular excision, 6–7, 7f Circulation, upper limb surgery and, 739 Circumferential lipectomy, 544–547 Circumferential lower truncal dermatolipectomy, 544–547 Clark levels, malignant melanoma and, 124, 126f Class I occlusion, 254, 257 Class II malocclusion, 254 Class III malocclusion, 254 Cleft hand, correcting, 855 Cleft lip. See also Microform cleft lip hair transplantation and, 568f Cleft lip and palate, 182, 184f, 185, 202 epidemiology and etiopathogenesis, 199 maxillary Le Fort I distraction, 101 multidisciplinary care, 199, 200t presurgical orthopedics, 202–206 surgical treatment, by age, 199, 200t Cleft palate. See also Primary cleft palate repair embryologic basis of, 184 prostheses, 353–354 repair, complications following, 216–217 Clindamycin, acne vulgaris and, 111

medwedi.ru

905

Clinical observation, replantation in upper extremity and, 875 Clinical studies breast cancer, 622 fascicular repair, 78 melanoma and, radiation for, 130 unrepaired cleft palate and, 217 Clinodactyly, 857 Closed nerve injury, algorithm for, 79f Closed plaster technique, open tibial fractures and, 674–675 Closed rhinoplasty approach, rationale, 523, 523t Clostridial collagenase injection, Dupuytren disease and, 865 Clostridium, necrotizing fasciitis, 821 Closure. See Skin Clotting cascade, activation, 17 CLVM. See Combined capillary-lymphaticocovenous malformation CM. See Capillary malformation CMF (Cyclophosphamide, methotrexate, 5-fluorouracil), breast cancer, 622 CMN. See Congenital melanocytic nevi CNS. See Central nervous system CO2 laser, 461, 462, 464 Erbium: YAG laser v., advantages v. disadvantages, 463t tuberous sclerosis, 174 wrinkles and, 175, 175f Coagulopathy, connective tissue disorders, 703 Cocaine, 91, 94–95 Coherent light, laser physics and, 169 Cold injury, treatment, 147 Cold intolerance, replantation in upper extremity, 880, 881t Collagen dermabrasion and, 461 implants, 63 laser treatments and, 175 radiofrequency and, 171 remodeling, 20, 20f z-plasty and, 155 Romberg disease and, 285 Collapse deformity, degenerative arthritis of basal joints of thumb, 884 Collar button abscess, 819 Colloid, fluid resuscitation and, 138 Colonized bacteria, wound healing and, 25 Columella reconstruction, second stage, 213 Columellar-labial angle, 522, 522f Columellar tip graft, 527, 527f Combined capillary-lymphaticocovenous malformation (CLVM), 197 Combined nerve palsies, tendon transfers for, 851 Combined vascular malformation syndromes, 197–198, 197t treatment, 198 Comedo DCIS, 619 Commissural burns, self-retaining spring dental retractors, 371 Common canthopexy, 412–413 Common canthoplasty, 412–413, 413f Common warts, 822, 823 Compartment syndrome, signs of, 676 Complement cascade (C5a), wound healing and, 17 Complete bilateral cleft lip, 201–202, 201f Complete blood count (CBC), malignant melanoma and, 124 Complete capsulectomy, latissimus dorsi flap breast reconstruction, 636 Complete conduction block, upper limb compression and, 828–829


906

Index

Complex syndactyly, Apert syndrome and, 855–857 Complex wounds, 49, 50f, 51, 51f Component boney dorsum reduction, 524 Component loss, thumb deficiencies as, 833–835, 836f Composite autogenous/alloplastic reconstruction, prosthetic auricular reconstruction, microtia and, 305–306 Composite loss, soft tissue and, 834, 834f Composite rhytidectomy, 503 Composite venous grafts, replantation in upper extremity and, 873 Compound nevi, 105 Compression neuropathies specific upper limb, 829–832 in upper limb, electrophysiologic studies of, 828–832 Compression sites, peroneal nerves, 703, 703f Compression therapy venous stasis ulcers and, 32 wound healing and, 25 Compressive stockings, combined vascular malformation syndromes, 198 Computed tomography. See CT Concentric mastopexy procedures, 583–584, 584f Concha type microtia, 303 Conchal alteration, 297, 298f Conchal resection, otoplasty and, 298 Concomitant neurovascular injury, flexor tendon injuries and, 804 Condylar fractures, 788, 790 Condyle, craniofacial microsomia and, 246–247 Congenital absence of vagina, 707 Congenital anomalies of hand and wrist, CT and, 755 Congenital breast anomalies, tissue expansion and, treatment of, 87–88 Congenital constriction band syndrome, 860, 860f Congenital dermoid inclusion cysts groups of, 288–289 treatment, 290 Congenital dermoid tumors, 288–290 Congenital hand abnormalities, 854–861 classification of, 854, 855t embryology and, 854 Congenital hand loss. See Hand agenesis Congenital hemangioma, 190–191 Congenital lymphedema, 715 genes for, 193 Congenital malformations of tongue, 185–186 Congenital melanocytic nevi (CMN), 120–123 bathing trunk distribution, 120, 121f clinical characteristics, 120 differential diagnosis, 120–122 epidemiology of, 120 histologic characteristics, 120 malignant transformation of, 120–122 management of, 122 Congenital microtia, acquired deformity v., 308 Congenital nevi, 105, 107f melanoblasts and, 120 pigmented lesion lasers and, 171 serial excisions for, 7 Congenital pigmented lesions, CMN v., 120–122 Congenital ptosis, lagophthalmos and, 404 Congenital trigger thumb, 825, 857 Conjunctiva, anatomy, 486 Connective tissue, 37 disorders, wounds and, 703–704 framework

of body, vessels following, 36–39 vessel relationship to, clinical applications of, 38–39 Consolidation period, 96 Constricted ears, 295, 296f, 298, 298f Contact burn, 132 Contaminated tissue, midline abdominal wall defects and, 671–672, 671f Contamination, wound healing and, 25 Continuous over-and-over suture, 5f, 6 Continuous positive airway pressure (CPAP), craniosynostosis and, 226 Contour deformity burn reconstruction surgery, 150 fat aspiration, 534, 535f prosthetic breast reconstruction with, 631 Contour irregularity, categories of, liposuction and, 535, 539 Contracture releases burn reconstruction surgery, 150 pressure sores and, 723 Contractures burn reconstruction surgery and, 153 treating, Dupuytren disease and, 864 Z-plasty and, 158 Contralateral mucoperichondrial flap, nasal reconstruction and, 393f Contrast-enhanced computed tomography, vascular malformations, 194 Conventional flap harvest, 452 Converse/Wood-Smith technique, antihelical fold manipulation, 296 Corneal ulcer, treatment, 20 Coronal images, MRI and, 758f, 760 Coronal suture of skull, craniosynostosis and, 235 Coronal synostosis bilateral, 224 skull in, 230–231, 230f, 231f deformational plagiocephaly v., 232t Coronal technique foreheadplasty, 511–512 incision placement, 511f Corrosion, vitallium and, 58 Corset platysmaplasty, 503 Corticosteroid, infantile hemangioma, 192 Cosmetic conditions, lasers for, 175–176, 175f Cosmetic surgery, reconstructive surgery v., 3 Cosmetics facial burn reconstruction, 161 reconstructive surgery v., 3 Cowden syndrome, 198 nevus sebaceous of Jadassohn and, 109, 109f CPAP. See Continuous positive airway pressure Cranial anatomy, anomaly development, 224–226 Cranial bone struts, lambdoid synostosis, 232 Cranial distraction, 101 Cranial skeleton, transcription factor Runx2/Cbfa1, 187–188 Cranial sutures craniofacial distraction and, 96 minor and major, 224, 225f Cranial vault, 224 remodeling, fronto-orbital advancement, 242 Craniectomy in infancy, craniosynostosis syndromes and, 241 Cranio-orbital disorders, management of, 293 Craniofacial clefts, 266–278 defining features, 266 hypertelorbitism and, 266–278 palate development and, 187 treatment of, 278

Craniofacial deformity, skull base defects and, 442 Craniofacial distraction future of, 101 history, 96 principles of, 96–102 Craniofacial microsomia 3-D CT scan, 250, 250f classifications, 249–250 clinical findings, 246–250, 247f epidemiology, 246 etiology of, 246 facial reconstruction, 252f preoperative assessment, 250 severity levels, 250f treatment, patient age and, 250–251, 253 Craniofacial morphogenesis, 186 Craniofacial plating systems, titanium and, 58 Craniofacial prosthetics, 348–355 Craniofacial skeleton, gunshot wounds to, 327f, 328f, 329 Craniofacial surgery, 224 Craniomaxillofacial internal fixation, metals, 58 Cranioplasty, craniosynostosis, 233 Craniosynostosis complications of, 233 history and pathogenesis of, 224 ICP and, 225 positional plagiocephaly of occiput v., 225 preoperative considerations, 226–227 surgical timing, 226 surgical type, 226–227 treatment options, 239t types of, 224–225 Craniosynostosis syndromes, 235–245 brain size and, 238 fronto-orbital advancement in, 239f genetic predisposition, 235 ICP in, 238–239 Crescent mastopexy, 588f Crohn disease, 823 Cross-facial nerve graft, facial paralysis and, 421f, 422f Cross-finger flap, 770, 771f Cross-tunneling, liposuction and, 535f Crouzon syndrome (Acrocephalosyndactyly type II), 235, 236f craniosynostosis and, 226 Crow’s feet, botulinum toxins and, 475 Crush injury, scarring and, 4 Crusting lesions, laser treatments for, 173 Cryotherapy, basal cell carcinomas and, 112 Cryptotia, 295, 297f, 298–299 Crystalloid, fluid resuscitation and, 138 CT (Computed tomography) chest wall irradiation, 167 craniosynostosis and, 226 facial trauma and, 315, 315f hand and wrist, 753–757 malignant melanoma and, 124 mandible fractures and, 324 MMS and, 117 orbitozygomatic fractures, 319 osteomyelitis, 822 scaphoid fractures, 782, 784f technical limitations, 756–757 therapeutic inguinal lymphadenectomy, 130 three-dimensional, wrist, 752f titanium and, 58 Cubital tunnel syndrome, 830 Curreri formula, burn injuries and, 140 Curvilinear dorsal aesthetic lines, 519, 519f Cushing General Hospital, hand specialization and, 736, 737f Cutaneous arteries, 33, 34f Cutaneous blood supply, classification of, 41 Cutaneous circulation, classifying, 33


Index Cutaneous defects, reconstructive ladder in, 14, 14f Cutaneous malignancies, SKs and, 106 Cutaneous perforators, 33, 38f fasciocutaneous flap, 689, 692f schematic of, 37f Cutaneous psoriasis, hyperkeratosis and, 21 Cutaneous resurfacing, 457–465 patient selection for, 457 Cutaneous tags, 110 Cutaneous tumors, MMS and, 115–116, 116t Cutaneous veins, 33, 35f Cutaneous-visceral hemangiomatosis, 191 Cutis hyperelastica. See Ehlers-Danlos syndrome Cutis laxa, 110 Cutis marmorata telangiectatica congenita, 195 Cutler-Beard advancement flap, upper eyelid reconstruction, zone 1 defects, 399, 400 CVS. See Cardiovascular system Cyanoacrylate tissue adhesives, 62–63 Cyanoacrylates, 62–63 Cyclic adenosine monophosphate. See cCAMP cAMP (Cyclic adenosine monophosphate), fibrous dysplasia, 279 Cyclophosphamide graft rejection and, 53 infantile hemangioma, 192 Cyclophosphamide, methotrexate, 5-fluorouracil. See CMF Cyclosporine, allografts and, 53 Cylindroma (Turban tumor), 109 Cymetra, 63 filler materials and, 468 Cystic acne, 111 Cystic erosions of carpal bones, CT and, 756, 757f Cysts. See also specific cysts ultrasound and, 753 Cytokines, wound healing and, 18t, 19 Cytotoxic drugs, graft rejection and, 53 Dacarbazine (DTIC), melanoma and, 130 Dacron (Polyethylene terephthalate), 60–61 Dactylitis, 823 Dantrolene, spasm, 723 DCIS. See Ductal carcinoma in situ DCs. See Dendritic cells De Quervain tenosynovitis, 825 Debridement amputated body part and, replantation surgery, 870–871 chest wall irradiation, 167 chronic wound, 684f cold injury, 147 history of, 674 necrotizing fasciitis, 821 osteomyelitis, 49, 50f pressure sores, 723 of pseudoeschar, 27 radiation wounds and, 164 wound healing and, 24 wound reconstruction, foot and ankle, 693–694 wound treatment, 25 Decompression of second dorsal compartment, intersection syndrome and, 825 Deep fascia, 37–38 cutaneous arteries and, 35, 36f of leg, 675–676, 676f, 676t skin attachment to, 38, 39f Deep fat layers, 531, 532f

Deep inferior epigastric perforator flap (DIEP flap), 639 TRAM flap v., 651 Deep lobe tumors, 342 Deep partial-thickness burns, 133 Deep peroneal nerve, foot and ankle, 688, 690f Deep plane rhytidectomy, 503 Deep posterior compartment of leg, 676 Deep venous thrombosis, burn injuries and, 140–141 Defatting of neck, 503 Deficiency of central labial sulculus, 221 Deficient tubercle, unilateral cleft lip repair and, 220 Definitive maxillary obturator prosthesis, 353, 353f Deformational plagiocephaly coronal synostosis v., 231, 231f, 232t nonsyndromic craniosynostosis and, 224–234 Degenerative arthritis, 882, 883f of basal joints of thumb, 882 incidence and clinical presentation, 882 pathogenesis of, 882 radiographic imaging and, 744 Degenerative disorders, CT and, 756, 757f Degenerative joint disease, 882–887 Degloving, 834 Dehiscence of abdominal closure, 669 wound healing and, 4 Delay phenomenon flaps and, 43 tissue expansion and, 84 Delayed healing wounds, 16 Delayed phase, bone scintigraphy and, 752 Delayed-primary breast reconstruction, 87 Delayed tissue expanders, expansion of, prosthetic breast reconstruction and, 626–627 Deltopectoral flap of Bakamjian, Law of Equilibrium and, 40 Demyelination, upper limb compression and, 829 Dendritic cells (DCs), 52 allogeneic transplantation and, 53 Dental models, orthognathic surgery and, 255–256 Dental restoration, osseointegrated implant reconstruction, 434 Dental terminology, orthognathic surgery and, 254 Dentistry, cleft lip and palate and, 202 Depressor anguli oris, botulinum toxins, 477 Dermabond cyanoacrylate, FDA and, 62, 63 Dermabrasion, 457, 461 acne vulgaris and, 111 CMN and, 122 CO2 laser, 176 Dermagraft, burn wound and, 148 Dermal papilla, hair transplantation and, 570f Dermal replacement, burn wound and, 147, 148f Dermal sutures, scar and, 4 DermaLive/DermaDeep, filler materials and, 468 Dermalogan filler materials and, 468 wrinkles and, 466 Dermatitis, Renova and, 113 Dermatofibrosarcoma protuberances, 110 MMS and, 116–117 Dermatology, for plastic surgeons, 105–114 DermiCol, filler materials and, 468 Dermis closure, vertical breast reduction, 607 Dermis layer, 105

medwedi.ru

907

Dermofasciectomy, Dupuytren disease and, 864 Dermoid sinus cysts, 289, 289f skull base defects and, 442 Desmoid tumors, 663 Detached retroauricular flap, 301f middle-third auricle defects, 301, 301f Developmental arrest. See Failure of formation of parts Dexamethasone, peripheral nerve allotransplantation, 82 Dextran, fluid resuscitation and, 138 Diabetes mellitus, wounds and, 702 Diabetic patients, wound care of, 31–32 Diagnostic studies, foot and ankle wound care, 690–691, 693 Diazepam, hyperventilation and, 94 DIC. See Disseminated intravascular coagulopathy Diclofenac, AK and, 107 Die-punch fracture, bone scintigraphy and, 752 DIEP flap. See Deep inferior epigastric perforator flap Differentiation of parts. See Failure of separation Differin, 113 Digastric muscle resection, neck rejuvenation and, 503 Digital fascia, normal anatomy of, 862 Digital fibro-osseous sheath, pulley system of, 802 Digital flexor tenosynovitis (Trigger finger), 824–825, 826f, 887 Digital nerve block, wrist and, 741, 742f Digital tendon lesions, MRI and, 761–762, 761f Dimethylsiloxane. See Silicone Diphosphonate compounds, bone scintigraphy and, 751 Diplopia, orbital floor surgery and, 319 Direct cutaneous vessels, 41 Disorders, generalized dermis, 110–111 Dissection, congenital dermoid inclusion cysts, 290 Disseminated intravascular coagulopathy (DIC), VMs and, 196 Distal, 254 Distal interphalangeal joint (PIP joint), injuries, 795–796 Distal phalanx fractures, 795 classification, 788 replantation, 875–876, 875f sub-mini digital prosthesis and, 897f Distal radial fractures, CT and, 752f, 753 Distal radioulnar joint (DRUJ) injuries, CT and, 753–754 synovitis, 887 Distant flap(s) reconstructive surgery and, 45 transfers, nasal reconstruction, 392 types of, 774 Distraction gap, temporal zones in, 97 Distraction osteogenesis bimolecular regulation of, 97–98 biomechanics of, 98 of midface, 244–245 types of, 96, 97f Distraction zone, 96 biomolecular analysis of, 97 histologic analysis of, 97 Diver’s test, abdominal laxity, 543f DNA alternations, head and neck cancer, 332 mutations, craniosynostosis syndromes, 245 radiation damage and, 162


908

Index

Do-not-Resuscitate decision, 139–140 Dominant pedicles type II pattern of circulation, vascular anatomy and, 44 type III pattern of circulation, vascular anatomy and, 44 Donor density, hair transplantation and, 562, 562t Donor hair follicles, harvest technique, 562 Donor nerve grafts, 80 Donor nerve morbidity, 81, 82f Donor scars, cheek reconstruction and, 375 Donor site burn reconstruction surgery and, 153 care of, 9 fascia lata and, 671 hair transplantation, 561–563, 562t microsurgery and, 68, 68f for nasal reconstruction, 388 postoperative care of, 8–9 selection and care, burn injury and, 143 Donor site morbidity, TRAM techniques and, 644 Donor tissue, hair transplantation and, 564, 565f Dopamine, anesthetic toxicity and, 94 Doppler ultrasonic probe flap monitoring and, 70, 72 perforators and, 39 Dorsal hand degloving injuries, 813–814, 814f Dorsal nasal flap, nasal reconstruction, 389, 390f Dorsal palpitation test, 525 Dorsal periosteum, replantation in upper extremity and, 872 Dorsal synovial cyst, 886 Dorsal wrist compartments, retinaculum and, 808, 809f Dorsalis pedis flap, 690 Dorsum analyzation, 520, 521f Dorsum of foot defects, 701 Dose range topical cocaine and, 95 toxicity anesthetic agents and, 93 Double-bubble deformity, breast implants, 580f Double central reverse Abbe flap, lower-lip defects and, 370, 370f Double-level osteotomy, 529, 529f Drainage, Palmar space infection and, 818, 821f Drains, vertical breast reduction, 607, 610 Dressings hand surgery and, 743 meshed skin grafts, 143 types of, characteristics and applications, 29t venous stasis ulcers and, 32 wound healing and, 28 Drugs. See specific type/category drug i.e. Antibiotics DRUJ. See Distal radioulnar joint Dry desquamation, radiation damage and, 162 Dry eye syndrome, blepharoplasty and, 489, 490 DTIC. See Dacarbazine Dual plane implant, capsular contracture, 578, 578f Ductal carcinoma in situ (DCIS), 619 treatment of, 621 Ductal preservation, breast, 602 Duplex imaging, deep venous thrombosis and, burns and, 141 Duplications, hand reconstruction and, 858–860

Dupuytren contracture, 862 Dupuytren disease, 862–865, 864 alternative treatment for, 865 Dupuytren contracture v., 862 initial consultation for, 863 pathologic anatomy, 862 patient counseling, 864 risk factors for, 862–863 surgical technique for, 864 treatment results, 864–865 Dural plication, unilateral coronal synostosis, 230, 230f Dural tear with cerebrospinal fluid leak, craniosynostosis and, 233 Duration of action, local anesthetic agent and, 91 Dynamic reconstructions, facial paralysis and, 420–423, 421f, 422f, 423f Dynamic rhytides, 466 Dynamic study, hand and wrist, 749–750 Dysplastic nevi, 105, 106f Dystrophic epidermolysis bullosa, 110 Earlobe prominence correction, 297–298 reconstruction, 302f Early Breast Cancer Trialists Collaborative Group, breast cancer, 622 Earring complications, 309–310 Ear(s). See also External ear craniofacial microsomia and, 249 reconstruction, otoplasty and, 295–312 soft-tissue injury, 316–317 Treacher Collins syndrome and, 287 Eccrine hidrocystoma, 109 Eccrine poromas, 109 Eccrine spiradenoma, 109 Eccrine tumors, 109 Econazole, onychomycosis, 822 Economics, TRAM flap procedure, 653–654 ECRB. See Tenosynovitis of extensor carpi radialis brevis ECRL. See Tenosynovitis of extensor carpi radialis longus Ectropion, eyelid ptosis correction, 408 Edema, pressure sores and, 722 EGFR. See Epidermal growth factor EHL. See Extensor hallucis longus Ehlers-Danlos syndrome (Cutis hyperelastica), 110 Elbow flexion, double fascicular transfer and, 81, 82f paralysis of triceps and, 852 Elderly replantation in, 866 wound healing and, 23–24, 32 Elective incisions, lines of tension, 4, 4f Elective lymph node dissection (ELND), melanoma and, 127–128 Elective reconstruction, thumb and, 833 Electrical injuries, 132–149, 146–147, 146f Electrocautery, fascial excision, 142, 142f Electrodesiccation, basal cell carcinomas and, 112 Electrodiagnostic studies (EDSs), CTS and, 829 Electromyelogram (EMG), upper limb compression and, 829 Electrons, laser physics and, 169 Electrophysiologic testing, upper limb compression and, 828 Elevation hand infection, 815–816 hand surgery and, 743 Elliptical excision, 6, 6f ELND. See Elective lymph node dissection

Embryo developing auricle of, 186f face of, late somite period, 183f head and neck region, 178f, 181f venous drainage of skin, 34 Embryology aortic arch artery, 177 branchial apparatus, 177–178, 181 congenital hand abnormalities, 854 cysts, 185 external ear, 186 facial development, 181–183 head, primary palate, 183f head and neck, 177–181 mandible, 183f, 184 microtia and, 303 microtia deformity, 303 muscles, 177–178 nasal cavities, 186 palate, 184–185 pharyngeal pouches, 178, 178f Pierre Robin sequence, 184 programmed cell death, 183f, 184 skin, 105 tongue, 184 transcription factor Runx2/Cbfa1, 187–188 EMG. See Electromyelogram EMLA. See Eutectic mixture of local anesthetics Encapsulation, facial skeletal augmentation, 549–554 Enchondromas, Maffucci syndrome and, 198 End-to-end anastomosis history of, 66 sutures, 68, 69, 69f End-to-side anastomosis, sutures, 68, 69, 69f Endocrine glands, head and neck embryology and, 185 Endoplast-50, filler materials and, 468 Endoscopic technique, foreheadplasty, 512 incision placement, 512, 512f Endotenon, 801 Endotine Forehead fixation device, 61 Endotine Midface ST, 61 Endotracheal tube, face burn and, 143, 144f Enophthalmos facial trauma, 326–327 orbital floor surgery and, 319 orbitozygomatic fractures, 321 Enteral feeding, burn injuries and, 140 Entropion, eyelid ptosis correction, 408 Enzymatic fasciotomy, Dupuytren disease, 865 Enzymes, wound healing and, 28 Epidermal growth factor (EGFR) palate development and, 187 receptor, head and neck cancer and, 338 Epidermal lesions, 106–110 Epidermal nevi, laser treatments for, 174 Epidermis, 105 basal cell carcinomas and, 112 Epidermoid carcinoma, mandible reconstruction, 426 Epidural sensor, ICP and, 225 Epinephrine addition local anesthetic agents, 92 minor nerve blocks, 92 digital nerve block, 741, 742f hypertension and, 93 soft tissue injuries, 316 topical cocaine and, 94 Epithelial appendages, dermis thickness and, 7 EPL. See Extensor pollicis longus Eponychia, 816, 818f Epstein pearls, palates and, 184 ePTFE, filler materials and, 468 Equipment, microsurgery and, 67


Index Erbium:YAG laser, 169, 172, 174, 461–462, 463–464, 463f AK and, 107 CO2 laser v., advantages v. disadvantages, 463t light, wrinkles and, 175 Erythema Baker-Gordon formula, 460 laser resurfacing and, 464 Erythrocyte-type glucose transporter protein-1 (GLUT-1), infantile hemangioma, 190, 191 Erythroplasia of Queyrat, MMS and, 117 Eschar, 25, 26 topical wound agents, 136 Escharotomy, burn injuries, 134–135 Esters local anesthetics and, 91 metabolism of, 91 Estlander flaps, lower-lip defects, 370, 371f Etidocaine cardiovascular compromise and, 94 duration and potency of, 91 Eutectic mixture of local anesthetics (EMLA), 92 Evisceration, abdominal wall reconstruction, 669 Excessive regeneration, abnormal response to injury and, 21 Excimer lasers, 169 Excision burn reconstruction surgery, 150 CMN and, 122 malignant melanoma and, 125 methods of, 6–7, 6f Excision margins, for melanoma, 127, 127t Excisional biopsy, malignant melanoma and, 124 Excisional instruments, hair transplantation and, 564, 565f Excisional release, burns and, 152f Exercise, healing and, 722 Exorbitism, craniosynostosis syndromes and, 240 Expanded flap design, 84–85 vascularity of, 84 Expanded polytetrafluoroethylene mesh, midline abdominal wall defects and, 670 Expanded TRAM flaps (Transverse rectus abdominis musculocutaneous flaps), 86 Expander-implant reconstruction, breast and, 87–88 Extensor carpi ulnaris tenosynovitis, 826 Extensor digitorum brevis muscle flaps, 689, 693f Extensor digitorum longus muscle, medial malleolus, 688 Extensor hallucis longus (EHL), ankle defects and, 688 Extensor pollicis longus (EPL), tendonitis, 825 Extensor tendon system anatomic pearls, 808 anatomy, 808 repair of, 808–814 Extensor tendons amputated body part and, replantation surgery, 871 reconstructive problems, 811–814 replantation in upper extremity and, 872 rupture, 813, 813f External acoustic meatus, external ear and, 186, 186f External auditory canal, 300 External ear, head and neck embryology and, 186

External fixation, fractures and, 680 External fixator, wound reconstruction, foot and ankle, 694 External head frame (RED), maxillary Le Fort I distraction, 100f, 101 External oblique flap, soft-tissue reconstruction and, 665–666 Extraoral craniofacial prostheses, 348–351 Extremities, radiation and, 165 Extremity salvage, 674 Extrinsic coagulation cascades, 17 Eyedrops facial paralysis and, 417 hydroxypropyl cellulose, facial paralysis and, 417 Eyelid. See also Upper eyelid anatomy, 484–488 and physiology, 395–397 cross-sectional of, 484, 485f elevation, anatomy and physiology of, 403 embryonic development of, 182f, 183 inflammatory disorders, blepharoplasty and, 490 innervation of, 484, 485f ptosis, classification of, 403, 403t ptosis correction, 403–408 complications and management for, 408 operation selection for, 404–408 preoperative evaluation for, 403–404 reconstruction, 395–414, 397–403 Type 1 maxillary defect, 437 Type III maxillary defect and, 438 zones in, 397–403 Treacher Collins syndrome and, 287 vascular system, 396 FAC (5-fluorouracil, doxorubicin, cyclophosphamide), breast cancer, 622 Face contouring, osteotomies and, 245 current transplantation and, 57 development embryologic stages of, 182, 182f head and neck embryology and, 181–183 division of, for rhinoplasty, 517, 518f evaluation, orthognathic surgery and, 254 fractures, 317–326 injuries initial management, 313–314 soft tissue and, 313–330 lidocaine and, 94 reconstructions, GoreTex and, 63, 65f skeletal injuries of, 313–330 skin grafts, 143 tissue expansion and, 85–86 Face burns categories, 161t excising, 144 intermediate phase scar manipulation and, 151 management of, 143–144 reconstruction, 159, 160f summary, 161 Facelift anatomy, 498–500 anatomic layers, 498–499, 499f facial nerve, 498–500 retaining ligaments, 500 Facelifting, 496–514 anesthesia during, 498 benefits v. limitations of, 496 complications, 505–506 in men, 504–505 nonsurgical, 171 patient safety, 505 postoperative care, 505

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preoperative preparation, 496–498 counseling, 497 instructions, 497–498 state of art, 496 techniques and alternatives, 500–505 Facial envelope, expanding, 257 Facial expression, facial nerve and, 416f Facial hemangioma, malformative anomalies and, 191 Facial musculature, 416f, 417 Romberg disease and, 283, 284f seventh cranial nerve, 415 Facial nerve dysfunction, gold weight and, 58 facelift anatomy and, 498–500 forehead, 357, 357f parotid gland tumors, 343–344 Facial palsy, craniofacial microsomia and, 249 Facial paralysis, 415 bilateral, 416f nonsurgical management of, 417 preoperative appraisal of, 417, 422f Ramsay Hunt syndrome, 423f reconstruction, 415–425 smiling, preprocedure v. postprocedure, 424f surgical management of, 418–425 Facial prominences, facial development and, 182, 182f Facial prosthesis, 58 Facial reanimation surgery, Moebius syndrome and, 283 Facial skeletal augmentation aesthetics and, 549, 550f anesthesia, 551 areas for, 551–553, 551f complications, 554 with implants, 549–554 preoperative planning, 549, 550f Facial trauma evaluation, 314–315 patient history and, 314 secondary deformities in, 326–329 Failure of formation of parts (Developmental arrest), congenital hand abnormalities, 854–855 Failure of separation (Differentiation of parts), 855–856 Famciclovir, laser abrasion, 464 Familial cutaneous-mucosal venous malformation, 196 Fasanella-Servat procedure. See Tarsal conjunctival mullerectomy Fascia lata, midline abdominal wall defects and, 671 Fascial excision, burn wounds and, 141–142 Fascial planes, forehead lift, 507–508 Fascial zones of adherence, lower truncal contouring, 540, 542f Fascian, filler materials and, 468 Fascicular identification, 76–77 Fasciocutaneous flaps, 38 cutaneous perforators, 689, 692f lower extremity, 688–690 neurovascular flaps v., 39 Fasciotomy, electrical injuries, 146, 146f Fast-flow combined malformations, 198 Fat, filler materials and, 469 Fat aspiration. See Aspiration of fat Fat grafting, 478–483 complications of, 482–483 patient examples, 483 drug-related lipoatrophy, 482f, 483 liposuction patient, 479f, 483 preprocedure markings, 481f, 483 thigh depression, 480f, 483 preparation for, 478


910

Index

Fat grafting (contd.) technique, 478–482 fat placement, 480f, 481, 481f, 482f harvesting, 478–479 postoperative care, 481–482 refinement and transfer, 479–481 Fat necrosis free TRAM flap and, 651 latissimus dorsi flap breast reconstruction, 636 TRAM techniques and, 644, 645 FCR. See Flexor carpi radialis FCU tendon. See Flexor carpi ulnaris tendon FDA. See Food and Drug Administration FDS. See Flexor digitorum superficialis Feeding aid appliance, 353 Felon, drainage of, 818, 819f Fentanyl, burn patient, 141 FGFR genes, craniosynostosis syndromes and, 235 Fiberoptic technology cervical esophagus reconstruction and, 453 endoscopic skull base surgery and, 347 Fibrel, wrinkles and, 466 Fibrin matrix, wound healing and, 17 Fibroblast growth factor palate development and, 187 pressure sores and, 727 Fibroblasts, radiation damage and, 163 Fibrous central zone, 97 Fibrous dysplasia, 281f–282f, 663 categories of, 279 pathogenesis of, 279–280 treatment, 280 Fibrous tumors, 110 Fibula donor site, mandible reconstruction and, 430 harvest, muscles and, 47f osteocutaneous flap, microsurgical techniques and, 386 Filet of toe flap, 690 Filler materials, 462t, 466–472. See also specific type filler material i.e. Aquamid injectable current, 467–472 indications for, 467 longevity of, 469 looking ahead with, 474 Fine-line scar, 3–4 Fine-needle aspiration biopsy (FNAB), parotid mass, 342 Fingernail deformity, osteoarthritis at DIP and, 886 prosthesis, 896f, 897 Finger(s) metacarpals fractures, 790–795 prosthesis, 896f, 897 radiographs, 747 rheumatoid disease of, 888 First extensor compartment tenosynovitis, 825 Fistulae, abdominal wall reconstruction and, 670 Fitzpatrick skin classification, 458t laser abrasion, 464 5-fluorouracil, doxorubicin, cyclophosphamide. See FAC 5-fluorouracil cream, AK and, 107 Fixation amputated body part and, replantation surgery, 871 Champy’s lines of osteosynthesis and, 325, 325f mandible fractures and, 324–325, 324t Fixation devices, fractures and, 680 Fixed-skin sites, 36f, 39

Fixture osseointegration, orbital prostheses and, 351 FK506. See Tacrolimus Flag flap, 771, 772f Flame burns, 132 Flap-delay procedure, 41 Flap necrosis, 42 Flap tissue coverage, indications for, hands, 769–774 Flap(s), 42. See also specific type flap i.e. Innervated flaps cervical contractures and, 159 design continuous vessel network and, 40–417 cutaneous circulation and, 33 microvascular transplantation, 48, 48f elevation, latissimus dorsi flap breast reconstruction, 632 harvest, microsurgery and, 67 modifications, reconstructive surgery and, 45–49 morbidity, TRAM techniques and, 644 neurovascular relationship and, 39 FLASH. See T2-weighted images Flash burns, 132 Flat warts, 823 Fleur-de-lis procedures, 548 Flexor carpi radialis (FCR), 801 tenosynovitis, 826 Flexor carpi ulnaris tendon (FCU tendon), 779 Flexor digitorum superficialis (FDS), 829 Flexor pollicis longus (FPL), 801 congenital trigger thumb, 825 digital flexor tenosynovitis, 825 Flexor pollicis longus tendon (FPL tendon), thumb fractures, 795 Flexor retinaculum release, tarsal tunnel exposure, 704 Flexor tendon amputated body part and, replantation surgery, 871 injuries, diagnosis of, 803–804 pulley system v., anatomic relationship, 826f replantation in upper extremity and, 872 sheath pulley system, 802f surgery history of, 801 tendon healing and, 801–807 Flexor tendon continuity postoperative therapy, 806 Stricklands adjusted system, 806 surgical reconstruction of, 804–805 contraindications for, 805 suture technique for, 805, 805f Stricklands preference for, 805, 805f Flexor tenosynovitis, 887 of index finger, 825 Floor of mouth cancer, 333 reconstruction, 445–446 Floppy eyelid syndrome, blepharoplasty, 489 Florid gynecomastia, 614 Fluid collections, ultrasound and, 753 Fluid resuscitation burn injury and, 134, 138–139 Parkland formula for, 138, 138t Fluorescein dyes, burn depth, 134 FNAB. See Fine-needle aspiration biopsy Foam dressings, wound healing and, 28 Focal contracture, facial burn reconstruction, 161 Focal demyelination, upper limb compression and, 828 Folded forehead flap, for lining, nasal reconstruction and, 394 Foley catheter, perineum burns, 145

Follicular unit extraction (FUE), hair transplantation and, 563 Follicular unit transplant (FUT), hair transplantation and, 560 Follicular units (FU), hair transplantation and, 560, 561f Food and Drug Administration (FDA) IFN alpha 2-b, 130 liquid silicone and, 60 polyurethane and, 63 TransCyte, 148 Foot fillet dissection, 685f fillet flap, below-knee amputation, 686 flaps, 689–690, 693 reconstruction, 687–705 ulcer, 690–691, 693 vascular supply, 688 wound care, 690–696 wound treatment, conclusions on, 704–705 Foot and ankle anatomy, 687–690 wound care, 690–696 Forceps countertraction, microsurgery and, 70, 70f Forearm free-flap design, phalloplasty, 731, 731f Forearm replantation, 879, 880f Forefoot reconstruction, 697–699, 701 Forehead anatomic layers of, 356, 357f anatomic relationships, 357f anatomy, 486–487 botulinum toxins, 474 flap, 392f nasal reconstruction, 389, 392 muscles of, 507, 508f, 509f nerve supply of, 357–358 reconstruction, 356–364 soft tissue defects and, 362–363, 363f tissue expansion and, 85, 88f Forehead lift, 507–514 historical perspective, 507 indications for, 507 muscles, 507, 508f, 509f preoperative evaluation, 507 preperative preparation for, 507–510 safe zone, 510f Foreheadplasty complications, 513 postoperative care, 513 surgical goals of, 510 techniques of, 511–513 Foreign bodies, MRI and, 765 Four-compartment fasciotomy, 676 FPL. See Flexor pollicis longus FPL tendon. See Flexor pollicis longus tendon Fraction healing, distraction and, 96 Fractures. See also Nonunion classification, 677 comparison of grades, 677, 677f dislocations, classification, 796 fixation, techniques available, 680 management, 680–686 of wrist, 779–787 Free-flap(s), 777, 778f breast reconstruction, free TRAM flap and, 651 chest wall reconstruction and, 667 donor site, 777 donor site selection, mandible reconstruction and, 428t failure, mandible reconstruction, 433–434 oral cavity reconstruction, 445, 446f, 448 phalloplasty, 731, 731f reconstruction, maxillary defect reconstruction and, 436


Index reconstructive surgery and, 47–48 salvage, of below-knee amputation, 686 subcomponents of, mandible reconstruction, 435 techniques, breast reconstruction and, 646–654 indications and contraindications, 647 wound reconstruction of foot and ankle, 696 Free latissimus dorsi flap reconstruction, scalp defect, 362f Free platysma transfer, eyelid reconstruction and, 419 Free pulp flap harvesting, thumb reconstruction and, 833, 835f Free radial forearm flap, thumb reconstruction, 834, 838f Free tissue transfers, 67 high-energy lower extremity injuries and, 681, 683 indications for, 66 in reconstructive surgery, 67t lateral skull base and, 444 skull base defects reconstruction, 443 Free TRAM flap, 639–640 aesthetics, 643f–644f free flap breast reconstruction, 651 preoperatively, 654f technical details, 640, 640f Free TRAM procedure, 647–649 Fresh frozen plasma, fluid resuscitation and, 138 Fresh tissue technique, 115 Frey syndrome, 344 Frontal sinus fracture, 322–323, 323f mucocele, 323, 324f Frontalis muscle botulinum toxins and, 474 forehead lift, 507, 508f Frontalis muscle palsy, foreheadplasty, 513 Frontalis sling, 409f levator function and, 408 Fronto-orbital advancement, 242–243, 242f craniosynostosis syndromes and, 239f Frontofacial detraction. See Monobloc detraction Frontonasal prominence, facial development and, 181 Frostbite, 147 FU. See Follicular units FUE. See Follicular unit extraction Full-thickness burns, 134, 136f burn reconstruction surgery and, 153 immersion time for, 133t Full-thickness defects, zone II, lower eyelid reconstruction, 401 Full-thickness incisions, antihelical fold manipulation, 296 Full-thickness skin grafts burn injury and, 143 burn reconstruction surgery and, 150, 156 perineum, 708, 708f sensory return for, 7 Full-width platysma transection, 504, 504f Functional microangiopathy, 31 Fungal cultures, onychomycosis, 822 Furans conchal mastoid sutures, otoplasty and, 298, 298f Furfuryladenine, 113 Furlow palatoplasty, VPI and, 218 FUT. See Follicular unit transplant G3139, melanoma and, 130 G-protein, fibrous dysplasia, 279 Gadolinium, MRI and, 760 Galactorrhea, augmentation mammoplasty, 576

Galderma, 113 Galea aponeurotica, 356 scoring of, scalp flap and, 358f Galeotti articulator, 261, 263f isolated mandibular surgery, 260 Gall bladder metastasis, systemic melanoma, 130 Ganglion cyst, MRI and, 764f, 765 Gangrene, forefoot and, 697 Gastrocnemius recession, ulceration of metatarsal head, 697f, 698 Gastrointestinal lesions, Blue rubber bleb nevus and, 196 Gastrointestinal prophylaxis, burn injuries and, 140–141 Gastrulation, germ layers in, 186 Gauze, wound healing and, 28 GCS. See Glasgow Coma Score GDP. See Guanosine diphosphate Gender dysphoria, penis reconstruction and, 728 Gene therapy, craniosynostosis syndromes, 245 General anesthesia, cocaine, 94–95 Generalized essential telangiectasia, 195 Genes, palate development and, 187 Genital ambiguity penis reconstruction and, 728 surgical correction, 728 Gentamicin, 30 Germ layers, head and neck embryology and, 177 Giant nevi, 120 CMN and, 120, 121f tissue expansion and, 86, 88f, 89f Gigantism, 859 Glabella botulinum toxins and, 474 muscles of, 507, 508f, 509f Glabella flap eyelid reconstruction, 400 upper eyelid reconstruction, 400 Glabellar muscles, transblepharoplasty approach, 513f Glanular ptosis, 583, 584f Glasgow Coma Score (GCS), 313, 314t facial injuries and, 313 GLUT-1. See Erythrocyte-type glucose transporter protein-1 Gluteal flap technique, 649, 650f, 651 Glycolic acid, 458 Goes-technique, vertical incision mastopexy and, 584, 586f Gold, implant materials and, 58 Gold weight, upper eyelid paralysis and, 418, 418f Golfer’s elbow. See Medial epicondylitis GORE, filler materials and, 468 Gore-Tex, 63 facial skeletal augmentation, 549 midline abdominal wall defects and, 670 skeleton of chest wall reconstruction, 665 Gorlin syndrome, basal cell carcinomas, 111, 112 Gorneygram, 517f Goulian knife, tangential excision and, 142 Gout, 744 Gouty arthritis, 888–890 Government regulations, augmentation mammoplasty and, 573 Gracilis flap, vaginal defects, 710, 710f, 711f Gracilis muscle facial paralysis and, 421f, 422f smiling and, 424f Graft donor site, wound reconstruction of foot and ankle, 696 Graft placement, methods for, hair transplantation and, 566

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Graft production. See Microdissection procedure Graft sheering, Jobst skin featureless face mask garment, 143 Grafts. See also specific type graft i.e. Skin graft nipple-areola reconstruction, 656 Gram-negative organisms, post burn period and, 136, 137 Gram-positive organisms, post burn period and, 137 Granulating wounds, 16 hypertrophic scarring and, 7 Granulation tissue, wound reconstruction, foot and ankle, 695 Grave’s disease, blepharoplasty and, 490 Grease burns, 132 Greasy gauze, donor site, burn injury and, 143 Great auricular nerve, facelift anatomy and, 500 Green light lasers, benign pigmented lesions, 175–176 Griseofulvin, onychomycosis, 822 Groin flaps. See Superficial circumflex iliac artery flap Growth factors. See also Vascular endothelial growth factor wound healing and, 18t, 19, 28 GTP. See Guanosine triphosphate Guanosine diphosphate (GDP), fibrous dysplasia and, 279 Guanosine triphosphate (GTP), fibrous dysplasia, 279 Guiding elastics, 262 Gunshot wounds craniofacial skeleton and, 327f, 328f, 329 mandible reconstruction, 426 Gustilo classification of open fractures of tibia, 677, 677t fracture grade comparison, 677f Gut suture, traumatic wounds, 316 Guyon tunnel syndrome, 830 Gynecologic malignancy, perineum irradiation and, 167 Gynecomastia, 614–618 causes of, 615t classification, 614–615 complications, 618 diagnosis, 614 etiology, 614 evaluation and treatment, algorithm for, 615, 615f pathology, 614 treatment of, 615–616, 618 H-zone of face, MMS and, 115 Haemophilus influenzae, septic arthritis, 820 Hair follicles, full-thickness skin grafts, 7–8 follicular tumors, 109 removal, laser treatments and, 176 volume, hair transplantation and, 560, 561f Hair transplantation, 560–570 adjunctive therapy, 566–567 future, 568, 570 initial consultation and screening, 560 lip reconstruction and, 371 medications, 560 operation, 561 postoperative period, 566–567 preoperative period, 560–561 recipient site and, 563–566 reconstructive and corrective, 567–568, 568f, 569f spiral/helical hair texture, 567, 567f Hairline, hair transplantation and, 563–566 Half-buried horizontal mattress suture, 5f, 6


912

Index

Halo head pattern, donor site and, 564 Hamate hook fractures, CT and, 755, 755f, 756f Hand amputations aesthetic considerations, 890 classification of, 890, 892 unilateral v. bilateral, prostheses, 893 anatomy, understanding and illustration of, 735 burn, management, 144 chronic infections of, 821–823 flap tissue coverage, indications for, 769–774 function restoration, nerve transfer and, 81 infection acute processes in, 816–820, 817–821 antibiotics for, 817t general principles, 815 inpatient hospital care, 816 operative principles, 815 rest/heat/elevation of limb, 815–816 injury, 800 prostheses aesthetic considerations and, 895 levels of amputation and, 895, 895f types of, 895, 897 radiographic imaging, 744–768 reconstruction, spinal cord injuries, paralysis and, 851–852 skin grafts, 769 soft-tissue reconstruction, 769–778 specialization evolution of, 735–736 reflections on, 738 surgery development of, plastic surgeons and, 735–747 metals and, 58 postoperative principles, 743 transplantation, 57 Hand agenesis, acquired amputation v., 893, 894f, 895 Hand and wrist pathology, imaging algorithms for, 766f–767f, 768 Hand views, standard radiographs, 745f, 746–747, 746f Hard palate malignancy, 333 Hard tissue replacement (HTR) polymer, 60 Harvest sites fat grafting, 478–479, 480f split-thickness skin graft and, 9 Harvesting vein grafts, replantation in upper extremity and, 873, 874f HBO. See Hyperbaric oxygen Head and neck anatomy, staging and, 331 cancer, 331–347, 332–339 distribution in U.S., 342f recent and future developments, 338–339 staging, 331, 341f survival rates, stage and site specific, 340t developmental biology of, 186–188 embryology, early development, 177 examination, facial trauma and, 314–315, 315f interdisciplinary team, 331 irradiation, reconstruction of, 166 Head frames, 100f, 101 Healing by secondary intention, cheek reconstruction and, 373 Healing wound. See Wound(s) Heat, hand infection and, 815 Helical rim loss, 300 skin cancer of, 309 Helical rim reconstruction, 300, 300f Hemangioma, 189

differential diagnosis for, 191 laser treatments for, 171, 172f MRI and, 765 radiologic characteristics of, 191 ulcerated, laser treatments for, 171 Hematoma acute auricular trauma, 308, 308f augmentation mammoplasty, 576 facelifting and, 505 gynecomastia, 618 otoplasty and, 299 prosthetic breast reconstruction with, 630 skin flaps and, 85 vertical breast reduction, 610 Hemifacial microsomia, microtia in, 303 Hemisoleus flap, tibial fracture, 682f Hemorrhage, facial injuries and, 313 Hemostasis amputated body part and, replantation surgery, 871 amputation stump, replantation surgery, 872 Herbert scaphoid fractures classification, 782, 785f Herbs, hair transplantation, 560 Hereditary hemorrhagic telangiectasia (HHT), 193, 195 Hereditary melanoma, genes for, 124 Hernia repair, goal, 668, 669f Herpes virus, TCA peel and, 459 Herpetic whitlow, 818, 820f Heterotopic ossification, burn injuries and, 148–149 Heterotopic transplant, 52 HHT. See Hereditary hemorrhagic telangiectasia High combined median ulnar palsies, 851 High-dose interferon alpha 2-b (IFN alpha 2-b) infantile hemangioma and, 192 melanoma and, 130 High-frequency oscillatory ventilators, ARDs and, 149 High median nerve palsies, 851 High-pressure injection injury, upper limb surgery and, 740 Hindfoot defects, 701 Histiocytosis, 663 HLAs. See Human leukocyte antigens Holevich flap, thumb reconstruction, 834, 837f Homograft, 52 Hook of hamate fracture, 786–787 Horizontal mattress suture, 5, 5f Horner syndrome, Romberg disease and, 285 HTR polymer. See Hard tissue replacement polymer Human acellular dermis, midline abdominal wall defects and, 671 Human bites, of hand, 820, 822f Human leukocyte antigens (HLAs), 53 Human papillomavirus (HPV), 106, 822 basal cell carcinomas and, 112 oropharyngeal tumors and, 332 Human placental collagen, filler materials and, 469 Human platelet-derived growth factor BB, pressure sores and, 727 Human tissue equivalents, wound healing and, 30 Hyacell, filler materials and, 469 Hyal-System, filler materials and, 469 Hyaluronic acid AK and, 107 derivatives, Romberg disease and, 285 Hydradenitis suppurativa, 111, 111f Hydrocephalus, 240–241 craniosynostosis and, 225

Hydrocodone/acetaminophen, rhinoplasty and, 530 Hydrocolloids, wound healing and, 28 Hydrofluoric acid injury, 146 Hydrogel dressings, wound healing and, 28 Hydroquinone, 458 bleaching agents, 114 laser abrasion, 464 Hydroxyapatite, bone grafts substitutes and, 59 Hydroxyproply cellulose eyedrops, facial paralysis and, 417 Hylaform, filler materials and, 469 Hylan Rofilan Gel, filler materials and, 469 Hyperbaric oxygen inhalation injury, 139–140 necrotizing fasciitis, 821 Hypercarbia, CNS toxicity and, 94 Hypercatabolism, burn injuries and, 140 Hyperextension injuries, 795 of PIP, 796 Hyperextension of MCP joint, 883f, 884 Hyperhidrosis, botulinum toxins and, 477 Hyperkeratosis, cutaneous psoriasis and, 21 Hypermetabolism, burn injuries and, 140 Hypernasal speech, head and neck embryology and, 185 Hyperpigmentation bleaching agents, retinoids and, 113 chemical peel, 461 laser resurfacing and, 464 TCA peel and, 459 Hypertelorbitism, 277 craniofacial clefts and, 266–278 Hypertension epinephrine and, anesthetic solution and, 93 topical cocaine and, 95 Hypertrophic scarring, 21 burn injuries, 148 burn reconstruction surgery and, 155 facelifting and, 506 granulating wounds and, 7 radiation therapy and, 165 TCA peel and, 459 Z-plasty and, 158, 159f Hyperventilation, seizure and, 94 Hypoglossal nerve, head and neck embryology and, 185, 185f Hypopharynx cancer, 334–335 anatomy and T staging, 331, 336f site locations, 331, 335t functional anatomy of, 451 Hypopigmentation chemical peel, 461 laser resurfacing and, 464 Hypoplasia brachial arches and, 246, 247t Romberg disease and, 284, 284f Hypoplastic thumb, 859 classification of, 859, 860t Hypoplastic zygoma, Treacher Collins syndrome and, 285 Hypotrichosis-lymphedema telangiectasia, genes for, 193 Hypovolemia, fluid resuscitation and, 139 Hypoxia, wound healing and, 23–24 Iatrogenic deformity, burns and, 153f ICP. See Intracranial pressure ICU. See Intensive care unit IFN alpha 2-b. See High-dose interferon alpha 2-b Ilium donor site, mandible reconstruction and, 427–428 ILP. See Isolated limb perfusion


Index Imaging. See also specific type imaging i.e. Radiographic imaging cervical esophagus reconstruction and, 453 facial trauma and, 315, 315f lymphedema, 715 osseous genioplasty and, 557 Imaging algorithms, hand and wrist pathology, 766f–767f, 768 IMF. See Inframammary fold Imiquimod (Aldara), AK and, 107 Immediate surgical obturator prosthesis, maxillary defects, 352–353, 352f Immobilization, hand surgery and, 743 Immune system, nerve allograft and, 82 Immunologic tolerance, 54 Immunosuppression, 53–54 MMS and, 115–116, 116t organ allograft transplantation and, 52 Immunosuppressive therapy, connective tissue disorders, 703 Implant arthroplasty, 885 Implantable-pulsed ultrasonic Doppler, oral cavity reconstruction and, 448 Implant(s) augmentation, sliding genioplasty v., 553 capsule, releasing, 628, 628f facial skeletal augmentation and, 549–554, 550, 550f, 551f immobilization, facial skeletal augmentation, 550, 551f latissimus dorsi flap breast reconstruction, 632 materials, 58–65, 59t discontinued, 63, 65 facial skeletal augmentation, 549–554 history, 58 positioning, facial skeletal augmentation, 550 shape, facial skeletal augmentation, 550 for soft-tissue depression, 553–554 Incisional instruments, hair transplantation and, 564, 565f Incisional release, burn reconstruction surgery and, 154f Incisional wound, scar from, 4 Incision(s). See also specific type incision i.e. Transcutaneous incisions amputated part and, replantation surgery, 870 augmentation mammoplasty and, 574, 574f closed rhinoplasty approach, 523–524, 524f escharotomy, 134–135 open rhinoplasty approach, 524 Palmar space infection and, 818, 821f principles of, felon and, 818, 819f pyogenic flexor tenosynovitis and, 819–820, 822f Inclusion cysts, burn management and, 145 Incomplete bilateral cleft lip, 201f, 202 Incremental component cartilaginous dorsal septal reduction, 524 Index finger amputation, 896f Indirect cutaneous vessels, 40f, 41 Induction radiation therapy, 166 Indwelling catheters, deep venous thrombosis, 140–141 Infancy AVM in, 197 infantile hemangioma in, 193 otoplasty in, nonoperative technique, 299 phalloplasty, 732 Infantile hemangioma clinical features of, 191 etiology, 190 management of, 191–193 natural history of, 191f skeletal alterations, 191

Infantile tumors, hemangioma v., 191 Infection augmentation mammoplasty, 576 burn injuries and, 141 chest wall defects, 664 congenital dermoid inclusion cysts, 290 craniosynostosis, 233 earrings, 310 frontal sinus fracture, 323, 324f hair transplantation, 566 head and neck irradiation, 166 mandibular fracture, 326 otoplasty and, 299 pressure sores and, 721–722 preoperative care, 722–723 prosthesis, 51 prosthetic breast reconstruction with, 630 of upper limbs, 815–823 vertical breast reduction, 612 wound healing and, 25 Inferior epigastric artery flaps, 775, 775f Inferior pedicle technique, reduction mammoplasty, 593–594, 595f, 596f Inferior turbinate hypertrophy, causes of, 522t, 523 Inferior turbinoplasty, 525 Infiltration anesthesia, 91–92 dosage and duration characteristics of, 93t Inflammation, pressure sores and, 722 Inflammatory arthritis, radiographic imaging and, 744 Inflammatory breast cancer, 620 Inflammatory cascades, wound-healing and, 15 Inflammatory cells, wound healing and, 19 Inflammatory phase, wound healing and, 16–17, 16–19, 17f Informed consent, liposuction and, 532 Inframammary fold (IMF), breast ptosis and, 583 Inframammary incision, 574, 574f Infraorbital rim augmentation, 551–552 Infratip lobular graft, 527, 527f Infraumbilical midline hernia, obese patient and, 672 Inhalation injury burns, 139–140 high-frequency oscillatory ventilators, 149 Injectable substance therapy, 466 Injection location, local anesthetic agents, 92 Injury. See also specific type injury i.e. Avulsion injuries abnormal response to, 20–21 inadequate regeneration and, 21 response to, 15 Innervated flaps, component losses and, 834 Inpatient hospital care, hand infection and, 816 Integra neodermis, burn wound and, 147, 148f Intense pulsed light, 171 Intensity-modulated radiation therapy (IRMT), head and neck cancer and, 338 Intensive care unit (ICU), burn patient, 133 Intercalary deficiency, congenital hand abnormalities, 855 Intercarpal ligament tears, MRI and, 760f, 761 Intercompartmental pressure, measurement, 676 Interdisciplinary team, head and neck, 331 Interdomal sutures, nasal tip projection alteration, 526, 526f Interferon alfa-2a, infantile hemangioma, 192 Intergroup Melanoma Surgical Trial, ELND and, 128 Intergroup Melanoma Trial, 125–126

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Interleuken-2, melanoma and, 130 Intermediate gynecomastia, 614 Intermediate phase scar manipulation, facial burns and, 151 Internal fixation, fractures and, 680 Internal nasal valve, 517f Internal topography, peripheral nerves and, 76 International Society for Study of Vascular Anomalies (ISSVA), vascular neoplasms and, 189, 190t Interphalangeal joint arthritis, 885–886 associated disorders, 886, 886f Interposition grafts, replantation in upper extremity and, 873 Intersection syndrome, 825 Intra-abdominal pressure, hernias and, 668 Intracranial pressure (ICP) craniosynostosis and, 225 craniosynostosis syndromes and, 238–239 Intradermal nevi, 105 Intramedullary nailing, fractures and, 680 Intranasal lining flaps, nasal reconstruction and, 393 Intranasal Z-plasty, cleft lip repair and, 223 Intraoral incisions. See Transcutaneous incisions Intraoral maxillofacial prostheses, 352–355 Intraoral mucosal incision, alloplastic augmentation of mandibular ramus, 553 Intraoral vertical ramus osteotomy, 264 Intrathoracic muscle flaps, chest wall irradiation, 167 Intravelar veloplasty, primary cleft palate repair, 215 Intravenous (IV) access, burn injuries, 134 Intubation, burn patient and, 132 Invasive ductal carcinoma, 619 Inverted cross-finger flap, 771 Inverted-T mastopexy procedures, 583 Inverted-T technique, breast reduction, 591–601 IRMT. See Intensity-modulated radiation therapy Irradiated breast, radiation and, 165–166 Irradiated skin, wound care of, 31 Irradiated wounds, treatment principles, 163–167 Irradiation, immunosuppression and, 53 Ischemia upper limb surgery and, 740 wounds and, 703 Ischemia-reperfusion injury, wound healing and, 24–25 Ischemia time, replantation in upper extremity, 867 Ischial pressure sores, 724 skin flaps for, 724f Isolagen, filler materials and, 469 Isolated cleft palate, 202 Isolated craniosynostosis, clinical observations and management, 227–233 Isolated limb perfusion (ILP), melanoma and, 130 Isolated mandibular surgery, 260 Isolated maxillary and Two-Jaw surgery, 260–261 Isosulfan blue, SNB and, 128 Isotretinoin, 113 ISSVA. See International Society for Study of Vascular Anomalies Itraconazole, onychomycosis, 822 IV. See Intravenous Jackson-Weiss syndromes, 235


914

Index

Jaw surgery complications, 264–265 principles, 262–263 Jaws, craniofacial microsomia and, 246–247 Jejunal autograft, cervical esophagus reconstruction and, 453 Jejunal free flap, 453f dissection technique, 452–453 Jessner solution, 457, 458 Jobst skin featureless face mask garment, graft sheering and, 143 Joint dislocations, 795–800 Joints replantation in upper extremity, 879, 881t upper limb surgery and, 740 Junctional nevi, 105 Juvederm, filler materials and, 469–470 K-wires (Kirschner wires), 58 fixation metacarpal head fractures, 792 metacarpal shaft fractures, 793, 794f shaft fracture of phalanx and, 790, 791f Kaban-Mulliken classification, Treacher Collins syndrome and, 288f Karapandzic flaps bilateral lower-lip defects and, 370, 370f lower-lip defects and, 370, 370f Kasabach-Merritt phenomenon, 191 DIC v., 196 IFN and, 192 Keloid(s) formation, 21 earring complications, 309–310 radiation therapy and, 165 Keratin, phenol and, 459 Keratinocytes, skin and, 105 Keratoacanthoma (KA), 108, 108f, 109 Keratolytic therapy, warts and, 822 Ketamine, topical cocaine and, 94 Ketoconazole, onychomycosis, 822 Key pinch reconstructions, hand and, 852, 852f Kidney, phenol and, 460 ¨ disease Kienbock lunate fractures with, 785, 786 MRI and, 763f, 764 staging of, 786, 787f Kinematics, of wrist, 779 Kinerase, 113 Kirk, N., hand specialization and, 736 Kirschner wires. See K-wires Klippel-Trenaunay syndrome, 173 Kojic acid, hydroquinone v., 114 Koken Atelocollagen implant, filler materials and, 470 KTP laser, 171, 172, 173, 174 L-Ascorbic acid, skin and, 113–114 LABC. See Locally advanced breast cancer Labial, 254 Lacrimal gland anatomy, 486 eyelid and, 396, 396f Lacrimal papilla, eyelid and, 395 Lacrimal system, eyelid and, 396, 396f Lactation, silicone, 578 Lagophthalmos, congenital ptosis and, 404 LAHSHAL acronym, cleft lip and palate, 200 Lambdoid synostosis, 224–225, 231–233, 231f, 232f operational procedure, 232–233, 232f Lambdoidal suture of skull, craniosynostosis and, 235 Langerhans cells, skin and, 105 Language, VPI and, 217 Laparoscopic flap harvesting, 452–453

Large-plug graft procedure, hair transplantation and, 569f Larynx anatomy and T staging, 331, 337f cancer, 335–336 site locations, 331, 336t Laser abrasion CMN and, 122 indications for, 464 photocoagulation, 172 phototherapy devices and, 171, 171t physics, 169–171 in plastic surgery, 169–176 with plastic surgery applications, 170t resurfacing, 457, 461–464 acne vulgaris and, 111 safety, 176 terminology, 462, 462t therapy CM and, 195 infantile hemangioma, 193 tube, 169, 170t laser physics and, 169 types of, 169 wounds, 464 Laser Doppler burn depth, 134 oral cavity reconstruction and, 448 Laser-generated recipient sites, hair transplantation and, 565 Laser in situ keratomileusis (LASIK surgery), blepharoplasty and, 490 Laser-tissue interactions, 169–171 LASIK surgery. See Laser in situ keratomileusis Late phase reconstructive surgery, burns and, 151 Latency period, 96 Lateral abdominal wall defects, 671 Lateral amputations, 890, 892 Lateral calcaneal flap, 690, 696f Lateral canthal anchoring, 492–493, 492f Lateral canthal reconstruction, zone IV defects, 401–402 Lateral circumflex femoral artery (LCFA), anterior lateral thigh flap, 450 Lateral compartment of leg, 675 Lateral epicondylitis (Tennis elbow), 827 Lateral extensor compartments, 827f Lateral graft, mandible reconstruction, 432, 432f Lateral nasal osteotomies complication of, 529t types of, 528–529, 528f Lateral palatine processes, head and neck embryology and, 183f, 184 Lateral platysma modification, 504f Lateral projection, standard radiographs, 746f, 747 Lateral resection, circumferential lipectomy and, 545, 547f Lateral skull base (Middle cranial fossa) lesions, 345 reconstruction, 443–444 Lateral throracic artery flap, 777, 777f Lateral transverse thigh flap (LTTF), 647, 649, 651, 651f, 652f Latham device NAM v., 205 PSIO and, 203 Latissimus dorsi musculocutaneous flap (LDF) breast reconstruction, 632–638 complications, 636 expander v. implant in, 635–636 operative strategy, 632 operative technique, 634–635, 635f

results, 636, 636f, 637f summary, 638 operative technique and, 632, 634 results, 636, 636f, 637f soft-tissue reconstruction and, 665 Law of Equilibrium, vessels and, 40 LCFA. See Lateral circumflex femoral artery LDF. See Latissimus dorsi musculocutaneous flap LDH. See Serum lactic dehydrogenase LeFort I fracture, 322f LeFort I osteotomy, 259f, 263 Treacher Collins syndrome and, 288 LeFort III distractor, 3-D CT scan, 243f LeFort III procedure, 240f, 243, 244 midface advancement, 241f Leg anatomy of, 675–676, 676f compartments of, 676t length measurement, combined vascular malformation syndromes, 198 Leiomyomas, 110 Leiomyosarcomas, 664 MMS and, 117 Lejour and Lassus method, vertical-incision mastopexy and, 584, 586f LeMesurier repair long upper lip, 220 primary unilateral cleft lip, 206, 207f Lentigines laser treatments and, 175–176 pigmented lesion lasers and, 171 Lesions, 105, 106. See also Malignant lesions; specific type lesions i.e. Pigmented lesions hair transplantation, 566 Leukopenia, silver sulfadiazine, 136–137 Leukoplakia, 108 Levator advancement procedure, 405–406 Levator dehiscence, 403, 404t Levator function assessment of, 404, 405f classification of, 403, 403t frontalis sling procedure, 408 Levator plication, ptosis and, 406–407 Levulan photodynamic therapy, 171 LIC. See Localized intravascular coagulopathy Lid crease asymmetry, eyelid ptosis correction, 408 Lidocaine, 91 allergic reaction, 91 soft tissue injuries, 316 toxicity, signs and symptoms, liposuction and, 539, 539t tumescent technique and, 94 Ligament reconstruction thumb basal joint arthritis and, 884 Ligamentous injuries to hand, 795–800 wrist and, 779–787 Light energy, laser physics and, 169 Light reflection, laser-tissue interactions, 169–170 Limb salvage, below-knee amputation stumps, 683–685 Limberg flap. See Rhomboid flap Limbs current transplantation and, 56 tissue expansion and, 88 Limited fasciectomy, Dupuytren disease and, 864 Limited-incision foreheadplasty technique, 512–513 incision placement, 512f Limited maxillary defect (Type 1 maxillary defect), 437, 437f eyelid reconstruction and, 438


Index Lingual, 254 Lining flaps, nasal reconstruction and, 393–394 Lip. See also Lower-lip; Upper lip defects; Vermilion adhesion, 203, 211 anatomy of, 366f construction, unilateral cleft lip repair, 209, 210 cross-section, 366f defects, 366–371 etiology of, 366 expansion, 371, 372f function of, 366 long upper, unilateral cleft lip repair and, 220 reconstruction, 365–372 facial paralysis and, 420 key points, 371–372 reconstruction flaps, 367 SCC of, 332 short upper, unilateral cleft lip repair and, 220 soft-tissue injury, 317 tight upper, unilateral cleft lip repair and, 220–221 Lip-sharing procedures, microstomia, 371 Lipid solubility, local anesthetic agent and, 91 Lipofuscin, Kinerase and, 113 Lipoma, MRI and, 763f, 765 Liposarcomas, 664 MMS and, 117 Liposuction, 531–539 anesthesia for, 532 deformities, fat grafting and, 478, 479f history, 531 incisions, gynecomastia, 616, 617f informed consent for, 532 marking and positioning, 533–534, 533f patient evaluation for, 531–532 patient selection, 531 postoperative course, 535 risk and complications, 535, 539 surgical planning and instrumentation, 532–533 treatable body areas, 535, 536f–538f tumescent technique for, 94 vertical breast reduction, 607, 608f wetting solution, 534, 534t Liquid silicone, FDA and, 60 Lisfranc amputation, 701 Liver amides and, 91 phenol and, 460 LMs. See Lymphatic malformations Lobular carcinoma in situ (LCIS), 619–620 Lobule type microtia, 303 Local anesthetic agent, 91–95 anesthetic profile, 91–92 dosage and duration characteristics, 92t, 93t facelifting and, 498 pharmacology, 91 toxicity, 93–94 treatment, 94 Local composite flaps, cheek reconstruction and, 378 Local flaps cheek reconstruction and, 374–379 hands, 769–774 nipple reconstruction, 655, 656f, 657f, 658f wound reconstruction of foot and ankle, 696, 699f, 700f Local muscle flaps, open tibial fractures and, 681 Local recurrence, melanoma and, 130 Localized intravascular coagulopathy (LIC), VMs and, 196

Locally advanced breast cancer (LABC), 620 Lockwood ligament, eyelid and, 396 Low median nerve compressions, 829 Low median nerve palsies, 850–851 Low ulnar nerve compression, 830 Lower extremity. See also Mangled extremity amputation, algorithm for, 683, 684f burns, 145 reconstruction, 674–686 trauma, 674–677 history, 674–675 treatment algorithm, 678f Lower eyelid blepharoplasty, 491–492, 492f botulinum toxins and, 475 facial paralysis and, 419–420 markings, blepharoplasty, 491 reconstruction, zone II defects, 400–401 retraction, orbital floor surgery and, 319 retractors, 484–485 Lower leg flaps, 688–689, 691f vascular supply, 688 Lower-lip defects, 369–371 double central reverse Abbe flap, 370, 370f Estlander flaps, 370, 371f Karapandzic flaps, 370, 370f deformity, 423–424 paresthesia, osseous genioplasty and, 557 position, 518, 518f Lower orbit, preoperative evaluation of, 489 Lower-third auricular defects, 302, 302f Lower truncal contouring abdominoplasty for, 540–548 complications from, 547–548, 547t history of, 540 patient presentation, 540, 541t patient selection, 541 relevant anatomy, 540–541, 541f, 542f LTTF. See Lateral transverse thigh flap Lumpectomy, DCIS and, 621 Lunate fractures, 785–786 Lund and Browder charts, burn size, age-based diagram, 133, 135f Lung metastasis, systemic melanoma, 130 Lunotriquetral instability, 781–782 Lunotriquetral ligament tears, MRI and, 760f, 761 Lymph nodes head and neck, 130 malignant melanoma and, 124 Lymphadenectomy for melanoma, 127–130 squamous cell carcinomas and, 113 Lymphangiosarcoma, 718 Lymphangitis, 816 Lymphatic drainage, SNB and, 128 Lymphatic malformations (LMs), 193 laser treatments for, 172–173 treatment, 196 Lymphatic mapping, SNB and, 128 Lymphedema, 715–719 classification, 715 etiology, 715 fascial excision, 142 medical management, 715, 715t pathophysiology, 715 summary of, 718 surgical management, 716–718 Lymphedema-distichiasis syndrome, genes for, 193 Lymphocyte, wound healing and, 18t, 19 Lymphomas of salivary glands, 340 Lymphoscintigraphy

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malignant melanomas of frontotemporal region, 342 preoperative, 128 sentinel nodes and, 129f SNB and, 128 M. bovis, typical mycobacterial infections, 823 M. tuberculosis, typical mycobacterial infections, 823 Macroarteriovenous fistulas (AVFs), 197 Macrocephaly-cutis marmorata syndrome, 195 Macrodactyly, hand reconstruction and, 859 Macrolane filler materials, 470 Macrotia, 295, 298, 298f MACS lift, facelifting and, 504 Mafenide, post burn period and, 137 Maffucci syndrome, 198 Maggot therapy debridement, 27 wound reconstruction, foot and ankle, 694 Magna-Site device, prosthetic breast reconstruction, 624f, 625f Magnetic resonance angiography, 760 Magnification equipment hand and wrist surgery, 742 microsurgery and, 67 Magnification technology, history of, 66 Major histocompatibility complex (MHC), transplantation antigens and, 52 Major nerve blocks, 92 local anesthetic agent, dosage and duration characteristics, 93t Major salivary glands, location, 343f Malar augmentation, 551 Malar fat pad, facelift anatomy and, 500 Male genitalia reconstruction, 710–714 Malformations, 189 Malignancy, 189. See also Basal cell carcinomas; Metastasis Malignant bone tumors, of chest wall, 663 Malignant degeneration, peripheral nerve sheath tumors, 292 Malignant lesions. See also specific type malignant lesions i.e. Malignant bone tumors benign lesions v., 105 of lymphatics, 718 Malignant melanoma, 124–131 of frontotemporal region, lymphoscintigraphy and, 342 of helical rim, 301f, 309 staging, 124 Malignant soft-tissue tumors, MRI and, 765 Mallet injury of thumb, 795 Malocclusion facial trauma, 327–328 mandibular fracture, 326 VMs and, 197 Malunion orthognathic surgery, 265 replantation in upper extremity, 879, 881t Mammography, 619 Mandible anatomy, 262 angle fractures, 325 body fractures, 325 craniofacial microsomia and, 246–247 defects classification, 426, 427f restoration of, 354–355 fibrous dysplasia, 280 fractures, 324–326 complications, 326 head and neck embryology and, 183f, 184 resection, 166, 431f


916

Index

Mandible (contd.) Romberg disease and, 284, 285 surgery, cephalometric tracing, 259 Mandible distraction, 98–101 craniofacial microsomia and, 251f devices, 98f, 99 technique, 99 treatment goals of, 99–101 vectors of, 99f Mandible reconstruction, 426–435 cancer and, 426 complications from, 433–434 free-flap donor-site selection, 427–430, 428f, 428t methods, 426–427 postoperative care, 433 postoperative issues, 434, 435 preoperative planning, 430 resection, 431f surgical technique, 430, 432–433 Mandibular advancement, sagittal splitting procedure for, 258f Mandibular prominences, facial development and, 181 Mandibular ramus augmentation, operative technique, 553 Mandibulofacial dysostosis. See Treacher Collins syndrome Mandibulomaxillary fixation (MMF), LeFort I osteotomy and, 263 Mangled extremity initial evaluation of, 677–679 reconstructive plan for, 679 special problems with, 679–680 MAO inhibitors. See Monoamine oxidase inhibitors Marcaine. See Bupivacaine Marjolin ulcer, 113 burn injuries and, 148 Markings breast amputation with free nipple graft, Spear technique, 598, 601f latissimus dorsi flap breast reconstruction, 632–634, 634f MMS and, 117, 117f nipple reconstruction, 655–659 vertical breast reduction, 604–605 vertical pedicle technique, 592, 592f Marlex mesh midline abdominal wall defects and, 670 skeleton of chest wall reconstruction, 665 Masseter motor nerve identifying, facial paralysis, 422, 422f Moebius syndrome, 424–425 Massive contamination, replantation in upper extremity, 867 Mast cells, infantile hemangioma, 190 Mastectomy defect. See also Total mastectomy intraoperative appearance, 624f Mastoid, blood supply to, 357 Mastopexy, mastopexy augmentation and, 583–590 Matrix metalloproteinases (MMPs) palate development and, 187 pressure sores and, 722 Mature bone zone, 97 Maxilla fibrous dysplasia, 280 number 1 Tessier craniofacial clefts and, 267, 269f Maxillary cast anatomy, 262 production, 261, 262f Maxillary constriction, 258 Maxillary defects classification system, 437–438, 437f, 438f reconstruction, 436–442 goals of, 436

restoration, autogenous reconstruction and, 354 trauma and, 352–354 Maxillary distraction, 101 craniofacial microsomia and, 247 Maxillary fractures, 321 Maxillary growth, PSIO and, 204 Maxillary hypoplasia, Apert syndrome and, 236 Maxillary Le Fort I distraction, 101 Maxillary reconstruction, algorithm for, 442f Maxillary surgery, cephalometric tracing, 259, 260f Maxillectomy defects, classification, 438, 440 Maxillofacial prosthetics, 348–355 Maxillomandibular fixation, subcondylar fractures and, 326 McComb method, bilateral cleft, 214 McCune-Albright syndrome, 279 McIndoe technique, reconstruction of absent vagina, 707 McKissock technique, reduction mammoplasty, 594, 594f, 595f MCP. See Metacarpophalangeal joint Mechanical creep, tissue expansion and, 84 Mechanical stress, tissue expansion and, 84 Medi-Sol, tar burn and, 137f Medial amputations, 892, 892f Medial antebrachial cutaneous nerve (MABC), harvesting, 80 Medial canthal reconstruction, zone III defects, 401 Medial crural septal sutures, nasal tip projection alteration, 526, 526f Medial epicondylitis (Golfer’s elbow), 827 Medial nasal prominences, head and neck embryology and, 183f, 184 Medial plantar flap, 690, 695f Medial plantar nerve, foot and ankle, 688, 690f Medial platysma, treatment of, 503f Medially based pedicle, vertical breast reduction, 604–612 Median nasal process, palate development and, 187 Median nerve blocks, wrist reconstruction and, 741, 742f compression, 829–830 sensory loss, 80 topography, 76 wrist reconstruction and, 741, 742f Median nerve palsies, tendon transfers for, 850–851 Medicolegal considerations, breast implants, 581–582 Medpor (Porex), 61 auricular reconstruction, 306, 308 facial skeletal augmentation, 550 Medpor (Porex) implant, 63f Medrol. See Methylprednisolone Dosepak Medullary carcinoma, 619 Melanin, pigmented lesion lasers and, 171 Melanoblasts, congenital nevi and, 120 Melanocytes malignant melanoma and, 124 skin and, 105 Melanoma. See also Advanced melanoma chemotherapy for, 130 CMN to, 120–122 diagnosing, 105, 106f excision margins, 127, 127t lips and, 366 MMS and, technique for, 117–119, 117f, 118f pigmented lesion lasers and, 171 recurrence, 130–131 scalp flap reconstruction, 360f

SNB and, 128–129, 128f stage groupings for, 126t Melanoma TNM classification, 124, 125t Melanoma tumorigenesis, 130 Mental retardation, craniosynostosis and, 225 Mentalis muscles, 371 botulinum toxins, 476–477 of lip, 365 Mepivacaine, 91 Merkel cells, skin and, 105 Mersilene mesh, 60, 61 Mesenchymal migration, facial development and, 182, 182f Mesenchymal syndrome, 824 Mesh implants, 61. See also specific type of mesh i.e. Prolene mesh Meshed skin grafts dressings for, 143 sheet skin grafts v., 8 Mesial, 254 Metabolic arthritis, radiographic imaging and, 744 Metabolic images, bone scintigraphy and, 752 Metabolism, local anesthetics, 91 Metacarpal base fractures, 793, 795 Metacarpal distraction lengthening, 838–839, 843f Metacarpal head fractures, 790–792 Metacarpal injury, 788 Metacarpal neck fractures, 792, 793 Metacarpal shaft fractures, 793, 794f Metacarpophalangeal joint (MCP), 808, 809f amputation distal to, 835, 839f amputation proximal to, 835, 839f dislocation, 800 Dupuytren disease and, 864 injuries, 798, 799f sagittal band injuries, 811–812 Metal eye shields, periorbital laser therapy and, 172 Metal reconstruction plates, mandible defects, 426, 427f Metallic artifacts, CT and, 756, 757f Metals, implantation and, 58–59 Metastasis, Marjolin ulcer, 113 Metastatic breast cancer, chest wall reconstructions and, 666f Metastectomy, systemic melanoma, 130 Metatarsal head, CAM Walker and, 698–699 Methadone, burn patient, 141 Methamphetamine injury, escharotomy, 134–135 Methicillin-resistant Staphylococcus aureus (MRSA) antimicrobials and, 30 hand infection and, 816 post burn period and, 137 Methotrexate, graft rejection and, 53 Methylprednisolone Dosepak (Medrol), rhinoplasty and, 530 Metoidioplasty, 729, 729f, 730f Metopic suture of skull, craniosynostosis and, 235 Metopic synostosis, 62f, 224, 227–228, 227f operative procedure, 227–228, 228f patient positioning, 227, 228f skull shape abnormalities, 227f Metronidazole, 30 Meyer-Rokitansky syndrome, 707 MHC. See Major histocompatibility complex Microanastomotic coupling device, 649, 649f Microdissection procedure (Graft production), hair transplantation and, 563 Microform cleft lip, 200, 201f operative technique, 210–211 postoperative care, 211 Micrognathia, 184


Index Microneurovascular muscle transfer, dynamic reconstructions, 420 Microstomia, lip-sharing procedures and, 371 Microsurgery equipment and operative preparation, 67 free tissue transfers, indications for, 66 history, 66 lymphedema and, 717 operative technique in, 67–70 patient education and, 66–67 peripheral nerve repair, 73–83 postoperative management in, 70, 72 principles of, 66–72 techniques cheek and, 382–386 nerve repair and grafting, summary, 82 Microtia deformity, 348 anatomy and surgical challenge, 302–303 embryology, 303 in hemifacial microsomia, 303 history, 302 middle ear reconstruction, canaloplasty and, 303 Nagata classification of, 303 surgical reconstruction, 304–308 Microvascular clamps, 68, 68f Microvascular free tissue transfer high-energy lower extremity injuries and, 681, 683 Romberg disease and, 285 Microvascular surgery principles in, oral cavity reconstruction, 447–448 salvage of extremities and, 685 Microvascular transplantation, 48, 48f Middle cranial fossa. See Lateral skull base Middle cranial fossa tumors, endoscopic approach, 347f Middle ear reconstruction, canaloplasty and, 303 Middle phalanx, replantation, 875–876, 875f Middle phalanx fractures, proximal phalanx fractures and, 788, 790 Middle-third auricular tumors, 301 Middle-third defects, 300–301 Midface anatomy, 487–488, 487f defects, classification, 438, 440 deficiency, craniosynostosis syndromes and, 241, 241f deformity, surgical correction, 243–244 distraction, 101 distraction devices, 100f hypoplasia, infraorbital rim augmentation, 551–552 osteotomies, craniosynostosis syndromes and, 241, 241f preoperative evaluation of, 489 structure, loss of, 436 Midfoot defects, 701 Midline abdominal wall defects contaminated tissue, 671–672, 671f stable soft tissues and, 670–671 unstable soft tissue and, 671–672, 671f Midline hernia, 672 Midline palatal microcysts, 184 Midline structure deficiency, 266, 268f Midline tissue, 266, 268f Millard technique primary unilateral cleft lip, 206, 207 short upper lip, 220 Mimics of infection, 823 Mini-abdominoplasty abdominal flap elevation, 543f technique for, 541, 543 Minigraft, hair transplantation and, 560 Miniplate fixation, mandible reconstruction, 432f

Minor nerve blocks, 92 Minor vascular pedicle, type II pattern of circulation, 44 MMF. See Mandibulomaxillary fixation MMPs. See Matrix metalloproteinases MMS. See Mohs micrographic surgery Moberg flap. See Volar neurovascular advancement flap Model block, 261, 262f Model surgery, occlusion casts and, 260 Modified Cutler-Beard advancement flap, upper eyelid reconstruction, zone 1 defects, 399, 399f Modified lateral tarsal strip procedure, 410–412, 412f advantages of, 411 Modified Mahler rotation-advancement repair, 210f microform cleft lip, 210–211 Modified Mohler rotation-advancement repair, operative technique, markings for, 208f Modified Mohler technique, primary unilateral cleft lip and, 207 Moebius syndrome, 280–281, 283 etiology and pathogenesis of, 281, 283, 283f masseter motor nerve and, 424–425 treatment, 283 Mohs chemosurgery, 115 SCCs and, 116 Mohs micrographic surgery (MMS), 115–119 conclusions on, 119 features of, 116t history of, 115 indications for, 115–116, 116t melanoma and, 117–119, 117f, 118f tumors treated with, 116t Molded shoes, plantar heel ulcers, 701 Molecular genetics, vascular malformations, 193, 194t Molecules, biologically active, wound healing and, 18, 18t Moles, types of, 105 excision scar, 3–4 Mondor disease, augmentation mammoplasty, 576 Monitoring, replantation in upper extremity and, 875 Monk head hairline, 564f Monks, G., hand specialization and, 736, 736f Monoamine oxidase inhibitors (MAO inhibitors), topical cocaine and, 94 Monobloc advancement 3-D CT scan, 243f craniosynostosis syndromes and, 240 Monobloc detraction (Frontofacial detraction), 101 Monobloc osteotomy, craniosynostosis syndromes and, 240 Monocryl, traumatic facial wounds, 316 Monocytes/macrophages, wound healing and, 18, 19 Morbidity, skull base resection, 444 Morphine, burn patient, 141 Mortality burn care and, 139 skull base resection, 444 Motion views (Instability series), wrist and, 749, 749f Motivation, tendon transfers and, 846 Motor anatomy, foot and ankle, 687–688 Motor nerve injury. See Nerve(s) Motor nerve transfers, applications of, 81 Motor nerves, forehead lift, 509–510, 509f Mouse studies, cranial skeleton, transcription factor Runx2/Cbfa1, 187–188

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917

Moving 2PD (Moving two-point discrimination), upper limb surgery and, 739 Moving two-point discrimination. See Moving 2PD MRA (Magnetic resonance angiography), vascular channels and, 765, 766f MRI (Magnetic resonance imaging) burn depth, 134 cervical spine injury, 314 chest wall irradiation, 167 contraindications for, 765 demonstrated anatomy, 760 hand and wrist, 757–767 lunotriquetral instability, 782 MMS and, 117 osteomyelitis, 822 parotid mass, 342 pathologic disorders and, 760–765 technique for, hand and wrist, 759–760 titanium and, 58 tumors and, 756 vascular malformations, 194 VMs and, 196 MRSA. See Methicillin-resistant Staphylococcus aureus Mucinous carcinoma, 619 Mucocele, skull base defects and, 442 Mucositis, head and neck cancer and, 338 Mucous cyst, 886 Mulliken method, bilateral cleft, 214 Multidisciplinary care cleft lip and palate, 199, 200t craniosynostosis and, 226 Multimodal scar manipulation, burns and, 152f Multiple skin cancers, treatment of, MMS and, 116t Multiple trichoepitheliomas, 109 Mupirocin, 30 Muscle flaps ARC of rotation and, 44 blood supply of, 42–43, 42–51 history of, 42 lower extremity, 688–690 perineum irradiation and, 167 thumb reconstruction, 834, 838f wound reconstruction of foot and ankle, 696, 699f Muscle free flaps, below-knee amputation, 686 Muscle-tendon unit loss, tendon transfers and, 845 Muscle-tendon units, tendon transfers and, 847, 848f, 849f Muscle transfer, facial paralysis and, 421 Muscles circulation, patterns of, 43–44 compartments, of leg, 675–676, 676f, 676t contractures, replantation in upper extremity, 880, 881t forehead lift, 507, 508f, 509f function, upper limb surgery and, 740 head and neck embryology and, 177–178 of nose, 515 power output of, muscle length v., 846f, 847 Muscles of mastication, craniofacial microsomia and, 248–249 Musculocutaneous flaps complex wounds and, 51 perineum irradiation and, 167 random skin flaps v., 9, 9f skin territory and, 44–45 Mustarde sutures, otoplasty and, 298 Mycobacterial infection, 823 Myelinated nerve fibers, upper limb compression and, 828


918

Index

Myelinated nerves, 73 Myocutaneous flap, ARC of rotation, 44 Nagata classification, microtia, 303 Nagata technique, 306, 307f, 308f complications, 305 microtia, 304, 305 Nail plate, onychomycosis and, 822 NAM. See Nasoalveolar molding Nasal base, 519, 520f Nasal cavities anatomy and T staging, 331, 338t head and neck embryology and, 186 malignancy, 336 site locations, 331, 337t Nasal deformity, 213 bilateral, NAM and, 205 cleft lip and palate, 200 NAM and, 204–205 Treacher Collins syndrome and, 287 Nasal dermoid inclusion cysts, 290 Nasal dorsal bone, secondary cleft lip and nose surgery, 222 Nasal dorsal cartilage, secondary cleft lip and nose surgery, 222 Nasal dorsum, rhinoplasty and, 524 Nasal fractures, 321 Nasal length, 520, 520f ideal, 518, 518f Nasal lining release, unilateral cleft lip repair, 209f Nasal pits, head and neck embryology and, 186 Nasal placodes, head and neck embryology and, 182f, 186 Nasal prostheses, 350, 351f Nasal reconstruction facial paralysis and, 420 general repair principles, 388 grafts, 392f lining flaps, 393 planning, 387–388 supporting framework for, 392–393 surgical techniques, 389–394 Nasal splints, rhinoplasty and, 530 Nasal stents, cleft lip repair and, 223 Nasal tip grafts, 527 modification, altering tip projection, 525–527 projection alar base width v., 520, 521f altering, 525–527 rotation, altering, 527–528 Nasal tip cartilage deformity, 214 secondary cleft lip and nose surgery, 222–223 Nasendoscopy, speech bulb appliance, 353 Nasoalveolar molding (NAM) bilateral cleft lip, 205, 206f bilateral nasal deformity, 205 complete bilateral cleft lip, 202 evaluation of, 205–206 nasal deformity correction, 204–205 Nasofacial analysis, rhinoplasty and, 517–523 Nasolabial angle, 522, 522f Nasolabial flap, nasal reconstruction, 389, 390f Nasolabial fold, botulinum toxins and, 476 Nasoorbitoethmoid fractures (NOE fractures), 321–322 Nasopharynx cancer, 333 anatomy and T staging, 331, 334f primary site locations, 331, 333t Neck botulinum toxins and, 475–476 T-staging classification system, 331, 338t

Neck burn, management, 144 Neck cancer, management, 336, 338 Neck rejuvenation, 503–504 Necrotizing fasciitis, 821 Negative pressure dressings lower-extremity trauma, 675 wounds and, 683 Negative-pressure wound therapy (NPWT), mechanism of, 27 Negative sculpting, 204 Neoadjuvant chemotherapy, breast cancer, 622 Neomycin, 30 post burn period and, 137 Neonatalhood, infantile hemangioma and, 191 Neoplasms chest wall defects, 663–664 as mimic of infection, 823 Nerve(s) allograft, 82 current transplantation and, 56 autograft, current transplantation and, 56 axons, regeneration, 73, 74f blocks dermabrasion, 461 dosage and duration characteristics, 92t conduction blockade, local anesthetics, 91 conduit characteristics of, 81 synthetic, 82 current transplantation and, 56 damage, orthognathic surgery, 265 grafts, 78–79 facial paralysis and, 421 microsurgery for, 73–83 head and neck embryology and, 177 injury, 73 classifying, 73–74, 75f, 76 facelifting and, 506 mangled extremity and, 680 nerve entrapment and, 79f lesions, median nerve palsies, 850 Moebius syndrome and, 283 regeneration, 82 repair, 80f principles of, 76 replantation in upper extremity and, 873 timing, 77–78 sheath, neurofibromatosis and, 291 supply, breast, 602 topography, 79f transfers, 80–81 vessels and, 39 vessels hitchhiking with, 39 Nervous system, craniofacial microsomia and, 249 Neural crest cellular origin of, 186–187 development interruption, 187 head and neck embryology and, 177, 178f Neural fold formation, 187 Neural plate formation, 186 Neurapraxia, 73, 75f Neurocutaneous melanosis, CMN and, 122 Neurofibromatosis, 290–294, 291f, 292f clinical presentation, 291–292 diagnostic criteria, 290t treatment, 292–293 Neurologic deficits, tendon transfers and, 845 Neurologic injury, facial injuries and, 313 Neuroma in continuity, 79, 81f Neuromuscular retraining, facial paralysis and, 417 Neuropathic ulcers, 31 Neurotized-functional muscle flap, reconstructive surgery and, 46, 46f Neurotmesis, 74, 75f

Neurotrophism, 73 Neurovascular compression syndromes, 347 Neurovascular flaps, 39 fasciocutaneous flaps v., 39 Neurovascular island flaps, thumb pulp, 772, 774, 774f Nevi, 105 Nevus cells, 120 Nevus of Ota, 105 pigmented lesion lasers and, 171 Nevus sebaceous of Jadassohn, 109, 109f laser treatments for, 174 New-fill (Sculptra), filler materials and, 470 NF-1 gene, 292 neurofibromatosis and, 291 NICH. See Noninvoluting congenital hemangioma Nidus, AVM and, 197 Nipple blood supply, augmentation mastopexy, 589 position, vertical breast reduction, 604 reconstruction conclusions, 659 methods for, 655–659 secondary cases, 659 Nipple-areola reconstruction, prosthetic breast reconstruction with, 630f Nipple-areolar complex, blood supply, 602, 603f Nipple-areolar necrosis, vertical breast reduction, 610, 612 Nodal neck metastases, 336, 338 Node-negative tumors, breast cancer, 622 NOE fractures. See Nasoorbitoethmoid fractures Nonablative lasers, 462 Nonablative resurfacing, patient selection for, 464 Noncomedo DCIS, 619 Noninnervated regional flaps, component losses and, 834, 834f Noninvoluting congenital hemangioma (NICH), 191 Nonlaser phototherapy, 171 Nonsteroidal anti-inflammatory agents (NSAIDS), tenosynovitis, 824 Nonsyndromic craniosynostosis, 224 deformational plagiocephaly and, 224–234 history and pathogenesis of, 224 Nonunion replantation in upper extremity, 879, 881t of Scaphoid fractures, CT and, 755, 755f Nose anatomy of, 515–517 cartilaginous framework of, ligamentous support of, 516f characteristics, 387, 388f aesthetic units of, 388f function, 516–517 soft-tissue injury, 317 vascular supply to, 516f Nose tip assessment, 519, 520f Nostril shape, unilateral cleft lip repair and, 209, 210 Nostril stenosis, cleft lip repair and, 223 NPWT. See Negative-pressure wound therapy NSAIDs. See Nonsteroidal anti-inflammatory agents Number 0 Tessier craniofacial clefts, 266, 268f Number 1 Tessier craniofacial clefts, 266–267, 269f Number 2 Tessier craniofacial clefts, 267, 269f Number 3 Tessier craniofacial clefts, 267, 270f


Index Number 4 Tessier craniofacial clefts, 267–268, 271f, 272f Number 5 Tessier craniofacial clefts, 269–270 Number 6 Tessier craniofacial clefts, 270–271, 272f Number 7 Tessier craniofacial clefts, 271–272, 273f Number 8 Tessier craniofacial clefts, 272–274, 273f Number 9 Tessier craniofacial clefts, 274, 274f Number 10 Tessier craniofacial clefts, 274, 275f Number 11 Tessier craniofacial clefts, 275, 275f Number 12 Tessier craniofacial clefts, 275, 276f Number 13 Tessier craniofacial clefts, 276, 276f Number 14 Tessier craniofacial clefts, 276–277, 277f Number 30 Tessier craniofacial clefts, 277, 278f Nutrition burn injuries and, 140 healing and, 722 Nylamid, 61 Nystatin, onychomycosis, 822 Obese patient, infraumbilical midline hernia and, 672 Obesity, abdominal wall, forces on, 668 Oblique facial cleft, 182, 184f Oblique vector, mandible distraction, 99 Oblique view of hamate, standard radiographs, 748, 748f Occipital arteries, scalp and, 356 Occlusal classification, orthognathic surgery and, 254 Occlusion casts, model surgery and, 260 Occlusion examination, osseous genioplasty and, 556 Occupational exposures, malignant melanoma and, 124 Ocular examination, facial trauma, 314 Ocular motility, craniosynostosis syndromes and, 240 Ocular prosthesis, 350 OMENS classification system, craniofacial microsomia and, 249 Omental flap, soft-tissue reconstruction and, 666–667 On-top plasty, 839–840 damaged finger remnant transfer, 836f Onlay tip graft, 527, 527f Onset of Action, local anesthetic agent and, 91 Onychomycosis (Tinea unguium), 822 Open fractures, free flap coverage, outcome, 679t Open knee wound, 682f Open nerve injuries, algorithm for, 80f Open rhinoplasty approach incision for, 523–524 rationale, 523, 523t, 524 Open tibial fracture, 683f treatment goal, 674 Open wounds. See Wound(s) OpSite, donor site, burn injury and, 143 Optic atrophy, 226 Optic disk edema, craniosynostosis and, 226 Oral cavity cancer, 332–333 anatomy and T staging, 331, 333f site locations, 331, 332t facial trauma and, 314 functional anatomy of, 445

Oral cavity reconstruction, 445–451. See also Soft-tissue methods of, 445–446 microvascular surgery principles in, procedure and postoperative management, 447–448 principles of, 445–451 Oral closure, primary cleft palate repair, 216 Oral communication, cervical esophagus reconstruction and, 453 Oral sphincter, 445 Oral tongue, 445 Orbicularis oculi muscle anatomy of, 484, 485f cadaver dissection, 486f innervation of, 484, 485f Orbital dermoid inclusion cysts, 288, 289 Orbital examination, orbital fractures and, 317–318 Orbital fat pads, 487f Orbital floor implants, 318–319 incorrectly placed, 319, 319f maxillary defect reconstruction and, 436, 437f Orbital floor surgery complications of, 319 floor implants, 318–319 incisions/technique in, 318, 318f indications for, 318 Orbital fractures, 317–319. See also Orbital floor surgery orbital examination in, 317–318 Orbital osteotomy, bilateral coronal synostosis and, 231f Orbital prostheses, 350–351, 352f Orbital septum anatomy, 485–486 eyelid and, 395 Orbitomaxillary defects (Type IV maxillary defect), 438, 442f Orbitozygomatic fractures, 319–321 complications, 321 diagnosis/exam, 319 operative techniques, 319–320, 321f Organ allograft transplantation, immunosuppression and, 52 Organ systems injury, response of, 15, 16f Orientation sutures, 69f Orofacial development, defects of, 184f Oronasal fistulas, cleft palate repair, 217 Oropharyngeal tumors, HPV-DNA, 332 Oropharynx cancer, 333–334 anatomy and T staging, 331, 335f site locations, 331, 334t Orthodontic treatment cleft palate repair and, 217 craniofacial microsomia, 253 Orthognathic surgery, 245, 254–265 complications, 264–265 dental terminology in, 254 diagnosis, 254 overview of treatment, presurgical, 261–262 physical examination, 254–255 procedures, 262–264 treatment plan, 256–257, 257f Orthognathic treatment, cleft palate repair and, 217 Orthopedic fixation devices, metallic artifacts and, 756–757, 757f Orthotics, plantar heel ulcers, 701 Orthotopic transplant, 52 Osseocartilaginous framework, of nose, 515 Osseointegrated implant reconstruction, dental restoration and, 434, 434f Osseointegrated implants, metals and, 58 Osseointegration, auricular prostheses, 349

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Osseous genioplasty, 555–559 alloplastic augmentation v., chin implants and, 555 location and orientation of, 556f patient examples, 557f, 558f, 559 surgical technique, 557–559 Osseous lesions, bone scintigraphy and, 753 Osseous reconstruction, of head and neck, 166 Osteoarthritis, 744 Osteoarthritis at DIP, dorsal synovial cyst and, 886 Osteocalcin, bone remodeling and, 97 Osteochondroma, 663 Osteocutaneous forearm flap, mandible reconstruction and, 429f Osteocutaneous free-flap, mandible reconstruction, 427 Osteocutaneous iliac crest flap, mandible reconstruction and, 429f Osteofasciocutaneous radial forearm flap, 449 Osteogenic sarcoma, mandible reconstruction, 426 Osteoid osteoma, CT and, 756, 757f Osteomyelitis, 49, 50f congenital dermoid inclusion cysts, 290 foot and ankle wound care, 691, 693 musculocutaneous flaps and, 51 Osteoplastic thumb reconstruction, 835–836, 842f Osteoradionecrosis, muscle transposition and, 50, 51f Osteotomies, 528–529 types of, 528–529, 528f Otoplasty ear reconstruction and, 295–312 goals of, 295 postoperative care, 299 procedure, 295–298 technique, 298f choice of, 298–299 timing, 295 Overcorrection, eyelid ptosis correction, 408 Overcorrection/unnatural contours, otoplasty and, 299 Overdose, cocaine, 94 Overgrowth, 859 Overjet, maxillary Le Fort I distraction, 101 Overresection aspiration of fat, 534 of tissue, gynecomastia, 618 Oxycodone, burn patient, 141 Oxygen tension, skin flaps and, 9–10 Oxygenation, wound healing and, 24 PABA, sunscreens and, 114 Paget disease, MMS and, 117 Pain control burn patient, 141 gluteal flap technique and, 651 rhinoplasty and, 530 Palatal closure, maxillary defect reconstruction and, 438, 439f Palatal fistulas, 254 cleft palate repair, 217 Palatal shelves, palate development and, 187 Palate development, 187 facial development and, 182, 182f head and neck embryology and, 184–185 Palatoplasty, techniques, 216 Palmar fascia, normal anatomy of, 862 Palmar space infection, 818–819, 821f Palpebral commissures, eyelid and, 395 Palpebral conjunctiva, eyelid and, 395 Palpebral fissure, eyelid and, 395 Palsies, tendon transfers for, 847–851


920

Index

Paneva-Holevich two-stage tendon reconstruction, 807 Panniculus, hanging, circumferential lipectomy and, 545 Papaverine, vasospasm and, microsurgery and, 70 Papilledema, craniosynostosis and, 226 Papillomas, names for, 110 Paranasal augmentation, 551, 552f Paranasal sinuses anatomy and T staging, 331, 338t cancer, 336 site locations, 331, 337t Parascapular flap microsurgical techniques and, 382, 385f soft-tissue reconstruction and, 665 Parasymphysis fractures, operative technique, 325 Paratenon, 801 Parathyroid glands, head and neck embryology and, 181 Parenchymal resection design skin resection patterns, 605 vertical breast reduction, 606–607 Parenteral nutrition, burn injuries and, 140 Parkes Weber syndrome, 195, 198 Parkland formula, fluid resuscitation, 138, 138t Paronychia hand and, 816, 818f hand infection, 816, 818f Parotid gland/duct injury, soft-tissue injury and, 317 Parotid gland tumors, treatment, 343–344 Parotid glands, 339 Parotid mass, evaluation, 342 Partial acquired defects, 300–302 Partial calcanectomy, plantar heel ulcers, 701 Partial defect reconstruction, 301f Partial flexor tendon severance, 804 Partial hand prosthesis, 896f, 897 Partial-thickness burns, 133 Passive flexion, flexor tendon continuity, 806 Passive molding, PSIO and, 203 Passive prostheses, hand, 895–896 Pasteurella multocida animal bites, 820 hand infection and, 816 Patch test, hydroquinone and, 114 Patient counseling Dupuytren disease and, 864 electrical injuries and, 147 education, microsurgery and, 66–67 evaluation, liposuction and, 531 history facelifting and, 496–497 forehead lift, 507 initial consultation, rhinoplasty, 517–523 management, burns and, 140–141 positioning hand surgery and, 743 for liposuction, 533–534, 533f microsurgery and, 67 selection cutaneous resurfacing, 457 liposuction and, 531 lower truncal contouring, 541 transport, burn center, 132, 133t Paucity of central lip, bilateral cleft lip, 221 PDGF. See Platelet-derived growth factor PDT. See Photodynamic therapy Pectoralis major flap, soft-tissue reconstruction and, 665 Pectoralis major myocutaneous flap (PMMCF), cervical esophagus reconstruction, 452

Pediatric intravenous insertion, topical anesthesia, 92 Pediatric patients, deep venous thrombosis, burns and, 141 Pedicle TRAM flap aesthetics, 641f, 642f free flap v., 646 reconstruction, microsurgical options, 647, 648f technical details in, 639, 640f Pedicled digital transfer, to thumb position, 833, 836f Pedicled flaps oral cavity reconstruction, 445 skull base defects reconstruction, 443 wound reconstruction of foot and ankle, 696 Pedicled greater omental flap, chest wall irradiation, 167 Pedicled rectus abdominis musculocutaneous flap, perineum irradiation and, 167 Pedicles design, skin resection patterns, 605 insertion, vertical breast reduction, 607 vertical breast reduction, 602, 603f, 606 Peeling agents, destruction depth of, 459f Pelvic floor, defects of, 712–713 Penicillin G, peripheral nerve allotransplantation, 82 Penile loss, penis reconstruction and, 728 Penile reconstruction, 710–711, 712f, 728–732. See also Total penile reconstruction author comments, 731–732 indications and requirements for, 728 surgical techniques, 728–731 Penny flaps, areolar tattooing and, nipple reconstruction and, 658–659, 658f Perforator flaps, 39, 39f reconstructive surgery and, 48, 49f Perforator TRAM, reconstructive surgery and, 49f Periareolar incision, 574, 574f gynecomastia, 616, 616f Periareolar mastopexy, 583, 584, 584f, 585f, 586f and augmentation, 589f Pericranial flap, 323f Pericranium, 356 Perineal reconstruction, in male patient, 711–712 Perineal structure deformities, causes of, 706 Perineum acquired defects of female, 707–708 burns, 144–145 defects of, 712–713 irradiation, 167 reconstruction female patient, 707–710 general principles of, 706 Periocular defect reconstruction, zone V defects, 402–403 Periocular zones, eyelid reconstruction, 397, 397f, 398f Perioral lines, botulinum toxins and, 476 Periorbital burns, management of, 143 Periorbital dermoid inclusion cysts, 288, 289 Periorbital laser therapy, metal eye shields for, 172 Periorbital region of eye, cross-sectional of, 484, 485f Periosteum, deep fascia and, 38 Peripheral nerve, 73, 74f allotransplantation, candidates for, 82 entrapment, upper limb compression and, 828 injury, nerve allograft, 82

neuromas, organ system regeneration and, 16 reconstruction, vascularized nerve grafts and, 80 repair, microsurgery for, 73–83 sheath tumors, malignant degeneration, 292 tissue, wound healing and, 21 Peripheral nerve blocks, types, 92 Peripheral nervous system (CNS), electrical injuries and, 147 Peripheral neuroma, treatment, 20 Peripheral neuropathy, wounds and, 702 Peripheral tolerance, 54 Peripheral vascular disease, foot ulcers, 703 Peroneal nerves, compression sites, 703, 703f PET scan (Positron emission tomography) head and neck cancer and, 338 malignant melanoma and, 124 Pfeiffer syndrome (Acrocephalosyndactyly type V), 235, 236–237, 237f broad thumbs in, 238f fronto-orbital advancement, 242–243, 242f PGA. See Polyglycolic acid PHA. See Romberg disease PHACES, 191 Phakomatosis pigmentovascularis, 195 Phalanges injury, 788, 789f Phalangization, 838, 840f Phalen test, FDS and, 829 Phalloplasty, 729, 730f, 731 Pharmacologic therapy, infantile hemangioma, 192 Pharyngeal arches, head and neck embryology and, 177, 178f Pharyngeal endoderm, head and neck embryology and, 177, 178f Pharyngeal flap sphincter pharyngoplasty v., 219 surgery, complications, 218 Pharyngeal pouches adult derivatives of, 180f head and neck embryology and, 178, 178f, 181 migration paths of, 180f Pharyngeal surgery, VPI and, 218–219 Pharyngoesophageal reconstruction goals of, 451–452, 451t options for, 452t Pharynx reconstruction, 451–454 principles of, 451–452 Phenol-croton oil peels, 457, 459–461 Phenol peel, 459–461 Phenol rhizotomy, spasm, 723 Phocomelia, congenital hand abnormalities, 855 Photodynamic therapy (PDT), 171 AK and, 108 Photograph consent, hair transplantation, 560 Photographs forehead lift, 507 hair transplantation, 561 preoperative, facelifting and, 497 Phototherapy devices, lasers and, 171, 171t Physical examination craniosynostosis and, 226 facial skeletal augmentation and, 549 osseous genioplasty and, 555–556 upper limb surgery and, 739–740 Physical therapy, mandible reconstruction, 433 Pierre Robin sequence, head and neck embryology and, 184 Pigmented lesion lasers, 171, 174 Pigmented lesions, 105–106 melanoma and, 122 Pillar closure, vertical breast reduction, 607 Pilomatricoma, 109


Index Pin tract infection, fractures and, 681 Pinch test, aspiration of fat, 534 PIP joint. See Distal interphalangeal joint Pisiforms anterior margin, standard radiographs, 746f, 747 Pivot point, skin flaps and, 10–12, 11f Plantar ulceration, 693 Plasmagel, filler materials and, 470 Plasmapheresis, burn care and, 149 Plastic surgeons dermatology for, 105–114 radiation wounds and, 163 Plastic surgery applications, lasers for, 170t current transplantation in, 54–57 history of, 52 lasers in, 169–176 techniques and principles in, 3–14 Plate fixation, metacarpal shaft fractures, 793, 794f Platelet-derived growth factor (PDGF) clotting cascade, 17 wound healing and, 28 wound reconstruction, foot and ankle, 694 Platysma bands, treatment of, 503f Platysma muscle, facelift anatomy and, 500 Pleomorphic adenoma, 339, 341–342 Plexiform neurofibroma, 292 of face, 293–294 Plum evacuator, CO2 laser, 176 PMMA. See Polymethylmethacrylate PMMCF. See Pectoralis major myocutaneous flap PMS-350, filler materials and, 471 Pneumatic tourniquets, wrist/hand surgery and, 742 Pneumocystis carinii prophylaxis, peripheral nerve allotransplantation, 82 Pollicization, 836f, 840–841 Polyamide, 61 Polyclonal antithyroglobulin (ATG), immunosuppression and, 54 Polyesters, 60–61 Polyethylene, 61 facial skeletal augmentation, 550 Polyethylene terephthalate. See Dacron Polyglycolic acid (PGA), 61 Polymers, bone reconstruction and, 60–63 Polymethylmethacrylate (PMMA) bone replacement and, 60 calvarial reconstruction, 364 Polymyxin B ointment, post burn period and, 137 Polypropylene, 61 Polypropylene mesh, 62 midline abdominal wall defects and, 670–671 Polytetrafluoroethylene polymer (PTFE polymer), 63 facial skeletal augmentation, 549 Polyurethane, FDA and, 63 POPLA group, PSIO and, 204 Porcine submucosa, midline abdominal wall defects and, 671 Porcine xenograft, 54–55 Porex. See Medpor Port-wine stains, laser treatments for, 171, 172, 172f Positional plagiocephaly of occiput, craniosynostosis v., 225 Positron emission tomography. See PET scan Post radiation fibrosis, chest wall irradiation, 167 Postburn alopecia, tissue expansion and, 159 Posterior cranial fossa. See Posterior skull base Posterior interosseous nerve compressions, 831

Posterior lamella, anatomy, 486f, 487f Posterior skull base (Posterior cranial fossa), lesions, 345–346 Posterior thigh flap, vaginal defects and, 710, 710f, 711f Posteroanterior oblique projection, standard radiographs, 746f, 747 Postmastectomy radiotherapy, 621–622 Postoperative adjuvant radiation therapy, parotid gland tumors, 344 Postoperative management, microsurgery and, 70, 72 Potency, local anesthetic agent and, 91–92 Povidine-iodine, wound healing and, 30 Power-assisted liposuction (PAL), 533, 538f PPD skin test. See Purified protein derivative skin test Preanesthesia, hair transplantation, 561 Preaxial deficiency, radial club hand as, congenital hand abnormalities, 854–855, 856f Prednisolone, graft rejection, 53 Prednisone, immunosuppression and, 53 Prefabricated flaps, reconstructive surgery and, 49 Pregnancy, silicone, 578 Pregnant patient, bupivacaine and, 94 Prehension, congenital hand abnormalities, 854–855 Prelaminated skin graft and cartilage, lining of forehead flap, nasal reconstruction and, 393 Premalignant skin lesion, 107, 108f Premaxillary setback, bilateral cleft lip, 221 Preoperative counseling, facelifting and, 497 Preoperative cutaneous lymphoscintigraphy, melanoma and, 128 Preoperative nasoalveolar molding, primary unilateral cleft lip and, 207 Pressure distribution, 720, 721f sitting, 720, 721f Pressure relief, wound healing, 723 Pressure sores, 720–727 closure, 723 epidemiology, 720, 721t multiple, 726 nonsurgical treatment, 727 pathophysiology of, 720–722 postoperative care for, 726 preoperative care, 722–723 recurrence, 726 staging, 720, 721t surgical treatment of, 723–726 time/pressure relationship with, 721, 722f treatment complications for, 726–727 wound care of, 31 Pressure-specified sensory device (PSSD), wounds and, 702 Pressurized water jet, debridement with, 27 Presurgical columella elongation, bilateral cleft, 214 Presurgical infant orthopedics (PSIO), 203–206 controversy in, 204 Presurgical nasoalveolar molding, PSIO and, 204–206 Presurgical orthopedics, cleft lip and palate, 202–206 Prilocaine, 91 Primary bilateral cleft lip repair, 211–214, 212f Primary bone tumors of chest, 663 Primary cleft palate repair, 214–217 operative technique, 215–216 timing of, 214–215

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Primary closure cheek reconstruction and, 374, 374f oral cavity reconstruction, 445 Primary contraction, 7 Primary lymphedema, 715 Primary tip rhinoplasty, unilateral cleft lip repair, 209f Primary unilateral cleft lip, repair, 206–211 anesthesia for, 207 timing and treatment planning, 207 Procaine, 91 Procedural pain, burn patient, 141 Procerus muscle, transblepharoplasty approach, 513f Proclination, 254 Profill, filler materials and, 470 Programmed cell death, head and neck embryology and, 183f, 184 Progressive hemifacial atrophy. See Romberg disease Prolabial unwinding flap, bilateral cleft, 214 Prolene, skeleton of chest wall reconstruction, 665 Prolene mesh, midline abdominal wall defects and, 670 Proliferative phase, wound healing and, 19–20, 19f Prominent ears, anatomic causes, 295, 296f Proplast, 63 Prostatectomy, cavernous nerve grafting following, 714 Prostheses. See also specific body part i.e. Hand aesthetic considerations and, 895 Bio-Chromatic coloring system for, 897 breast reconstruction and, 623–631 hand agenesis, 893, 894f, 895 infected/exposed, wounds and, 51 levels of amputation and, 895, 895f maxillary defect reconstruction, 436 skull base defects reconstruction, 443 specificity of, 893 types of, 895, 897 tissue expansion and, 84 unilateral v. bilateral, hand amputations, 893 Prosthetic auricular reconstruction, microtia and, 305–306 Prosthetic breast reconstruction complications, 630–631 patient selection, 623 postoperative care, 629–630 technique, 623–625 timing, 623 Prosthetic mandible replacement, mandible defects, 426 Protective positioning, elements of, hand surgery and, 743 Protein, burn injuries and, 140 Protein binding, local anesthetic agent and, 91 Protein solutions, fluid resuscitation and, 138 Proteus syndrome, 197–198 Proximal forearm median compression neuropathies, 829–830 Proximal forefoot amputation, Lisfranc amputation and, 701 Proximal interphalangeal joint (PIP joint) collateral ligament injuries, 798 dorsal dislocations, 796–797, 797f Dupuytren disease and, 864 volar dislocations, 797–798 Proximal phalanx, replantation, 876–877 Proximal radial nerve compressions, 831 Pruritus, burn management, 145 Pruzansky type III deformity, treatment, 251 Pruzansky’s mandibular deformity classification, 247, 248f Pseudoeschar, 27


922

Index

Pseudogout, 744 characterization of, 746 Pseudoptosis, augmentation mammoplasty, 576f Pseudosarcomatous lesions, 110 Pseudoxanthoma elasticum, 110 PSIO. See Presurgical infant orthopedics Psoriasis isotretinoin, 113 Tazarotene gel for, 113 Psoriatic arthritis, 888 PSSD. See Pressure-specified sensory device Psychological considerations breast implants, 580f facelifting and, 497 vertical breast reduction, 612 Psychological problems, replantation in upper extremity, 867 PTFE polymer. See Polytetrafluoroethylene polymer Puckers, vertical breast reduction, 612 Pulley system, flexor tendon v., anatomic relationship, 826f Pullthrough resection, gynecomastia, 616, 618f Pulsed-dye laser CM and, 195 facial burn reconstruction, 161 Pulsed lasers, laser-tissue interactions, 170 Punch biopsy, malignant melanoma and, 124 Puncture wound, felon, 818, 819f Purified protein derivative skin test (PPD skin test), typical mycobacterial infections, 823 Pushback technique, primary cleft palate repair, 216 Pyoderma gangrenosum, 111 Pyogenic flexor tenosynovitis, signs of, 819–820, 822f Pyogenic granulomas hemangioma v., 191 laser treatments for, 173 Q-PCR. See Quantitative polymerase chain reaction Q-switched YAG laser, tattoos and, 176 Quality-of-Life assessments, cervical esophagus reconstruction and, 453 Quantitative polymerase chain reaction (Q-PCR), wound-healing and, 15 Question mark ears, 295, 299 R115777, melanoma and, 130 R. See Roentgen Rad, 162 Radial aplasia, classification of, 854, 855t Radial club hand, congenital hand abnormalities, 854–855, 856f Radial compression neuropathies, 830–831 Radial forearm flap, 774 Radial forearm free flap dissection technique, 448–449 microsurgical techniques and, 382, 384f pertinent anatomy for, 448 total lip defects and, 369 Radial nerve, 808 block, wrist and, 741, 742f compressions, at elbow, 831 fascicular anatomy, 76, 78f repair, 76, 78f upper limb compression and, 828 wrist and, 741, 742f Radial nerve palsies, tendon transfers for, 847–848, 849f Radial polydactyly, 858–859 Radiance/Radiance FN/Radiesse, filler materials and, 470

Radiation, 162–168 breast and, 165–166 exposure, types, 162 injuries, 162–168 melanoma and, 130 Radiation dermatitis of breast, 111f Radiation necrosis, musculocutaneous flaps and, 51 Radiation therapy chest wall defects, 664 delivery, 162 head and neck cancer and, 338 irradiation summary, 167–168 prosthetic breast reconstruction with, 631 skin and, 165 Radiation wound, 49, 51, 51f chest wall, 164f sample, 163f Radiocolloid, lymphoscintigraphy and, 128 Radiofrequency, 171 Radiographic imaging. See also Chest radiography craniosynostosis and, 226 of hand and wrist, 744–768 metacarpal head fractures, 790–792 normal hand, 745f, 746f standard, 746–749 Radiologic imaging, vascular malformations, 194 Radionuclide angiogram, bone scintigraphy and, 751, 753 Radionuclide studies, inhalation injury, 139 Radiotherapy basal cell carcinomas and, 112 squamous cell carcinomas and, 113 Radius donor site, mandible reconstruction and, 428–429 Radius free flap, mandible reconstruction and, 429 Ramsay Hunt syndrome, facial paralysis, 423f Ramus, craniofacial microsomia and, 247 Random-pattern flaps, 42 Random skin flaps, 777 blood supply of, 42 musculocutaneous flaps v., 9, 9f Range of motion, tendon transfers and, 846 Rapidly involuting congenital hemangioma (RICH), 191 RARs. See Retinoic acid receptors Raynaud syndrome, 765 Raynaud’s disease, wounds and, 703 Recipient site hair transplantation and, 563–566 microsurgery and, 68, 68f Reconstruction of absent vagina, 707 Reconstructive ladder algorithm, 66 wound closure and, 14, 14f Reconstructive surgery. See also Burn(s) cosmetic surgery v., 3 flap modifications and, 45–49 free tissue transfers in, indications for, 67t Rectus abdominus flap, 449 microsurgical techniques and, 382–383 soft-tissue reconstruction and, 666 Rectus abdominus myocutaneous flap (VRAM), 713f perineal reconstruction, 711–712 vaginal reconstruction, 709–710, 710f Recurrence, pressure sores, 726 Recurrent pleomorphic adenoma, 340–341 Recurrent tumors, 341 chest wall irradiation, 167 MMS and, 115–116, 116t RED. See External head frame Reduction mammoplasty. See also Vertical breast reduction indications for, 591

inferior pedicle technique, 593–594, 595f inverted-T technique and, 591–601 Spear technique, 512f, 513f, 595–598, 598f tissue and, 39 Reflex sympathetic dystrophy (RSD), bone scintigraphy and, 753 Regeneration, 15–16, 21, 22 inadequate, abnormal response to injury and, 21 Regional lymph nodes dissection, lymphedema, 715 melanoma and, 127 Regional myocutaneous flaps, oral cavity reconstruction, 445 Regnault grading system, breast ptosis and, 586, 587 Regranex. See Becaplermin Regression, infantile hemangioma, 190 Rehabilitation, burn injuries and, 149 Release, burn reconstruction surgery and, 154 Remodeling phase, wound healing and, 20, 20f Remodeling zone, 97 Renova, 113 Reossified bone, craniosynostosis syndromes and, 241 Reperfusion, of amputated part, replantation in upper extremity and, 874 Reperfusion damage, wound healing and, 24–25 Replantation levels of amputation, 875–879 multiple digits, 877 postoperative result, 877f Replantation in upper extremity, 866–881 absolute contraindications for, 866, 867t multiple injuries within amputated part, 866 significant associated injury and, 866 systemic illness, 866 complications, 879, 881t contraindications for, 866 indications for, 866 postoperative care and monitoring, 874–875 re-exploration, 875 relative contraindications for, 866, 867t age, 866 avulsion injuries, 866–867 technique of, 872–874 Replantation service, transfer to, 867, 869 Replantation surgery, evaluation for, 870 Resoplast, filler materials and, 467, 470 Respiratory obstruction, cleft palate repair, 217 Rest, hand infection and, 815 Restylane, 92 filler materials and, 470–471 Resuscitation, decisions, 139–140 Retaining ligaments, facelift anatomy and, 500 Reticular dermis, 105 Retin-A micro, 113 Retin-A (Retinol), 457 Retin-A (Tretinoin), 113 laser abrasion, 464 Retinaculum, dorsal wrist compartments and, 808, 809f Retinal dermatitis, 113 Retinoic acid, acne vulgaris and, 111 Retinoic acid receptors (RARs), 113 Retinoids, 457 skin and, 113 Retinol, vitamin A and, 113 Retrograde sural nerve flap, 689, 692f Retromolar trigone tumors, 333


Index Revascularization foot ulcers, 703 muscle transplantation and, 50f skin grafting and, burn injury and, 142 Reverse Abbe flap, dip defect and, 366 Reversed cross-finger flap, 771 Reviderm-intra, filler materials and, 471 Rheumatoid arthritis (RA), 887–888 radiographic signs of, 744 Rheumatoid disease of fingers, 888 of thumb, 888 Rheumatoid synovitis, 887–888 Rhinophyma, 111, 111f Rhinoplasty, 515–530. See also Secondary rhinoplasty closure, 529 in infancy, skin envelope, 223 operative technique, 523–529 postoperative management, 530 preoperative assessment, 517–523 Rhizotomy, spasm, 723 Rhomboid defect, Limberg flap and, 12, 12f Rhomboid flap (Limberg flap) cheek reconstruction and, 375–376, 379f transposition flap as, 12, 12f Rhytides. See Wrinkles Rib grafts, 363 RICH. See Rapidly involuting congenital hemangioma Rigid internal fixation, amputated body part and, replantation surgery, 871 Ring avulsion injuries, classification of, 870t Rodent ulcer, 112 Roentgen (R), 162 Rolando-type fracture, 795, 797f Romberg disease (Progressive hemifacial atrophy; PHA), 283–285, 284f Rosacea, laser treatments for, 173 Rotation advancement flap ARC of rotation and, 44 cheek reconstruction and, 376–378, 379f, 382f Rotation skin flap, planning, 10, 10f RSD. See Reflex sympathetic dystrophy Rubens flap, 651 positioning for, 653f preoperatively, 654f Rule of Nines, burns and, 134f Runaround abscess, 816, 818f paronychia and, 816 Russ scaphoid fractures classification, 782–783, 785f S. epidermidis, Hydradenitis suppurativa, 111, 111f Sacral pressure sores, 725 flaps for, 725, 725f Saethre-Chotzen craniosynostosis, Twist transcription factor, 188 Saethre-Chotzen syndrome (Acrocephalosyndactyly type III), 237, 238f Safe zone, forehead lift, 510f Sagittal band injuries, 811–812 ruptures, 812 Sagittal split osteotomy, bilateral, 264 Sagittal splitting procedure, mandibular advancement and, 258f Sagittal suture of skull, craniosynostosis and, 235 Sagittal synostosis, 224 operative procedure, 228–229, 229f Sagittal T1-weighted images, MRI and, 759f, 760 SAL. See Suction-assisted lipoplasty

Salicylic acid (SA), 457, 458 skin and, 113 warts and, 822 Saline breast implants, 628, 628f, 629f augmentation mammoplasty and, 574–575 complications, 580f permanent, 628, 628f Salivary glands, 339 tumors, 339–344 benign v. malignant, 340–342 pathology, 340 Saphenous nerve, foot and ankle, 688, 690f SARPE. See Surgically assisted rapid palatal expansion Saucer-type deformity, gynecomastia, 618 SC. See Sulfur colloid Scald burn, 136f. See also Perineum depth of, 132, 133t Scalp anatomic layers of, 356, 357f anatomy, 356–362 autograft for, 143 defect, free latissimus dorsi flap reconstruction, 362f flap, scoring of galea, 358f flap reconstruction melanoma and, 360f posterior skull, 361f lymphatics, 357 reconstruction, 356–364, 358–362 defects 6 to 9 cm, 360–361 defects greater 9 cm, 361–362, 363f defects less than 3 cm, 358 defects less than 6 cm, 358–360 tissue expansion and, 85, 86f–87f scarring, foreheadplasty, 513 SCCs, 116 sensation, foreheadplasty, 513 temporal region, anatomic relationships, 357f vessels, 356 Scaphoid fractures classification, 782, 785f CT and, 754–755, 754f, 755f nonunion of CT and, 755, 755f no degenerative changes, treatment, 784–785 types of, 784, 786t treatment, 783–785 Scaphoid nonunion advanced collapse (SNAC) wrist, treatment, 785 Scaphoid projection, 748, 748f Scapholunate instability radiographic examination, 780, 784f stages of, 780, 783f Scapholunate ligament tears, MRI and, 760f, 761 Scapula donor site, mandible reconstruction and, 429–430 Scapular flap, dissection technique, 450 Scar formation excessive, abnormal response to injury and, 21 inadequate, abnormal response to injury and, 21 tissue regeneration v., 15–16 widening, 3 Scar therapy, wound healing and, 30 Scarpa’s fascia, lower truncal contouring, 540, 541f, 542f Scar(s). See also Hypertrophic scarring; Multimodal scar manipulation appearance of, factors affecting, 3 burn reconstruction surgery and, 150, 153 capsule, osseous genioplasty, 555–559

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technique and, 4 unfavorable, unilateral cleft lip repair and, 221 vitamin E and, 114 SCCs. See Squamous cell carcinomas Schirmer test, canthoplasty, 408, 411f Schuchardt procedure, cheek and lip, 369, 369f Schwann cells, nerve allograft and, 56 Sciatic nerve, foot and ankle, 687 Sclerotherapy LMs and, 196 spider veins and, 174 VMs and, 196–197 Screw fixation metacarpal shaft fractures, 793 shaft fracture of phalanx and, 790, 791f Scrotal reconstruction, 711 Sculptra. See New-fill Sebaceous carcinoma, MMS and, 117 Sebaceous epithelioma, 109–110 Sebaceous nevi laser treatments for, 174 Levulan photodynamic therapy, 171 Sebaceous tumors, 109–110 Sebaceus nevus of Jadassohn, 109 Seborrheic keratoses (SKs), 106 actinic cheilitis v., 107, 108f Secondary cleft lip and nose surgery, 219–223, 221–223, 222f indications for, 219 skeletal base of nose, 222 timing, 219–220 Secondary contracture, 7 Secondary facelifting, 504 Secondary lymphedema, 715 Secondary rhinoplasty, 221–223, 222f, 530 Segmental aponeurectomy, Dupuytren disease and, 864 Segmental flaps, reconstructive surgery and, 45 Segmental vascular pedicles, type IV pattern of circulation, vascular anatomy and, 44 Seizure, hyperventilation and, 94 Selective photothermolysis, laser-tissue interactions, 170 Self-retaining spring dental retractors, commissural burns and, 371 Sella-nasion-subspinale (SNA), orthognathic surgery and, 255, 256f Sella-nasion-supramentale (SNB), 255, 256f Semiocclusive dressings, wound healing and, 28 Senile sebaceous hyperplasia, 110 Sensibility restoration, tendon transfers and, 846 Sensory anatomy, foot and ankle, 687–688, 690f Sensory examination, foot and ankle wound care, 691 Sensory flap reconstructive surgery and, 46–47 thumb reconstruction, 834, 837f Sensory groups, 76, 77f Sensory innervation, of lip, 365 Sensory nerves foot and ankle, 687–688, 690f forehead lift, 509, 510f Sensory return, replantation in upper extremity, 880, 881t Sensory testing, nerve injury and, 76, 76t Sentinel node biopsy (SNB) indications for, 129 malignant melanoma and, 124 parotid gland tumors and, 343–344 Sentinel nodes, 128 lymphoscintigraphy of, 129f


924

Index

Separation of parts procedure, infraumbilical midline hernia and, 672, 672f Septal composite flap, nasal reconstruction and, 394f Septal reconstruction, cartilage graft harvest and, 525 Septic arthritis, 820–821 Septic joints, 820–821 Septocutaneous flaps, 38 Septum constituents of, 516f ULCs and, separation of, 524 Serial excision, 7 Seromas gluteal flap technique, 651 latissimus dorsi flap breast reconstruction, 636 lower truncal contouring and, 547 Serratus anterior flap, soft-tissue reconstruction and, 665 Serum lactic dehydrogenase (LDH), malignant melanoma and, 124 Seventh cranial nerve anatomy of, 415, 417, 417f essential functions of, 415 Severe facial asymmetry, microtia and, 308 Shaft fracture of phalanx, 790, 791f Shave biopsy, malignant melanoma and, 124 Shearing injuries, staging, 720, 721t Sheen graft, nasal tip cartilage, 223 Sheet autograft, face burn and, 143 Sheet skin grafts burn injury and, 143 meshed skin grafts v., 8 Short lower face, correction, 259 Short-scar technique, facelifting and, 504 Shoulder abduction, nerve transfer and, 81 Shunting, hydrocephalus, 241 SIEA. See Superficial inferior epigastric artery Sievert (Sv), 162 Silicone (dimethylsiloxane), 60 effects, 578 facial skeletal augmentation, 549 filler materials and, 471 Silicone elastomer implants, capsule formation and, 60 Silicone gel implants, 574, 575–576, 623 prosthetic breast reconstruction, 627 Silikon-1000, filler materials and, 471 Silvadene, donor site, burn injury and, 143 Silver nitrate, post burn period and, 137 Silver sulfadiazine, 30 post burn period and, 136 Simon grade 3 gynecomastia, 618 Simon stage 1 lesions, 615, 616f Simple interrupted suture, 4–5 Single blade method, donor hair follicles and, harvest technique, 562, 562f, 563f Single-digit amputations, replantation in upper extremity, 867 Single follicular units (FU), hair transplantation and, 560, 561f Single vascular pedicle, type I pattern of circulation, vascular anatomy and, 44 Sinonasal tract squamous cell carcinoma, 336 Sirolimus, graft rejection and, 53 Sizers, saline filled, prosthetic breast reconstruction, 627–628, 627f Skeletal class II occlusion, 258 Skeletal class III malocclusion, 258 Skeletal deformity, 3-D CT scan, 250, 250f Skeletal injuries, face and, 313–330 Skeletal molding, history, 96 Skeletal stabilization, tendon transfers and, 846 Skeleton, Number 2 Tessier craniofacial clefts and, 267

Skeleton of chest wall reconstruction, 664–665 Skin adhesives, wound closure and, 6 anatomy, 105 blood supply of, 33–41 closure replantation in upper extremity and, 874 vertical breast reduction, 607 vertical reduction mammaplasty, 603 current transplantation and, 54–55 embryology, 105 envelope dissection, rhinoplasty and, 524 rhinoplasty in infancy and, 223 histology of, 458f layers of, 105, 106f, 457 lesions, laser treatments for, 174 lymphedema and, 717 of nose, 515 plastic surgery and, 3 products, 113–114 radiation therapy and, 165 replacement burn wound and, 147–148 technology, 149 resection patterns vertical breast reduction, 604–605 vertical reduction mammaplasty, 602, 603f resurfacing laser, 175f Rhinophyma, 111, 111f Romberg disease and, 283 of scalp, 356 slough, facelifting and, 505–506 staples, 6 substitutes, wound healing and, 30 territory, musculocutaneous flaps and, 44–45 tumors, categorizations of, 106 type, scar type v., 3 Skin allograft, 54 Skin autograft, 54 Skin bridges, abdominal surgery and, 669 Skin cancer. See also Basal cell carcinomas; Malignant melanoma; Squamous cell carcinoma of helical rim, 309 Skin flap necrosis, prosthetic breast reconstruction with, 630 Skin flaps, 9–12. See also Flap(s); Muscle flaps; specific type flap i.e. Cervical flaps burn reconstruction surgery and, 157–158 classification of, 9f connective tissue framework and, 36 nerves, vessels hitchhiking with, 39 pivot point and, 10–12, 10f planning, 10 Skin graft, 7–9, 52 adherence, 8 burn injury and, 141 burn reconstruction surgery and, 150, 154, 156 cheek reconstruction and, 374 CM and, 195 donor sites, 8 dorsum of foot defects, 701 face burn and, 143 hands and, 769 hydradenitis suppurativa and, 111, 111f late, burn reconstruction surgery and, 151f for lining flaps, nasal reconstruction and, 393 midfoot defects, 701 nipple-areola reconstruction, 656 oral cavity reconstruction, 445

postoperative care of, 8–9 radiation wounds and, 163 rejection, drugs for, 53 scalp, 359f survival requirements for, 8 technical aspects of, burn injury and, 142–143 tie-over bolster dressing for, 9, 9f types, 7–8, 8f wound reconstruction of foot and ankle, 696 Skin island bleeding response, mandible reconstruction, 433 latissimus dorsi flap breast reconstruction, 634, 635f Skin marker. See Markings Skin paradigm bilateral cleft nose repair, 212–213 criticisms of, 213 Skin wounds closure of, 4–7 flexor tendon injuries and, 804, 804f Skin xenograft, 54–55 SKs. See Seborrheic keratoses Skull base anatomic subdivisions, 346f reconstruction, 363 Skull base defects reconstruction, 442–444 complications of, 443 goals of, 442–443 tumor resection and, 442 Skull base surgery, 345–347 Sleeping position, Cubital tunnel syndrome, 830 Sliding genioplasty disadvantage of, 553 implant augmentation v., 553 Sliding tarsoconjunctival flap, lower eyelid reconstruction, 401 Sliver, hair transplantation and, 563f Slough, 27 Slow-flow combined malformations, 197–198 Small concha type microtia, 303 Small skull base defects, summary, 444 SMAS. See Subcutaneous musculoaponeurotic system SMAS. See Superficial musculoponeurotic system SMAS plication, 502–503 SMASectomy, 502, 502f Smiling, facial paralysis and, 422, 423, 423f Smooth implants, smooth-walled capsules, 549 Smooth muscle tumors, 110 SNA. See Sella-nasion-subspinale SNAC. See Scaphoid nonunion advanced collapse Snap-back test, canthoplasty, 408, 411f SNB. See Sella-nasion-supramentale SNB. See Sentinel node biopsy Soap, phenol and, 459 Sodium carbonate, soft tissue injuries, 316 Sodium tetradecyl sulfate, VMs and, 196 Soft-tissue arthroplasty, carpometacarpal injuries and, 834, 834f augmentation, 466–472 future of, 472 avulsion, mangled extremity and, 679 coverage tendon transfers and, 846 upper limb surgery and, 739 craniofacial microsomia and, 249 defects, forehead reconstruction, 362–363 defects of thumb, flap selection for, 834, 839t


Index depression, implants for, 553–554 facial injuries and, 313–330 fillers, fat grafting as, 478–483 free flap, mandible reconstruction, 427 infection, cold injury, 147 injuries, 769 treatment of, 315–317 loss, of thumb, 834, 834f management, open tibial fractures and, 681 midline excess, 266 movement, osseous genioplasty and, 556 neurofibroma, 292 number 1 Tessier craniofacial clefts and, 266–267 number 2 Tessier craniofacial clefts and, 267 oral cavity reconstruction, 445 plexiform neurofibromas, of forehead, 294 reconstruction chest wall reconstructions and, 665–667 goals, 165 of hand, 769–778 polymers and, 60–63 sarcomas of extremities, radiation therapy and, 165 SoftForm, wrinkles and, 466 Solar lentigo, 105, 107f bleaching agents, 114 Soleus muscle, 689 Sommerlad’s intravelar veloplasty, primary cleft palate repair, 215 Spasm. See also Antispasmodic agents control of, 31 pressure sores and, 723 Spastic disorders, tendon transfers and, 845 Spear technique, reduction mammoplasty, 595–598, 598f, 599f, 600f Speech oral cavity reconstruction, 450 VPI and, 217 Speech bulb appliance, 353, 354f Sphenoid wing tumors, endoscopic approach, 347f Sphincter pharyngoplasty, 218–219 pharyngeal flap v., 219 Spider telangiectasia, 195 Spider veins, laser treatments for, 173, 174 Spinal cord injuries, paralysis and, hand reconstruction for, 851–852 Splinting flexor tendon continuity, 806 hand burn, 144 tenosynovitis, 824 Split-finger graft, eyelid reconstruction, 400f Split-hook active prostheses, hand, 895, 895f Split-thickness skin graft, 7 burn reconstruction surgery and, 150 EMLA for, 92 hands, 769 open tibial fractures and, 681 Spontaneous ulceration, infantile hemangioma, 192 Spreader grafts, 525, 525f Springboard graft, unilateral deformity and, 223 Squamous cell carcinomas (SCCs), 105, 107, 112–113, 112f, 116, 340 histologic grading and, 113 of lip, 332 sebaceus nevus of Jadassohn, 109 Stability in solution, local anesthetics, 91 Stable undisplaced fracture, treatment, scaphoid fractures, 783 Staged subcutaneous excision beneath flaps, lymphedema and, 717, 718f Stahl classification system, lunate fractures and, 786, 787f Stahl ear deformity, 295, 297f, 298, 298f

Stainless steel, biomedical implants and, 58 Staphylococci, post burn period and, 136 Staphylococcus animal bites, 820 septic arthritis, 820 Staphylococcus aureus hand infection and, 816 hydradenitis suppurativa and, 111, 111f skin flaps and, 9 Staples, skin grafts and, 143 Static rhytides, 466 Stenstrom technique, antihelical fold manipulation, 296, 298f Steroids graft rejection, 53 inhalation injury, 139 problem wounds and, 31 Stewart-Treves syndrome, 718 Stigmata of facial burns, 161t STN. See Supratrochlear nerve Straight line closure lip adhesion, 211 primary unilateral cleft lip, 206, 207f Streptococci, post burn period and, 136 Streptococcus necrotizing fasciitis, 821 septic arthritis, 820 Stress views, wrist and digits, 749–750 Stretch marks, abdominoplasty, 543 Strickland classification, total active motion formula, 806 Strickland method, for flexor tendon continuity, 805 Sturge-Weber syndrome, 195 Sub-mini digital prosthesis, distal phalanx and, 897, 897f Subacute reconstruction, thumb and, 833 Subcondylar fractures, 325–326 Subcranial Le Fort III distraction. See Midface Subcutaneous facelift, 500, 501f redraping, 501 undermined skin flap and, 501 Subcutaneous musculoaponeurotic system (SMAS), 356 dissections, 501–502 extended dissections, 502, 502f traditional dissections, 501–502 Subcuticular skin suture, 5–6, 5f traumatic facial wounds, 316 Submandibular gland stones, 342 Submandibular glands, neck rejuvenation and, 503 Submental dissection and platysmaplasty, 503, 503f Submucous cleft plate, 202 Subperiosteal facelift, 504 Subtotal maxillary defect (Type II maxillary defect), 437, 438f Subtotal resection, VMs and, 197 Subungual melanoma, amputation for, level of, 127, 127f Suction-assisted lipoplasty (SAL), 532–533, 538f Sulfur colloid (SC), lymphoscintigraphy and, 128 Sunlight basal cell carcinomas, 111–112, 112f retinoids and, 113 squamous cell carcinomas and, 112 Sunscreen, 114 Superficial burns, 133 Superficial circumflex iliac artery flap (Groin flaps), 774–775, 776f Superficial fascia, 37 Superficial fat layers, 531, 532f Superficial inferior epigastric artery (SIEA), 646 flap, 774, 775f

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Superficial liposuction, 532 Superficial musculoaponeurotic system-muscle layer, facial nerve and, 499 Superficial musculoaponeurotic system (SMAS), facelift anatomy, 498, 499 Superficial partial-thickness burns, 133, 136f Superficial peeling agents, 458 Superficial rhytides, 466 Superficial temporal arteries, scalp and, 356 Superior oblique medial osteotomy, 529, 529f Support stockings, VMs and, 197 Supporting framework, nasal reconstruction, 392 Supratrochlear nerve (STN), forehead lift, 509, 510f Sural nerve, foot and ankle, 688, 690f Sural nerve grafts, replantation, 879, 980f Surface orbital anatomy, age-related changes and, 488 Surgeon, preoperative preparation for, forehead lift and, 507–510 Surgery, 3. See also Microsurgery; specific type surgery i.e. Two-Jaw surgery cleft lip and palate, 199, 200t, 203 complications, botulinum toxins and, 477 complications of, lymphedema and, 718 craniofacial clefting, 278 craniofacial microsomia, 253, 253f craniosynostosis syndromes and, 241–245 CTS and, 829 evaluation and classification, cleft lip and palate, 199, 200t infantile hemangioma, 193 lymphedema and, 716–718 operative preparation for, microsurgery, 67 pressure sores, 723–726 pyogenic flexor tenosynovitis and, 819, 822f results of, lymphedema and, 717–718 syndactyly and, 855–857 thumb basal joint arthritis, 884 upper limb injury, 740–743 Surgical algorithms, CMN and, 122 Surgical clips, MRI and, 765 Surgical decompression, Guyon tunnel syndrome, 830 Surgical excision basal cell carcinomas and, 112 of distant metastases, melanoma and, 130 squamous cell carcinomas and, 113 warts and, 822 Surgical management, burn patient, 141–148 Surgical obturator, maxillary defects and, 352–353 Surgical reconstruction, microtia, 304–308 Surgical resection LMs and, 196 VMs and, 197 Surgically assisted rapid palatal expansion (SARPE), 263–264 Surgisis filler materials and, 471 midline abdominal wall defects and, 671 Survival head and neck cancers and, 344 ILP and, 130 melanoma and, radiation for, 130 Survival rates, head and neck cancer, stage and site specific, 340t Suture(s) antihelical fold manipulation, 296 microsurgery and, 68, 69, 69f otoplasty and, 299 removal, scarring and, 4 scarring and, 3–4


926

Index

Suture(s) (contd.) technique, flexor tendon continuity, 805, 805f techniques, 4–7, 5f Sv. See Sievert Swan neck deformity, 812, 812f Swanson classification of congenital upper limb abnormalities, 855, 855t Sweat duct carcinoma, MMS and, 117 Symes amputation, hindfoot and, 701 Symmetry, determination, 518, 518f Symphalangism, 857 Symphysis fractures, operative technique, 325 Syndactyly, hand reconstruction and, 855–857, 857f Syndactyly of digits, Apert syndrome and, 237f Syndromic craniofacial synostosis, midface distraction, 101 Syndromic craniosynostosis, 188 genetic predisposition, 235 treatment options, 239t Synkinesis, 417 Synovial venous malformations, of knee, 196 Synthetic ruby rod, 169 Synthetic skin substitutes, CMN and, 122 Syringocystadenoma papilliferum, 109 Syringomas, 109 laser treatments for, 174 Systemic conditions, blepharoplasty and, 489–490 Systemic lupus erythematosus, arthritis of, 888 Systemic melanoma, 130 clinical course of, 130 Systemic retinoids, 113 Systemic therapy, breast cancer, 622 T-cells, immunosuppression and, 53, 54 T-skin resection, vertical reduction mammaplasty, 603 T-Type procedures, 548 T1-weighted images, 759 T2-weighted images (FLASH), 759, 760 Tachycardia, fluid resuscitation and, 139 Tacrolimus (FK506) graft rejection and, 53 nerve allograft and, 82 Tagging neurovascular structures, amputated body part and, replantation surgery, 871 Tamoxifen, DCIS and, 621 Tangential excision, burn wounds and, 141–142 Tanzer/Brent technique, auricular reconstruction, 306 Tar burn, Medi-Sol and, 137f Tarsal conjunctival mullerectomy (Fasanella-Servat procedure), ptosis and, 406–408, 407f Tarsal plates, eyelid and, 395 Tarsal tuck canthopexy, 410 Tarsal tunnel exposure, flexor retinaculum release, 704 Tarsofascial layer, eyelid and, 395 Tarsoligamentous sling, 486f Tarsorrhaphy face burn, 143 paralyzed eyelid and, 418 Task analysis, tendon transfers and, 846 Tattoo removal, laser treatments and, 176 Tazarotene gel, 113 TBSA. See Total body surface area TCA. See Trichloroacetic acid TCOF 1 gene, Treacher Collins syndrome and, 286–287 Tear breakup time, canthoplasty, 408, 411f

Tear trough deformity, 487f facelift anatomy and, 500 Tears, eyelid and, 396 Technetium-99m, lymphoscintigraphy and, 128 Technetium-99m bone scintigraphy, phases of, 751–753, 751f Teflon, skeleton of chest wall reconstruction, 665 Telangiectasias, 195 laser treatments for, 173 Telecanthus, soft-tissue injury and, 329 Temperature, skin and, 33 Temperature strip, free TRAM procedure, 649, 649f Templates, mandible reconstruction, 432f Temporal bone, craniofacial microsomia and, 247 Temporal hollowing, 327f, 329 Temporalis transfer, eyelids and, 419, 419f Temporomandibular joint disease. See TMJ disease Temporoparietal fascia free flap, hand reconstruction and, 778 Temporoparietal flap, dissection technique, 450 Ten test, nerve injury, 76 Tendon adhesions, replantation in upper extremity, 880, 881t anatomy, zones of hand, 801, 802f avulsion injuries, 804 grafts, 807 healing, 803–803 flexor tendon surgery and, 801–807 repair surgical prerequisites, 846 tendon transfers v., 845 ruptures, 804 transfers basic tenets of, 845 for combined nerve palsies, 851 evaluation and goal establishment, 845 indications for, 845 muscle selection for, 847 muscle-tendon units and, 847, 848f, 849f palsies and, 847–851 postoperative management for, 852–853 Tendon sheath injection technique, tenosynovitis, 824 Tendon sling, lower eyelid, facial paralysis and, 419, 420f Tendon zones, 802, 802f of injury, 808–809, 809f Tendonitis, 824 MRI and, 762, 762f Tennis elbow. See Lateral epicondylitis Tennison repair, long upper lip, 220 Tenocytes, 801 Tenolysis, 807 Tenosynovitis, 824–827 edema and inflammation cycle, 824, 825f MRI and, 762, 762f Tenosynovitis of extensor carpi radialis brevis (ECRB), 825 radial nerve compressions and, 831 Tenosynovitis of extensor carpi radialis longus (ECRL), 825 Tensile strain, distraction osteogenesis, 98 Tension, burn reconstruction surgery and, 153 Tensor fascia lata (TFL) flaps infraumbilical midline hernia and, 672, 672f ischial pressure sores, 724, 724f trochanteric ulcers, 726f

Tessier classification craniofacial clefts and, 266, 267f facial clefts of, 183 Tessier craniofacial clefts, combination numbers, 274f Testicular autotransplantation, 713–714 Tetanus prophylaxis, 23 Tetracaine, 91 TFCC. See Triangular fibrocartilage complex TFL flaps. See Tensor fascia lata flaps TGF-ß. See Transforming growth factor-beta Thenar flap, 772, 773f, 774f Therapeutic axillary lymphadenectomy, 130 Therapeutic inguinal lymphadenectomy, complications from, 130 Therapeutic lymphadenectomy, 129–130 Thermal injuries, 132–149 Thermal relaxation time, pulsed lasers, 170 Thiopental, hyperventilation and, 94 Thoracic outlet syndrome (TOS), 831–832 Thoracic reconstruction, 663–667 Threshold potential, local anesthetics, 91 Thrombocytopenia, Kasabach-Merritt phenomenon, 191 Thumb amputation, 834–835, 839f, 891f, 896f basal joint arthritis, treatment of, 884–885, 886f basal joint degenerative disease, stages of, 883f, 884 deficiencies, types of, 833–835 dislocations of joints, 800 duplication, Wassel classification, 858f fractures, 795 joint injuries, 798–800, 798f MCP joint, stress view, 798f metacarpal fractures, treatment, 795 phalanges fractures, 795 reconstructions, 737, 833–844 evaluation, 833 indications, 833 procedures, 835–844 technique, choices of, 835, 840t replantation, 868f, 877 Thumb loss classification, 833, 836f Thumb opposition restoration, 737 Thumb ulnar collateral ligament tears, MRI and, 760–761 Thyroglossal duct cyst, head and neck embryology and, 185 Thyroid gland, head and neck embryology and, 185 Tibial fracture chronic osteomyelitis and, 683, 684f hemisoleus flap, 682f Tie-over bolster dressing, skin graft and, 9, 9f TIMP-1. See Tissue inhibitor metalloproteinase Tinea unguium. See Onychomycosis Tinel sign, axonotmesis and, 73 Tissue cellular origin of, 186–187 debridement, electrical injuries and, 147 differentiation, vessel size and, 39–40, 40f expander exchange, to permanent implant, 626f, 627–628 expanders, 84, 85f cheek reconstruction and, 379–382 latissimus dorsi flap breast reconstruction, 632 postoperative care, 629–630 prosthetic breast reconstruction, 624, 624f, 625f, 626f types, 84 expansion, 39, 84–90 burn reconstruction surgery, 158, 158f complications, 90


Index physiology of, 84 postburn alopecia and, 159 reconstructive surgery and, 47 growth, vessel size and, 39–40 heating, surgical effects of, 170 injury, determining, 147 regeneration pathways, 21 scar formation v., 15–16, 16f Tissue inhibitor metalloproteinase (TIMP-1) infantile hemangioma, 190 pressure sores and, 721–722, 722 Titanium, craniofacial plating systems and, 58 TMJ disease (Temporomandibular joint disease), 254 TNM classification (Tumor, node, metastases classification), 331 Toe-to-thumb transfers, 841–842, 841f, 843f Toe ulcers, 697 Toes, preservation of, 697–698 Tolerance, 54 Tongue head and neck embryology and, 184, 185–186, 185f oral cavity reconstruction and, 450 Tongue reconstruction, 446 Tonsillar pillars, tumors and, 445 Topical anesthesia, 92 Topical wound agents burns and, 135–137 eschar and, 136 TOS. See Thoracic outlet syndrome Total body surface area (TBSA) burn patient, 133 infection and, 141 fluid resuscitation and, 138 Total contact casting, wound healing and, 25 Total dose, effect of, local anesthetic agents, 92 Total left facial paralysis, 416f Total mastectomy, 621 Total maxillary defect (Type III maxillary defect), 437 eyelid reconstruction and, 438 type IIIA and, 437–438 type IIIB and, 438 Total maxillectomy, 441f Total parotidectomy, 340 Total penile reconstruction, 711 Tourniquets, wrist surgery and, 742 Toxic shock syndrome, lower truncal contouring and, 547 Toxicity, local anesthetics, 91, 93–94 TPF. See Traumatic palmar fascitis Tracheostomy, Treacher Collins syndrome and, 287 Tracheotomy, facial injuries and, 313 Traction alopecia, hair transplantation and, 568f Traction fixation, fractures and, 680 Traction sutures, face burn and, 143 TRAM flap (Transverse rectus abdominus musculocutaneous flap), 43. See also Expanded TRAM flaps; Perforator TRAM contraindications for, 647 contrast of techniques, 651, 653 future, 653–654 indications for, 639, 647 irradiated breast and, 165–166 latissimus dorsi flap breast reconstruction, 636 risk factors, 647t techniques, 647–651 tissue expansion and, 90 Trans-sutural distraction Transblepharoplasty, approach to glabellar muscles, 513f

Transcaphoid perilunate dislocation, 747f, 748, 748f Transconjunctival lower blepharoplasty, 492 Transcription factor Runx2/Cbfa1, embryology and, 187–188 Transcutaneous incisions (Intraoral incisions) chin augmentation and, 553 mandible distraction, 99 orbitozygomatic fractures, 320, 320f TransCyte, burn wound and, 148 Transdomal sutures, nasal tip projection alteration, 526, 526f Transfer of regional flaps, wound complications, 675 Transfer of single functional units, hand and, 737 Transferred muscles, re-education of, 853 Transforming growth factor-α, palate development and, 187 Transforming growth factor-beta1 , distraction osteogenesis, 97–98 Transforming growth factor-beta (TGF-ß) clotting cascade, 17 signaling, embryologic development and, 187 Transition zone, 97 Transmetacarpal replantation, 877, 878f, 879 Transmetatarsal amputation, 701 Transnasal medial canthoplasty, 322 Transosteotomy distraction, 96 Transplant biology history, 52 plastic surgery applications and, 52–57 Transplant immunology, 52–54 Transplantation. See also Donor site antigens, 52–53 current plastic surgery and, 54–57 future, 57 nomenclature, 52 Transport segment, 96 Transposition skin flap cheek reconstruction and, 375–376 planning, 10, 10f, 11f Transverse amputations, 892 Transverse rectus abdominis musculocutaneous flap. See TRAM flap Trapezial resection arthroplasty, with ligament reconstruction, 885, 885f Trapezium fracture, 787 Trapezius flap cheek reconstruction and, 378–379 soft-tissue reconstruction and, 665 Trapezius muscle, latissimus dorsi flap breast reconstruction, 634 Traumatic arthritis, 882 Traumatic palmar fascitis (TPF), 863, 863f Traumatic wounds, 316 Treacher Collins syndrome (Mandibulofacial dysostosis), 285–288, 286f Kaban-Mulliken classification, 288f pathogenesis of, 286–288 Tretinoin. See Retin-A Triangular fibrocartilage complex (TFCC), 779 acute traumatic tear, 759f, 760 arthrography, 750 lunotriquetral instability, 782 tears, MRI and, 759f, 760 Tricalcium phosphate-osteogenic composite, bone grafts substitutes and, 59 Trichloroacetic acid (TCA) peel, 457, 458–459, 460, 460f destruction depth of, 459f pretreatment, 459 Trichofolliculoma, 109 Tricholemmoma, 109 Trichophyton rubrum, onychomycosis, 822

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Trigeminal nerve, temporal region of scalp, 357, 357f Trigger finger. See Digital flexor tenosynovitis Triphasic Doppler, foot and ankle wound care, 691 Tripier flap canthal reconstruction, 402f lower eyelid reconstruction, 400, 401 Tripod-type reconstruction, hand and, 852 Trisulfide, lymphoscintigraphy and, 128 Trochanteric ulcers, 725–726 Trott method, bilateral cleft, 214 Truncal deformity, weight-loss patients, circumferential lipectomy and, 545, 546f Trunk, tissue expansion and, 86 Tubed radial forearm flap, 453, 453f Tuberous sclerosis, laser treatments for, 174 Tubiana, R., hand surgery and, 737, 738f Tubigrip, lower extremity burns and, 145 Tubular carcinoma, 619 Tuft fractures, 795 Tumescent technique, liposuction and, 94 Tumor, node, metastases classification. See TNM classification Tumor map, MMS and, 117, 118, 118f Tumor suppressor genes p16, head and neck cancer and, 338 Tumor(s). See also specific type tumors i.e. Parotid gland tumors of bone, MRI and, 763f, 764–765, 764f, 765f CT and, 756, 757f extirpation, nerve reconstruction after, 76 face and body, MMS and, 115–116, 116t mandible reconstruction, 434 margin assessment, MMS and, 117 MMS and, 116–117 MOHS technique, 115 MRI and, 756 resection, skull base defects and, 442 of sella turcica, endoscopic approach, 346f spill, 341 tonsillar pillars, 445 treatment of, MMS and, 116, 116t ulceration, 663 malignant melanoma and, 124 Turban tumor. See Cylindroma Turribrachycephaly, 230, 230f Twist transcription factor, Saethre-Chotzen craniosynostosis and, 188 Two-flap palatoplasty, 216 Two-Jaw surgery, 260, 264 Two-layer plication, mini-abdominoplasty, 541, 543 Two-stage nasolabial flap, nasal reconstruction, 389, 391f Type 1 maxillary defect. See Limited maxillary defect Type I deformities, facial burn reconstruction, 161 Type I muscles, segmental flaps and, 45 Type II deformities, facial burn reconstruction, 161 Type II maxillary defect. See Subtotal maxillary defect Type II muscles, segmental flaps and, 45 Type III mandibles, Treacher Collins syndrome and, 287 Type III maxillary defect. See Total maxillary defect Type III muscles, segmental flaps and, 45 Type IV maxillary defect. See Orbitomaxillary defects Type IV muscles, segmental flaps and, 45


928

Index

Typical mycobacterial infections, 823 Tzanck smear, Herpetic whitlow and, 818, 820f Ulceration. See also specific type ulcer i.e. Marjolin ulcer infantile hemangioma and, 192 metatarsal head, 698 midfoot defects, 701 pressure distribution, 721 ULCs. See Upper lateral cartilages Ulnar collateral ligament (UCL) injury, 798, 799, 799f tear treatment, 799, 799f Ulnar nerve, 830 compressions neuropathies, 830 fascicular topography, 76, 77f harvesting, 80 palsies, tendon transfers for, 848–850 wrist and, 741, 742f Ulnar nerve block, wrist and, 741, 742f Ulnar polydactyly, 859 Ulnar styloid, standard radiographs, 746f, 747 Ultrasonography, vascular malformations, 194 Ultrasound-assisted liposuction (UAL), 533, 536f, 537f Ultrasound (US) burn depth, 134 hand and wrist, 753 Ultraviolet light, basal cell carcinomas, 111–112, 112f Umbilical incision, 574, 574f Undercorrection, eyelid ptosis correction, 408 Undermined skin flap redraping of, subcutaneous facelift, 501 subcutaneous facelift, 501 Underresection of tissue gynecomastia, 618 vertical breast reduction, 612 Unilateral cleft lip repair, 220–221 nasal lining release, 209f operative technique, 207–210 primary tip rhinoplasty, 209f Unilateral complete cleft lip, 201, 201f correcting, 204–205 Unilateral coronal synostosis, 224, 229–230, 230f skull deformities, 229f Unilateral incomplete cleft lip, 200–201, 201f operative technique, 210 Unilateral mandibular distraction, 100 Unna boot burn injury and, 143 lower extremity burns and, 145 venous stasis ulcers, 32 Unna paste, 457, 458 Upper arm, replantation, 879 Upper auricular pole, position alteration, 298 Upper eyelid, 395 facial paralysis and, 418–419, 419f reconstruction, zone 1 defects, 397, 398f, 399 structural elements of, cross-section, 396f Upper eyelid paralysis, gold weight, 418, 418f Upper eyelid retractors, 484–485 Upper lateral cartilages (ULCs), septum and, separation of, 524 Upper lid blepharoplasty, 491 Asian, 491 Upper lid markings, blepharoplasty, 490, 490f Upper limb(s) amputations aesthetic considerations, 890 patient response to, 890 prostheses and, 890–897

arthritis, 882–897 compression, overview of, 828–829 infections of, 815–823 injury, categories of, 740 prostheses, 892–897 reconstruction algorithm for, 88 operative principles, 741–743 surgery physical examination in, 739–740 principles of, 739–743 Upper lip defects, 368–369 Upper orbit, preoperative evaluation of, 488–489 Upper-third auricle defects, 300, 301f Upper-third auricular defects, 300, 301f Urine output, fluid resuscitation and, 139 UV radiation, malignant melanoma and, 124 UVB rays, sunscreens and, 114 V-Y advancement flap bilateral, hands, 769, 770f closure, LeFort I osteotomy and, 263 technique applications for, 12, 13f cheek reconstruction and, 375, 375f wound reconstruction of foot and ankle, 696, 699f VAC device. See Vacuum-assisted wound closure device Vacuum-assisted wound closure device (VAC device), 27 burn injury and, 143 wound reconstruction, foot and ankle, 693 wound reconstruction of foot and ankle, 695–696 Vagina, acquired defects of, 709 Vaginal reconstruction, rectus abdominus flap and, 709–710 Valacyclovir herpes virus, TCA peel and, 459 laser abrasion, 464 Valium, spasm, 723 Van Nuys Prognostic Index, DCIS and, 621 Vancomycin-resistant Enterococcus (VRE), antimicrobials and, 30 Varicose veins, laser treatments for, 172, 173–174 Vascular anatomy foot and ankle, 687, 689f patterns of, 43, 43f Vascular anomalies, 189–198 nomenclature of, 189 nosology of, 189 Vascular Anomalies Centers, 198 Vascular channels, MRA and, 765, 766f Vascular compromise, lower truncal contouring and, 548 Vascular delay, axial-pattern flaps and, 43 Vascular endothelial growth factor (VEGF) distraction osteogenesis, 97–98 infantile hemangioma, 190 tissue expansion and, 84 Vascular injury, mangled extremity and, 679–680 Vascular insufficiency, nonhealing wounds and, 49, 50f Vascular lesion(s) laser treatments for, 171–174 lasers, 170–171 Vascular malformations categories of, 193 molecular genetics in, 193, 194t subcategories for, 193, 194t Vascular neoplasms, 189, 190t ISSVA and, 189, 190t Vascular repair technique, history of, 66

Vascular supply, foot and ankle wound care, 691 Vascular system, development, embryo and, 36–37 Vascular territories, three dimensional, 37f Vascularized bone, reconstructive surgery and, 47, 47f Vascularized graft, 52 Vasodilatory activity, local anesthetic agent and, 91 Vasospasm, papaverine for, microsurgery and, 70 Vector of distraction, 96 Vectors, mandible distraction and, 99, 99f VEGF. See Vascular endothelial growth factor Vein graft anastomoses, replantation in upper extremity and, 873–874 Vein grafts, 81–82 head and neck irradiation, 166 Velopharyngeal insufficiency (VPI) operative treatment of, 217–219 pharyngeal surgery for, 218–219 preoperative evaluation, 218 submucous cleft palate and, 202 Venolymphatic malformations, laser treatments for, 173 Venous anastomoses, replantation in upper extremity and, 873 Venous hum, mandible reconstruction, 433 Venous malformations (VMs), 193, 196–197 laser treatments for, 172, 173f Venous stasis ulcers, wound care of, 32 Venous system, development, 34, 35f Ventral hernia repair, 670–672 Vermilion, 367–368 advancement flap, 367f deficiency, unilateral cleft lip repair and, 220 lip defect and, 366 switch flaps, 367, 368f Verruca vulgaris, 106–107 laser treatments for, 174 Verrucous carcinoma, MMS and, 117 VersaJet water dissector, burn-wound excision, 142, 142f Vertical breast reduction breast meridian, 604 complications, 610, 612 medially based pedicle and, 604–612 operative technique, 605–607, 606f, 610 postoperative course, 608f, 609f, 610, 610f–611f summary, 612–613 Vertical deficiency of ramus, vertical vector, 99, 99f Vertical-incision mastopexy, 584–586, 586f Vertical limb, vertical-incision mastopexy and, 584–586, 586f Vertical mastopexy, 583, 584f Vertical mattress suture, 5, 5f Vertical maxillary excess, 259 Vertical pedicle technique, reduction mammoplasty, 592–593, 592f preoperative markings, 592, 592f–593f Vertical reduction mammaplasty, 602–613 procedure design, 602–604 Vertical resection pattern, skin resection patterns, 604–605, 605f Vertical scar augmentation mastopexy, 589, 590f Vertical skin resection pattern, vertical breast reduction, 604 Vertical vector, mandible distraction, 99 Vessel segment, microsurgery and, 68, 68f Vessels areas fixed to mobile, 39 origin, 40


Index size and tissue growth, 39–40, 41f tissue planes and, 39 Vicryl, skeleton of chest wall reconstruction, 665 Videofluoroscopy, hand and wrist motion, 750 Villonodular synovitis, 887 Vinca alkaloid, infantile hemangioma, 192 Vincristine, infantile hemangioma, 192 Vincula, 803f Vincular mesentery system, 803f Viral infection, of hand, 822–823 Virus, CO2 laser and, 176 VISI. See Volar intercalated segment instability Vision craniosynostosis and, 226 craniosynostosis syndromes and, 239–240 Visual acuity, 411f craniosynostosis and, 226 Vitallium, corrosion and, 58 Vitamin A connective tissue disorders, 703 skin and, 113 Vitamin C, topical, skin and, 113–114 Vitamin E, scars and, 114 Volar cross-finger flap, 772, 773f thumb amputation, 891f, 892 Volar intercalated segment instability (VISI) deformity, lunotriquetral instability, 782 Volar neurovascular advancement flap (Moberg flap), hands, 769–770 Volar V-Y advancement flaps, hands, 769, 770f von Langenbeck two-flap technique, primary cleft palate repair, 216 VPI. See Velopharyngeal insufficiency VRAM. See Rectus abdominus myocutaneous flap VRE. See Vancomycin-resistant Enterococcus Vulva, surface defects of, 708–709 W-plasty, scar and, 13, 14, 14f Wallerian degeneration, 73, 828 Wartenberg syndrome, 831 Warthin tumor, 341 Warts, 106–107 hands and, 822 Wassel classification, thumb duplication, 858f Watson knife, tangential excision, 142 Weber-Ferguson approach, plexiform neurofibromas of face, 294 Webster-Bernard operation, lower-lip defects and, 371, 371f Webster technique, otoplasty and, 298 Webster’s triangle, preservation, 528, 528f Wedge excision, 6, 7f, 301f Weight-loss, massive, circumferential lipectomy and, 545 Wetting solution, liposuction and, 534, 534t Whistle deformity, bilateral cleft lip, 221 Whitnall tubercle, eyelid and, 395 WHO. See World Health Organization Wood lamp examination, face burn, 143 Workhorse flap, anterior skull base defects and, 441f, 443 World Health Organization (WHO), malignant melanoma and, 125

World War II hand specialization and, 736–737 post-war era, hand surgery and, 737–738, 738f Worsening organ dysfunction, fluid resuscitation and, 139 Wound care, 23–32. See also Dressings; specific type wound i.e. Radiation wound adjuncts to, 25, 27–28, 30–32 advances in, 23, 24t agents, burns and, 135–137 foot and ankle, 690–696 diagnostic studies, 690–691, 693 fundamentals, 23–25 problem wounds, timing and, 30–32 products, pressure sores and, 727 of uncomplicated wounds, 30 Wound-edge eversion, scar and, 4 Wound reconstruction. See also Flap(s); Grafts foot and ankle biomechanics, 696 postsurgical care, 697 preparing for, 693–696 treatment options, 695–696 Wound remodeling. See Remodeling phase Wound(s). See also Delayed healing wounds; Skin wounds; Ulceration closure abdominal surgery and, 669 abdominal wall reconstruction, 668–670 hand surgery and, 743 mandible reconstruction, 433 radiation wounds and, 164 reconstructive ladder in, 14, 14f comorbidities and, 702–704 complications, 675 dehiscence eyelid ptosis correction, 408 head and neck irradiation, 166 extensions, hand surgery and, 742–743 facial burns and, 151 healing, 4 abnormal response to, 20–21 bacteria and, 25 future modalities in, 32 hypoxia and, 24 immobilization, 743 impairments in, conditions contributing to, 23, 25t inflammatory cascade of, 26f inflammatory phase, 16–19, 17f injury response and, 15 ischemia-reperfusion injury, 24–25 lower truncal contouring and, 547 normal, phases of, 16–20, 17f normal and abnormal, 15–22 pressure relief and, 723 proliferative phase of, 19–20, 19f reconstruction of absent vagina, 707 remodeling phase, 20, 20f semantics of, 16 vertical breast reduction, 612 vitamin C, 114 wound reconstruction to, foot and ankle, 694 infection, chemical peel, 461 measurement, foot and ankle wound care, 691 moist v. dry, healing of, 9 from nasal reconstruction, 387–388

929

negative pressure dressings, 675, 683 open burn reconstruction surgery, 150 tendon transfers and, 846 reconstruction, preparing for, foot and ankle, 693–696 scar therapy, 30 shape and position, abdominal surgery and, 670 Wraparound toe transfer, 842, 844 technique, 841f, 844 Wrinkle lines dermabrasion, 461 incisions and, 4 Wrinkles (Rhytides) laser treatments for, 175, 175f types of, 466 Wrist anatomy, 779 arthrodesis, 887 arthroscopy, lunotriquetral instability, 782 disarticulation, 896f extension, radial nerve palsies and, 847–848 fractures of, 779–787 ligamentous injuries of, 779–787 normal axial MRI of, 758f coronal MRI of, 758f sagittal MRI of, 759f radiographic imaging, 744–768 reconstruction, median nerve and, 741, 742f replantation, 879 synovitis, 887 views, standard radiographs, 747–749, 747f Xenogeneic transplantation, 53 Xenograft, 52 Xenon flashlamps, 171 Xeroderma pigmentosum, 110 basal cell carcinomas, 111 Y-shaped vein grafts, replantation in upper extremity and, 873, 874f Yellow dye laser, 169 Z-plasty, 12–14 burn reconstruction surgery and, 153, 154–155, 154f, 155f, 156 burns and, 151 geometric principle of, 12–13, 13t classic 60 degree angle, 13, 13f hypertrophic scarring and, 158, 159f lower eyelid reconstruction, 401 multiple, 157f phalangization, 838 planning and uses of, 13–14 rotation advancement flap, 377 short upper lip, 220 type I deformities, 161 vermilion deficiency, 220 Zyderm collagen implants, filler materials and, 471–472 Zygomatic arch fractures, 320–321 complications, 321 reduction of, 320, 320f Zygomatic complex, craniofacial microsomia and, 247 Zyplast collagen implants, filler materials and, 471, 472

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