Complications in Cardiothoracic Surgery: Avoidance and Treatment

Complications in Cardiothoracic Surgery AVOIDANCE AND TREATMENT Editor

Alex G. Little, MD The Elizabeth Berry Gray Chairman and Professor Department of Surgery Wright State University School of Medicine Dayton, Ohio

Complications in Cardiothoracic Surgery AVOIDANCE AND TREATMENT

Complications in Cardiothoracic Surgery AVOIDANCE AND TREATMENT Editor

Alex G. Little, MD The Elizabeth Berry Gray Chairman and Professor Department of Surgery Wright State University School of Medicine Dayton, Ohio

© 2004 by Futura, an imprint of Blackwell Publishing Blackwell Publishing, Inc./Futura Division, 3 West Main Street, Elmsford, New York 10523, USA Blackwell Publishing, Inc., 350 Main Street, Malden, Massachusetts 02148-5020, USA Blackwell Publishing Ltd, 9600 Garsington Road, Oxford OX4 2DQ, UK Blackwell Publishing Asia Pty Ltd, 550 Swanston Street, Carlton, Victoria 3053, Australia All rights reserved. No part of this publication may be reproduced in any form or by any electronic or mechanical means, including information storage and retrieval systems, without permission in writing from the publisher, except by a reviewer who may quote brief passages in a review. 04 05 06 07 5 4 3 2 1 ISBN: 0-87993-427-1 Complications in cardiothoracic surgery : avoidance and treatment / editor, Alex G. Little. — 1st ed. p. ; cm. Includes bibliographical references and index. ISBN 0-87993-427-1 1. Heart—Surgery—Complications. 2. Chest—Surgery—Complications. [DNLM : 1. Thoracic Surgical Procedures—adverse effects. 2. Intraoperative Complications—prevention & control. 3. Postoperative Complications—prevention & control. WF 980 C73683 2004] I. Little, —Alex G. RD597.C645 2004 617.4′1201— dc22 2003024723 A catalogue record for this title is available from the British Library Acquisitions: Steven Korn Production: Julie Elliott Typesetter: Graphicraft Limited, Hong Kong, in 9.5/12pt Palatino Printed and bound by MPG Books Ltd, Bodmin, Cornwall, UK For further information on Blackwell Publishing, visit our website: www.blackwellfutura.com The publisher’s policy is to use permanent paper from mills that operate a sustainable forestry policy, and which has been manufactured from pulp processed using acid-free and elementary chlorine-free practices. Furthermore, the publisher ensures that the text paper and cover board used have met acceptable environmental accreditation standards. Notice: The indications and dosages of all drugs in this book have been recommended in the medical literature and conform to the practices of the general community. The medications described do not necessarily have specific approval by the Food and Drug Administration for use in the diseases and dosages for which they are recommended. The package insert for each drug should be consulted for use and dosage as approved by the FDA. Because standards for usage change, it is advisable to keep abreast of revised recommendations, particularly those concerning new drugs.

Contents

List of contributors, vii Introduction, ix Acknowledgments, x Part I General complications 1 Complications of thoracic incisions, 3

Norman J. Snow, MD, Malek G. Massad, MD, and Alexander S. Geha, MD, MS 2 Respiratory complications of thoracic operations, 36

Hani Shennib, MD 3 Arrhythmias following cardiothoracic operations, 48

Adam E. Saltman, MD, PhD and Joseph LoCicero III, MD Part II Complications of general thoracic surgery 4 Complications of pulmonary resection, 67

Stephen J. Burke, MD and L. Penfield Faber, MD 5 Complications of tracheobronchial resection, 92

Douglas J. Mathisen, MD 6 Complications of lung volume reduction procedures, 108

Robert J. Burnett, MD and Douglas E. Wood, MD 7 Complications of lung transplantation, 128

Paul F. Waters, MD, FRCS(C), FACS 8 Pleural space problems, 135

Sudish Murthy, MD, PhD and Thomas W. Rice, MD 9 Complications of chest wall reconstruction, 155

M. Bulent Tirnaksiz, MD and Claude Deschamps, MD 10 Complications of esophageal resection, 161

Richard J. Battafarano, MD, PhD and Nasser K. Altorki, MD 11 Complications of esophageal reconstruction, 173

Alex G. Little, MD v

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Contents

12 Complications of antireflux surgery, 183

Riivo Ilves, MD, FRCS(C), FACS and Mark R. Dylewski, MD 13 Complications of esophageal instrumentation, 202

Donald E. Low, MD 14 Complications of mediastinal surgery, 230

Thomas A. D’Amico, MD Part III Cardiac surgery 15 Complications of coronary artery bypass surgery, 257

Nader Moazami, MD and Hendrick Barner, MD 16 Complications of cardiopulmonary bypass and cardioplegia, 280

Lawrence L. Creswell, MD 17 Complications of aortic surgery, 349

Thoralf M. Sundt, III, MD and Whitney M. Burrows, MD 18 Complications of valvular surgery, 362

Jeffrey T. Sugimoto, MD, Anthony D. Bruno, MD, and Karen A. Gersch, MD 19 Postpericardiotomy syndrome, 385

William A. Gay, Jr., MD 20 Pulmonary and pleural complications after cardiac surgery, 390

Jeffrey E. Everett, MD 21 Neurological complications in cardiac surgery, 405

George J. Koullias, MD, PhD and John A. Elefteriades, MD Index, 437

List of contributors

Nasser K. Altorki, MD Attending Cardiothoracic Surgeon, Professor of Cardiothoracic Surgery, Department of Cardiothoracic Surgery, New York-Presbyterian Hospital-Cornell Medical Center, New York, NY Hendrick Barner, MD Professor of Surgery, Department of Surgery, Division of Cardiothoracic Surgery, Washington University School of Medicine, St. Louis, MO

Mark R. Dylewski, MD Division of Cardiovascular Surgery, West Florida Hospital, Pensacola, FL

John A. Elefteriades, MD Professor of Surgery (Cardiothoracic), Yale University School of Medicine; Chief of Cardiothoracic Surgery, Yale-New Haven Hospital, New Haven, CT Jeffrey E. Everett, MD

Richard J. Battafarano, MD, PhD Assistant Professor of Surgery, Division of Cardiothoracic Surgery, Department of Surgery, Washington University School of Medicine, St. Louis, MO

Anthony D. Bruno, MD Chief Resident in General Surgery, Creighton University Medical Center, Omaha, NE

Stephen J. Burke, MD Fellow, Division of Cardiothoracic Surgery, Rush-Presbyterian-St. Luke’s Medical Center, Chicago, IL

Robert J. Burnett, MD Chief Resident, Division of Cardiothoracic Surgery, University of Washington, Seattle, WA

Whitney M. Burrows, MD Assistant Professor of Surgery, Division of Thoracic Surgery, University of Maryland, Baltimore, MD

Assistant Professor, Department of Surgery, Division of Cardiothoracic Surgery, University of Iowa Health Care, Iowa City, IA

L. Penfield Faber, MD Director of Thoracic Surgery, Department of Cardiovascular-Thoracic Surgery, RushPresbyterian-St. Luke’s Medical Center; Professor of Surgery, Rush Medical College Chicago, IL

William A. Gay, Jr., MD Professor of Surgery, Department of Surgery, Division of Cardiothoracic Surgery, Washington University School of Medicine, St. Louis, MO Alexander S. Geha, MD, MS Professor and Chief, Division of Cardiothoracic Surgery, The University of Illinois College of Medicine at Chicago, Chicago, IL Karen A. Gersch, MD Chief Resident in General Surgery, Creighton University Medical Center, Omaha, NE

Lawrence L. Creswell, MD Associate Professor of Surgery, Division of Cardiothoracic Surgery, University of Mississippi Medical Center, Jackson, MS

Thomas A. D’Amico, MD Associate Professor of Surgery, Department of Surgery, Division of Cardiovascular and Thoracic Surgery, Duke University Medical Center, Durham, NC

Riivo Ilves, MD, FRCS(C), FACS Director of General Thoracic Surgery, Albany Medical Center Hospital; Professor of Surgery, Albany Medical Center, Albany, NY

George J. Koullias, MD, PhD Resident in Cardiothoracic Surgery, Yale-New Haven Hospital, Yale University School of Medicine, New Haven, CT

Claude Deschamps, MD

Alex G. Little, MD

Professor of Surgery, Division of General Thoracic Surgery, Mayo Clinic and Mayo Foundation, Rochester, MN

The Elizabeth Berry Gray Chairman and Professor, Department of Surgery, Wright State University School of Medicine, Dayton, OH

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viii List of Contributors

Joseph LoCicero III, MD Professor and Chair, Department of Surgery, University of South Alabama College of Medicine, Mobile, AL

Hani Shennib, MD Professor, Department of Surgery, McGill University, Montreal, Quebec, Canada

Head, Section of General Thoracic Surgery, Virginia Mason Medical Center; Clinical Instructor, Department of Surgery, University of Washington School of Medicine, Seattle, WA

Norman J. Snow, MD Professor of Surgery, Division of Cardiothoracic Surgery, Section Chief, General Thoracic Surgery, The University of Illinois College of Medicine at Chicago; Chief, Thoracic Surgery, West Side Veterans Administration Hospital, Chicago, IL

Malek G. Massad, MD

Jeffrey T. Sugimoto, MD

Associate Professor of Surgery, Division of Cardiothoracic Surgery, Director, Heart and Lung Transplant Programs, The University of Illinois College of Medicine at Chicago, Chicago, IL

Professor of Surgery, Vice-Chairman Department of Surgery, Chief, Cardiothoracic Surgery, Creighton University Medical Center, Omaha, NE

Douglas J. Mathisen, MD Chief of Thoracic Surgery, Massachusetts General Hospital; Hermes Grillo Professor of Thoracic Surgery, Harvard Medical School, Boston, MA

Thoralf M. Sundt, III, MD

Donald E. Low, MD

Senior Associate Consultant, Division of Cardiovascular Surgery, Mayo Clinic; Associate Professor of Surgery, Mayo Medical School, Rochester, MN

Nader Moazami, MD Assistant Professor of Surgery, Department of Surgery, Division of Cardiothoracic Surgery, Washington University School of Medicine, St. Louis, MO

M. Bulent Tirnaksiz, MD Fellow in General Thoracic Surgery, Division of General Thoracic Surgery, Mayo Clinic and Mayo Foundation, Rochester, MN

Sudish Murthy, MD, PhD

Paul F. Waters, MD, FRCS(C), FACS

Department of Thoracic and Cardiovascular Surgery, The Cleveland Clinic Foundation, Cleveland, OH

Professor of Surgery, Mount Sinai School of Medicine, New York, NY

Thomas W. Rice, MD Head, Section of Thoracic and Cardiovascular Surgery, The Cleveland Clinic Foundation, Cleveland, OH

Adam E. Saltman, MD, PhD Associate Professor of Surgery and Physiology, Department of Cardiothoracic Surgery, University of Massachusetts Memorial Medical Center, Worcester, MA

Douglas E. Wood, MD Professor and Chief, Section of General Thoracic Surgery, Endowed Chair, Lung Cancer Research, University of Washington, Seattle, WA

Introduction

Cardiothoracic surgery, including operative techniques and postoperative care, can and should be read about in the several available textbooks by both residents in training and active practitioners. This activity provides the fund of knowledge which is the foundation of surgical competence. However, it is the practical experience gained in the operating room and on the wards dealing with complications and deviations from the typical or average scenario that matures and fully develops a surgeon. The typical textbook demonstrates the ‘right’ or standard way to do things and the implicit assumption is that if these guidelines are followed then the patient and the surgeon’s life will be complication free. This is not the case and reminds me of the observation that good results come from experience and experience is gained by making mistakes. The goal of this book is to minimize the frequency of surgical complications and maximize the outcome when they do occur by allowing the reader to learn from the operative and clinical experience of those who have gone before so that each generation can collectively stand on the shoulders of the preceding generation without the need to learn from one’s own complications. This book is therefore designed less to address indications for operations than how to carry them out and provide postoperative care without complications. While the authors of the various chapters address the correct or right way to perform operations and care for patients after surgery, they have also been tasked to address and emphasize specific do’s and don’t s for both intra operative techniques and postoperative care that will reduce the incidence of complications. As some complications, alas, are inevitable, also addressed are the issues of timely recognition and appropriate treatment of complications when they do occur despite best efforts. In sum, I hope the reader will see and use this book as a supplement to, not a replacement for, standard text books and operative atlases and that it will contribute to an ongoing commitment to excellence in cardiothoracic surgery.

ix

Acknowledgments

The editor is grateful to the authors of the various chapters who have sacrificed professional and personal time to produce their thoughtful and well-written chapters. Two people deserve my special thanks. The first is Steven Korn, an incredibly patient, supportive and wise Publisher without whose encouragement and friendship this book would not have occurred. Secondly, special thanks go to Lorraine Rinaldi my Administrative Assistant for many years. Her energy, zeal and commitment to excellence in this project have been invaluable and always appreciated.

x

PA RT I

General complications

CHAPTER 1

Complications of thoracic incisions Norman J Snow, Malek G Massad, Alexander S Geha

Introduction The history of thoracic incisions dates to the Hippocratic era when trephination of empyema cavities was first reported. Subsequent reports primarily documented the use of incisional drainage of chest infections since intrapleural surgery was inevitably associated with respiratory failure due to open pneumothorax. Evolution of thoracic incisions evolved gradually until our avoidance of intrapleural surgery was overcome by recognition of the safety of endotracheal intubation, positive pressure ventilation and the ability to operate safely within the pleural cavity. The choice of which incision to use is guided by such considerations as the surface landmarks, a knowledge of intrathoracic anatomy and the relationships between the two. Incisions performed anteriorly are rarely useful for operations on dorsal organs such as the bronchus, the esophagus or the aorta. Conversely anteriorly placed incisions are often appropriate for operations on the anterior pulmonary hilum, the pericardium and the heart. The guiding principle regarding the choice of a thoracic incision should be the provision of adequate exposure necessary to accomplish the operation safely balanced by the approach which least disrupts the thoracic anatomy and least impairs thoracic function. Cosmetic considerations are important in certain situations. Widely accepted surgical principles such as the use of Langer’s lines of tension for placement of incisions, gentle handling of tissues, pinpoint hemostasis when employing electrocautery and precise anatomic closure are encouraged.

Sternotomy incisions Median sternotomy The road to the heart is only two or three centimeters in a direct line, but it has taken surgery nearly 2400 years to travel it [Hehrlein] [1]. The median vertical sternal approach was first suggested by Milton in 1897 [2]. At the time when cardiac operations were performed through a transverse bilateral thoracotomy, Shumaker reported use of the vertical sternotomy incision for pulmonary valvulotomy [3,4], and Blalock used it for the same lesion in some of his initial cases [5]. In 1956 Julian and coworkers from our 3

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institution described their initial experience for intracardiac procedures requiring hypothermia and inflow occlusion. A year later, they described its use in four patients with intracardiac lesions that required extracorporeal circulation and advocated its use for these purposes [5–7]. Julian et al. stressed the importance of firm closure and the use of non-absorbable sutures [5]. The advantages of the median sternotomy incision far outweigh its disadvantages. It provides access to all the cardiac chambers and the major vessels in the event of an emergency or traumatic injury. It is less painful than the bilateral transverse thoracotomy incision, and by maintaining the integrity of the pleural spaces and lungs, it compromises pulmonary function less, particularly in the immediate postoperative period [8]. The median sternotomy incision has been advocated for lower cervical procedures including tracheal resection and reconstruction, and for exposure of mediastinal structures for resection of mediastinal pathology and for exposure of the heart and great vessels [9]. The incision also provides access to both pleural cavities and both lungs without the complications associated with the transverse trans-sternal bilateral thoracotomy exposure [10]. Thal extended its utilization to include bilateral pulmonary resections such as for pulmonary metastatectomy [11]. Most importantly, the median sternotomy incision has greatly facilitated the performance of cardiovascular procedures requiring cardiopulmonary bypass including heart and heart–lung transplantation. More recently, the median sternotomy approach allowed off-pump beating heart coronary artery bypass operations (MIDCAB) to be performed with ease [12]. All patients undergoing a median sternotomy should be shaved or clipped on the morning of the operation and the operative field scrubbed and painted with povidone-iodine. We utilize what we called the ‘universal scrub and drape’ from neck to toes on all patients undergoing open heart surgery. We continue to use a routine 10-min scrub rather than the Hibiscrub paint and we apply disposable Iodophor-impregnated adhesive drapes to all exposed skin surfaces. All patients receive routine antibiotic prophylaxis consisting of a single intravenous preoperative dose just before the skin incision and two or three postoperative doses to cover the patient during the initial 24-h period after the operation. We use a second generation cephalosporin for our coronary operations and a combination of vancomycin and an aminoglycoside for patients undergoing valve operations. The operative technique of the vertical midline sternotomy and the methods of closure play a significant role in the process of healing of the sternotomy incision. For routine first time exposure, the midline skin incision extends from just below the suprasternal notch down to the end of the xyphoid. While dissecting the subcutaneous tissue with the electrocautery, it is important to provide exposure by applying traction on both sides of the incision in order to avoid a paramedian dissection. For a right-handed surgeon, this is best achieved by placing the left thumb and index fingers on both sides of the incision and applying equal traction on either side. In the majority of patients, midline dissection leads to the anterior presternal fascia which is quite vascular.

Complications of thoracic incisions 5

Exposure of one of the edges of the pectoralis major muscle on either side alerts the surgeon that the incision is deviating from the midline. In some patients, the pectoral muscles are well developed and enlarged so that the midline incision will inadvertently cut through them. As the anterior presternal fascia is exposed, the sternochondral junctions on both sides of the sternum are palpated with the left thumb and index fingers. Once the midline of the sternum is outlined, the submanubrial and subxyphoid spaces are developed using blunt dissection with the fingertip. The incision is carried upward a short distance under the skin into the deep cervical fascia and the interclavicular ligament formed by fibers of the superior sternoclavicular ligament from each side is transected. Venous plexuses near the suprasternal notch are identified and clipped or ligated. A constantly present venous plexus overlying the sternoxyphoid junction is identified and cauterized. The sternotomy incision is then performed, using the oscillating Stryker saw for cutting the sternum. The cordless battery-driven saw is practical and easy to handle without the fear of cross contamination during connection and handling. Once the sternum is divided, bleeding from the sternal edges is controlled. Pinpoint hemostasis of the anterior presternal fascia is achieved with the electrocautery under vision whereas the edges of the posterior sternal fascia on both sides are cauterized throughout the length of the sternum to assure control of all the bleeding sites. Bleeding from the bone marrow is controlled with bone-wax, although we have found that rubbing the sternal marrow on both sides with Gel-foam provides good control of bleeding without the added risk of infection or other complications [13]. The thymus and pericardium are divided with the electrocautery and the venous branches at the inferior border of the innominate vein are clipped or ligated. It is important to preserve the viability of the presternal soft tissues to maintain maximum tissue viability between the skin and the sternum. Discriminatory use of the electrocautery also plays an important role in minimizing the amount of burned tissue and decreasing the rate of infections. Nishida and colleagues utilized the technique of pinpoint hemostasis on presternal soft tissues on over 3000 patients who underwent a median sternotomy and achieved a sternotomy wound infection rate as low as 0.16% [14]. For spreading of the sternal edges and exposure of the anterior mediastinal structures, it is advisable to use a sternal retractor with blades designed to distribute evenly the traction along the cut sternal edges rather than using the regular rib spreader [11]. The retractor should not be placed too high along the sternum to avoid injury to the innominate vein or the brachial plexus [11]. When procedures require exposure of the posterior plate of one or both sternal edges such as during internal mammary artery harvest, the sternal edges should not be forcefully retracted upwards in order to avoid sternal and rib fractures or dislocations. At the conclusion of the operation, the sternal edges are checked again for any bleeding source. In patients undergoing coronary bypass operations with the internal mammary artery, the mammary artery bed is checked and any active bleeding is controlled. The sternum is re-approximated with six to eight

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Chapter 1

Figure 1.1 An interlocking wire suture technique for sternal closure is illustrated which provides lateral sternal reinforcement, and uses a figure-of-eight suture technique which reduces perpendicular wire shear. (Reprinted by permission: Ann Thorac Surg 1989; 47: 927–929. Courtesy of Elsevier Science, Inc.)

stainless steel wires that are passed immediately adjacent to the sternal borders in order to avoid injury to the internal mammary vessels. When the sternum is soft or osteoporotic, it is advisable to wrap the entire sternum with eight stainless steel wires to distribute the load throughout the sternum and to assure a sturdy approximation of the two sternal segments. We apply two to three wires as wide as possible through the manubrium and then encircle the sternum by applying an additional four to five wires through the intercostal spaces at the level of the sternochondral junction. We avoid placing sutures through the sternomanubrial joint or through the costal cartilage or ribs to minimize the chance of inflammation and pain during ambulation. Another useful method of closure of the sternal edges is using three or four interlocking figure-of-eight (butterfly) wire sutures also wrapped around the sternum and passed through the intercostal spaces as described by DiMarco et al. (Figure 1.1) [15]. The wires are twisted by hand, tightened and buried in the soft tissue, avoiding any over-riding of the sternal edges. We avoid the use of nonabsorbable multifilament sutures such as heavy Mersilene for closure of the sternum as they do not provide any particular advantage to the stainless steel wires. Following re-approximation of the sternal edges, the edges of the linea alba at the inferior border of the incision and the anterior presternal fascia are re-approximated with a continuous heavy absorbable suture such as an 0-Dexon or 0-Maxon. The overlying soft tissue is also re-approximated to obliterate any potential space, particularly over the lower part of the incision near the xyphoid process. In obese women, we have found it useful to add another layer of closure by applying deep subcuticular sutures in order to decrease the amount of tension on the skin suture line which is typically closed with subcuticular sutures or skin staples. Lamm et al. recommend use of additional retention sutures in this group of patients where the sutures are placed parallel on both sides of the skin incision so that they capture the complete

Complications of thoracic incisions 7 Table 1.1 Guidelines for the surgical management of median sternotomy complications. Median sternotomy complication

Recommended treatment

Skin disruption, intact anterior presternal fascia Intact skin, sternal separation, no infection Skin disruption, sternal separation, no infection Sternal dehiscence, mediastinitis Chronic osteomyelitis of sternum

Drainage, debridement, wound care Sternal rewiring, Robicsek technique Sternal rewiring, continuous irrigation Sternal debridement, muscle flap coverage Partial/ complete resection and local coverage

suprasternal tissue including fascia, subcutaneous fat, and skin [16]. This will place the tension on the retention sutures that are then removed 1–2 weeks after the operation. All dressings are kept for 24 h after the operation and the patients are allowed to shower by the third or fourth postoperative day. In obese women or in women with large breasts, we recommend that they wear a supportive brassiere or corset immediately after the operation in order to minimize lateral tension on the incision generated by pendulous breasts and to keep the lower part of the incision covered for the initial few days after the operation. Physical therapy is initiated during the early postoperative period, commencing with a range of motion exercises of both upper extremities. The patients are instructed to avoid any extraneous activity or active exercises involving the upper extremities or shoulders, and to avoid lifting heavy objects for at least 6–8 weeks from the time of their operation. Delayed healing of part or all of the sternum has been observed a year or more after the operation manifesting as an audible or palpable click on physical examination. Sternal wound complications occur infrequently with an estimated incidence of 1–5% depending on the series [7,17,18]. When they do occur, they are associated with a substantial morbidity and mortality. Minor complications include skin separation and superficial soft tissue seroma or infection without bone involvement. These usually respond to conservative treatment such as oral or intravenous antibiotics, local drainage and debridement and frequent wound care (Table 1.1). Once the infection clears and healthy granulation tissue starts forming, the wound may be closed secondarily. Major complications include sternal dehiscence, acute mediastinitis and sternal osteomyelitis. They usually require more extensive management including systemic antibiotics, wound and sternal debridement and tissue coverage of the wound. These can have grave consequences and are associated with a mortality of 5–27% depending on the series reported [7,17,18]. In a large series of patients undergoing open heart procedures through median sternotomy, Breyer and associates compared the incidence of minor and major sternal complications in patients whose sternum was closed with wire and those whose sternum was closed with heavy Dacron sutures and found no difference. A theoretical concern is that eradication of a deep infection would be more difficult in presence of the multifilament braided sutures. However, this was not shown to be true

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in their series. Major complications occurred in 0.8% of the patients whose sternum was closed with wire and in 0.9% of those whose sternum was closed with Dacron [17]. Many predisposing factors for sternal complications have been implicated. These can be classified into preoperative factors, intraoperative factors, and postoperative factors [14,19]. Although it is difficult to control preoperative factors such as diabetes, obesity, chronic obstructive lung disease, previous chest radiation, immunosuppressed state, renal failure or other comorbid conditions, the surgeon can have direct impact on the intraoperative factors such as strict aseptic technique, precise midline osteotomy, selection of good closure material, optimal hemostasis, prophylactic antibiotics, meticulous atraumatic surgical technique and avoidance of prolonged operative time [14,20]. Finally, certain factors or complications may arise in the postoperative period and may lead to sternal instability or disruption such as external cardiac compression, mediastinal bleeding requiring re-exploration and prolonged mechanical ventilatory support. Sternal dehiscence is associated with one or more of the following: an unusual amount of incisional pain, skin incision separation, serous or cloudy drainage through the separated sternal edges, a clicking sound upon movement of the upper trunk or upper extremities, and an otherwise unexplained fever or leukocytosis. Physical examination often demonstrates a clicking sound that is elicited by exerting pressure on one of the two sternal edges or less frequently palpable separation of the sternal edges [7]. Early postoperative sternal instability may lead to skin separation, ingress of bacteria, and subsequent wound infection [21]. In extreme cases, paradoxical movement of the chest on deep inspiration may be visible to the examining physician. The almost uniformly painful unstable sternum has a cardiac tamponade and flail chest effect on the cardiac and respiratory functions [22]. These acutely ill patients can be retrieved from a progressive downhill course characterized by low cardiac output, atelectasis, and progressive respiratory failure [22]. Based on the physical examination alone, it is sometimes difficult to determine the extent of tissue and sternal involvement and radiographic examination is helpful. An upright chest radiograph in the posteroanterior and lateral projections or sternal views may show evidence of sternal overriding, separation or fracture. A broken or loosened wire may also suggest a sternal problem. Identification of a vertically oriented midsternal lucency on plain radiograph may be the first clue to the diagnosis of sternal separation [23]. However, as many as 30% of patients may develop such a midsternal stripe following median sternotomy without having sternal separation, and therefore its visualization does not necessarily indicate impending sternal dehiscence but rather warrants a careful clinical evaluation of the operative site [24]. Computed axial tomography (CAT scan) of the chest may also show sternal separation, a non-drained substernal fluid collection, or bone resorption suggestive of osteomyelitis. A white blood cell tagged nuclear scan may also demonstrate increased uptake in the sternum suggestive of osteomyelitis.

Complications of thoracic incisions 9

Figure 1.2 Conventional Robicsek sternal weave. (Reprinted by permission: J Thorac Cardiovasc Surg 1977; 73: 267–268. Courtesy of Mosby, Inc.)

The diagnosis of sternal wound infection is often supported by bacteriologic assays with Gram stain and cultures. Staphylococcus aureus and S. epidermidis are the two principal offending microorganisms. Gram-negative organisms and enteric flora have been also cultured from sternal wounds, particularly Pseudomonas aeruginosa, Klebsiella, Serratia marcescens and enterobacter. More recently, we have been encountering resistant organisms such as methicillinresistant S. aureus (MRSA) and vancomycin-resistant enterococcus (VRE). Systemic antibiotics are started empirically until the offending organism(s) are identified and the proper bacterial antibiotic sensitivity results become available. It has been our observation and that of others [7] that in almost every instance of sternal separation, the wires cut through a sternal edge. Once the sternal dehiscence is complicated by wound infection, important therapeutic principles include: mandatory wide drainage, debridement and coverage of the sternal wound, adequate ventilatory support and prolonged systemic antibiotic coverage. When dehiscence of the sternal closure is detected early, the sternum is still viable and the infection has not deepened into the mediastinum, an attempt may be made at rewiring the sternum utilizing the Robicsek weaving technique (Figure 1.2) [25]. The chest incision is then closed after thorough irrigation with antibiotic or a diluted povidone iodine containing solution [26]. Continuous irrigation of the mediastinal space with an antibiotic solution through an irrigation suction system for a period of 3–5 days has been advocated with satisfactory results [8,27–29]. However, when this conservative approach fails or when radical debridement makes primary

10

Chapter 1 Table 1.2 Available tissue transfer for coverage of anterior mediastinum following sternal debridement. Left and/or right pectoralis major muscle or myocutaneous flap Left and/or right rectus abdominis muscle or myocutaneous flap Left or right latissimus dorsi muscle or myocutaneous flap Free muscle transfer (rectus abdominis, latissimus) Omentum Skin and soft tissue of anterior chest wall

closure of the wound impossible, then muscle flap coverage is indicated [30]. In most instances, the actual sternal involvement is more severe than what is anticipated clinically. Signs of cartilage or bone resorption secondary to osteochondritis or acute osteomyelitis mandate removal of much, if not all of the sternum. We have found it useful to co-ordinate the operative care with the plastic surgeons beforehand in order to plan single-stage coverage [30–33]. Several options are available for the surgical team for adequate coverage of the anterior mediastinal structures following sternal debridement or resection. These include pedicled and free myocutaneous flaps and omentum and are listed in Table 1.2 [6,30,33–35]. Chronic osteomyelitis of the sternum is a very serious complication, particularly in patients with prosthetic valves. A prolonged course (4–6 weeks) of intravenous antibiotics may bring the infection under control. However, it is sometimes advisable to proceed with total or subtotal resection of the infected sternum or sternal segment with excision of the cartilage of the adjacent ribs. Utilization of a muscle flap might be necessary to secure coverage of the exposed mediastinal structures. A chronic draining sinus or sinuses from a healed sternum have been observed several months following median sternotomy, some of which may be attributed to an underlying foreign body such as an adjacent wire or suture. This may be associated with surrounding cellulitis and tissue inflammation. Treatment entails obtaining cultures from the draining site and administration of oral or intravenous antibiotics. Frequently, this condition requires local debridement of the sternal segment along with removal of the foreign body followed by local coverage. A rare complication is the occasional patient who presents weeks to months after the operation with a partial separation of the sternum and a healed skin incision (Figure 1.3a). In these instances, Robicsek et al. recommend a modification of the sternal weaving closure technique in which the separated part of the sternum, often being the lower end, is exposed. An osteotomy is made on one side of the sternum to realign the sternal segments and two weaving wires are passed along each of the two sternal borders in the area of sternal separation. This allows easy approximation of the two halves, that are then united by three or four transverse wire sutures buttressed by this peristernal weave (Figure 1.3b). Detaching the sternal edges from the pectoralis major muscles on either side and re-approximating them over the sternum will

Complications of thoracic incisions 11

Figure 1.3 (a,b) Modified sternum weave applied in partial sternal separation. (a) Before repair. (b) After repair. (Reprinted by permission: J Thorac Cardiovasc Surg 1998; 116: 361–362. Courtesy of Mosby, Inc.)

provide adequate soft tissue coverage of the re-wired sternum for proper healing [36]. Incisional hernias develop in about 4% of patients undergoing operations through median sternotomy [37]. These are usually located in the linea alba near the lower border of the xyphoid process. The main predisposing factors are wound infections, use of absorbable suture material, obesity and pulmonary complications. In one series, 35% of these hernias became symptomatic and required a later repair [37]. Median sternotomy complications also occur in children following open heart surgery. The same principles of management apply with some modifications. In reconstructing sternotomy wounds in female patients, wide mobilization of the pectoralis major muscles is relatively contraindicated to prevent damage to the undeveloped breast buds [38]. Closure of the wound with limited mobilization only of the sternal edge of the adjacent pectoral cutaneous tissue or a rectus abdominus muscle or myocutaneous flap may be more appropriate.

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Chapter 1

Redo sternotomy The redo sternotomy or re-sternotomy incision is utilized for cardiac pathology that requires reoperative intervention. The need for this approach has increased over the past two decades since an increasing number of patients are undergoing a second (or third, fourth) coronary revascularization procedure. Reoperations are also utilized in patients with prosthetic valve complications, and in patients who have previously undergone a commissurotomy or valve repair and who return for valve replacement. The use of the re-sternotomy incision has also increased among infants and children who undergo corrective operations for congenital heart defects after they have been managed initially with palliative procedures. The re-sternotomy incision is also utilized to provide access to the in-patients with previous heart or heart–lung transplants who require re-transplantation. The re-sternotomy incision may also be utilized for debulking of previously resected retrosternal or mediastinal tumors. The approach also provides access to both pleural spaces and both lungs and may be utilized for resection of recurrent benign and malignant pulmonary disease. At our center, about 15% of adult cardiac surgical procedures and 25% of congenital cardiac procedures are performed through a previous sternotomy incision. When a re-sternotomy is contemplated, attention should be given to a proper history and physical examination. It is important to obtain the previous operative report which provides a ‘road map’ for the surgeon. If the previous sternotomy was for a coronary bypass or a valve operation, it is important to know whether the internal mammary artery or arteries were used. A plane chest radiogram in the posteroanterior and lateral positions will identify the proximity of the heart to the sternum. It may also identify the course of the internal mammary artery through previously applied clips at the divided mammary branches. It will also provide information about the number of sternal wires and the technique of sternal closure; whether the previous sternotomy incision was paramedian and required weaving wire(s) for closure or whether figure-of-eight butterfly sutures have been placed. In the operating room, it is advisable that percutaneous defibrillating pads be placed in the event the patient develops ventricular tachycardia or fibrillation and becomes unstable before dissecting the heart away from the surrounding pericardium and mediastinal structures. It is also advisable to have a guide wire placed in the common femoral artery prior to the sternotomy in order to access the femoral vessels for cannulation for cardiopulmonary bypass or for intra-aortic balloon pump placement if needed. The chest is entered through the previous sternotomy scar. Prior to initiating the sternotomy, minimizing ventilation with high tidal volumes and positive-end expiratory pressures serves to avoid displacement of the heart towards the operative incision [38]. In most redo operations, the sternum is divided with the use of an oscillating cast cutter or occasionally a Lebsche knife. Garrett and Mathews have described the technique of retaining the sternotomy wires after untwisting to provide upward traction on the sternum and to limit the

Complications of thoracic incisions 13

depth of penetration of the oscillating saw [39]. We have found this technique helpful, particularly in second and third-time redo operations or in the elderly patient with osteoporosis or a brittle sternum. The suprasternal area is dissected with the electrocautery to expose the manubrium over its most superior portion. Dissection commences over the lower part of the incision to re-expose the linea alba and xyphoid. With upward and lateral traction on the costal arch and xyphoid, the retrosternal space is freed to a safe distance that will allow division of the lower end of the sternum with the oscillating saw. The anterior periosteal plate and spongiosa of the sternum are then divided with the oscillating saw starting from the lower sternal edge upwards. Once this is done, the posterior periosteum of the sternum is divided in a similar fashion starting at the lower end of the sternum. After the retrosternal space is entered, upward traction is applied on either side of the sternal edges and with gentle downward countertraction with a sponge or forceps, the mediastinal tissues are dissected away from the sternum. The dissection is continued laterally on both sides of the sternal edges until about an inch or more of the costal margin is exposed. It is helpful to enter one or both pleural spaces, as that frees the mediastinal structures and facilitates the dissection. The sternal spreader is then placed. The heart and major vessels are then exposed in a systematic fashion starting at the diaphragm, the right atrium and aorta. It is advisable to delay total mobilization of the left side of the heart until cardiopulmonary bypass is instituted and occasionally until the heart is arrested to minimize bleeding and tearing of the epicardial surfaces. The main complications relating to the redo sternotomy include major cardiac lacerations and injury to the native coronary vessels or to the previously implanted coronary bypass grafts, intraoperative hemorrhage during bypass with subsequent development of bleeding diathesis, and multiple sternal fractures with postoperative sternal instability. It is therefore important to inspect all the dissected surfaces for hemostasis prior to heparinization and again after reversal of heparin and before closure of the sternal incision. When the sternum is brittle or has one or more fractures or is off center we apply figureof-eight wire sutures around the fracture or around the area where the incision is off center [8]. When the sternum is too thin and osteoporotic or when the sternotomy cut was paramedian rather than in the midline, vertical wires are woven in and out laterally alongside the sternal borders as described by Robicsek [25]. The encircling wires are then applied around the Robicsek wires to decrease the amount of tension on the sternum and to minimize the chance that the encircling wires cut through the thinned out sternum (Figure 1.2).

Bilateral submammary vertical sternotomy incision One disadvantage of the median sternotomy incision is the clearly visible vertical scar in the skin since the incision is at right angles to Langer’s lines [8]. Moreover, and for unknown reasons, the sternal region is known for a high incidence of hypertrophied and keloid scars [8]. The bilateral submammary skin incision in women and young females provides a nice alternative. With

14

Chapter 1

the patient supine, an anterior incision is made along the inferior skin creases of both breasts and joined transversely. The skin and subcutaneous tissue flaps are raised to expose the sternum which is divided vertically. The main limitation of this exposure is the need for retraction of the subcutaneous tissues of the anterior chest wall and both breasts in addition to the sternal spreader. The incision may also require suction drains to be placed in the subcutaneous spaces to avoid hematomas. This incision provides an aesthetic scar that is not as apparent as the vertical scar and can be obscured by a brassiere or a swim suit top.

Partial sternotomy In 1949, Holman and Willete reported on the use of the partial or incomplete vertical sternotomy with transection of the sternum at the second intercostal space for pericardiectomy [5,40]. The same approach was also applied for removal of lesions of the anterior mediastinum, such as substernal thyroid adenoma, and for exposure of the trachea and upper thoracic esophagus [41,42]. The partial sternotomy incision may be modified to provide exposure of the anterior superior mediastinum, aorta and arch (partial upper sternotomy or manubrial split) or to provide exposure of the heart through a partial lower sternotomy. To achieve this latter exposure, the lower sternum is split vertically up to the second intercostal space with bilateral transection of the sternum at the top of the incision [43,44]. A variety of operations may be performed through this approach, including coronary bypass operations, resection of left ventricular aneurysms, valve operations, closure of atrial and ventricular septal defects, resection of atrial myxomas and combined cardiac operations [44,45]. A standard sternal retractor is inserted to spread the lower sternal edges. With the lower sternotomy, exposure of the aorta and the most superior part of the operative field may be enhanced by lifting the intact upper sternomanubrial segment with a Rultrac retractor (Rultrac, Inc., Mentor, OH, USA) or a Favaloro Type retractor [44]. Sternal closure is usually done with standard peristernal wires. An additional set of two vertical wires are applied to approximate the upper and lower sternal segments. Alternatively, a figureof-eight wire is placed around the transversely transected sternal segment for the same purpose. Walterbusch recommends transecting the manubrium along an inverted V-shaped line (Figure 1.4) [45]. This provides the advantage of cannulating the aorta near the pericardial fold superiorly, and prevents horizontal dislocation of the sternal coaptation. The main advantage of the partial sternotomy is less postoperative pain compared with full sternotomy or anterolateral thoracotomy, particularly with the lower sternotomy when the manubrium and both clavicular heads as well as the attachments of the first and second ribs remain intact. Other potential advantages include decreased blood loss compared with complete sternotomy and a shorter skin incision with a better aesthetic appearance of the scar. These advantages make the partial sternotomy a worthwhile alternative to complete sternotomy [43]. The main disadvantages of the partial sternotomy are the need to sacrifice one or both internal mammary arteries,

Complications of thoracic incisions 15

(b)

(a)

(c) Figure 1.4 (a) In partial sternotomy, only the corpus is divided longitudinally. Transection of the manubrium follows an inverted V-shaped line. The xyphoid is simply cut off with bone scissors. (b,c) The sternum is closed by twisting paired sternal wires together. (Reprinted by permission: J Thorac Cardiovasc Surg 1998; 115: 256–257. Courtesy of Mosby, Inc.)

possible injury to one or more intercostal neurovascular bundles, inadequate exposure of the aortic arch with the lower sternotomy, and the need to rewire three separated segments of the sternum in contrast to only two segments with the full sternotomy.

Median sternotomy–bilateral subcostal (chevron) incision A useful incision is the combined vertical sternotomy and bilateral subcostal (chevron) incision. The incision provides excellent exposure for patients undergoing combined thoracic and abdominal operations such as resection of hypernephroma with extension into the inferior vena cava and right atrium. The incision is also utilized in patients undergoing combined heart–liver or heart–lung–liver transplants. We have also used this incision for a combined triple vessel coronary artery bypass and orthotopic liver transplant in a patient with Child C liver cirrhosis who was found to have multivessel coronary artery disease on pretransplant workup [46,47]. Subsequently, with increasing experience with off-pump coronary artery bypass, we have staged the two operations in cirrhotic patients requiring coronary artery bypass whereby we

16

Chapter 1

perform the coronary bypass on a beating heart and follow that by the liver transplant at a separate setting. The bilateral subcostal incision is made about one and a half inches below the costal margin. The incision is extended to the left side either halfway to the midclavicular line for exposure of the liver and upper midline abdominal structures or all the way to the anterior axillary line for exposure of the entire upper abdomen. The incision is then extended as a midline vertical sternotomy to expose the anterior mediastinum and heart. Retraction is achieved by applying a standard sternal spreader and an upper arm or Book–Walter retractor to expose the abdominal organs. Wound closure entails standard closure of the median sternotomy along with closure of the bilateral subcostal portion and re-approximation of the abdominal musculature. The retrosternal space is drained through two chest tubes exteriorized through the upper abdominal wall. It is important to re-approximate the linea alba in the midline with heavy non-absorbable sutures and follow that with another layer to re-approximate the anterior presternal fascia and soft tissue. The skin closure is completed with surgical clips or inverted mattress nylon sutures. It is advisable to keep the skin clips or sutures for 3–4 weeks to avoid skin separation and wound dehiscence, particularly in the immunosuppressed transplant patient.

Thoracotomy incisions Posterolateral thoracotomy The posterolateral thoracotomy is the standard approach to a variety of intrathoracic operations such as pulmonary resection, esophageal surgery, aortic reconstruction and posterior mediastinal surgery. It offers wide exposure but requires division of large groups of chest wall muscles, including the latissimus dorsi, occasionally the serratus anterior, trapezius, and rhomboids. Prevention of complications begins with proper positioning of the patient on the operating table. Padding all exposed surfaces is mandatory. This includes lateral malleolus, elbow, hip and knee. Neurological injury due to pressure-induced ischemia or necrosis is wholly preventable. We prefer padded cloth bolsters rather than the ‘bean bag’ because of concerns regarding the prolonged exposure of vulnerable prominences to the rigid surface of this device. There are no definitive data favoring one method over the other and it remains an issue of personal preference. Care must be taken to avoid hyperextension of the arm at the shoulder joint. Brachial plexus stretch injuries are often disabling and can be avoided if proper positioning is utilized. An ‘airplane device’ or cloth blankets are both suitable to support the ipsilateral arm if attention is given to arm position and protection of exposed surfaces. Foam padding placed under the dependent arm and contiguous to body surface areas at risk is useful and effective. An axillary roll is placed under the thorax both to protect against brachial plexus injury and to elevate the thorax off the table to permit adequate respiratory excursion of the dependent lung. This may be important with single lung ventilation. Postoperative examination is

Complications of thoracic incisions 17

routine to assess for cutaneous or neurological injuries, both to intervene early and to satisfy quality assurance concerns. The technique of the incision may have consequences postoperatively. Meticulous hemostasis is most important, especially in this incision which divides large muscle masses. Use of the electrocautery is common and one should avoid the production of excess ‘char’ and necrotic tissue so as to minimize the possibility of subsequent wound infection. Blood vessels may retract into the muscle and later bleed, so patient and methodical cautery use is best. Entry into the pleural space may be accomplished using a variety of techniques including via the intercostal space or through the bed of a rib which is either resected or stripped of its periosteum. Simple incision of the intercostal muscle has been utilized, as has reflection of the periosteum and entry over the top of the rib. The lower margin of the rib is never used in order to avoid injury to the neurovascular bundle (Figure 1.5). Troublesome bleeding from intercostal

Figure 1.5 Options for entering the pleural space: (a) dividing the intercostal muscle from the superior edge of the ribs with cautery; (b) reflecting the periosteum from the superior rib edge and entering through the periosteal bed; (c) subperiosteal rib resection; (d) intercostal approach with short segment posterior rib resection. (Reprinted with permission: Heitmiller RF. Thoracic incisions. In: Baue AE, Geha AS, Hammond GL et al., eds. Glenn’s Thoracic and Cardiovascular Surgery. Stamford, CT: Appleton & Lange, Inc., 1996; 73–89. With permission of The McGraw-Hill Companies.)

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Chapter 1

vessel injury and neurogenic pain (intercostal neuralgia) from intercostal nerve injury may thus be prevented. Intercostal artery bleeding is not an uncommon source of hemorrhage requiring reoperation after thoracotomy [48]. The bleeding may not be readily apparent due to impaired visibility, so placement of a sponge inside the pleural cavity under the incision to assess for hemorrhage is useful. Rib resection is seldom utilized unless fibrosis and adhesions limit entry into the chest or the rib is needed for a bone graft [49]. During reoperative thoracotomy, rib removal offers increased exposure for safe dissection of pleural adhesions and adherent lung. There is some evidence to suggest that intercostal space entry results in less pain due to intercostal neuralgia than rib resection [50]. Excessive retraction of the ribs during thoracotomy predisposes to tearing and bleeding at the costo-vertebral angle. Division of the posterior rib with excision of a 1 cm length will allow the rib to ‘hinge’ and avoid traction at the angle which probably causes the bleeding. This is not associated with measurable morbidity and may actually reduce postoperative pain associated with a rib fracture and painful respiratory motion at the fracture site. The posterolateral thoracotomy has been associated with considerable postoperative pain and some disability. Division of the shoulder girdle musculature results in at least transient muscle dysfunction. Significant neurological pathology has been seen after posterolateral thoracotomy in children resulting in shoulder asymmetry and electromyographic evidence of injury to nerves of the serratus and latissimus dorsi muscles. The deficits were seen more frequently in children operated upon within the first year of life. The higher the incision, the more frequent was the incidence of sequelae. Fortunately, most were not functionally significant but there is the potential for abnormal joint wear. The authors concluded that the incisions should be as low as possible to avoid denervating significant muscle mass and operations should be performed after the first year of life if possible [51]. Another report examining the sequelae of thoracotomy in children documented a surprising incidence of breast and pectoral maldevelopment after anterolateral thoracotomy [52]. Placing the incision in the seventh intercostal space anteriorly, below the level generally thought that breast migration might occur in adulthood, should avoid this complication, as will elevating the pectoralis muscle from the chest wall rather than incising and therefore denervating it. Closure of the posterolateral thoracotomy, and indeed all thoracic incisions, should be as meticulous and as attentive to detail as the opening. Restoration of chest wall integrity and strength minimizes postoperative disability and pain. We prefer large no. 2 absorbable pericostal sutures. These are placed carefully around the ribs so as to avoid the neurovascular bundle, since encirclement of the bundle will aggravate intercostal neuralgia. We have not drilled the sutures through the ribs. If there is a rib fracture, two choices are available: either excision of a short segment of rib to eliminate painful motion, or placement of pericostal sutures on either side of the fracture in a figure-of-eight fashion to tightly ‘splint’ and immobilize it. An anatomic layered closure is

Complications of thoracic incisions 19

preferred, both to strengthen the incision and to insulate against leakage of fluid or air into the chest wall. We prefer subcuticular closure of the skin and normally utilize a running technique. Monofilament absorbable sutures seem to incite less erythema and local cutaneous reaction than the braided suture which we previously employed. Daily inspection of the incision permits early recognition of a wound infection and early intervention may limit the extent of this complication. Full-thickness infections and dehiscence of a thoracotomy are very rare, even when the thoracotomy is performed for drainage of infections or resection of infected tissue.

Muscle-sparing thoracotomy The anatomic magnitude of the standard posterolateral thoracotomy as well as early observations that sparing the large shoulder girdle muscles results in less pain and perioperative morbidity has encouraged the development of various muscle-sparing incisions to gain access to the thorax [53–55]. Computed tomography (CT) has documented muscle atrophy directly related to posterolateral as opposed to anterolateral thoracotomy [56]. The various musclesparing incisions differ in their location on the surface of the chest and as to which muscles are actually spared rather than divided. Anterior incisions may divide or reflect the pectoralis major muscle while anterolateral thoracotomy requires reflection of the latissimus dorsi posteriorly and division of the serratus in the direction of its fibers (Figure 1.6). The incision in the serratus is always placed anterior to the long thoracic nerve. The muscle may then be elevated and thus the surgeon preserves the innervation to the muscle, preventing ‘winging’ of the scapula, a very debilitating complication. Alternatively, the serratus may be reflected from the anterior rib attachments. Most musclesparing incisions require development of subcutaneous flaps which permit the mobility necessary for retraction of the muscle to provide adequate exposure. Often two rib retractors are used, with placement in opposite planes. This effectively separates the ribs in one plane and the muscles in the other. A posterior or auscultatory triangle incision necessitates reflection of the latissimus dorsi forward and the serratus anterior upward (Figure 1.7). The dissection of these flaps may lead to seroma formation [57]. Tacking the underlying fascial closure to the latissimus dorsi muscle may minimize seroma formation. Most seromas require little or no therapy and resolve spontaneously. Occasionally, aspiration of the seroma is indicated for treatment and for reassurance that they are not the source of infection. Some authors have recommended routine placement of suction drains in the subcutaneous space to prevent seroma formation [58]. We have not routinely employed these drains, since the clinical sequelae of the occasional seroma are limited and in most cases no specific treatment is necessary. Another variant is the vertical axillary thoracotomy [59]. This incision may be very small or may be extended to allow excellent visualization for pulmonary resection procedures. It requires elevation and dorsal retraction of the latissimus dorsi. The serratus is again split in the direction of its fibers. The

20

Chapter 1

(a)

(b)

Figure 1.6 (a) Dissection and mobilization of the latissimus dorsi muscle so it can be retracted rather than divided. (b) The serratus anterior has been divided in the direction of its fibers to expose the intercostal space. (Reprinted by permission: J Thorac Cardiovasc Surg 1990; 99: 592. Courtesy of Mosby, Inc.)

long thoracic nerve may be vulnerable to injury and a thorough knowledge of its anatomy is necessary. The nerve is closest to the anterior border of the scapula at the level of the higher intercostal spaces. Therefore placement of certain thoracic incisions must be carefully planned in order to avoid nerve injury and subsequent winging of the scapula (Figure 1.8). If the serratus is to be divided, it is mandatory to do so as low as possible. Division below the scapular tip assures sufficient innervated and functional muscle mass to prevent the loss of scapular support. Winging of the scapula occurs when there is a loss of serratus muscle tension which pulls the scapula downward and the counterbalancing muscles dominate. This results in outward and upward scapular rotation. Positioning the arm posteriorly moves the scapula dorsally, thus further exposing the long thoracic nerve to operative trauma. Salazar et al. have studied the long thoracic nerve in cadavers and proposed guidelines to minimize the potential for its injury [60]. Scapular winging, shoulder pain and inability to raise or rotate the shoulder forward result in significant morbidity, patient distress and prolonged disability [61]. Prevention is paramount.

Complications of thoracic incisions 21

(a)

(b) Figure 1.7 (a) The latissimus dorsi and serratus anterior are mobilized to expose the intercostal spaces. (b) Generous exposure is provided through the auscultatory triangle by mobilization and retraction of the major muscles. (Reprinted by permission: Ann Thorac Surg 1989; 47: 782–783. Courtesy of Elsevier Sciences, Inc.)

Despite the hope that sparing of large muscles on the chest wall would diminish perioperative morbidity, limit hospital stay and improve postoperative pulmonary function [54,62–64], such results have been difficult to document. Lemmer et al. [65] found differences in early postoperative spirometric measurements favoring the muscle-sparing group but no differences in length of stay, pain control, complications, or seroma formation. Ponn et al. [66] in an uncontrolled study reported no differences in complications, length of stay, atelectasis or dysrhythmias but found differences in certain spirometric values

22

Chapter 1

Figure 1.8 Proximity of the long thoracic nerve to the scapular border is demonstrated. Incisions should avoid the nerve, including video-assisted thoracic surgery (VATS) and axillary thoracotomy incisions. (Reprinted by permission; J Thorac Cardiovasc Surg 1998; 116: 961. Courtesy Mosby, Inc.)

and seroma formation. Hazelrigg et al. [58] prospectively randomized patients to muscle sparing or posterolateral thoracotomy and concluded that although there was less narcotic requirement and pain in the muscle-sparing group, there were no significant differences in pulmonary function, shoulder range of motion, morbidity or mortality or length of stay. Seroma formation in the muscle-sparing group was 23%, but was of little clinical significance. They noted early postoperative shoulder strength advantage for the muscle-sparing group but at 30 days the groups were similar. Visual analog scale pain assessment and narcotic requirements consistently favored the muscle-sparing patients. Long-term studies have shown little difference in postoperative pain leading to the conclusion that factors other than muscle transsection must be responsible for much of the postoperative pain. Factors such as excessive rib distraction, intercostal nerve injury both by the retractor and the pericostal sutures, inadequate early pain control, and trauma to other muscle groups may be important factors [67,68]. Efforts to minimize intercostal nerve trauma, avoidance of excessive rib distraction, attention to patient positioning, careful placement of pericostal sutures to avoid neurovascular bundle entrapment and thoughtful postoperative analgesic regimens may help control if not

Complications of thoracic incisions 23

eliminate some of these common operative sequelae. Landreneau and colleagues [69] have concluded that the principal advantage of muscle-sparing incisions is the preservation of the large muscle groups that may be used as rotational flaps for patients requiring tissue transfers to augment suture lines and to fill infected spaces. We currently employ muscle-sparing incisions as often as possible. Only rarely does concern for the adequacy of exposure cause us to convert from an anterolateral or auscultatory triangle musclesparing incision to a conventional incision with muscle division. All types of pulmonary resections, decortications, mediastinal procedures and simple biopsies are routinely accomplished with muscle-sparing techniques.

Thoracoabdominal incision The left thoracoabdominal incision has been utilized for many years when exposure of the lower thorax and upper abdomen is required. The incision is performed by extending the intercostal incision, usually in the 7th or 8th interspace, across the costal arch into the abdomen. The diaphragm is incised radially to avoid damage to the phrenic nerve and resultant diaphragmatic dysfunction. The most frequent clinical scenario involves resection of the middle or lower esophagus and the proximal stomach. The advantages of this incision include excellent exposure, the ability to operate upon varying lengths of stomach or esophagus, and the fact that it affords a single position and incision [70]. The major problem associated with this approach is the propensity for infection at the level of costal arch transection. The infection presents with erythema, fluctuance and often a purulent draining sinus at the site. There may be systemic signs of infection including fever, leukocytosis and malaise. The cartilage derives its principal blood supply from the perichondrium, and surgical disruption may render the cartilage segment ischemic and subject to infection, after which it behaves as a foreign body. The cartilage should be divided sharply, since overuse of the electrocautery will cause necrosis of the cartilage and further predispose it to infection. Superficial infections can be locally drained and treated with conventional techniques such as wet to dry saline dressing changes. However, deeper infections and those with an infected sequestrum of cartilage must be surgically drained and the cartilage excised. There is controversy regarding whether the entire costal arch must be excised if the infection involves the 6th through 10th cartilages because of the common tissue involved [71,72]. In our experience, sequential debridement of individual sinus tracts is usually unsuccessful in eradicating the infection within the costal arch. Wide total or subtotal excision of the arch with primary closure (with or without muscle flap coverage) is preferred. Suction drainage is usually employed after debridement. Prevention of this vexing problem may be possible by employing several strategies, including appropriate use of perioperative prophylactic antibiotics (short course, intravenously administered beginning within 1 h of the incision). A precise anatomic closure should include secure restoration of the costal arch with absorbable suture which virtually eliminates the suture as a nidus for chronic infection. Excision of a

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Chapter 1

short segment of the transected cartilage eliminates malunion and painful motion at the site as well as an ischemic sequestrum. A secure closure utilizing the diaphragmatic sutures to close the abdominal and chest wall muscles helps to prevent herniation of abdominal viscera through a weakened area by drawing the diaphragm up to the undersurface of the costal arch [70].

Bilateral thoracosternotomy: the clamshell incision Early cardiac surgery was frequently performed through the thoracosternotomy or clamshell incision. Subsequent conversion to the median sternotomy relegated this incision to the archives, but new indications have surfaced. Bilateral sequential lung transplantation is performed with this approach, as is the resection of anterior malignancies, especially those with significant lateral extension requiring intrapleural dissection [73]. The procedure begins with proper positioning. Since there is considerable distraction of the ribs bilaterally, the arms should be carefully padded and placed either at the patient’s side or abducted on arm boards, care being taken to avoid traction on the brachial plexus. Intercostal incisions are made in the 4th or 5th interspace. The incision must follow the interspace and must not be made transversely in order to avoid oblique division of ribs and cartilages. In men, a submammary incision suffices, with transverse division of the sternum at the selected interspace level. The skin incision is placed in the inframammary crease for women (Figure 1.9). Secure ligation of the mammary vessels will prevent postoperative bleeding. Closure is accomplished by using traditional sternal wires to close the sternum. Alternatives include K-wires and various plating devices. Thoracotomy closure is completed as per the surgeon’s preference. The incision is more uncomfortable than median sternotomy and it should not be utilized if sternotomy provides adequate exposure. Epidural analgesia is helpful for postoperative pain control.

Figure 1.9 Proper placement of the skin incision for the ‘clamshell’ approach. Note that the intercostal incisions follow the interspace and are not made transversely. (Reprinted by permission: Ann Thorac Surg 1994; 58: 31. Courtesy of Elsevier Science, Inc.)

Complications of thoracic incisions 25

Figure 1.10 Excellent exposure via a right hemiclamshell incision for a superior mediastinal tumor. (Reprinted by permission: Ann Thorac Surg 1994; 58: 31. Courtesy of Elsevier Science, Inc.)

Complications specific to this approach include mammary vessel hemorrhage, and sternal overriding. The former is preventable by careful operative technique, and the latter has occurred rarely, but can be painful and cosmetically unappealing. Secure wiring of the sternal bone should be all that is needed to avoid this complication, but some authors have favored placing K-wires into the sternum to eliminate the possibility [74]. The ‘hemi-clamshell’ (trap door) incision is utilized to expose the cervicothoracic junction and the anterior mediastinum. The incision includes an anterior thoracotomy (usually in the 4th or 5th intercostal space) and a partial median sternotomy from the selected interspace to the jugular notch. Cervical extension is performed if needed and division of the first rib from within can also improve cervical exposure. Clinical indications have included chest trauma, tumors of the anterior cervicothoracic junction, and tumors involving the upper mediastinum and one lung [75] (Figure 1.10). Careful attention to the internal mammary vessels should prevent hemorrhagic complications. Despite the nature of the incision, few complications have been reported. Sternal stability has been regularly observed following proper wire reapproximation. Musculoskeletal and somatic complaints seem no more prevalent than with conventional thoracotomy [75].

Mediastinoscopy and mediastinotomy Surgical exploration of the mediastinum is an invaluable clinical tool in the diagnosis and staging of thoracic malignancies. Early reports described unilateral cervicothoracic exploration. Carlens [76] is credited with the initial description of the midline mediastinoscopy in 1959. The current technique is similar to the original descriptions with few modifications. Since the superior mediastinum is a space within which are many vital and easily injured structures,

26

Chapter 1

adequate training and experience, as well as surgical patience are necessary to avoid catastrophic complications. Mediastinoscopy is begun with a transverse incision just above the sternal notch. It proceeds in the avascular midline plane to the pretracheal space which is developed by blunt dissection. Injuries to the trachea, pulmonary artery, azygous vein, bronchus, left recurrent laryngeal nerve and even the aorta have been described. The overall complication rate is about 3%, with less than a 1% mortality rate. Serious complications with lasting sequelae are 0.5% or less. Thorough knowledge of the anatomy, suction dissection of the lymph nodes so they appear in relief and consistent and aspiration prior to biopsy (to assess for bleeding potential) should prevent catastrophic complications. Although most problems are not caused by the incision per se, but by the operative adventure within, their occurrence is to be acknowledged and avoided. The two most common incisional complications are wound infection and tumor seeding. Fortunately, both are quite rare. Wound infection occurs in approximately 0.1–0.15% of cases [77,78]. Mediastinal extension of the infection has been reported only sporadically. Our preference has been to close the platysma with an absorbable 3–0 suture and to perform a running subcuticular skin closure. Most isolated mediastinoscopy procedures are today performed on an out-patient basis. When erythema and swelling occur, we advise warm compresses and oral antibiotics. Rarely does the incision require open drainage but this can be safely accomplished with no significant side-effects. Tumor implantation in the mediastinoscopy incision is exceedingly unusual. An early analysis showed an incidence of 0.12% in over 6400 cases [79]. Neither cell type nor stage of disease seem to influence occurrence of tumor implantation. Both chemotherapy and radiation have been used to treat this complication, but the numbers are too small to assess efficacy [80]. Both direct implantation secondary to tumor extraction and hematogenous deposition in the wound have been implicated. In at least one case the mediastinoscopy was actually negative although the patient had tumor in the subcarinal fatty tissue. Due to the paucity of information it is not possible to state how to avoid this complication. The report of parasternal mediastinotomy by McNeill and Chamberlain [81] in 1966 was the first of many to demonstrate the utility of this incision to provide access to the superior mediastinum. The procedure is performed through the second or third intercostal space, depending on the site of the target lesion. Generally the costal cartilage is removed and mediastinal entry occurs via the bed of the cartilage, which we prefer to excise since it leaves patients with little, if any morbidity or disability. Reassurance is offered that the small bulge with forced exhalation or Valsalva maneuver is of no consequence. Extrapleural or intrapleural examination, either directly or with a mediastinoscope, results in high diagnostic yields. If the lung is not biopsied or injured, chest tubes are not required. Catheter aspiration of air, with a Valsalva maneuver supplied by the anesthesiologist, evacuates the ambient air. Closure

Complications of thoracic incisions 27

is with absorbable suture to the pectoralis muscle, subcutaneous tissue and skin. Most Chamberlain operations are performed as out-patient procedures. Admission is advised if there are complications, pneumothorax, or slow anesthetic recovery [82]. As with mediastinoscopy, complications after mediastinotomy are uncommon. Superficial wound infection has been reported in as high as 2.4% of cases. Local measures almost always suffice, particularly if there is no retained cartilage sequestrum. Other complications are hemorrhage, pneumothorax, and recurrent laryngeal nerve injury, but these are independent of the incision itself. There is essentially no mortality reported for this procedure. A postoperative upright chest X-ray should be performed to assess for pneumothorax and bleeding after both mediastinoscopy and mediastinotomy.

Thoracoscopy or video-assisted thoracic surgery incisions Video-assisted thoracic surgery (VATS) allows operative exposure via a small camera and monitor linkage so that only small incisions are required. Multiple ports are placed so that operating instruments can be introduced into the pleural cavity. The ostensible advantages include shorter length of stay, faster recovery and return to work, less systemic inflammatory response, and less pain and disability when compared with standard thoracotomy access. VATS does not depend upon an airtight seal as does laparoscopy. In fact, pneumothorax is necessary if the lung is to fall away from the chest wall to provide adequate exposure. The camera is usually inserted first, after which working ports may be placed under direct vision for safety. These rigid instruments often fulcrum on the rib and periosteum and as such may be the source of considerable postoperative pain, presumably because of their injury to the periosteum. Some studies have suggested that there is little difference between postthoracotomy pain and pain following VATS [83,84]. One could speculate that smaller instrumentation might be less traumatic to insert and manipulate. Wound infections do occur in VATS incisions [85,86], as does port site implantation of metastasis [87]. Extraction within an endobag should virtually eliminate the port site recurrence. All nodules with malignant potential should be removed within the bag. Overall the complication rate is 4–5% following VATS. Most are minor in nature [86]. An unexpectedly high rate of dehiscences, hernias and wound infection has been associated with the anterior thoracotomy used for ‘minimally invasive’ coronary artery bypass grafting [88–90]. Wound ischemia due to internal mammary artery harvesting has been implicated as a cause. It may be that median sternotomy is preferable to minithoracotomy, whether the operation is conducted with or without the heart lung machine. We have occasionally noted subcutaneous emphysema after VATS. As these small incisions are sometimes difficult to close with precision, we have opted for a heavy 0-Vicryl closure of the chest wall muscles, usually placing them in a figure-of-eight fashion. Air-tight closure and adequate pleural drainage should prevent troublesome subcutaneous air in the majority of patients.

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Figure 1.11 Subcutaneous air is seen within an intercostal hernia in a patient taking steroids who had undergone an anterior thoracotomy for lung biopsy. (Reprinted by permission: Chest 1995; 107: 878. Courtesy American College of Chest Physicians.)

Miscellaneous complications Lung hernia Herniation of the lung through the intercostal space is an uncommon cause of post-thoracotomy pain. It is produced by chest wall trauma, either societal or surgical. Loss of chest wall integrity may be due to the primary injury or dehiscence of a thoracotomy. Interestingly, traumatic hernias rarely present early, perhaps due to muscle spasm and splinting of the area which mask the hernia bulge. The hernias are often located anteriorly, since there is less chest wall musculature in this location and because the interspaces are wider. It may be difficult to distinguish pain secondary to lung hernia from intercostal neuralgia. The parietal pleura is innervated by the intercostal nerves and there is overlap between the two syndromes [91]. Pain is located over a soft, spongy swelling on the chest wall which is maximally appreciated during forced exhalation. Quiet breathing may mask the hernia and physical examination and radiography should be performed with a Valsalva maneuver (Figure 1.11). Plane radiography, especially tangentially across the swelling, or CT will demonstrate the hernia, although physical examination is sufficient for clinical decision making [92]. Prevention is preferable to repair. Careful closure and avoidance of wound infection should diminish the incidence. Small (< 5 cm) defects which are asymptomatic or minimally so, may be managed safely nonoperatively. Enlargement, persistent symptoms and large size are clinically problematic and repair is usually indicated. Wound closure can be effected using local tissues such as rib struts, periosteal flaps, fascia or muscle. If this is not possible, prostheses such as Gore-Tex or Marlex mesh may be implanted to obdurate the defect.

Complications of thoracic incisions 29

Neurological sequelae of thoracotomy When neurological complications are seen after surgery on the thoracic aorta, spinal cord ischemia is thought to be the cause. However, non-aortic surgery involving a posteriorly placed thoracotomy can also result in paraplegia [93], meningitis [94] and subarachnoid-pleural fistula with pneumocephalus [95]. The principal causal factor is excessive traction with resultant bleeding at the costo-vertebral junction. Attempts at control lead to disruptive dissection, use of cautery and packing. There have been reported instances of migration and swelling of topical oxidized cellulose resulting in a mass effect within the spinal canal. Cautery-induced trauma, ligation of intercostal arteries and epidural hematoma formation have also been implicated in the development of postthoracotomy paraplegia. The incidence of paraplegia after thoracotomy at the University of Maryland was 0.08% over a 40-year period [93]. Recognition of postoperative neurological damage must be made quickly to minimize permanent sequelae. Routine neurological assessment in the recovery room or ICU is mandatory. Since most thoracotomy patients are now extubated ‘early’ if not in the operating room, opportunity exists for rapid diagnosis. Once the physical examination confirms injury, urgent magnetic resonance imaging or CT scan is indicated, followed by timely consultation with the spine service. If indicated, operative intervention is immediately carried out. Despite all best efforts, complete neurological reversal is seldom achieved. The hazards of operating in the costo-vertebral recess must be appreciated if such misadventures are to be avoided. Excessive retraction and bleeding can be avoided in most instances by dividing the posterior rib and allowing it to hinge rather than tear at the costo-vertebral angle. Should bleeding occur despite careful operative technique, then minimal topical hemostatic cellulose should be applied and intercostal ligation should be avoided if at all possible.

Thoracic infection and antibiotics The incidence of wound infection in thoracotomy incisions is low. A Mayo Clinic series [96] noted an infection rate of 1.6%. Factors influencing the incidence of thoracotomy infection include the length of surgery, immune status of the patient and the size of the infecting inoculum. Presence of prosthetic material and any devitalized tissue adversely affects the clinical course. Optimization of the patients’ nutrition and immune status as well as limiting the surgical and perioperative factors are the goal of the surgeon. Several early observations encouraged the routine use of prophylactic antibiotics and claimed that such a practice was responsible for the low infection rate [97,98]. More recent studies have shown that the routine use of properly administered systemic antibiotics prior to thoracotomy reduces the wound infection rate [99,100]. The timing of the antibiotic administration is important, since delay after inoculation decreases the efficacy. We begin the intravenous antibiotic infusion in the operating room so we are assured that the drug has circulated within 1 h of the thoracic incision. Some authors differentiate between wound infection (well controlled with antibiotics) and other thoracic infections such

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as empyema or pneumonia. It may be that the two require different considerations, such as preoperative cultures or vigilance that infections elsewhere on the patient are properly addressed. If there is endobronchial obstruction with distal pneumonitis, we obtain preoperative sputum cultures and plan the perioperative antibiotic regimen accordingly [101]. Short courses of antibiotics (one to four doses) are as effective as prolonged use [102] and may obviate some of the sequelae such as Clostridium difficile colitis and antibiotic resistance. Our current protocol includes the preoperative treatment of any documented infections (bronchitis, post obstructive pneumonia, skin infections), preoperative antibacterial soap for in-patients and out-patients as well as intravenously administered antibiotics (usually cefazolin) in the operating room and for 24–48 h postoperatively. Special consideration is accorded patients submitted to esophageal resection, since their flora may be different and require coverage for upper aerodigestive tract organisms [103]. Cephalosporins with anaerobic coverage are utilized, with or without concomitant metronidazole. Body hair is clipped immediately prior to the operation. A betadine skin preparation is used in surgery, and dressings are maintained for 48 h in the ICU or recovery area. There is a tendency for personnel to neglect to scrutinize the wound if the wound dressing is connected to the chest tube dressing and the two dressings should be separated. With thoracic wound infections there may be erythema, swelling, pain and drainage. Intraoperatively, efforts are made to avoid or contain spillage of contaminated material. We routinely utilize antibiotic irrigation prior to closure, although no studies have found this to be necessary. Drainage of an infected area and application of wet to dry dressings usually suffice for superficial wound infections. Deeper infections require mechanical debridement of all necrotic tissue and excision of infected bone or cartilage. Healing by secondary intention or secondary wound closure are both satisfactory when the wound is clean. Dehiscence of a thoracotomy incision may be caused by local infection, inadequate surgical technique or compromise of the patient’s ability to heal [104]. Recognition is facilitated by careful observation with notation of a widening of the intercostal spaces, often made worse by coughing. There may be a fluid wave or subcutaneous air beneath the incision. Respiratory insufficiency may ensue in patients with marginal respiratory status. Unless there is frank necrosis or infection, thoracotomy wounds which break down are usually closed primarily after debridement and cleansing. Occasionally open packing is necessary. Monofilament absorbable sutures are used to prevent chronic infections from the sutures themselves. Satisfactory healing of a thoracotomy dehiscence can be expected following surgical repair.

References 1 Hehrlein FW, Herrmann H, Kraus J. Complications of median sternotomy in cardiovascular surgery. J Cardiovasc Surg (Torino) 1972; 13: 390–393.

Complications of thoracic incisions 31 2 Milton H. Mediastinal surgery. Lancet 1897; 1: 872–875. 3 Shumaker HB, Lurie PR. Pulmonary valvulotomy. J Thorac Surg 1953; 25: 173–186. 4 Julian OC, Dye WS, Grove WJ et al. Hypothermia in open heart surgery. Arch Surg 1956; 73: 493–502. 5 Julian OC, Lopez-Belio M, Dye WS et al. The median sternal incision in intracardiac surgery with extracorporeal circulation: a general evaluation of its use in heart surgery. Surgery 1957; 42: 753–761. 6 Brown AH, Braimbridge MV, Panagopoulos P et al. The complications of median sternotomy. J Thorac Cardiovasc Surg 1969; 58: 189–197. 7 Stoney WS, Alford WC Jr, Burrus GR et al. Median sternotomy dehiscence. Ann Thorac Surg 1978; 26: 421– 426. 8 Ochsner JL, Mills NL, Woolverton WC. Disruption and infection of the median sternotomy incision. J Cardiovasc Surg (Torino) 1972; 13: 394 –399. 9 Grillo HC. Surgical treatment of postintubation tracheal injuries. J Thorac Cardiovasc Surg 1979; 78: 860–875. 10 Falor WH, Traylor R. Extended indication for the median sternotomy incision. Am Surg 1982; 48: 582–583. 11 Heitmiller RF. Thoracic incisions. In: Baue AE, Geha AS, Hammond GL, Laks H, Naunheim KS, eds. Glenn’s Thoracic and Cardiovascular Surgery, 6th edn. Stamford, CT: Appleton & Lange, Inc., 1996; 73–89. 12 Oz MC, Argenziano M, Rose EA. What is ‘minimally invasive’ coronary bypass surgery? Experience with a variety of surgical revascularization procedures for single vessel disease. Chest 1997; 112: 1409–1416. 13 Robicsek F, Masters TN, Littman L et al. The embolization of bone wax from sternotomy incisions. Ann Thorac Surg 1981; 31: 357–359. 14 Nishida H, Grooters RK, Soltanzadeh H et al. Discriminate use of electrocautery on the median sternotomy incision: a 0.16% wound infection rate. J Thorac Cardiovasc Surg 1991; 101: 488–494. 15 DiMarco RF Jr, Lee MW, Bekoe S et al. Interlocking figure-of-eight closure of the sternum. Ann Thorac Surg 1989; 47: 927–929. 16 Lamm P, Godje OL, Lange T et al. Reduction of wound healing problems after median sternotomy by use of retention sutures. Ann Thorac Surg 1998; 66: 2125–2126. 17 Breyer RH, Mills SA, Hudspeth AS et al. A prospective study of sternal wound complications. Ann Thorac Surg 1984; 37: 412– 416. 18 Serry C, Bleck PC, Javid H et al. Sternal wound complications: management and results. J Thorac Cardiovasc Surg 1982; 80: 861. 19 Kontos GJ Jr, Starr MG, Orszulak TA. Etiology of mediastinal infection after cardiac surgery. In: Salem TJV, ed. Mediastinal and Sternal Infections. Cardiac Surgery: State of the Art Review. Philadelphia: Hanley and Belfus, Inc., 1988; 519–530. 20 Shafir R, Weiss J, Herman O et al. Faulty sternotomy and complications after median sternotomy. J Thorac Cardiovasc Surg 1988; 96: 310–313. 21 Demmy TL, Park SB, Liebler GA et al. Recent experience with major sternal wound complications. Ann Thorac Surg 1990; 49: 458– 462. 22 Sommerhaug RG, Wolfe SF, Red DA et al. Infected median sternotomy wounds. Ann Thorac Surg 1987; 43: 461 (letter). 23 Adams GW, Ravin CE. Midline lucency following median sternotomy. Chest 1983; 83: 793–794. 24 Escovitz ES, Okulski TA, Lapaywker MS. The midsternal stripe: a sign of dehiscence following median sternotomy. Radiology 1976; 121: 521–524.

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25 Robicsek F, Cook JW, Rizzoni W. Sternoplasty for incomplete sternum separation. J Thorac Cardiovasc Surg 1998; 116: 361–362. 26 Angelini GD, Lamarra M, Azzu AA et al. Wound infection following early repeat sternotomy for postoperative bleeding. An experience utilizing intraoperative irrigation with povidone iodine. J Cardiovasc Surg (Torino) 1990; 31: 793–795. 27 Grossi EA, Culliford AT, Krieger KH et al. A survey of major infectious complications of median sternotomy: a review of 7,949 consecutive operative procedures. Ann Thorac Surg 1985; 40: 214–223. 28 Wong PS, Youhana A, Magee PG et al. Primary closure of infected sternum. Ann Thorac Surg 1993; 56: 1005–1006. 29 Bryant LR, Spencer FC, Trinkle JK. Treatment of median sternotomy infection by mediastinal irrigation with an antibiotic solution. Ann Surg 1969; 169: 914 –920. 30 Cohen M, Silverman NA, Goldfaden DM et al. Reconstruction of infected median sternotomy wounds. Arch Surg 1987; 122: 323–327. 31 Miller JI, Nahai F. Repair of the dehisced median sternotomy incision. Surg Clin North Am 1989; 69: 1091–1102. 32 Pearl SN, Dibbell DG. Reconstruction after median sternotomy infection. Surg Gynecol Obstet 1984; 159: 47–52. 33 Weinzweig N, Yetman R. Transposition of the greater omentum for recalcitrant median sternotomy wound infections. Ann Plast Surg 1995; 34: 471– 477. 34 Tizian C, Borst HG, Berger A. Treatment of total sternal necrosis using the latissimus dorsi muscle flap. Plast Reconstr Surg 1985; 76: 703–707. 35 Trotter MC, Ilabaca PA, Economides NG et al. Muscle flaps for repair of dehisced or infected sternotomy wounds. J Tenn Med Assoc 1994; 87: 511–513. 36 Robicsek F, Cook JW, Rizzoni W. Sternoplasty for incomplete sternum separation. J Thorac Cardiovasc Surg 1998; 116: 361–362. 37 Davidson BR, Bailey JS. Incisional herniae following median sternotomy incisions: their incidence and etiology. Br J Surg 1986; 73: 995–996. 38 Stahl RS, Kopf G. Sternotomy infections in infants. Ann Thorac Surg 1990; 50920: 337 (letter). 39 Garrett HE Jr, Mathews J. Reoperative median sternotomy. Ann Thorac Surg 1989; 48: 305. 40 Holman E, Willete F. The surgical correction of constrictive pericarditis. Surg Gyncol Obstet 1949; 89: 129–144. 41 Orringer MB. Partial median sternotomy: anterior approach to the upper thoracic esophagus. J Thorac Cardiovasc Surg 1984; 87: 124 –129. 42 Gitter R, Daniel TM, Kesser BW et al. Membranous tracheobronchial injury repaired with gastric serosal patch. Ann Thorac Surg 1999; 67: 1159–1160. 43 Zwart H. Partial sternotomy: a mini approach for a maxi exposure. J Thorac Cardiovasc Surg 1997; 114: 686 (letter). 44 Moreno-Cabral. Mini-T sternotomy for cardiac operations. J Thorac Cardiovasc Surg 1997; 113: 810–811 (letter). 45 Walterbusch G. Partial sternotomy for cardiac operations. J Thorac Cardiovasc Surg 1998; 115: 256–257 (letter). 46 Massad M, Benedetti E, Pollak R et al. Combined coronary bypass and orthotopic liver transplantation: technical considerations. Ann Thorac Surg 1998; 65: 1130–1132. 47 Benedetti E, Massad M, Chami Y, Wiley T, Layden M. Is the presence of surgically treatable coronary artery disease a contraindication to liver transplantation. Clin Transplant 1999; 13 (Part 1): 59–61. 48 Sirbu H, Busch T, Aleksic I et al. Chest re-exploration for complication after lung surgery. Thoracic Cardiovascular Surg 1999; 47: 73–76.

Complications of thoracic incisions 33 49 Kittle CF. Which way in? The thoracotomy incision. Ann Thorac Surg 1988; 45: 234. 50 Weinberg JA, Krause AR. Intercostal incisions in transpleural operations. J Thorac Surg 1950; 19: 769–778. 51 Emmel M, Ulbach P, Herse B et al. Neurogenic lesions after posterolateral thoracotomy in young children. Thorac Cardiovasc Surg 1996; 44: 86–91. 52 Cherup L, Siewers R, Futrell J. Breast and pectoral muscle maldevelopment after anterolateral and posterolateral thoracotomies in children. Ann Thorac Surg 1986; 41: 492–497. 53 Bethancourt DM, Holmes EC. Muscle sparing thoracotomy. Ann Thorac Surg 1988; 45: 337–339. 54 Horowitz MD, Ancalmo N, Ochsner JL. Thoracotomy through the auscultatory triangle. Ann Thorac Surg 1989; 47: 780–781. 55 Noirclerc M, Dor V, Chauvin G et al. Extensive thoracotomy without muscle section. Ann Chir Cardiovasc 1973; 12: 181–184. 56 Frola C, Serrano J, Cantoni S et al. CT findings of atrophy of chest wall muscle after thoracotomy: relationship between muscles involved and type of surgery. Am J Roentgenol 1995; 164: 599–601. 57 Mitchell RL. The lateral limited thoracotomy incision: standard for pulmonary operations. J Thor Cardiovasc Surg 1990; 99: 590–596. 58 Hazelrigg S, Landrenau R, Boley J et al. The effect of muscle-sparing versus standard posterolateral thoracotomy on pulmonary function, muscle strength and postoperative pain. J Thorac Cardiovasc Surg 1991; 101: 394 – 401. 59 Fry W, Kehoe T, McGee J. Axillary thoracotomy. Amer Surgeon 1990; 460– 463. 60 Salazar J, Ditz J, Tseng E et al. Relationship of the long thoracic nerve to the scapulan tip: an aid to prevention of proximal nerve injury. J Thorac Cardiovasc Surg 1998; 116: 960–964. 61 Kauppila L, Vastamaki M. Latrogenic serratus anterior paralysis long-term outcome in 26 patients. Chest 1996; 109: 31–34. 62 Van Raemdonck D, Coosemans W, Lerut T. Vertical axillary thoracotomy: a muscle sparing approach for routine thoracic operations. Acta Chirurgie Belgica 1993; 93: 207–211. 63 Siegel T, Steiger Z. Axillary thoracotomy. SGO 1982; 155: 725–727. 64 Khan I, McManus K, McCraith A, McGuigan J. Muscle sparing thoracotomy: a biomechanical analysis confirms preservation of muscle strength but no improvement in wound discomfort. Eur J Cardiothorac Surg 2000; 18: 656–661. 65 Lemmer J, Gomez M, Symreng T et al. Limited lateral thoracotomy. Arch Surg 1990; 125: 873–877. 66 Ponn R, Ferneini A, D’Agostino R et al. Comparison of late pulmonary function after posterolateral and muscle-sparing thoracotomy. Ann Thorac Surg 1992; 53: 675–679. 67 Ashour M. Modified muscle-sparing posterolateral thoracotomy. Thorax 1990; 45: 935–938. 68 Benedetti F, Vighetti S, Ricco C et al. Physiologic assessment of nerve impairment in posterolateral and muscle-sparing thoracotomy. J Thorac Cardiovasc Surg 1998; 115: 841– 847. 69 Landrenau R, Pigula F, Luketich R et al. Acute and chronic morbidity differences between muscle-sparing and standard lateral thoracotomies. J Thorac Cardiovasc Surg 1996; 112: 1346–1350. 70 Heitmiller R. Results of standard left thoracoabdominal esophagogastrectomy. Semin Thorac Cardiovasc Surg 1992; 4: 314–319. 71 Talucci R, Webb W. Costal chondritis: the costal arch. Ann Thorac Surg 1983; 35: 318–321. 72 McLaughlin J, Hankins J. Thoracic infections. In: Cordell RA, Ellison RG, eds. Complications of Intra Thoracic Surgery. Boston: Little Brown and Co., 1979; 335–345. 73 Bains M, Ginsberg R, Jones W et al. The Clamshell incision: an improved approach to bilateral pulmonary and mediastinal tumor. Ann Thorac Surg 1994; 58: 30–33.

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74 Wright C. Transverse sternothoracotomy. Chest Surg Clinics N America 1996; 6: 149–156. 75 Lardinois D, Sippel M, Gugger M et al. Morbidity and validity of the hemiclamshell approach for thoracic surgery. Eur J Cardiothorac Surg 1999; 16: 194 –199. 76 Carlens E. Mediastinoscopy. A method for inspection and tissue biopsy in the superior mediastinum. Dis Chest 1959; 36: 343. 77 Foster E, Munro D, Dobell A. Mediastinoscopy. Ann Thorac Surg 1972; 13: 273–286. 78 Puhakka H. Complications of mediastinoscopy. J Laryngol Otol 1989; 103: 312–315. 79 Ashbaugh D. Mediastinoscopy. Arch Surg 1970; 100: 568–573. 80 Al-Sotyani M, Maziak D, Shamji F. Cervical mediastinoscopy: incisional metastasis. Ann Thorac Surg 2000; 69: 1255–1257. 81 McNeill T, Chamberlain J. Diagnostic anterior mediastinal exploration. Ann Thorac Surg 1966; 2: 532. 82 Olak J. Parasternal mediastinotomy (Chamberlain procedure). Chest Surg Clin N America 1996; 6: 31–39. 83 Furrer M, Rechsteiner R, Eigenmann C et al. Thoracotomy and thoracoscopy: postoperative pulmonary function, pain and chest wall complaints. Eur J Cardiothorac Surg 1997; 12: 82–87. 84 Hutter J, Miller K, Moritz E. Chronic sequelae after thoracoscopic procedures for benign diseases. Eur J Cardiothor Surg 2000; 17: 687–690. 85 Yim A, Liv H. Complication and failures of video-assisted thoracic surgery: experience from two centers in Asia. Ann Thorac Surg 1996; 61: 538–541. 86 Kaiser L, Bavaria J. Complications of thoracoscopy. Ann Thorac Surg 1993; 56: 796–798. 87 Yim A. Port-site recurrence following video-assisted thoracoscopic surgery. Surg Endosc 1995; 9: 1133–1135. 88 Pagni S, Salloum E, Tobin GR et al. Serious wound infections after minimally invasive coronary bypass procedures. Ann Thorac Surg 1998; 66: 92–94. 89 Hake U, Hilker M. Deep wound infection following minithoracotomy for coronary bypass grafting. Ann Thorac Surg 1999; 67: 595. 90 Ng P, Chua A, Swanson M. Anterior thoracotomy wound complications in minimally invasive direct coronary bypass. Ann Thorac Surg 2000; 69: 1338–1340. 91 DiMarco A, Oca O, Renston J. Lung herniation. A cause of chronic chest pain following thoracotomy. Chest 1995; 107: 877–879. 92 Minai O, Hammond G, Curtis A. Hernia of the lung: a case report and review of the literature. Connecticut Med 1997; 61: 77–81. 93 Attar S, Hankins J, Turney S et al. Paraplegia after thoracotomy: Report of five cases and review of the literature. Ann Thorac Surg 1995; 59: 1410–1416. 94 Saldana R, Srikrishna S, Pais P et al. Pyogenic meningitis after posterolateral thoracotomy. Ann Thorac Surg 1996; 62: 1573–1574. 95 Brown W, Symbas P. Pneumocephalus complications, routine thoracotomy: symptoms, diagnosis and management. Ann Thorac Surg 1995; 59: 234 –236. 96 Trastek V, Pairolero P, Allen M, Deschamps C. Unusual complications of pulmonary resection. Chest Surg Clinc N America 1992; 2: 853–860. 97 Bryant LR, Dillon M, Mobin-Uddin K. Prophylactic antibiotics in noncardiac thoracic operations. Ann Thorac Surg 1975; 19: 670–676. 98 Cooper D. Incidence of postoperative infection and the role of antibiotic prophylaxis in pulmonary surgery: a review of 221 consecutive patients undergoing thoracotomy. Chest 1981; 75: 154–160. 99 Aznar R, Mateu M, Miro JM et al. Antibiotic prophylaxis in non cardiac thoracic surgery: cefazolin v. placebo. Eur J Cardiothorac Surg 1991; 5: 515–518.

Complications of thoracic incisions 35 100 Kvale P, Ranga V, Kopacz M. Pulmonary resection. Southern Med J 1977; 70 (Suppl. I): 64–68. 101 Ferdinand B, Shennib H. Postoperative pneumonia. Chest Surg Clin N Am 1998; 8: 529–539. 102 Olak J, Jeyasingham K, Forrester-Wood C et al. Randomized trial of one-dose versus six dose cefazolin prophylaxis in elective general thoracic surgery. Ann Thorac Surg 1991; 51: 956–958. 103 Sharpe D, Renwick P, Matthews K, Moghissi K. Antibiotic prophylaxis in oesophageal surgery. Eur J Cardiothorac Surg 1992; 6: 5561–5564. 104 Douglas J. Complications related to patient positioning, thoracic incisions and chest tube placement. In: Wolfe W, ed. Complications in Thoracic Surgery. St Louis: Mosby Year Book, 1992; 76–87.

CHAPTER 2

Respiratory complications of thoracic operations Hani Shennib

Postoperative atelectasis The incidence of postoperative atelectasis or lung collapse varies from 6% to 76% based on the clinical and radiological criteria for assessment and on methods of surveillance [1–8] Plate-like atelectasis after thoracic surgery is quite frequent and usually associated with minimal clinical findings. However, in patients with borderline lung function atelectasis may lead to other serious sequela such as cardiac arrhythmia, pneumonia and respiratory failure. On the other hand, major collapse involving the whole lung or lobe can lead to significant shunt and decompensation.

Susceptibility to atelectasis Thoracic surgical patients are particularly vulnerable to pulmonary atelectasis as they are subjected both to general anesthesia and a thoracotomy [9–17]. Loss of upper airway reflexes, endotracheal intubation and active lung collapse in the course of many routine thoracic surgical procedures predispose to postoperative atelectasis. Administration of narcotic analgesics and postoperative pain impair respiratory mechanics, and accentuate atelectasis. Furthermore, pneumo and hemothorax, which often develop in the absence of adequate pleural drainage, may contribute to postoperative lung collapse. Retention of secretions within the airway secondary to inability to cough, pain, loss of lung compliance, and vocal cord dysfunction are all factors that would induce or compound atelectasis. Certain procedures are associated with a major risk of atelectasis and these include sleeve pulmonary resections, lung transplantation, and major chest wall resections. At a cellular level [14,15,17,18], atelectasis alters lung host defenses by impairing mucociliary function, pulmonary macrophage phagocytic, bactericidal and lymphocyte activity, thus impairing the lung host defenses and therefore making the patient susceptible to pneumonia [19–23]. Intraoperatively, atelectasis may occur due to malpositioning of an endotracheal tube, inadequate suctioning of endotracheal secretions, inadvertent creation of contralateral pneumothorax from pleural holes, and from unexplained airway reactivity. This may occur and progress intraoperatively and hence it is imperative that a chest radiograph be done on arrival to the recovery room. More 36

Respiratory complications of thoracic operations 37

important, however, is to have excellent rapport between the anesthesiologist and surgeon during the procedure to recognize ventilation difficulties encountered during surgery. Any hypoxia or decrease in measured end-tidal carbon dioxide should be investigated. Usually malpositioning of the endotracheal tubes can be avoided or corrected by the choice of the appropriate tube size and confirmation of its location by prompt bronchoscopy. Atelectasis may not be apparent on the initial postoperative radiograph. Oxygen which is routinely administered postoperatively will accentuate atelectasis as it displaces normally inhaled nitrogen, resulting in diffusion atelectasis [24]. Atelectasis should be suspected when the chest radiograph shows evidence of volume loss with increased opacification, diaphragmatic elevation and mediastinal shift. In patients with asthma and severe chronic obstructive pulmonary disease (COPD) it may take a longer time for hyperinflated lung segments to collapse. This is also true for patients with major airway obstruction, and chest radiographs may not be the most sensitive way to identify this. Surgeons must adopt a vigilant routine for assessing postoperative chest radiographs themselves, as often, radiologists are less familiar with surgical techniques and may misinterpret postoperative images. Surgical techniques such as creation of a pleural tent or temporary diaphragmatic eventration by phrenic nerve injection may be reported incorrectly by radiologist due to lack of operative information. Radiologically, it may be difficult to differentiate between atelectasis, pneumonia, and pulmonary infarction [25–27]. Shift of the mediastinum towards the atelectatic side helps differentiate between loss of lung volume and a pleural fluid collection which causes a contralateral shift. Clinical manifestations of atelectasis such as low-grade temperature and mild elevation of the white blood cell count also appear equally with pneumonia. Pulmonary infarction is notoriously misinterpreted and its associated lung consolidation is usually interpreted as pneumonia and treated as such. Earlier on, it may manifest clinically and radiologically as atelectasis. Clipping or ligature of segmental veins are often tolerated quite well. Inadvertent interruption of lobar veins, on the other hand, due to technical error or when lobar torsion occurs, results in full opacification of the lobe and will appear radiographically as a rounded and well-demarcated consolidated lobe. Remarkably, a bronchoscopic examination is often inconclusive and mild indentation of the affected bronchus due to some rotation may be undetected. It is hence important to differentiate atelectasis early after surgery from other more serious pulmonary complications. Management of atelectasis consists of anticipation, prevention and treatment [5,6,18,26,28–45]. It is important to identify those patients that are at high risk of atelectasis preoperatively. The obese, elderly, those with COPD, patients with restrictive chest wall or lung disease and those with head and neck surgery which affects the vocal cords, must be prepared and educated about postoperative respiratory therapy protocols prior to surgery. Such education and a physiotherapy program should be pursued vigorously in the postoperative

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Chapter 2

period with specific therapeutic measures added for any underlying disease. For example, asthma and COPD patients may benefit from an intensified regimen of pre- and postoperative steroid and bronchodilator prophylaxis. Postoperative optimization of analgesia, preferably by administration of regional epidural analgesics, must be considered with all major operations. Patient-controlled intravenous analgesics are superior to uncontrolled intravenous and subcutaneous analgesic administration. The negative effects of overdose, albeit less, will still lead to somnolence and reduction of overall patient activity. The main objective of postoperative physiotherapy is the incremental improvement in overall cardiovascular and chest function. Incentive spirometry techniques and other methods to improve respiratory mechanics are most effective in clearing the bronchopulmonary tree from secretions, expanding the lung, and decreasing the risk of atelectasis. The administration of inhaled bronchodilators may improve the efficacy of clapping, vibration and other chest physiotherapy techniques when given before surgery. The literature is full of studies comparing the efficacy of one method of chest physiotherapy with another. Regardless, chest physiotherapy has been shown to minimize the risk of postoperative atelectasis. The use of mucolytic agents remains controversial, but we do use it occasionally in patients with recurrent airway obstruction due to thick inspissated secretions. When atelectasis is established, aggressive chest physiotherapy should be continued. Incentive inspirometry is superior to the old blow bottles and causes better expansion of collapsed lung segments by alveolar recruitment. Several European centres have experience with the use of non-invasive mechanical ventilators for the treatment of major atelectasis. Intermittent, positive pressure breathing by pressure-cycled ventilators pushes a determined volume of air to a preset pressure. Contraindication for such a therapy includes bullous emphysema, and massive or persistent air leak. Side-effects of this ventilator modality such as abdominal distension and bloating have not been reported; however, controlled studies to substantiate the efficacy of this method are lacking. While some single-arm reports suggest a benefit in the incidence of pulmonary complication, one randomized study failed to show an advantage of intermittent positive pressure breathing over incentive inspirometry for prevention of pulmonary complications following open heart surgery. Caution should be exercised in subjecting patients who have had a sleeve resection as disruption of a bronchial anastomosis may cause an air leak. The presence of major lobar atelectasis or atelectasis of lesser extent, in patients with borderline lung function, warrants prompt use of fiberoptic bronchoscopy for diagnosis and therapy. In addition to permitting anatomic inspection for possible technical problems, it may be possible to identify and remove major obstructions due to retained secretions. The performance of deep bronchial secretion sampling for culture and sensitivity will also help to determine the need for administering antibiotics.

Respiratory complications of thoracic operations 39

In patients with compromised neurological status, the use of fiberoptic bronchoscopy to clear airways of secretions, particularly following aggressive physiotherapy, may be beneficial. Hypoxic patients require continuous oxygen monitoring and administration. Excessive utilization of suctioning in the course of fiberoptic bronchoscopy can lead to significant hypoxia. This can be remedied promptly by discontinuing the suctioning and if needed by purging oxygen through the working channel of the bronchoscope. On occasion, when retained secretions lead to repeat respiratory failure, prolonged endotracheal intubation and/or re-intubation, it is advisable to consider performing tracheostomy to facilitate pulmonary toilet. Percutaneous tracheostomy can be easily performed in the intensive care unit and has become increasingly the technique of choice in some centres.

Postoperative pneumonia This is one of the most common and potentially devastating of all postoperative complications. It has the same risk factors described previously for other pulmonary complications. In addition, its risk is higher following right as opposed to left pneumonectomy after extensive lung and chest wall resection and with prolonged operative time and increased transfusion requirement [5–7,46–52]. The diagnosis and treatment of postoperative pneumonia are extremely difficult [53–56], primarily because of the overlap in symptoms, hematological and radiological changes between atelectasis and pneumonia. Often it is overor underdiagnosed. Delayed treatment of postoperative pneumonia may lead to rapid progression to respiratory failure and death. It is hence advocated that aggressive antibiotic therapy be promptly initiated whenever the classic triad of fever, elevated white blood count and a radiological infiltrate manifest. This becomes even more pertinent in the presence of progressive decline in gas exchange. In the absence of reliable bacterial culture results, it is advocated to commence antibiotics on empiric basis. Immediate deep sample Gram stains and bacterial cultures must be obtained by endotracheal suction or bronchoscopy. Initial antibiotic therapy should cover Haemophilus influenzae, Staphylococcus aureus, Streptococcus pneumoniae, Enterobacteriaceae including Klebsiella pneumoniae, Escherichia coli and Pseudomonas eroginosa. The utilization of ampicillin and an aminoglycoside or a third-generation cephalosporin are currently the golden standard. While prevention of postoperative pneumonia has traditionally entailed administration of prophylactic doses of antibiotics [57,58], current regimens for thoracic surgery are outdated and rather reflect a general surgery practice aimed at decreasing wound infections [8]. Currently used second-generation cephalosporins are less likely to be effective in preventing bronchopneumonia or empyema. Wound infections in thoracic incisions on the other hand are unusual due to the excellent chest wall blood supply.

40

Chapter 2

Acute respiratory failure Acute adult respiratory failure following a cardiothoracic procedure is defined as respiratory decompensation requiring intubation and mechanical ventilation any time after initial extubation or failure to discontinue mechanical ventilation within 48 h of completing surgery. While there is a variation in the overall incidence of pulmonary complications following cardiothoracic surgery, the incidence of this serious respiratory complication ranges between 5% and 14%. The significance of development of respiratory failure following thoracic surgery is its associated mortality. Bush et al. reported that 14% of all patients ultimately required tracheostomies and 8% died. Ginsberg reported that 40–70% of all postoperative deaths after lung resections were attributed to respiratory complications [10]. Bousamara reported that up to 10% of patients undergoing lung volume reduction surgery may require prolonged mechanical ventilation [59] and Markos also reported an incidence of 10% of respiratory failure in patients undergoing lung resection for lung cancer [60]. Preoperative risk factors for pulmonary complications include smoking history, sputum production, obesity, old age and impaired cardiopulmonary function. Clearly, the patients overall and preoperative pulmonary functional status will contribute to determining any added risk of mortality from respiratory failure. As we operate on older frail patients with boderline lung functions, mortality will probably increase. Many factors contribute to the development of postoperative respiratory failure. Several insults occur routinely during surgery and may contribute to such injury: lung collapse during single lung ventilation, manipulation of the lung during dissection and positive pressure ventilation are contributors and prime the lung for membrane leakage following surgery. Redistribution of lung perfusion following major resection, early postoperative mechanical ventilation, excessive intravenous fluid and blood administration, silent aspiration, medications and cardiac events may also contribute to the development of capillary leak in the early postoperative period. Despite early extubation, lung injury often progresses over a few days following operation so that an injury may only manifest itself 48–72 h after. Frequently, this renders differential diagnosis of the etiology (pneumonia, embolism, cardiogenic, etc.) more complex. Existing underlying cardiopulmonary disease renders diagnosis and management of respiratory failure more difficult (e.g. pulmonary fibrosis organizing pneumonia, aortic valve and coronary artery disease). Moderate improvement in outcome of post-thoracotomy respiratory failure has recently been reported due to advances in supportive care [61–83]. New concepts which may have contributed to such improvement include minimization of inspired oxygen, avoiding hyperinflation, avoiding recruitment– rerecruitment, the use of airway pressure release ventilation, inverse ratio ventilation, permissive hypercapnea, better fluid management and intermittent utility of the prone position. The administration of antibiotics, antifungals, steroids, anti-inflammatory agents and surfactant have not shown convincing

Respiratory complications of thoracic operations 41

benefits. Inhaled nitric oxide, on the other hand, has been shown to lead to improvement in hemodynamics and gas exchange.

Post-pneumonectomy pulmonary edema This is the most dreaded and poorly understood complication following pneumonectomy. Flooding of the remaining lung with edematous transudate brings immediate respiratory failure and a mortality that is higher than 80%. Fortunately, it only occurs in less than 5% of all pneumonectomy patients [84]. It was originally described by Gibbon [85] in the early 1940s but only recently has it been recognized as a distinct entity. While originally it was assumed to be secondary to fluid overload, today it is thought to be of multifactorial etiology and probably related to some direct form of pulmonary vascular endothelial injury from increased capillary pressure and flow through the remaining lung. Progressive baro-trauma from mechanical ventilation in the course of supportive therapy accentuates this alveolar–capillary damage [86]. In an attempt to identify risk factors for post-pneumonectomy pulmonary edema Delaurier [84] et al. reviewed the course of 291 pneumonectomy cases and identified 13 patients who developed post-pneumonectomy edema following right pneumonectomy. The extent of surgery and duration of the operation were noted as risk factors for its development. Not surprisingly, excessive pleural drainage from patients with this form of injury was noted in comparison with patients who did not develop post-pneumonectomy edema. This occurred despite conservative fluid intake. Administration of blood products such as fresh frozen plasma, higher mechanical ventilation pressures during surgery, and performance of redo thoracotomy for completion pneumonectomy were considered additional risks [87]. Usually, post-pneumonectomy edema develops in the first 48–72 h after an otherwise routine uncomplicated pneumonectomy. Dyspnea and oxygen requirement progress rapidly leading to admission to the intensive care unit for mechanical ventilation. Physical examination and early chest radiographs are usually unremarkable; with rapid progression, examination will reveal the presence of diffuse lung crepitations and crackles and chest radiographs will manifest whiteout of the lung. Administration of diuretics is often of little value. Insertion of a pulmonary artery catheter and measurement of wedge pressure will suggest low-pressure edema. Care must be taken as expansion of a pulmonary artery balloon catheter in the course of hemodynamic measurement temporarily occludes a significant amount of the cross-sectional area of the single remaining pulmonary artery. This significant increase in pulmonary artery resistance may result in significant hemodynamic compromise and a drop in arterial pressure. Diagnosis is often made after exclusion of other pulmonary complications such as pulmonary embolism, bacterial and viral pneumonia and aspiration pneumonia. A bronchoscopy often reveals frothy clear bronchial secretions and bronchoalveolar lavage and bacterial workup

42

Chapter 2

are often negative. Perfusion scans or enhanced spiral computed tomography scans will rule out the presence of pulmonary embolism. Despite the lack of convincing evidence that excessive fluid intake is responsible for post-pneumonectomy pulmonary edema, caution about administering intravenous fluids following pneumonectomies should be practised and it is advisable that in the course of supporting these patients with mechanical ventilation, adequate sedation and analgesia be continued until the patient is ready to be weaned. Patients actively struggling against the ventilator create abrupt increases in airway pressures and add additional baro-trauma. Support must also include rotating patients in bed regularly in order to avoid hydrostatic pulmonary congestion. Many treating physicians would give diuretics, however, excessive dehydration may compromise perfusion of peripheral lung zones resulting in increased shunting and hypoxia. It is recommended that bacterial cultures of sputum be regularly obtained and any specific pneumonia be treated with the appropriate antimicrobial agent. Prophylactic antibiotics have no proven role, while prophylactic anticoagulation is merited in most intensive care patients unless contraindicated. Pulmonary vascular recruitment by utilization of inhaled nitric oxide has been shown to improve gas exchange and may benefit patients with post-pneumonectomy pulmonary edema. It is also likely that other new therapeutic agents such as prostanoid based drugs and endothelin receptor antagonists may be of benefit. Extracorporeal membrane oxygenation and liquid ventilation are considered a last resort and should be reserved for younger patients with convincing evidence of lung recoverability. It is likely that liquid ventilation may prove superior in supporting the lung by avoiding baro-trauma of positive pressure ventilation [88–98].

Recurrent laryngeal and phrenic nerve injuries Even though not traditionally classified under respiratory complications, recurrent laryngeal and phrenic nerve injuries can lead to serious pulmonary sequelae [99]. Recurrent laryngeal injury may occur in the course of mobilization of the upper thoracic esophagus during esophagectomy or the performance of a long myotomy, during radical left lung pneumonectomy when dissecting around the aortopulmonary window or during aortic surgery on the left side. Dissection along the tracheo–esophageal groove at the thoracic inlet may result in injury to the right recurrent laryngeal nerve as it swings around the right subclavian artery. Orringer has described principles of techniques during cervical esophagectomy to avoid recurrent laryngeal nerve injury which include careful placement of metal retractors for retraction of the trachea to expose the esophagus. Similarly, cervical tracheal resections require special attention to avoid injuring the recurrent nerve as it turns medially into the laryngeal muscle [99]. Phrenic nerve injury most commonly occurs in the course of routine primary or redo cardiac surgery and is attributed to nerve paresis or praxia during high

Respiratory complications of thoracic operations 43

dissection of the internal mammary artery due to tension on the pericardial stay sutures and the topical use of pericardial slush. In general thoracic surgery, the phrenic nerve may be injured or purposely resected during mobilization or radical resection of aggressive mediastinal tumors. When thoracoabdominal procedures require transdiaphragmatic access, it is advisable to divide the diaphragm along the perimeters or radially. Anterior mediastinotomy (Chamberlain procedure) may result in injury to either of the two nerves. Better visualization and magnification with video-assisted techniques may potentially decrease the risk of phrenic and laryngeal nerve injuries.

References 1 Canver C, Bhayana J, Lajos T et al. Pulmonary resection combined with cardiac operations. Ann Thorac Surg 1990; 50: 796–799. 2 Deron S, Kotler M. Noncardiac surgery in the cardiac patient. Am Heart J 1988; 116: 831–838. 3 Detsky A, Abrams H, Forbath N et al. Cardiac assessment for patients undergoing noncardiac surgery. Arch Intern Med 1986; 146: 231–234. 4 Freeman W, Gibbons R, Shub C. Preoperative assessment cardiac patients undergoing noncardiac surgical procedures. Mayo Clin Proc 1989; 64: 1105–1117. 5 Anderson WH, Dossett BE, Hamilton GL. Prevention of postoperative pulmonary complications; use of isoproterenol and intermittent positive pressure breathing on inspiration. JAMA 1963; 186: 763–767. 6 Dales RE, Dionne G, Leech JA et al. Preoperative prediction of pulmonary complications following thoracic surgery. Chest 1993; 104: 155–159. 7 Deslauriers J, Ginsberg RJ, Dubois P et al. Current operative morbidity associated with elective surgical resection for lung cancer. Can J Surg 1989; 32: 335–339. 8 Massard G, Wihlm J. Postoperative atelectasis. In: Shennib H, ed. Medical Complications of Thoracic Surgery. Chest Surgical Clinic of North America. Philadelphia: W.B. Saunders, 1998, 503–528. 9 Foster E, Davis K, Carpenter J et al. Risk of noncardiac operation in patients with defined coronary disease: The Coronary Artery Surgery Study (CASS) registry experience. Ann Thorac Surg 1986; 4: 42–50. 10 Ginsberg R, Hill L, Eagan E et al. Modern thirty-day operative mortality for surgical resections in lung cancer. J Thorac Cardiovasc Surg 1983; 86: 654 –658. 11 Goldman L, Caldera D, Nussbaum S et al. Multifactorial index of cardiac risk in noncardiac surgical procedures. N Engl J Med 1977; 297: 845–850. 12 Kirsh M, Rotman H, Behrent D et al. Complications of pulmonary resection. Ann Thorac Surg 1975; 20: 215–236. 13 Krowka M, Pairolero P, Trastek V et al. Cardiac dysrhythmia following pneumonectomy: clinical correlates and prognostic significance. Chest 1987; 91: 490–495. 14 Lewis J, Bastanfar M, Gavriel F et al. Right heart function and prediction of respiratory morbidity in patients undergoing pneumonectomy with moderately severe cardiopulmonary dysfunction. J Thorac Cardiovasc Surg 1994; 108: 169–175. 15 Mangano D, Browner W, Hollengerg M et al. Association of preoperative myocardial ischemia with cardiac morbidity and mortality in men undergoing noncardiac surgery. N Engl J Med 1990; 323: 1781–1788. 16 Miller D, Orszulak T, Pairolero P et al. Combined operation for lung cancer and cardiac disease. Ann Thorac Surg 1994; 58: 989–994.

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17 Mowry F, Reynolds E. Cardiac rhythm disturbances complicating resectional surgery of the lung. Ann Intern Med 1964; 61: 688–695. 18 Tarhan S, Moffit E, Taylor W et al. Myocardial infarction after general anesthesia. JAMA 1972; 220: 1451. 19 Gamsu G, Singer MM, Vincent HH et al. Postoperative impairment of mucous transport in the lung. Am Rev Respir Dis 1976; 114: 673–679. 20 Nelin LD, Rickaby DA, Linehan JH et al. Effect of atelectasis and surface tension on pulmonary vascular compliance. J Appl Physiol 1991; 70: 2401–2409. 21 Nguyen DM, Mulder DS, Shennib H. Altered cellular immune function in the atelectatic lung. Ann Thorac Surg 1991; 51: 76–80. 22 Paul A, Marelli D, Shennib H et al. Mucociliary function in autotransplanted, allotransplanted and sleeve resected lungs. J Thorac Cardiovasc Surg 1989; 98: 523–528. 23 Shennib H, Mudler DS, Chiu RCJ. The effects of pulmonary atelectasis and reexpansion on lung cellular immune defences. Arch Surg 1984; 119: 274 –277. 24 Rothen HU, Sporre B, Engberg G et al. Influence of gas composition on recurrence of atelectasis after a reexpansion maneuver during general anesthesia. Anesthesiology 1995; 82: 832–842. 25 Woodring JH, Reed JC. Types and mechanisms of pulmonary atelectasis. J Thorac Imaging 1996; 11: 92–108. 26 Yao Taso T, Huang Tsai Y, Shee Ian R et al. Treatment of collapsed lung in critically ill patients. Chest 1990; 97: 435– 438. 27 Young M, Marrie TJ. Interobserver variability interpretation of chest roentgenograms of patients with possible pneumonia. Arch Intern Med 1994; 154: 2729–2732. 28 Nagasaki F, Flehinger B, Martini N. Complications of surgery in the treatment of carcinoma of the lung. Chest 1982; 82: 25–29. 29 Patel R, Townsend E, Fountain S. Elective pneumonectomy. Factors associated with morbidity and operative mortality. Ann Thorac Surg 1992; 54: 84 –88. 30 Rao T, Jocobs K, El-Ete A. Reinfarction following anesthesia in patients with myocardial infarction. Anesthesiology 1983; 59: 499–505. 31 Reed C, Spinale F, Crawford F. Effect of pulmonary resection on right ventricular function. Ann Thorac Surg 1992; 53: 578–582. 32 Ritchie A, Bowe P, Gibbons J. Prophylactic digitalization for thoracotomy: a reassessment. Ann Thorac Surg 1992; 53: 578 –582. 33 Steen P, Tinker J, Tarhan S. Myocardial reinfarction after anesthesia and surgery. JAMA 1978; 239: 2566–2570. 34 von Knorring J. Postoperative myocardial infraction. A prospective study in a risk group of surgical patients. Surgery 1981; 90: 55–60. 35 von Knorring J, Lepantalo M, Lindgren L et al. Cardiac arrhythmias and myocardial ischemia after thoracotomy for lung cancer. Ann Thorac Surg 1992; 53: 642–647. 36 Wahi R, McMurtrey M, DeCaro L et al. Determinants of preoperative morbidity and mortality after pneumonectomy. Ann Thorac Surg 1989; 48: 33–37. 37 Yokoyama T, Derrick M, Lee A. Cardiac operation with associated pulmonary resection. J Thorac Cardiovasc Surg 1993; 105: 912–917. 38 Handelsman H. Intermittent positive pressure breathing therapy. Health Technol Assess Resp 1991; 1: 1–9. 39 Jaworski A, Goldberg SK, Walkenstein MF et al. Utility of immediate post lobectomy fiberoptic bronchoscopy in preventing atelectasis. Chest 1988; 94: 42. 40 Jonhson D, Kelm C, Thomson D et al. The effect of physical therapy on respiratory complications following cardiac valve surgery. Chest 1996; 109: 638–644.

Respiratory complications of thoracic operations 45 41 Marini J, Pierson D, Hudson L. Acute lobar atelectasis. A prospective comparison of bronchoscopy and respiratory therapy. Am Rev Respir Dis 1979; 119: 971–978. 42 Pedersen J, Schurizek BA, Melsen NC et al. Is minitracheostomy a simple and safe procedure? A prospective investigation in the intensive care unit. Intensive Care Med 1991; 17: 333–335. 43 Shennib H, Baslaim G. Bronchoscopy in the Intensive Care Unit. Chest Surgical Clinic of North America. Philadelphia: W.B. Saunders Co., 1996; 345–361. 44 Stiller K, Geake T, Taylor J et al. Acute lobar atelectasis. A comparison of two chest physiotherapy regimens. Chest 1990; 98: 1336–1340. 45 Van Heerden PV, Jacob W, Cameron PD et al. Bronchoscopic insufflation of room air for the treatment of lobar atelectasis in mechanically ventilated patients. Aneasth Intensive Care 1995; 23: 175–177. 46 Boushy SF, Billig DM, North LB et al. Clinical course related to preoperative and postoperative pulmonary function in patients with bronchogenic carcinoma. Chest 1971; 59: 383. 47 Busch E, Verazin G, Antkowiak JG et al. Pulmonary complications in patients undergoing thoracotomy for lung carcinoma. Chest 1994; 105: 760. 48 Craven DE, Kunches LM, Kilinsky V et al. Risk factors of pneumonia and fatality in patients receiving continuous mechanical intubation. Am Rev Respir Dis 1986; 133: 792. 49 Deslauriers J, Ginsberg RJ, Piantadosi S et al. Prospective assessment of 30-day operative morbidity for surgical resections in lung cancer. Chest 1994; 106: 329S. 50 Gaynes R, Bizek B, Mowry-Hanley J et al. Risk factors for nosocomial pneumonia after coronary artery bypass graft operations. Ann Thorac Surg 1991; 51: 215. 51 Girabaldi RA, Britt MR, Coleman ML et al. Risk factors for postoperative pneumonia. Am J Med 1981; 70: 677. 52 Harpole DH, Liptay MJ, DeCamp MM Jr. et al. Prospective analysis of pneumonectomy; risk factors for major morbidity and cardiac dysrhythmias. Ann Thorac Surg 1996; 61: 977. 53 Higuchi JH, Coalson JJ, Johanson WG. Bacteriological diagnosis of nosocomial pneumonia in primates. Am Rev Respir Dis 1982; 125: 53. 54 Huxley EJ, Viroslav J, Gray WR et al. Pharyngeal aspiration in normal adults and patients with depressed consciousness. Am J Med 1978; 64: 564. 55 Iwamoto K, Ichiyama S, Shimokata K et al. Postoperative pneumonia in elderly patients: incidence and mortality in comparison with young patients. Intern Med 1993; 32: 274 –277. 56 Mitsudomi T, Mizoue T, Yoshimatsu T et al. Postoperative complications after pneumonectomy for treatment of lung cancer: multivariate analysis. J Surg Oncol 1996; 61: 218. 57 Aznar R, Mateu M, Miro JM et al. Antibiotic prophylaxis in noncardiac thoracic surgery: cefazolin versus placebo. Eur J Cardiothorac Surg 1991; 5: 515. 58 Bernard A, Pillet M, Goudet P et al. Antibiotic prophylaxis in pulmonary surgery. J Thorac Cardiovasc Surg 1994; 107: 896. 59 Bousamra M, Presberg KW, Chammas JH. Early and late morbidity in patients undergoing pulmonary resection with low diffusion capacity. Ann Thorac Surg 1996; 62: 968. 60 Markos J, Mullan BP, Hillman DR et al. Preoperative assessment as predictor of mortality and morbidity after lung resection. Am J Resp Dis 1989; 39: 902. 61 Abraham E, Park YC, Covington P et al. Liposomal prostaglandin E1 in acute respiratory distress syndrome: a placebo-controlled randomized, double-blind multicenter clinical trial. Crit Care Med 1996; 24: 10–15. 62 Amato MBP, Barbas CVS, Medeiros DM et al. Beneficial effect of ‘open lung approach’ with low distending pressures in ARDS. Am J Respir Crit Care Med 1995; 152: 1835–1846. 63 Anderson HL, Delius RE, Sinard JM et al. Early experience with adult extracorporeal membrane oxygenation in the modern ear. Ann Thorac Surg 1992; 53: 553–563.

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64 Anzuete A, Baughman RP, Guntuplli KK et al. Aerosolized surfactant in adults with sepsisinduced ARDS. Exosurf ARDS sepsis study group. N Engl J Med 1996; 334: 1417–1421. 65 Armstrong BW, MacIntyre NR. Pressure-controlled inverse ratio ventilation that avoids air trapping in the adult respiratory distress syndrome. Crit Care Med 1995; 23: 279–285. 66 Bernard GR, Artigas A, Brigham KL et al. The American–European Consensus Conference on ARDS. Definitions, mechanisms, relevant outcomes, and clinical trial coordination. Am J Respir Crit Care Med 1994; 149: 818–824. 67 Broccard AF, Shapiro RS, Schmitz LL et al. Influence of prone position on the extent and distribution of lung injury in a high tidal volume oleic acid model or ARDS. Crit Care Med 1997; 25: 16–27. 68 Brunet F, Mira JP, Belghith M et al. Extracorporeal carbon dioxide removal technique improves oxygenation without causing overinflation. Am J Respir Crit Care Med 1994; 149: 1557–1562. 69 Chatte G, Sab JM, Dubois JM et al. Prone position mechanically ventilates patients with severe acute respiratory distress syndrome. Am J Respir Crit Care Med 1997; 155: 473– 478. 70 Dreyfuss D, Soler P, Basset G et al. High inflation pressure pulmonary edema. Respective effects of high airway pressure, high tidal volume and positive end-expiratory pressure. Am Rev Respir Dis 1988; 137: 1159–1164. 71 Dreyfuss D, Soler P, Saumon G. Mechanical ventilation-induced pulmonary edema. Crit Care Med 1995; 151: 1568–1575. 72 Falkenhain SK, Reilley TE, Gregory JS. Improvement in cardiac output during airway pressure release ventilation. Crit Care Med 1992; 20: 1358–1360. 73 Feihl F, Perret C. Permissive hypercapniaahow permissive should we be? Am J Respir Crit Care Med 1994; 150: 1722–1737. 74 Gauger PG, Pranikoff T, Schreihner RJ et al. Initial experience with partial liquid ventilation in pediatric patients with the acute respiratory distress syndrome. Crit Care Med 1996; 24: 16–22. 75 Gerlach H, Pappert D, Lewandowski K et al. Long-term inhalation with evaluated low doses of nitric oxide for selective improvement of oxygenation in patients with ARDS. Intens Care Med 1993; 19: 443– 449. 76 Hickling KG, Walsh J, Henderson S et al. Low mortality rate of ARDS using low-volume, pressure-limited ventilation with permissive hypercapnia: a prospective study. Crit Care Med 1994; 22: 1568–1578. 77 Hirschl RB, Prannikoff T, Gauger P et al. Liquid ventilation in adults, children and full term neonates. Lancet 1995; 346: 1201–1202. 78 Hirschl RB, Prannikoff T, Wise C et al. Initial experience with partial liquid ventilation in adult patients with acute respiratory distress syndrome. JAMA 1996; 275: 383–389. 79 Lewis JF, Jobe AH. Surfactant and the adult respiratory distress syndrome. Am Rev Respir Dis 1993; 147: 218–233. 80 Rossaint R, Falke KJ, Lopez F et al. Inhaled nitric oxide for ARDS. N Engl J Med 1993; 328: 399–405. 81 Slotman GJ, Burchard KW, D’Arezzo A et al. Ketoconazole prevents acute respiratory failure in critically ill surgical patients. J Trauma 1988; 28: 648–654. 82 Slutsky AS. Barotrauma and alveolar recruitment. Intensive Care Med 1993; 19: 369–371. 83 Swissler B, Kemming G, Habler O et al. Inhaled prostacyclin (PG12) versus inhaled nitric oxide in ARDS. Am J Respir Crit Care Med 1996; 154: 1671–1677. 84 Deslauriers J, Aucoin A, Gregoire J. Postpneumonectomy pulmonary edema. In: Shennib H, ed. Medical Complications of Thoracic Surgery. Chest Surgical Clinic of North America. Philadelphia: W.B. Saunders, 1998; 611–631.

Respiratory complications of thoracic operations 47 85 Gibbon JH, Gibbon MH. Experimental pulmonary edema following lobectomy and plasma infusion. Surgery 1942; 12: 694 –704. 86 Jansen JP, Brutel de la Riviere A, Carpentier-Alting MP et al. Postpneumonectomy syndrome in adulthood. Chest 1992; 101: 1167–1170. 87 Little AG, Langmuir VK, Singer AH et al. Hemodynamic pulmonary edema in dog lungs after contralateral pneumonectomy and mediastinal lymphatic interruption. Lung 1984; 162: 139–145. 88 Mathisen DJ, Kuo EY, Hahn C et al. Inhaled nitrous oxide for adult respiratory distress syndrome following pulmonary resection. Soc Thoracic Surgeons Annu Meeting 1998; 7: 68 (Abstract). 89 Mathru M, Blakeman B, Dries DJ et al. Permeability pulmonary edema following lung resection. Chest 1990; 98: 1216–1218. 90 Nabers J, Hoogsteden HC, Hilvering C. Postpneumonectomy pulmonary edema treated with continuous positive airway pressure face mask. Crit Care Med 1989; 17: 102–103. 91 Okada M, Ota T, Okada M et al. Right ventricular dysfunction after major pulmonary resection. J Thorac Cardiovasc Surg 1994; 108: 503–511. 92 Satur CMR, Robertson RH, DaCosta PE et al. Multiple pulmonary microemboli complicating pneumonectomy. Ann Thorac Surg 1991; 52: 122–126. 93 Shapira OM, Shanian DM. Postpneumonectomy pulmonary edema. Ann Thorac Surg 1993; 45: 190–195. 94 Slinger PD. Perioperative fluid management for thoracic surgery. The puzzle of postpneumonectomy edema. J Cardiothorac Vasc Anesth 1995; 9: 442– 451. 95 Turnage WS, Lunn JJ. Postpneumonectomy pulmonary edema. A retrospective analysis of associated variables. Chest 1993; 103: 1646–1650. 96 Van der Werff YD, van der Houwen HK, Heijmans PJM et al. Postpneumonectomy pulmonary edema. A retrospective analysis of incidence and possible risk factors. Chest 1997; 111: 1278–1284. 97 Waller DA, Keavey P, Woodfine L et al. Pulmonary endothelial permeability changes after major lung resection. Ann Thorac Surg 1996; 61: 1435–1440. 98 Wittnich C, Trudel J, Zidulka A et al. Misleading ‘pulmonary wedge pressure’ after pneumonectomy: its importance in postoperative fluid therapy. Ann Thorac Surg 1986; 42: 192–196. 99 Feins R. Neurological complications in thoracic surgery. In: Shennib H, ed. Medical Complications of Thoracic Surgery. Chest Surgery Clinic of North America. Philadelphia: W.B. Saunders, 1998; 633–643.

CHAPTER 3

Arrhythmias following cardiothoracic operations Adam E. Saltman, Joseph LoCicero III

Cardiac arrhythmia after thoracotomy is not a new problem. Since the first reports in 1943 [1,2], many communications concerning arrhythmias have appeared in the literature. For a comprehensive review, the reader is referred elsewhere. They may occur in the atrium or the ventricle, although supraventricular arrhythmias are far more common, usually accounting for over 80% of such disorders. Of these, atrial fibrillation occurs most frequently, although multifocal atrial tachycardia and atrial premature complexes are not unusual. The purposes of this chapter are (i) to describe the incidence and characteristics of cardiac arrhythmias that appear after thoracic surgery, (ii) to explain what is known about the etiology of these dysrhythmias, (iii) to report on which prophylactic regimens are thought currently to be effective against them, and (iv) to instruct the reader as to their treatment.

Incidence and characteristics of postoperative arrhythmias It has been well documented that cardiac arrhythmias, particularly atrial arrhythmias such as atrial fibrillation or flutter, occur in approximately 25–40% of patients undergoing open heart surgery [3]. The incidence of these arrhythmias following non-cardiac thoracic surgery is a bit more variable, depending upon the specific procedure. Most studies which have addressed the issue have concluded that postoperative arrhythmias serve as a marker for increased mortality, longer intensive care unit stay and longer length of hospital stay [4–6], although it is not clear if the arrhythmia itself is an independent predictor or rather a symptom of the patient’s illness.

Supraventricular As displayed in Table 3.1, atrial arrhythmias following thoracic surgery appear in 8–37% (average 20%) of all patients undergoing thoracotomy. Atrial fibrillation (AF) is by far the most common rhythm, accounting for at least 55% of supraventricular arrhythmias. The magnitude of operation plays an important role. After simple exploration or biopsy, anywhere from 4.6 to 23.5% (average 9.3%) of patients suffered an atrial arrhythmia. After lobectomy, the 48

Arrhythmias following cardiothoracic operations 49 Table 3.1 Postoperative cardiac arrhythmias.

Study

Patients

Borgeat et al. [14] Van Mieghem et al. [20] Von Knorring et al. [16] Ritchie et al. [25] Amar et al. [6] Harpole et al. [5] Wahi et al. [4] Keagy et al. [24] Amar et al. [17] Krowka et al. [7] Asamura et al. [8] Roth et al. [12] Amar et al. [15] Amar et al. [27]

30 30 598 140 100 136 197 369 100 236 267 75 78 70 (Total patients) 1000

Percent with arrhythmias 20 26 16 37 13 24 23 20 18 22 25 8 13 23 20

Percent atrial 67 57 100 69 100 100 100 81 100 100 89 100 100 100 ←(Averages)→ 91

Percent ventricular 33 43 0 18 0 0 0 15 0 0 6 0 0 0 6

Percent atrial, % of all patients with arrhythmias who demonstrated atrial fibrillation, atrial flutter, or other supraventricular tachycardia; percent ventricular, % of all patients with arrhythmias who demonstrated premature ventricular contractions, bigeminy or ventricular tachycardia or fibrillation.

incidence ranged from 1.6 to 59.1% (average 11.6%), and after pneumonectomy atrial arrhythmias appeared in 3.3–40.0% of patients (average 18.0%). After thoracotomy for esophagectomy, the incidence of supraventricular arrhythmias varied from 4.4 to 23.8% (average 17.6%). Atrial arrhythmias following pneumonectomy appear to be particularly worrisome. In a series of 236 consecutive pneumonectomies reported by the Mayo Clinic, 22% of patients experienced postoperative atrial arrhythmias, most often AF (64%) [7]. In 55%, the arrhythmia was persistent despite attempts at chemical and electrical cardioversion. In patients with refractory AF, 31% died during their hospitalization. Overall, 25% of patients in this series experiencing any kind of postoperative arrhythmia died within 30 days of surgery. This was independent of preoperative pulmonary function, postoperative diagnosis, cancer stage or arterial blood gas levels. Intrapericardial dissection and postoperative pulmonary edema increased the incidence of postoperative dysrhythmia, suggesting that cardiac manipulation and irritation may predispose to morbidity and mortality. These arrhythmias typically appear within the first 3 days of surgery, with a peak incidence around the second day [5,8]. Almost all will resolve spontaneously, as 90% disappear within the first three postoperative days, and 7.9% of the remainder will discontinue within the first week.

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Ventricular Ventricular arrhythmias, mainly appearing as either burst of extrasystoles or short runs of non-sustained tachycardia, are appearing more commonly as the acuity of illness and average patient age rise with time. Fortunately, they are much more rare than supraventricular arrhythmias, appearing in only 0–43% (average 6%) of all patients undergoing non-cardiac thoracic surgery of all types.

Risk factors Many investigators have attempted to determine the specific risks factors associated with postoperative cardiac arrhythmias. Unfortunately, no common element has emerged. In one study by Melendez and Carlon of 180 patients undergoing pneumonectomy, lobectomy, wedge resection or lesser pulmonary procedures, there was a 12% incidence of cardiac ‘complications’ [9]. The authors attempted to assign a Cardiopulmonary Risk Index (CPRI: the addition of the Goldman Cardiac Risk Index [10] to a Pulmonary Risk Index which included obesity, cough, elevated PaCO2, poor spirometric parameters, cigarette smoking and asthma) to each patient. There was no correlation between the CPRI and the incidence of cardiac arrhythmias. Furthermore, there was no correlation between postoperative arrhythmias and either the Cardiac Risk Index or the Pulmonary Risk Index when considered in isolation. Not too surprisingly, however, preoperative ‘rhythm alteration’, ‘cardiac disease’, an abnormal electrocardiogram and a forced expiratory volume in 1 s (FEV1) < 2.0 correlated positively with postoperative arrhythmias. This finding was echoed by Hasenbos and colleagues who attempted to compare differences in postoperative complications between patients given epidural or intramuscular narcotic pain medication [11]. Although this study found no differences in postoperative complications between groups according to method of pain relief, it did find that patients who were taking ‘cardiac drugs’ preoperatively had a higher risk of developing arrhythmias in the postoperative period (68% vs. 38%). This study suggests that patients with pre-existing cardiac disease are at higher risk of developing postoperative arrhythmias. In a search for anatomic risk factors for postoperative complications, Roth et al. attempted to quantify coronary artery calcifications found on chest computed tomography (CT) scan and use the Coronary Artery Calcification Index (CAC) to predict the occurrence of postoperative arrhythmias [12]. Although the CAC had 100% sensitivity for postoperative arrhythmias, its positive predictive value was only 23%, making it a weak index by which to screen patients for this complication. With a negative predictive value of 100%, however, it is helpful to know that a patient with no coronary calcifications present on chest CT will probably have a smoother postoperative course. Asamura and associates have undertaken the most complete study to date on preoperative risk factors for postoperative arrhythmias [8]. They studied

Arrhythmias following cardiothoracic operations 51

267 patients undergoing pneumonectomy, lobectomy bilobectomy, segmentectomy or wedge resection, and discovered 63 arrhythmias (23.6% incidence). Of those, 60 (95%) were supraventricular, and of that subset 33 (55%) were atrial fibrillation. Besides tabulating demographic variables such as sex, age, indication for operation, hypertension and preoperative ECG status, the authors also made note of the mode of thoracotomy, the extent of the pulmonary resection and the extent of the lymph node dissection. They found that only age > 70 years (P < 0.0008) and extent of pulmonary resection (P < 0.0001) were independent predictors for the appearance of postoperative atrial arrhythmias. There is recent evidence emerging that the side of operation may play a role in the genesis of arrhythmias following thoracic surgery, particularly pneumonectomy. In a series of 115 patients undergoing pneumonectomy, Yellin and Zeligson reported the incidence of dysrhythmias to be 4.2% in patients undergoing a left-sided operation, compared with 14% in those with a right pneumonectomy (P = 0.05) [13]. This has been supported by some studies [5], but not by others [4,14].

Influence on outcome A few studies have attempted to correlate the occurrence of postoperative arrhythmias with patient outcome. In a report of 78 patients undergoing pneumonectomy, lobectomy or wedge resection for non-small cell lung cancer, Amar et al. found 13% demonstrated postoperative dysrhythmias [15]. Somewhat surprisingly, neither the stage of the tumor, the extent of operation, nor the administration of preoperative radiation therapy influenced survival at the 30-month follow-up. This may have been due to the small study population. Survival at 30 months was, however, adversely affected by age > 70 years, perioperative chemotherapy and the occurrence of postoperative supraventricular tachycardia. The patients who died during the follow-up period did so as a result of their disease, and not from arrhythmias. In another study conducted by von Knorring and associates of 598 patients undergoing resection for lung cancer, atrial tachyarrhythmias occurred in 16% [16]. Of those patients with recurrent episodes, 17% died. This was significantly higher than the mortality rate observed in patients with limited episodes (2.5%, P < 0.01).

Specific arrhythmias and their mechanisms It is not currently known what causes atrial dysrhythmias in postoperative thoracic surgical patients. There have been many conjectures, including increased sympathetic discharge from postoperative pain, atrial fluid overload from intraoperative and postoperative resuscitation, and even increased atrial pressure from high pulmonary vascular resistance in the patient after parenchymal resection. In a study of 100 consecutive patients undergoing

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pulmonary resection at Memorial Sloan-Kettering Cancer Center, Amar et al. were able to show that patients with high right ventricular pressures (as determined by echocardiography) had a higher incidence of postoperative supraventricular tachycardias [17]. This was not associated with an elevated right atrial pressure, however, as measured by a central venous catheter. Also, the right and left atrial chambers were of normal size and did not differ between groups. These findings are partially supported by the work of Reed et al., who showed that right ventricular function is diminished following pulmonary resection [18]. They demonstrated that right ventricular end diastolic volume increased and ejection fraction decreased during the first 2 days after resection. In comparison with preoperative values, pulmonary artery systolic pressure and calculated pulmonary vascular resistance did not change. This corresponds to the period of highest risk for postoperative supraventricular tachycardia (SVT). They did not follow these patients out beyond the first 2 days, however. Also, for the 20% of patients who exhibited SVT, they did not discriminate the right ventricular variables between patients who suffered SVT and those who did not. Whether this results from a primary myocardial process or an alteration in right ventricular loading during the early postoperative period remains unclear. Although the same authors subsequently reported that right ventricular preload recruitable stroke work was unchanged during the first 24 h following surgery, which suggests that right ventricular contractility per se is unaffected [19].

Atrial premature contractions Atrial premature contractions (APCs) are characterized by a P wave appearing earlier in the cardiac cycle than anticipated, usually of a different morphology than the usual sinus P waves (Figure 3.1). This suggests that the ectopic beat originates in atrial tissue outside of the sinoatrial node. If the APC is early, it may encounter a refractory atrioventricular node (AVN), and either no impulse will be transmitted to the ventricle or the conducted impulse will depolarize the ventricle with a bundle branch pattern. If the APC enters the sinus node during electrical diastole, it may ‘reset’ the node and delay onset of the next sinus beat. The causes of APCs are legion, and they have been associated with congestive heart failure, electrolyte imbalances, myocardial ischemia and pericarditis. The use of temporary epicardial atrial wires or a transesophageal electrocardiogram can facilitate their diagnosis.

Atrial fibrillation Atrial fibrillation results from a chaotic, disorganized and irregular beating of the atrium at 400–600 times per minute. The sinus node no longer participates in the pacemaking process. The atrioventricular node, which is incapable of transmitting impulses so rapidly to the ventricle, blocks most of these beats. The ventricle therefore typically responds to atrial fibrillation by beating irre-

Arrhythmias following cardiothoracic operations 53

Figure 3.1 Premature atrial contractions. A 12-lead electrocardiogram is shown. Note the regular sinus rhythm for the first seven beats of the rhythm strip, below. On the 8th beat there is an early inverted P wave, indicating an ectopic origin. The QRS complex remains narrow and upright, indicating normal conduction through the AV node and subnodal conduction tissues.

gularly between 60 and 180 beats per minute, usually in the more rapid range (Figure 3.2). This results in the electrocardiographic hallmark of an undulating baseline with irregular, narrow QRS complexes. The subjective effect on the patient ranges from little more than a feeling of ‘doom’ or palpitations to frank hypotension and syncope. Treatment should be therefore tailored to each individual situation, depending upon the immediacy of the desired result. Most episodes of AF will resolve spontaneously within a few days of surgery. In fact, as discussed above, less than 10% of patients who experience postoperative AF will remain in it beyond 1 week. Therefore, it is uncommon to have to continue antiarrhythmic drugs beyond the first few days after surgery, even if their administration was required to convert the arrhythmia back to sinus rhythm.

Atrial flutter Atrial flutter (AFL) is a much less commonly encountered arrhythmia following thoracic surgery. It is a ‘well organized’ arrhythmia, with the atrium beating in a more regular, synchronous fashion at 200–400 beats per minute. The AV node can only transmit every second or third beat to the ventricle, usually resulting in a regular ventricular rate of 140–150 beats per minute (Figure 3.3). There is classically a ‘sawtooth’ or ‘F wave’ pattern in limb leads II, III and aVF. If the diagnosis is not clear, maneuvers to temporarily block the AV node (carotid sinus massage, Valsalva maneuver, or adenosine) will usually be helpful. Hemodynamically, this arrhythmia is usually better tolerated than AF, but occasionally ventricular rate control is required in order to allow more

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Figure 3.2 Atrial fibrillation. A 12-lead electrocardiogram is shown. Note the rapid rate of the ventricular response and the irregularity of the rhythm. There is no isoelectric baseline between QRS complexes. There is no discernible P wave. The QRS complexes are narrow, indicating normal conduction through the AV node and subnodal conduction tissues. (This patient has ECG evidence of an old anteroseptal myocardial infarction, as well as left ventricular hypertrophy.)

Figure 3.3 Atrial flutter. A 12-lead electrocardiogram is shown. Note the rapid ventricular rate, but this time with a very regular rhythm. There are clearly discernible P waves, each with a fixed relationship to the QRS complex. Flutter (‘F’) waves are visible in leads II, III, and aVF, indicating common atrial flutter with 2 : 1 conduction through the AV node. The QRS complexes here are also narrow, indicating normal conduction through the AV node and subnodal conduction tissues.

time for diastolic filling and ejection. Because AFL is much more rare than AF, less is known about its natural history. It stands to reason, however, that AFL in the postoperative period should follow the same time course as AF, as the immediate stimulus for this arrhythmia abates with time.

Arrhythmias following cardiothoracic operations 55

Figure 3.4 Multifocal atrial tachycardia.

Multifocal atrial tachycardia Multifocal atrial tachycardia (MAT) is an arrhythmia most often associated with chronic obstructive pulmonary disease, a disorder common to many patients undergoing thoracic surgery. Therefore, its appearance may be due to either the stimulus of surgery or as a baseline rhythm disturbance. Its cause is unknown and its treatment non-specific. It is defined as a rhythm with an atrial rate of between 100 and 200 beats per minute with at least three different P wave morphologies. The R–R and P–R intervals will usually vary, as there are multiple pacemaking sites in the atrium, each a different distance from the AV node (Figure 3.4). MAT may degenerate into AF.

Premature ventricular complexes Premature ventricular beats or complexes (PVB or PVC) are fortunately much less common in the postoperative period than are supraventricular rhythms (Figure 3.5). Their origin is more often traced to myocardial ischemia and/or electrolyte disturbances, typically as a result of microreentrant circuits in small areas of abnormal ventricular myocardium. The QRS complex will be wide and bizarre, mimicking a bundle branch pattern of conduction. There is no relationship to the P wave. If the PVC conducts in a retrograde manner through excitable tissue such as the AV node and SA node, then these pacemakers may be ‘reset’, and a compensatory pause will appear. PVCs may be classified as unifocal, if there is one morphology, or multifocal if there are two or more different morphologies. This implies that unifocal

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Figure 3.5 Premature ventricular complexes. A 12-lead electrocardiogram is presented. Note the normal appearance of the first, third, fourth and sixth through ninth beats. There is a P wave coupled to a narrow, upright QRS complex. The second and fifth beats, however, are very large, bizarre-looking, and appear similar to beats seen in bundle branch block. There is no fixed relationship between these beats and the preceding P wave. They are clearly of ventricular origin.

PVCs arise from a single locus in the ventricle, whereas multifocal ectopic beats arise from several sites. Occasionally, as mentioned above, a supraventricular impulse may encounter refractory conducting tissue and appear very similar to a PVC. If the bizarre QRS complex is preceded by a P wave and there has been a long–short sequence of R–R intervals, then it is likely that an APC or other supraventricular ectopic beat has encountered refractory conduction tissue. This is known as Ashman’s phenomenon.

Ventricular tachycardia Ventricular tachycardia (VT) is defined as three or more consecutive beats of ventricular origin at a rate of greater than 100 beats per minute. They are always wide-complex beats with no relationship to the P wave (Figure 3.6). Although it may sometimes be difficult to discriminate VT from SVT with aberrant conduction, VT typically will not terminate with vagal maneuvers, and is almost always associated with hemodynamic collapse. Therefore, resuscitation is paramount, and diagnosis can be established after a stable rhythm has returned.

Antiarrhythmic drug prophylaxis Since the description of postoperative arrhythmias, there have been attempts to prevent them. Drug trials using amiodarone, digoxin, diltiazam, flecainide and propranolol have all appeared in the literature, ranging from randomized, prospective studies to retrospective chart reviews. The results have, unfortunately, been mixed.

Arrhythmias following cardiothoracic operations 57

Figure 3.6 Ventricular tachycardia. A 12-lead electrocardiogram is presented. Note the rapid rate with a very regular rhythm. Each beat a wide QRS complex, of left bundle branch block configuration. The P waves are difficult to discern, but are indicated by the large solid arrows. There is no relationship between the P waves and QRS complexes. This is clearly of ventricular origin.

Amiodarone Amiodarone, which possesses all four of the Vaughan-Williams classifications of antiarrhythmic drug action (sodium channel, calcium channel, potassium channel and β-adrenergic receptor blockade), has been used increasingly frequently as an agent against atrial arrhythmias. Unfortunately, amiodarone is associated with thyroid, ophthalmic and pulmonary toxicities. Van Meighem et al. attempted to use amiodarone as a prophylactic agent against postoperative arrhythmias following pulmonary surgery [20]. They terminated their study prematurely, after three of 96 patients enrolled developed life-threatening adult respiratory distress syndrome (ARDS), with a mortality of 67%. This did not seem to result from toxic levels of amiodarone, as these patients demonstrated similar serum levels of drug to those patients without complication. In a review of their experience from 1987 to 1991, 552 major pulmonary resections had been performed, with an overall incidence of AF between 16% and 23%. The incidence of ARDS in patients receiving amiodarone was 11%, compared with 1.8% in patients who did not receive this drug. This particular adverse effect has not yet been reported in the cardiac surgical population, in whom amiodarone has been shown to effectively halve the rate of postoperative AF [21–24].

Digoxin Prophylactic ‘digitalization’ has been attempted several times in order to minimize the occurrence of postoperative arrhythmias, both in cardiac and in

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non-cardiac thoracic surgical patients. In a randomized controlled unblinded study of 80 consecutive patients undergoing thoracotomy for esophagectomy, Ritchie et al. randomly assigned half of the patients to receive digoxin and half to receive no treatment [25]. The drug was begun preoperatively and continued postoperatively for 9 days, with serum levels measured and adjusted appropriately. There was no difference in the occurrence of dysrhythmias between the patient groups. The authors did not discriminate between atrial and ventricular arrhythmias. They did, however, clearly demonstrate that patients undergoing resection for benign disease had a significantly lower incidence of arrhythmia than did those having an operation for malignancy (0% vs. 39%, P < 0.002). They extended their findings in a study of 140 patients undergoing thoracotomy for pulmonary and esophageal procedures [26]. The overall incidence of arrhythmias was 37%, with no differences between digoxin-treated patients and control.

Diltiazem In a small study of patients undergoing pneumonectomy at memorial SloanKettering Cancer Center, digoxin was compared with diltiazem for postoperative control of arrythmias [27]. Patients on digoxin had an incidence of 31% supraventricular arrythmias while those on diltiazem had an incidence of 14% (P = 0.09). However, in the subset of patients having an intrapericardial pneumonectomy, diltiazem patients had no supraventricular arrythmias compared with 32% in the digoxin arm (P < 0.005). No patients in the study had ventricular tachycardia, although most had occasional ventricular premature beats.

Flecainide In a randomized, placebo-controlled single-blinded study of 30 patients undergoing pneumonectomy, lobectomy or decortication, Borgeat et al. determined that flecainide administration immediately following operation resulted in a significant decrease in the use of additional antiarrhythmic drugs [14]. Because these authors did not consider the incidence of atrial arrhythmias as a separate endpoint, one cannot draw a conclusion about the efficacy of flecainide against this rhythm. There was, however, a significant decrease in the incidence of PVCs. In another study by this same group comparing the postoperative administration of flecainide with digoxin, the same group showed that flecainide significantly decreased the incidence of AF (by 50%) and PVCs (by 100%) [28].

Propranolol In 1999, Bayliff and associates conducted a randomized trial of propranolol vs. placebo in patients undergoing a major pulmonary resection [29]. This study was somewhat flawed because of a large number of patients (142 out of 242) who did not participate in the study. They were able to randomize 99 of the

Arrhythmias following cardiothoracic operations 59

100 patients in the study. Patients in the experimental arm received 10 mg of propranolol every 6 h. Arrythmias of any variety occurred in 62% of placebo patients and 72% in the propranolol group. However, rhythms that required treatment were 20% in the placebo patients and 6% in the propranolol patients. Only AF occurred in the propranolol group while every rhythm including ventricular tachycardia was seen in the placebo group. Hypotension and bradycardia were common in the propranolol group at 49% and 25%, respectively, while both were significantly less in the placebo group at 26% and 4%, respectively. Although it seemed to be effective, the side-effects argue against the routine use of propranolol in thoracic surgery.

Treatment The treatment of postoperative arrhythmias is controversial. A brief review of the most commonly used medications is presented in Table 3.2, and a suggested treatment algorithm is presented in Figure 3.7. Because atrial arrhythmias are far more common, their management is discussed in some detail below. In contrast, because the treatment of ventricular arrhythmias relies primarily upon resuscitation of the patient from a hemodynamically unstable situation, little else will be said about them. The principles of correcting electrolyte abnormalities and ruling out myocardial ischemia should be paramount for patients demonstrating ventricular ectopy and/or tachycardia. Once the diagnosis of an atrial tachyarrhythmia has been established, the first priority is to assess hemodynamic stability. If the patient experiences syncope, or if the blood pressure is < 80 mmHg systolic, then synchronous electrical cardioversion should be performed. The first shock is typically delivered at 200 J, with subsequent shocks at 300 J and 360 J, respectively. For the syncopal patient, no premedication is required. For the patient who is mentating, however, some sedation should be administered prior to cardioversion. Sometimes this will depress the blood pressure further, requiring intravenous fluid administration.

Table 3.2 Commonly used antiarrhythmic agents. Drug

Class

Loading dose

Maintenance dose

Adenosine Digoxin Procainamide Metoprolol* Verapamil Diltiazem

(Unassigned) (Unassigned) I-A II IV IV

6–12 mg rapid i.v. push 1.0–1.5 mg/4 doses/12 h 17 mg/kg (load over 20 min) 5–10 mg i.v. bolus 5–10 mg i.v. bolus 0.25 mg/kg (load over 10 min)

(None) 0.125–0.25 mg/day p.o. or i.v. 2 mg/min i.v. infusion 5–10 mg i.v. q 1–2 h 5–10 mg i.v. q 1–2 h 5–10 mg/min i.v. infusion

‘Class’ refers to Vaughan-Williams classification; i.v., intravenous. *b-Blockers are contraindicated in patients with bronchospastic disease or known hypersensitivity to the drug.

Diagnosis Atrial tachyarrhythmia

Hemodynamically stable? (BP > 80 mmHg systolic) NO YES

Electrically cardiovert***

Achieve ventricular rate control*

NO HR 60–100 bpm ?

YES

Resolved within 24 hours?

YES

No further treatment

NO Chemical cardioversion**

Sinus rhythm within 24 hours?

YES

NO

Electrical cardioversion

Sinus rhythm?

YES

Continue antiarrhythmic drug

NO

Start anticoagulation

Figure 3.7 Suggested treatment algorithm. Once the diagnosis of atrial tachyarrhythmia is established, this algorithm follows that suggested in the text. Key: *Ventricular rate control may be achieved through any combination of AV nodal blocking drugs, such as digoxin, verapamil and/or diltiazem. b-Adrenergic blocking drugs are generally discouraged in this patient population, due to bronchospasm. **Chemical cardioversion is typically undertaken first with procainamide, as described in the text. ***DC synchronous electrical cardioversion is initially attempted at 200 J. If unsuccessful, then another shock at 300 J and then 360 J may be required.

Arrhythmias following cardiothoracic operations 61

Ventricular rate control If the patient is hemodynamically stable and mentating, then the next priority should be to achieve control over the ventricular rate, as it is usually rapid (140–200 beats per minute). Drugs such as digoxin, verapamil, diltiazem or metoprolol all depress AV nodal conduction, and are most useful here. Many thoracic surgical patients exhibit bronchospasm, however, and therefore β-adrenergic blocking drugs are relatively contraindicated. Furthermore, β-blockers are frequently longer-acting than calcium channel blocking drugs and are not as easy to reverse should an adverse effect appear. For these reasons, this author prefers to use digoxin (0.5-mg i.v. bolus, followed by two 0.25-mg i.v. boluses spaced 4 h apart) combined with verapamil (5–10-mg i.v. bolus every 5–10 min) or diltiazem (0.25–0.35 mg/kg i.v. bolus every 5–10 min) to control ventricular rate. If these drugs are not successful, or if the patient’s hemodynamics deteriorate, then synchronous cardioversion should be undertaken immediately. Once rate control has been achieved, the patient may be transitioned over to equivalent doses of oral digoxin and verapamil or diltiazem over the next 24 h. During this period of time, electrolytes such as potassium and magnesium should be assayed and repleted. Myocardial ischemia should be ruled out by electrocardiography. In the absence of these factors, the natural history of postoperative atrial tachyarrhythmias is self-termination. Therefore, usually nothing more than a day or two of rate control is required. If the patient does, indeed, spontaneously convert back to normal sinus rhythm over the next 24 h, the digoxin and calcium channel blocker can be discontinued and no further treatment is required.

Cardioversion If, however, the patient remains in a rate-controlled fibrillation or flutter beyond 24 h, then cardioversion should be attempted. Usually this is begun as a trial of chemical cardioversion with antiarrhythmic medication. Unfortunately, there is no single drug which demonstrated high efficacy at converting postoperative AF or AFL to sinus rhythm. The class I-A agents such as procainamide and quinidine exhibit approximately a 30% conversion rate, similar to placebo. The class I-C agents such as flecainide and propafanone claim a somewhat higher conversion rate (about 40–60%), but their use is contraindicated in patients recently following a myocardial infarction or with a known depressed ejection fractionamany of the patients who are seen on thoracic surgical services. The new class III agent, ibutilide, claims a very high conversion rate of approximately 60%, but is associated with both a high relapse rate and also the appearance of malignant ventricular arrhythmias such as Torsades de Pointes. One of the older class III agents, d-sotalol, has been shown to be effective at converting AF to sinus rhythm, but the racemic mixture of d- and l-sotalol has significant β-blocking activity and is relatively contraindicated in thoracic surgical patients. Despite its relative lack of efficacy, the most often used and recommended drug for chemical cardioversion is procainamide. It is easy to load (17 mg/kg

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i.v. over 20 min), has relatively few acute limiting side-effects (hypotension, nausea), and is quickly metabolized. Unlike quinidine, which has anticholinergic side-effects, procainamide has some antiadrenergic effects, and can therefore ‘double’ as an AV nodal blocking drug. Once the patient has been given a procainamide load, they are started on a continuous infusion of 2–4 mg/min. If the patient is taking oral medications, then Procan SR® or ProcanBID® can be started by mouth once the loading dose is completed. The infusion is stopped after the second oral dose. If the patient converts to sinus rhythm, then the oral antiarrhythmic drug should be continued for at least 30 days after surgery. It may then be stopped as an out-patient, as the risk of relapsing into AF or AFL is extremely unlikely so far out from operation. If the arrhythmia persists, however, two options are available. First, a semielective electrical cardioversion may be undertaken at this time, with adequate serum levels of antiarrhythmic drug present. Second, the patient may be given anticoagulation with heparin and then maintained on warfarin. Typically, if a patient is discharged from the hospital in rate-controlled AF with adequate anticoagulation, they will spontaneously convert to sinus rhythm as an out-patient. If, however, they remain in AF beyond 30 postoperative days, then they should be at low risk for an out-patient electrical cardioversion, provided they have remained therapeutically anticoagulated.

Summary Cardiac arrhythmias are common after thoracic surgical procedures. Most arrhythmias are atrial in origin and typically are not life threatening, although there are some data which suggest that they adversely affect long-term prognosis. Their cause remains unclear, although there is some indication that acute right ventricular overload may contribute. Risk factors for atrial arrhythmias following thoracotomy appear to be increasing patient age, extent of operation and perhaps side of operation. These arrhythmias typically occur within the first 2–3 days after surgery, and usually abate by day 6. Treatment should initially be aimed at achieving ventricular rate, with the hope that most patients will spontaneously convert back to normal sinus rhythm. Should conservative measures fail at cardioversion, then anticoagulation should be instituted and electrical cardioversion can be attempted, either as an in-patient or later, as an out-patient.

References 1 Currens JH, White PD, Churchill ED. Cardiac arrhythmias following thoracic surgery. N Engl J Med 1943; 229: 360–364. 2 Baley CC, Betts RH. Cardiac arrhythmias following pneumonectomy. N Engl J Med 1943; 229: 356–360. 3 Ferguson TB Jr. Arrhythmias associated with thoracotomy. In: Wolfe WG, ed. Complications in Thoracic Surgery. Recognition and Management. St Louis: Mosby, 1992; 28–50.

Arrhythmias following cardiothoracic operations 63 4 Wahi R, McMurtrey MJ, DeCaro LF et al. Determinants of perioperative morbidity and mortality after pneumonectomy. Ann Thoracic Surg 1989; 48: 33 –37. 5 Harpole DH, Liptay MJ, DeCamp MM Jr, Mentzer SJ, Swanson SJ, Sugarbaker DJ. Prospective analysis of pneumonectomy: risk factors for major morbidity and cardiac dysrhythmias. Ann Thoracic Surg 1996; 61: 977–982. 6 Amar D, Burt ME, Bains MS, Leung DH. Symptomatic tachydysrhythmias after esophagectomy: incidence and outcome measures. Ann Thoracic Surg 1996; 61: 1506–1509. 7 Krowka MJ, Pairolero PC, Trastek VF, Payne WS, Bernatz PE. Cardiac dysrhythmia following pneumonectomy. Clinical correlates and prognostic significance. Chest 1987; 91: 490–495. 8 Asamura H, Naruke T, Tsuchiya R, Goya T, Kondo H, Suemasu K. What are the risk factors for arrhythmias after thoracic operations? A retrospective multivariate analysis of 267 consecutive thoracic operations. J Thoracic Cardiovasc Surg 1993; 106: 1104–1110. 9 Melendez JA, Carlon VA. Cardiopulmonary risk index does not predict complications after thoracic surgery. Chest 1998; 114: 69–75. 10 Goldman L, Caldera DL, Nussbaum SR et al. Multifactorial index of cardiac risk in noncardiac surgical procedures. N Engl J Med 1977; 297: 845–850. 11 Hasenbos M, van Egmond J, Gielen M, Crul JF. Post-operative analgesia by epidural versus intramuscular nicomorphine after thoracotomy. Part II. Acta Anesthesiologica Scand 1985; 29: 577–582. 12 Roth BJ, Meyer CA. Coronary artery calcification at CT as a predictor for cardiac complications of thoracic surgery. J Comp Assisted Tomogr 1997; 21: 619–622. 13 Yellin A, Zeligson E. Postpneumonectomy dysrhythmias. Chest 1988; 93: 669 (letter). 14 Borgeat A, Biollaz J, Bayer-Berger M, Kappenberger L, Chapuis G, Chiolero R. Prevention of arrhythmias by flecainide after noncardiac thoracic surgery. Ann Thoracic Surg 1989; 48: 232–234. 15 Amar D, Burt M, Reinsel RA, Leung DH. Relationship of early postoperative dysrhythmias and long-term outcome after resection of nonsmall cell lung cancer. Chest 1996; 110: 437–439. 16 von Knorring J, Lepantalo M, Lindgren L, Lindfors O. Cardiac arrhythmias and myocardial ischemia after thoracotomy for lung cancer. Ann Thoracic Surg 1992; 53: 642–647. 17 Amar D, Roistacher N, Burt M, Reinsel RA, Ginsberg RJ, Wilson RS. Clinical and echocardiographic correlates of symptomatic tachydysrhythmias after noncardiac thoracic surgery. Chest 1995; 108: 349–354. 18 Reed CE, Spinale FG, Crawford FA Jr. Effect of pulmonary resection on right ventricular function. Ann Thoracic Surg 1992; 53: 578–582. 19 Reed CE, Dorman BH, Spinale FG. Assessment of right ventricular contractile performance after pulmonary resection. Ann Thoracic Surg 1993; 56: 426–431; discussion 431–432. 20 Van Mieghem W, Coolen L, Malysse I, Lacquet LM, Deneffe GJ, Demedts MG. Amiodarone and the development of ARDS after lung surgery. Chest 1994; 105: 1642–1645. 21 Daoud EG, Strickberger SA, Man KC et al. Preoperative amiodarone as prophylaxis against atrial fibrillation after heart surgery. N Engl J Med 1997; 337: 1785–1791. 22 Rady MY, Ryan T, Starr NJ. Preoperative therapy with amiodarone and the incidence of acute organ dysfunction after cardiac surgery. Anesth Analg 1997; 85: 489–497. 23 Dimopoulou I, Marathias K, Daganou M et al. Low-dose amiodarone-related complications after cardiac operations. J Thorac Cardiovasc Surg 1997; 114: 31–37. 24 Keagy BA, Lores ME, Starek PJ, Murray GF, Lucas CL, Wilcox BR. Elective pulmonary lobectomy: factors associated with morbidity and operative mortality. Ann Thorac Surg 1985; 40: 349–352.

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25 Ritchie AJ, Bowe P, Gibbons JR. Prophylactic digitalization for thoracotomy: a reassessment. Ann Thorac Surg 1990; 50: 86–88. 26 Ritchie AJ, Tolan M, Whiteside M, McGuigan JA, Gibbons JR. Prophylactic digitalization fails to control dysrhythmia in thoracic esophageal operations. Ann Thorac Surg 1993; 55: 86–88. 27 Amar D, Roistacher N, Burt ME et al. Effects of diltiazem versus digoxin on dysrhythmias and cardiac function after pneumonectomy. Ann Thorac Surg 1997; 63: 1374–1381; discussion 1381–1382. 28 Borgeat A, Petropoulos P, Cavin R, Biollaz J, Munafo A, Schwander D. Prevention of arrhythmias after noncardiac thoracic operations: flecainide versus digoxin. Ann Thorac Surg 1991; 51: 964–967; discussion 967–968. 29 Bayliff CD, Massel DR, Inculet RI et al. Propranolol for the prevention of postoperative arrhythmias in general thoracic surgery. Ann Thorac Surg 1999; 67: 182–186.

PA RT II

Complications of general thoracic surgery

CHAPTER 4

Complications of pulmonary resection Stephen J Burke, L Penfield Faber

The avoidance of postoperative complications after pulmonary resection remains the goal of every thoracic surgeon. Many risk factors may contribute to the development of postoperative complications (Table 4.1). The major complications that more frequently occur are listed in Table 4.2. Intraoperative prevention, prompt diagnosis, and appropriate treatment will decrease morbidity. The following discussion will review common complications which need to be recognized early and managed efficiently in a busy thoracic service.

Atelectasis Partial or complete collapse of a segment of lung due to atelectasis and retained secretions plagues to some degree many pulmonary resections. The incidence of postoperative atelectasis varies in the literature with a range from 10% to 70% [1]. Atelectasis is one of the most common complications following thoracic surgery; the most average incidence being 20–30%. We reviewed our complications following pulmonary resection from 1 January 1994 to 1 January 1999. There were 194 complications in 1243 resections. Nearly 10% of postoperative complications requiring further intervention were due to atelectasis or retained secretions (Table 4.3).

Table 4.1 Risk factors for postoperative complications. 1 2 3 4 5 6 7 8 9 10 11 12

Extensive resection Right side vs. left side Diagnosis: inflammatory or cancer vs. benign Sex: male vs. female Adjuvant chemoradiation therapy FEV1 < 800 ml Dlco < 70% Comorbidity: CAD, COPD, poor nutrition Preoperative steroid use Postoperative infection Prolonged ventilatory support Surgical technique

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1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 19 20 21 22 23 24

1 2 3 4 5 6 7 8 9 10 11 12 13 14 15

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Arrhythmias Atelectasis/secretions Alveolopleural fistula Intrapleural space Bronchopleural fistula Hemorrhage Pulmonary edema Lobar torsion Pneumonia Wound infection Chylothorax Esophageal injury Cardiac herniation Recurrent/vagus nerve injury Tumor embolus Cerebrovascular accident Myocardial infarction GI bleed Bronchovascular fistula Empyema Subcutaneous emphysema Right pneumonectomy syndrome Pulmonary embolus ARDS

Event

Patients (%)

Atelectasis/secretions Alveolopleural fistula† Empyema Bronchopleural fistula Nerve injury Chylothorax Lobar torsion Cardiac herniation Hemorrhage Infection ARDS Death DVT/PE Aspiration pneumonitis Other

22 (11.3) 48 (24.7) 2 (1.0) 9 (4.6) 11 (5.6) 4 (2.0) 1 (0.5) 0 (0.0) 9 (4.6) 12 (6.7) 6 (3.1) 36 (18.5) 4 (2.0) 4 (2.0) 25 (13.0)

*1243 lung resections from January 1994 to January 1999 at a tertiary thoracic center. †Defined: air leak present after 7 days.

Table 4.2 Complications of pulmonary resection.

Table 4.3 Incidence of postoperative complications.*

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The etiology of atelectasis is complex and the understanding and treatment of postoperative atelectasis is of vital importance. The development of mucous plugs and eventual reabsorption of trapped alveolar gas is a major cause of atelectasis [2]. Contributing to the obstruction may be blood or bronchospasm. Ineffective pain relief may also contribute to shallow breathing and poor expansion of segments of the lung. Once collapsed, the alveoli surface tension make re-expansion difficult. Clinically, work of breathing increases and atelectasis manifests as tachypnea, fever, tachycardia, or hypoxia. Lung compliance, functional residual capacity, and vital capacity decrease with physiologically significant atelectasis [3]. Radiographically, atelectasis may present as linear densities, segmental or lobar collapse, or diffuse involvement. These are all signs that treatment is needed. Treatment of atelectasis begins with prevention. Preoperatively, patients should be strongly encouraged to stop smoking, even if only for a few days before surgery. Bronchospasm should be under control. Perioperative incentive spirometry combined with walking are encouraged for all patients. Adequate analgesia can be offered by many methods. We prefer the routine use of epidural anesthesia for 3 to 5 days postoperatively and have found excellent control of pain with this practice. Intraoperatively, visualizing reexpansion of all segments of the lung at the completion of the procedure is mandatory. If thick secretions are present intraoperatively or a sleeve resection has been performed, fiberoptic bronchoscopy is done at the completion of surgery to remove retained secretions. Postoperatively, treatment of atelectasis involves several interventions. Most patients are extubated in the operating room and prompt elevation of the head of the bed to 45° is begun in the recovery room. Patients are mobilized to a chair the night of surgery and ambulation is begun on postoperative day 1. Incentive spirometry begins in the recovery room and continues during hospitalization. Most patients respond to this treatment. If atelectasis persists with copious secretions, nasotracheal aspiration is begun to assist the removal of secretions and stimulate the patient to cough. In the presence of thick pulmonary secretions and physiologically significant collapse of the lung, fiberoptic bronchoscopy is performed at the bedside. Fiberoptic bronchoscopy with topical anesthesia may need to be repeated until full re-expansion can be achieved (Figure 4.1). In our review, 95% of patients needing intervention for atelectasis and retained secretions responded with bronchoscopy alone. Rarely do patients need further assistance by a tracheostomy or minitracheostomy [4]. Both allow direct passage of catheters into the airway with removal of secretions. The use of intermittent positive pressure breathing or selective hyperventilation of collapsed segments for the treatment of postoperative atelectasis has not been proven [1]. Most patients with atelectasis can be treated with prevention and minimal interventional techniques, and attention to prevention decreases its incidence.

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(a)

(b) Figure 4.1 (a) Atelectasis of right middle and lower lobes following right upper lobectomy. (b) Expansion following fiberoptic bronchoscopy. Note apical space.

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Intrapleural spaces When the lung fails to fill the intrathoracic cavity, an interpleural space will develop. This occurs in approximately 11–29% of pulmonary resections [5–7]. After pulmonary resection, the intrapleural space is normally compensated for by: (i) expansion of the remaining lung, (ii) mediastinal shift, (iii) narrowing of the intercostal spaces, and (iv) elevation of the diaphragm [8]. Failure of these compensatory mechanisms due to non-compliance of the remaining lung, mediastinal fibrosis, or persistent air leaks manifests as a postoperative space with its associated complications. Several studies have looked at the natural history of pleural spaces [5–9]. Kirsch and associates reported that 74% of pleural spaces undergo spontaneous resolution, 13% resolve with temporary tube drainage, and 7% persist after drainage, but do not become infected. Only 6% of pleural spaces go on to become infected [9]. Similarly, Silver and colleagues reported a postoperative space in 29% of patients with 12% developing an empyema [7]. Several steps can be used to prevent intrapleural spaces (Figure 4.2). Preoperative status may suggest intraoperative risk of pleural spaces. Pulmonary functions tests may indicate pulmonary fibrosis and loss of lung compliance. Also, patients with known inflammatory disease are at increased risk of postoperative spaces. These patients may benefit from more limited resections such as segmentectomy or wedge resection. Intraoperatively, separate chest tubes

Figure 4.2 Suggested management of the postoperative space. (From [1].)

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(a)

(b)

Figure 4.3 Persistence space seen in the frontal (a) and lateral (b) projections. Space will obliterate over several weeks.

should drain the apex and the base. Several intraoperative maneuvers exist to minimize postoperative space problems (Figure 4.3). These include pleural tent, phrenic nerve crush, transplantation of the diaphragm, thoracoplasty, or pneumoperitoneum. Pleural tents in our experience adhere to the lung surface and expedite the closure of parenchymal air leaks. The space above the pleural tent fills with fluid and becomes fibrotic (Figure 4.4). This effectively eliminates a space problem. Phrenic nerve crush and transplantation of the

Complications of pulmonary resection 73

(a)

(b) Figure 4.4 (a) Pleural tent constructed intraoperatively to minimize space complications following right upper lobectomy and superior segmentectomy of the right lower lobe. (b) Expansion of the residual lung with apical fibrosis above the pleural tent.

diaphragm elevate the diaphragm, but at the expense of its function. Its only indication may be following right middle and lower lobectomy. The disadvantage of a poor cough in the postoperative period usually outweighs its benefit in reducing an intrapleural space. If more extensive resection is planned or encountered, a thoracoplasty may be considered. A tailoring thoracoplasty involves subperiosteal resection of the first, second, and half of the

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third ribs. This will decrease the apical space and can be done at the time of surgery if a postero-lateral thoracotomy has been done. More extensive thoracoplasties are large operations, disfiguring, and often associated with inadequate postoperative ventilation. Pneumoperitoneum is one maneuver that can be used intraoperatively or postoperatively to reduce a pleural space. Our technique is to insufflate 1000–1500 cm3 of air into the peritoneal cavity to elevate the diaphragm. More air may be insufflated if the diaphragm has not risen and the patient is still comfortable. The elevated diaphragm pushes the lung to the apex and usually stops the air leak (Figure 4.5).

(a)

(b)

Figure 4.5 (a) Pneumoperitoneum carried out postoperatively for significant air leak and an apical space following right upper lobectomy in a patient with pulmonary fibrosis. (b) Lateral projection clearly shows the elevated diaphragm.

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If a pleural space is present postoperatively, several strategies can be used to eliminate or reduce the space. When chest tubes are in proper position at the apex and base, more suction can be applied to the chest tube. We routinely place chest tubes to 20 cm water suction at the completion of the resection; but this may be increased to 30–40 cm water suction. Suction pressure above this will often cause patient discomfort with minimum benefit. Moderate increases in suction of ≤ 10 cm are better tolerated when increasing suction. Removal of secretions is also important to reduce postoperative spaces. Cough and humidification are usually effective; but for persistent spaces, fiberoptic bronchoscopy has been effectively employed to clear the airway and further expand the lung. If no air leak is present with a pleural space, the chest tube is taken off suction. If no air leak or increase in size of the space is noted over 24 h, the chest tube can be removed. The great majority of these spaces will resolve and can be followed with serial chest X-rays. We do not send these patients home on antibiotics and the incidence of an infected space is small. When persistent air leaks or infection are present, the need for further surgical intervention is considered. During the first 2 weeks postoperatively, experience is used to guide whether air leaks will seal on their own or require surgical closure. Empyemas need to be drained (Figure 4.6). Small, infected spaces will often close with fibrin scar if chest tubes are slowly removed at weekly intervals. If the space is large or does not resolve, the space can be obliterated with a thoracoplasty or muscle flap closure. Muscle flaps commonly used include: pectoralis major, serratus anterior, and latissimus dorsi. Omentum has also been used to close bronchial fistula and obliterate pleural spaces. By using these guidelines most pleural spaces can be effectively resolved.

(a) Figure 4.6 (a) Chest tube connected to a Heimlich valve for prolonged air leak (continued p. 76).

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(b)

(c)

(d) Figure 4.6 (cont’d) (b) Patient presents 3 weeks after chest tube removal with apical empyema. (c) Pig-tail catheter is placed for drainage. (d) Follow-up chest film six months after catheter removal.

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Alveolopleural fistula (prolonged air leak) Many patients after pulmonary resection will have some degree of postoperative air leakage. Most small air leaks will close spontaneously within 2 to 5 days; those persisting beyond 1 week are considered to be complications because of their increased morbidity. The incidence of prolonged, postoperative air leaks is 4–15%. Prolonged air leaks were our most common complication and accounted for almost 25% of complications requiring further intervention (Table 4.3). Understanding the management of prolonged air leaks is fundamental to thoracic surgery. Most air leaks are termed alveolopleural fistula as they arise from exposed small bronchi or alveoli. Bronchopleural fistulas arise from larger bronchi and will be discussed separately. These alveolopleural fistulas usually close within 7 days. They occur where the visceral pleura has been torn or stripped from the lung, after transecting incomplete fissures, during non-anatomic resections, or from staple lines in emphysematous lung following wedge resections or bullectomy. These leaks can be minimized with careful surgical technique. Automatic stapling devices have reduced the incidence of air leak when dividing incomplete fissures; but care should still be used to define anatomical boundaries and avoid trauma when developing a window for the stapler. With emphysematous lungs, pericardial or GORE-TEX (W.L. Gore & Associates, Inc., Flagstaff, AZ, USA) guards over the stapler will reinforce the staple line. At completion of the operation, the lung is submerged in saline and inflated to 20–25 cm airway pressure. Air leaks in the staple line or lung parenchyma are reinforced with sutures. Most staple lines do not need to be reinforced. Small air leaks located at the window for insertion of the stapler should be controlled with well-placed sutures that avoid the major arteries and veins. Persistent air leaks following suture placement will often respond to pedicled flaps of either pleura or pericardial fat. Although not air-tight, these flaps along with complete expansion of the lung will allow apposition of the lung surfaces and minimize most air leaks. Fibrin glue can also be applied to the lung surface to minimize air leaks and is now commercially available [10]. If an air leak persists for longer than 7 days, several therapeutic maneuvers may be performed (Figure 4.7). All tubing and connections should be checked for possible air leaks in the tubing system. The chest tube may also be withdrawn a few centimeters in order for the holes in the chest tube to be repositioned. It has been postulated that suction applied to holes in the chest tube may keep air leaks open if positioned directly over the air leak. Moving the tube allows pleural surfaces to come in contact with each other and help to seal the air leak. After these maneuvers, the chest tube can be placed to water seal to see if the air leak continues and if a postoperative space develops. Suction is restarted if a space develops. If the lung remains expanded, the chest tube may be withdrawn in the presence of a small air leak, but the tube must be reinserted and the lung fully expanded if a large space reforms. Talc or a sclerosant

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Figure 4.7 Suggested management of prolonged air leak. (From [1].)

can be instilled through the chest tube to create an inflammatory reaction to stop the leak. If a large air leak persists or a recurrent space requires reinsertion of a chest tube, the air leak is managed with either long-term suction or placement of a Heimlich valve to one or both chest tubes. In our review, over 80% of persistent air leaks could be treated with Heimlich valves on an out-patient basis. The patient is seen in follow-up at weekly intervals to determine if the air leak has sealed. Usually the air leak has resolved in 1–3 weeks. If the air leak is present at 3 weeks after surgery, reoperation is strongly considered. If the air leak persists for more than 4 weeks after discharge from the hospital, the space is considered infected and the chest tube is converted to a chronic empyema tube that is slowly withdrawn over weeks. Heimlich valves were not appropriate for 8% of our persistent air leaks due to increased size of the space off of suction. Their chest tubes remained on suction to eliminate pleural spaces and all eventually closed spontaneously. Similarly, 10% (5/48) of patients with a prolonged air leak in our experience required re-exploration for surgical closure of persistent air leaks. Using these maneuvers, air leaks can be managed effectively with minimal need for further surgery.

Bronchopleural fistula/empyema Bronchopleural fistula implies a larger communication between the bronchi and the pleural space. The incidence of bronchopleural fistula after pulmonary resection has ranged from 1 to 5% in recent reviews [8,11–13]. Bronchopleural fistulas accounted for only 5% of our recent complications; but the morbidity and mortality still remains high. Our mortality was 20% (2/9) in patients with a bronchopleural fistula over the last 5 years. Several risks factors contribute to the development of bronchopleural fistulas. Older age at the time of resection increases the risk for postoperative bronchopleural fistula. Poor wound healing secondary to poor nutrition and adjuvant chemoradiotherapy also

Complications of pulmonary resection 79

contributes to postoperative fistula formation. Preoperative bronchoscopy may visualize inflammation or infection at the site of planned bronchial resection. Elective surgery may be delayed or special steps taken to adequately cover the bronchus with a vascularized flap. Bronchoscopy will also visualize the endobronchial extent of tumor invasion to plan a resection free of cancer and minimize fistula formation. Infection in the pleural space will also enhance poor healing of the bronchial stump with fistula formation. Technical factors may also influence the incidence of bronchopleural fistulas. An excessively long bronchial stump has the tendency to accumulate secretions leading to bronchial disruption. The bronchus should be resected as close to the trachea or bronchial lumen without compromise. Special care should be taken to avoid devascularizing the remaining tracheobronchial tree. Overzealous dissection during hilar mobilization or lymph node dissection should be minimized. The technique of bronchial closure continues to be debated. Forrester-Wood in 1980 showed superior results with stapled closure vs. sutured closures [14]. More recent reviews find no significant difference between handsewn and stapled bronchial closures [12]. Inadequate apposition of thick bronchial walls during stapled closure, sutures placed unevenly, or sutures tied improperly may lead to a fistula. Flap coverage is also considered after bronchial closure. Coverage for diseased or radiated bronchial stumps, as well as pneumonectomy stumps located on the right side, are routinely covered with tissue flaps. The left pneumonectomy stump retracts into the mediastinal soft tissue and is less prone to fistula formation. Wright and colleagues recommend flap closure of all pneumonectomy stumps [12]. Tissue from the pleura, intercostal muscle, pericardium, mediastinal fat, omentum, pectoralis major, serratus anterior, and latissimus dorsi muscle can be used for flap coverage of the bronchus. A broad-based pleural flap will reduce suture hole leaks, but brings very little new blood supply to the bronchial stump. Most muscle flaps need to be prepared when entering the chest to provide adequate length and viability. Muscle flaps provide the best coverage for preventing fistulas, but at the expense of increased time and morbidity. We commonly use a broad-based mediastinal fat pad to cover bronchial stumps (Figure 4.8). The mediastinal fat is easily harvested off the pericardium from the cardiophrenic angle to the upper mediastinum. The fat pad provides some new vascularity to the bronchial stump, although not as rich as the muscle flap. It is important to fix the fat pad to the peribronchial tissues, avoiding a full thickness bite of the bronchus. These maneuvers will help to avoid bronchopleural fistulas postoperatively. Bronchopleural fistulas usually occur 7–15 days postoperatively, but small fistulas after pneumonectomy may manifest themselves months following surgery [9]. Clinical manifestations include: fever, purulent or serosanguinous cough, persistent large air leak, a sudden increase in the size of an air leak, or development of a pleural space after chest tube removal. After pneumonectomy, subcutaneous emphysema, cough producing thin secretions, and

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Figure 4.8 Mediastinal fat pad sutured in placed to cover a right pneumonectomy stump. (From [8].)

increased dyspnea may indicate a bronchopleural fistula. Additional evidence of a bronchopleural fistula may be confirmed by chest radiography. Radiographic findings may include: new pleural space; development of an air-fluid level; or, after pneumonectomy, a decrease in the level of fluid on the pneumonectomy side of < 2 cm. These clinical signs suggest the presence of a fistula. Bronchoscopy should be carried out urgently and often assists with the diagnosis and treatment of bronchopleural fistulas. Large fistulas or complete separation of the anastomosis can be easily detected. Small fistulas are more difficult to visualize and may only appear as a back-and-forth motion of secretions, necrotic tissue, inflammation, or granulation tissue at the bronchial stump. Residual tumor, inflammation, or infection of the proximal bronchus are also important to note if bronchial closure is being considered. Treatment is dependent on the timing and circumstances of the bronchopleural fistula. Approximately 20–30% of small fistulas will close with drainage alone following pneumonectomy [9,15]. Results with conservative treatment are usually better following lobectomy than pneumonectomy. Fistulas after lobectomy are rare and usually occur after bilobectomy rather than standard lobectomy. Increased dissection for a bilobectomy may devascularize the bronchial stump, stressing the importance of careful closure and bronchial artery preservation in these circumstances. Surgical repair of a lobar bronchial fistula may require resection, if not, pneumonectomy. This

Complications of pulmonary resection 81

major surgery in a compromised patient and probable infection in the pleural space must be carefully weighed against the benefits of surgical closure. Conservative treatment is recommended for lobar bronchial fistula. This consists of tube drainage and space closure with a pedicled muscle flap. Timing is critical when a bronchopleural fistula is diagnosed. The space should be urgently drained with a chest tube to prevent aspiration of fluid into the remaining lung and appropriate antibiotics are begun to treat the underlying empyema. Chest tubes are placed to water-seal drainage without suction to minimize loss of tidal volume. Previously, primary closure of bronchopleural fistulas was recommended after only 48–72 h. With better antibiotics, irrigation treatment for empyema, and vascularized stump coverage, reoperation and reclosure of the bronchial stump can be considered up to 14 days after the original pneumonectomy [8]. A single lumen endotracheal tube placed into the contralateral bronchus under bronchoscopic guidance is used to prevent aspiration into the dependent lung during operative positioning. The technique of repair of the bronchial stump includes careful debridement and the use of monofilament sutures to re-approximate the bronchus. A vascularized flap, as previously discussed, is then used to cover the bronchial stump. Recently, Landreneau and colleagues have described the technique of videoassisted thoracoscopy (VATS) to treat empyemas [16]. They successfully closed the fistula and drained the infection in 98% of patients with VATS treatment alone when the empyema was treated early in the ‘fibrinopurulent’ phase. Early diagnosis and prompt treatment are paramount in the management of bronchopleural fistula and associated empyema. The management of a bronchopleural fistula that occurs several weeks or months after pneumonectomy requires the space to be drained and the infection controlled. This is best accomplished with the open thoracostomy or Eloesser flap [17]. The presence of a chronic bronchopleural fistula requires direct closure as the fistula will not heal spontaneously and the pneumonectomy space cannot be sterilized until the fistula has healed. Puskas [18] described successful closure of chronic bronchopleural fistulas following pneumonectomy in 47 patients (85%) using direct suture closure of the bronchial stump in 37 and suturing of tissue flaps over the fistula in 10 patients. All of these bronchial closures were buttressed with vascularized flaps of omentum, muscle or pleura. At the time of the bronchopleural fistula closure, the empyema cavity can also be partially obliterated using myoplasty and thoracoplasty techniques. Any residual cavity that remains can be successfully sterilized using the Claggett technique [19]. This antibiotic irrigation technique can be accomplished after the fistula is closed. It consists of irrigation of the empyema space with antibiotics and packing the space with sterile gauze to achieve healthy granulation tissue. When the cavity is clean, the patient is brought to surgery and the cavity is filled with an antibiotic solution and the open thoracostomy or Eloesser flap is closed. Approximately 60% of empyemas can be sterilized with this technique, but a repeat procedure may be required if the empyema recurs.

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A two-stage procedure is advocated by Deschamps [20] for fistula closure and sterilization of a pneumonectomy empyema space. The first stage consists of opening the thoracotomy incision with debridement and closure of the bronchial fistula and coverage with viable tissue. The empyema cavity is thoroughly debrided and the cavity is packed open with gauze soaked in Povidone iodine solution, diluted 20: 1. The packing is changed daily and when healthy granulation appears in the pleural space, the cavity is filled with antibiotic solution and a watertight chest wall closure is obtained. Satisfactory results are noted to be achieved in 80% of patients. If antibiotic irrigation and open thoracostomy closure fail to sterilize the empyema cavity, it can be managed with daily packing with expected decrease in size of the space by granulation tissue over several months. Pairolero [21] reported the use of muscle flaps along with omentum to achieve an 88% success rate in controlling intrathoracic empyema. Extrathoracic muscle transpositions, along with omentum, are now the accepted standard of therapy for treatment of the chronic bronchopleural fistula and empyema. The need for thoracoplasty has been significantly decreased with these described techniques. Other techniques are available to attempt to close a post-pneumonectomy bronchial fistula. If a long bronchial stump is present the trans-sternal approach can be utilized as described by Baldwin and Mark [22]. The bronchus is approached through the pericardium and stapled and transected. Following closure of the bronchus the empyema cavity is treated by antibiotic irrigation techniques. Fibrin glue can be used to close a small bronchial fistula up to 4 mm in size. Tissue glue can be made from cryoprecipitate and thrombin. Commercially made glues are available. Closure of small fistulas in both pneumonectomy and lobar stumps has been achieved [23]. The glue is instilled through catheters passed through the channel of a fiberoptic bronchoscope. This technique is associated with low morbidity and can be the initial therapeutic maneuver if the procedure is small. Fewer than 10% of our most recent bronchopleural fistulas were candidates for closure with fibrin glue.

Chylothorax Chylothorax is a rare complication after pulmonary resection that occurs more commonly after pneumonectomy than after lobectomy or segmentectomy. Cerfolio and associates found an incidence of < 0.5% for all thoracic cases [24]. Chylothorax is more common after esophageal surgery, accounting for almost two-thirds of the reported experience. Thoracic duct injury accounted for 2% of our recent complications. Resection of large central tumors and extensive lymphadenectomy increase the possibility of thoracic duct injury. Knowledge of the anatomy of the thoracic duct may prevent its injury and aid in its treatment. The thoracic duct begins as the cisterna chyli at the level of the second lumbar vertebrae, just lateral to the aorta. The most constant loca-

Complications of pulmonary resection 83

tion of the thoracic duct is at the diaphragm where it passes through the aortic hiatus with the aorta and azygous vein [25]. Often the favored site for elective ligation of the duct is here during its more constant path through the aortic hiatus. The thoracic duct then ascends to the right side of the aorta and anterior to the vertebrae. The duct crosses to the left side at the level of the fifth or sixth thoracic vertebrae. It remains posterior to the aortic arch and adjacent to the esophagus before it empties into the junction of the left subclavian and internal jugular veins. Almost 40% of individuals have multiple branches that are most common in the mid-thoracic region. Injury can occur anywhere in the mediastinum, but this variability makes injury more common. The close proximity to the esophagus and subcarinal space on the right make extensive lymphadenectomy in these areas prone to thoracic duct injury. Damage can also occur on the left side after the duct has crossed the thorax. Mobilization of the left main-stem bronchus or removal of lymph nodes along the left tracheo– esophageal groove may injure the thoracic duct. A knowledge of the location of the thoracic duct may prevent this complication. A chylous leak can often be diagnosed intraoperatively. Because the patient has not eaten the day of surgery, chyle from a ductal injury may appear thin and clear rather than milky. If golden-yellow fluid continues to fill the operative space, the surgeon should consider a possible thoracic duct injury and attempt to identify its site. Administration of cream or milk down a nasogastric tube may help to identify the leak. Whenever the ductal injury is identified intraoperatively, the injury should be repaired with fine interrupted permanent sutures. Many thoracic duct injuries are not identified until postoperatively. Because patients often do not eat postoperatively, the classic milky appearance of the pleural drainage is often absent. However, continuation of large amounts of pleural drainage should raise the suspicion of a ductal injury. Chest tube outputs measuring > 500 cm3/day are typical of chylous effusions. After the patient resumes a general diet, the milky appearance of the pleural fluid may become evident. It should be analyzed for cholesterol and triglycerides if the diagnosis is in question. Chyle typically has elevated cholesterol and triglyceride levels. Staats [26] in 1980 reported if the triglyceride level is > 110 mg/ 100 cm3, then there is a 99% chance that the effusion is chyle. Similarly, if the triglyceride level is < 50 mg/100 cm3, there is only a 5% chance that the pleural fluid is chyle. Large amounts of chest tube drainage confirmed by laboratory studies can identify chylous effusions. The initial treatment of a thoracic duct injury is conservative. If not present, chest tubes are placed to drain the involved pleural space completely and allow expansion of the lung. The chest tube output must be accurately measured. A trial with a specialized diet containing no fat and medium-chain triglycerides may be tried. A more conservative approach is allowing nothing orally and providing complete nutrition by central hyperalimentation. The success of this conservative approach varies. Cerfolio found non-operative therapy to be successful in 27% of patients [24]. Others have reported success

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in close to half of patients with conservative therapy [8]. We found that 75% responded to non-operative treatment in our last review. Guidelines for conservative management of thoracic duct injuries are becoming better defined. Because of the depletion of the patient’s nutrition from prolonged drainage and increased risk of infection, conservative management should never exceed 2 weeks’ duration. Earlier surgical intervention has been advocated by some groups. The Mayo clinic experience suggests that outputs > 1000 cm3/day for more than 7 days or any thoracic duct injury after esophageal surgery should be surgically repaired at 1 week [24]. With the good results from surgical ligation and the increased interest in less invasive techniques such as thoracoscopy, the trend may be toward earlier intervention at the time of diagnosis [25]. Surgical management of thoracic duct injuries remains very effective. The traditional approach is direct ligation of the duct near the diaphragm through either a thoracic or abdominal approach. This was first proposed by Lampson in 1948 and involves mass ligation of the soft tissues that include the thoracic duct between the aorta, azygous vein, and vertebrae at the diaphragm. Clips should be avoided because they can injure the duct. Our approach is through a low right thoracotomy, although a left thoracotomy may be used. Surgical ligation is effective in nearly 90–95% of cases. Other approaches have been to enter the chest on the side of the chylous leak. The leak itself is identified and sutured. Identification of the site of leak may be troublesome with this approach due to inflamed tissues. Fibrin glue has also been used to seal thoracic duct leaks and is gaining popularity with thoracoscopic approaches [25]. If primary surgical repair fails in the chest, the thoracic duct may be ligated through the abdomen. In a patient unable to tolerate surgery, pleurodesis may be attempted but often ineffectively obliterates the pleural space. Pleuroperitoneal shunts and stops the leak are effective and can prevent malnutrition in patients with advanced cancer causing chylous effusions. These options are rarely needed in postoperative chylous leaks and long term, conservative management should be avoided because of the associated malnutrition, infectious complications, and increased mortality.

Cardiac herniation Cardiac herniation is a rare event after pulmonary resection, but if not promptly managed is often fatal. The incidence is low and much of our understanding comes from isolated case reports. We experienced no cases over the last 5 years. Cardiac herniation is often associated with intrapericardial pneumonectomy with herniation of the heart through a large pericardial defect. Without prompt recognition and reoperation, death quickly ensues, accounting for a mortality rate approaching 50% [27]. Understanding of the mechanism of cardiac herniation may prevent and reduce its mortality. Cardiac herniation typically occurs shortly after the completion of the pulmonary resection on the operating table or in the immediate postoperative

Complications of pulmonary resection 85

Figure 4.9 Cardiac herniation following right pneumonectomy and pericardial resection.

period. The event may be heralded by such precipitating factors as: change in the patient’s position, coughing, extubation, positive pressure ventilation distributed to the remaining good lung, or excessive negative pressure administered to the pleural space after pneumonectomy. Typically, the blood pressure will drop with increased jugular venous distention and the heart impulse may be displaced laterally. The upper extremities may be cyanotic with right-sided herniation where displacement of the heart causes angulation and obstruction of the vena cava. Left-sided herniation may have ST-T wave changes on electrocardiogram resulting from compression of the myocardium against the pericardial defect. A chest radiograph will often be diagnostic in right-sided herniation, showing displacement of the heart into the right chest (Figure 4.9). Left-sided herniation is more difficult to detect on posteroanterior chest radiogram where the heart apex may be angulated against the lateral chest wall. The lateral radiograph will typically show posterior displacement of the heart. When cardiovascular collapse occurs shortly after large resections including the pericardium, radiographic findings and knowledge of this complication should help diagnose cardiac herniation. Prevention is key to avoiding this complication. We believe that small pericardial defects should be closed primarily. Large, left-sided pericardial defects are less worrisome because further displacement of the heart to the left is

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Figure 4.10 GORE-TEX patch reconstruction of a right-sided pericardial defect. The head of the patient is to the right.

rare and a large pericardial opening is less likely to strangulate the heart. Right-sided defects which are large are prone to herniation and all should be closed. We prefer patch closure of the pericardial defect (Figure 4.10). Pericardectomy may prevent strangulation of the heart on the left side, but will not prevent herniation of the heart on the right side. Closure of a large pericardial defect after a resection on the right side is mandatory. When cardiac herniation occurs, emergent re-exploration is necessary with reduction of the heart into the pericardial space. Thoracoscopy or fluoroscopy to confirm diagnosis will only delay repair. The pericardial defect must be closed to prevent reoccurrence. Pleura, Vicryl mesh, fascia, Dacron patch, and catgut sutures bridging the defect have been used to close the pericardium. We prefer to use a GORE-TEX pericardial patch because of its strength and pliability. Suturing the edge of the pericardium to the myocardium has been reported but risks bleeding or injury to the coronary vessels. If performed expeditiously, these techniques will give good surgical results.

Lobar torsion Lobar torsion after pulmonary resection remains a rare but significant complication. Although the exact cause of the complication is unknown, it is believed that rotation on the bronchovascular pedicle results in pulmonary venous

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obstruction and eventual gangrene. Rotation may occur intraoperatively or postoperatively. Angulation of the bronchus also compromises bronchial arterial circulation and contributes to the lung infarction. Lobar torsion must be differentiated from other causes of lobar gangrene such as pulmonary vein thrombosis or pulmonary artery occlusion combined with disruption of the bronchial circulation. Torsion is absent in these cases and circulatory compromise is usually associated with operative injury. Lobar torsion typically involves the right middle lobe after a right upper lobectomy. If the transverse fissure is complete, the right middle lobe has few attachments to the lower lobe and can move freely. The middle lobe can, then, rotate on its bronchovascular pedicle. Less commonly, lobar torsion can occur on the left side after either upper lobectomy or lower lobectomy. In our 5-year review, we identified one case of right middle lobe torsion that required surgical resection. Schuler reviewed lobar torsion and reported a 16% mortality in their 31 cases [28]. If not recognized early, circulatory embarrassment of the lobe can lead to infarction, lobar gangrene, and increased mortality. Prevention and early recognition are essential to the management of lobar torsion. In the presence of a complete transverse fissure, the right middle lobe should be secured to the remaining lobe to prevent torsion. Sutures can be used or the distal edges of the lung may be secured with staples. Careful surgical technique is mandatory to prevent interrupting circulation to the lung causing lobar gangrene without torsion. At the completion of the resection, the lung should be inspected while fully inflated to prevent intraoperative torsion. Early recognition of this complication is essential to prevent irreversible ischemia. Clinical symptoms of lobar torsion are few in the early stages. If left untreated, these patients become septic and develop fever, massive air leak, or foul smelling sputum or bloody chest tube drainage. A chest radiograph taken postoperatively may show signs of torsion (Figure 4.11). Radiographic findings may include: hilar displacement, bronchial cut-off, or lobar consolidation. Later, the radiograph may show enlargement of the lobe beyond that normally expected from hyperinflation. Over time, the lobe will gradually decrease in size due to consolidation and have a honeycomb pattern or ground-glass appearance [9]. Nuclear perfusion scans and angiography may demonstrate the obstruction to flow through the main lobar vessels or its branches, but are not diagnostic for lobar torsion. Atelectasis and intraparenchymal hematoma may have the same appearance. Urgent flexible bronchoscopy can be diagnostic and should be considered to identify lobar torsion or more commonly remove mucous plugs from an atelectatic lobe. The bronchoscopic features of lobar torsion are a ‘fish-mouth’ bronchus that allows passage of the bronchoscope, but quickly reobstructs when the bronchoscope is removed. This compressed bronchus with normal distal airways should raise the suspicion of lobar torsion and the need for surgical management. After prompt diagnosis, the treatment of lobar torsion is immediate surgical re-exploration. If lobar torsion is recognized before pulmonary infarction,

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(a)

(b) Figure 4.11 (a) Left upper lobe torsion following left lower lobectomy. (b) Chest X-ray following thoracotomy with repositioning of the left upper lobe and fixation with a pleural flap to prevent repeat torsion.

the lung is carefully repositioned and secured to prevent recurrence. Often surgical exploration is performed after pulmonary gangrene has started. The involved lung must be resected and the circulation to the remaining lobe inspected for circulatory compromise. The successful treatment of lobar torsion includes early recognition of clinical changes and prompt surgical treatment.

Complications of pulmonary resection 89

Nerve injury The recurrent laryngeal, phrenic and vagus nerves are the nerves most commonly involved in a thoracic surgical procedure. Each of these nerves can be invaded by a tumor or pathological process and the nerve is resected to achieve a complete resection. Injury to a nerve can also occur with the use of electrocautery or resection of tissues in close proximity to the nerve. The left recurrent laryngeal nerve wraps around the ligamentum arteriosum in the aorto–pulmonary window and can be damaged with lymph node dissection or during a difficult pneumonectomy. On occasion, the tumor invades the vagus nerve above the transverse aortic arch and resection of the vagus nerve with pleurectomy at this level results in vocal cord paralysis. The right recurrent laryngeal nerve can be damaged during the superior mediastinal lymph node dissection following right-sided lung cancer operations. Shields [29] reported injury to the left recurrent laryngeal nerve in 3/62 patients after extensive lymph node dissection. Unilateral vocal cord paralysis following pulmonary resection can be associated acutely with inadequate cough or airway aspiration. Retained secretions and aspiration can result in significant complications, particularly following a pneumonectomy. Signs of vocal cord paralysis include a breathy voice, a poor cough and/or aspiration of liquids. When vocal cord paralysis is known or suspected, fiberoptic visualization of the larynx should be carried out to determine the position of the affected vocal cord. A poor cough and aspiration with lateral positioning of the paralyzed vocal cord indicate a need for repositioning of the vocal cord. The paralyzed vocal cord can be repositioned toward the midline by injection of Gelfoam paste into its lateral aspect. This is temporary to achieve an improved cough and to diminish the complications of aspiration. Following discharge the patients is re-evaluated by fiberoptic techniques and Teflon is then injected for long-term benefit. Other methods of vocal cord medialization include neuromuscular transfer and the recently described thyroplasty technique [30]. Sacrifice or injury of the phrenic nerve may manifest itself as an asymptomatic elevated diaphragm or an ineffective cough with retained secretions. Special attention must be made to maintain a clear airway in this instance. Injury to a single vagus nerve rarely produces clinical symptoms and the true incidence of injury to this nerve is unknown. Dissection of apical lung cancers can result in sacrifice of the Stellate ganglion resulting in a Horner’s syndrome and branches of the brachial plexus can be damaged by resection of the cancer. The patient should be informed preoperatively of possible nerve damage whenever extensive central or apical cancers are resected.

References 1 Piccione W, Faber LP. Management of complications related to pulmonary resection. In: Waldhausen JA, Orringer MB, eds. Complications In Cardiothoracic Surgery. Mosby Year Book: St Louis, 1991; 336.

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2 Lewis FR. Management of atelectasis and pneumonia. Surg Clin N Am 1980; 67: 1391. 3 Stock MC, Downs JB, Gaver PK et al. Prevention of postoperative pulmonary complications with CPAP, incentive spirometry and conservative therapy. Chest 1985; 87: 151. 4 Mastboom WJ, Wobbes T, van den Dries A et al. Bronchial suction by minitracheostomy as an effective measure against sputum retention. Surg Gynecol Obstet 1991; 173: 187. 5 Shields TW, Lees WMM, Fox RT et al. Persistent pleural space following resection for pulmonary tuberculosis. J Thorac Cardiovasc Surg 1959; 38: 523–536. 6 Barker WL, Langston HT, Naffah P. Postresectional thoracic spaces. Ann Thorac Surg 1966; 2: 299. 7 Silver AW, Espinas EE, Byron FX. The fate of post-resection space. Ann Thorac Surg 1966; 2: 1311–1326. 8 Faber LP, Piccione W. Complication of surgery in the lung cancer patient. In: Mitchell JB, Johnson DH, Turrisi AT, eds. Lung Cancer: Principles and Practice. Lippincott-Raven, 1996. 9 Kirsch MM, Rotman H, Behrendt DM et al. Complications of pulmonary resection. Ann Thorac Surg 1975; 20: 215. 10 Spotnitz WD, Dalton MS, Baker JW et al. Successful use of fibrin glue during 2 years of surgery at a university medical center. Am Surg 1989; 55: 1660. 11 Yano T, Yokoyama H, Fukuyama Y et al. The current status of postoperative complications and risk factors after a pulmonary resection for primary lung cancer. A multivariate analysis. Eur Cardiothoracic Surg 1997; 11: 445–449. 12 Wright CD, Wain JC, Mathisen DJ, Grillo HC. Post-pneumonectomy bronchopleural fistula after sutured bronchial closure: incidence, risk factors and management. J Thoracic Cardio Surg 1996; 112: 1367–1371. 13 Vester SR, Faber LP, Kittle CF, Warren WH, Jensik RJ. Bronchopleural fistula after stapled closure of bronchus. Ann Thorac Surg 1991; 52: 1253–1258. 14 Forrester-Wood CP. Bronchopleural fistula following pneumonectomy for carcinoma of the bronchus. J Thorac Cardiovasc Surg 1980; 80: 406–409. 15 Wain JC. Management of late postpneumonectomy empyema and bronchopleural fistula. Chest Surg Clin N Am 1996; 6: 529–531. 16 Landreneau RJ, Keenan RJ, Hazelrigg S et al. Thoracoscopy for empyema and hemothorax. Chest 1995; 109: 18–24. 17 Eloesser L. An operation for tuberculosis empyema. Surg Gynecol Obstet 1935; 60: 1096. 18 Puskas JD, Mathisen DJ, Grillo HC et al. Treatment strategies for bronchopleural fistula. J Thorac Cardiovasc Surg 1995; 109: 989. 19 Claggett OT, Gerace JE. A procedure for the management of post-pneumonectomy empyema. J Thorac Cardiovasc Surg 1963; 45: 141. 20 Deschamps C, Pairolero PC, Allen MS et al. Early complications: broncholeural fistula and empyema. Chest Surg Clin N Am 1999; 9: 587–595. 21 Pairolero PC, Arnold PG, Piehler JM. Intrathoracic transposition of extrathoracic skeletal muscle. J Thorac Cardiovasc Surg 1983; 86: 806–809. 22 Baldwin JC, Mark JBD. Treatment of bronchopleural fistula after pneumonectomy. J Thorac Cardiovasc Surg 1985; 90: 813. 23 Torre M, Chiesa G, Ravini M et al. Endoscopic gluing of bronchopleural fistula. Ann Thorac Surg 1994; 58: 901. 24 Cerfolio RJ, Allen MS, Deschamps C et al. Postoperative chylothorax. J Thorac Cardiovasc Surg 1996; 112: 1361–1365. 25 Merrigan BA, Winter DC, O’Sullivan GC. Chylothorax. Br J Surg 1997; 84: 15–20. 26 Staats RA, et al. The lipoprotein profile of chylous and unchylous pleural effusion. Mayo Clin Proc 1980; 55: 700.

Complications of pulmonary resection 91 27 Deiraniya AK. Cardiac herniation following intrapericardial pneumonectomy. Thorax 1974; 29: 545–552. 28 Schuler JG. Intraoperative lobar torsion producing pulmonary infarction. J Thorac Cardiovasc Surg 1973; 65: 951. 29 Shields TW. General features and complications of pulmonary resections. In: General Thoracic Surgery. Williams and Wilkins, 1994; 391–414. 30 Carew JF, Kraus DH, Ginsberg RJ. Early complications: recurrent nerve palsy. Chest Surg Clinics N Am 1999; 9: 597–608.

CHAPTER 5

Complications of tracheobronchial resection Douglas J Mathisen

Management of complications of bronchoplasty Techniques have been developed to allow sleeve resection of any lobe of the lung. These techniques allow both surgery for individuals who could not tolerate more extensive operations and an improved quality of life because of the preservation of functioning lung parenchyma. For these reasons, practicing thoracic surgeons should be familiar with technical details of the operation. The technical demands of the operation are such that there is an increased risk of complications. These can be minimized by strict attention to technical details. Complications, however, are inevitable and one should be familiar with their presentation and management possibilities. Like most surgery, the management of complications starts in the operating room, doing everything possible to avoid them!

Indications for sleeve lobectomy Knowing the indications for bronchoplasty will help in patient selection and improve results. The most common indication for sleeve lobectomy is the presence of a neoplasm originating at the origin of a lobar bronchus. The neoplasm can be either benign or malignant. It is the rare neoplasm that can be managed by endoscopic methods with the expectation of cure. Hamartoma and papilloma may be the exceptions. One should not be tempted to try laser ablation or removal of benign or low-grade neoplasms. The biology of these tumors is such that they always involve the bronchial wall deeply enough that complete removal or obliteration is impossible. Extensive lasering can lead to bronchial stricturing and also to bronchial perforation, inflammation and growth of the neoplasm, possibly precluding a future bronchoplastic procedure. There are other conditions that may be amenable to bronchoplastic techniques. At the time of thoracotomy, the origin of the bronchus may be found to be involved with malignant lymph nodes, or positive frozen section margins may document direct extension of the primary neoplasm. These are conditions not identifiable by bronchoscopy and underscore the need for thoracic surgeons to be familiar with bronchoplastic techniques. Other indications are post-traumatic, postinflammatory, and postsurgical strictures. 92

Complications of tracheobronchial resection 93

Evaluation of patients for bronchoplastic procedures The evaluation of patients for possible bronchoplastic procedures should proceed on many levels. The advanced knowledge provided by thorough evaluation will help in planning the operation and improving overall results. In addition to general medical evaluation to determine the ability to tolerate a pulmonary resection, it is essential to evaluate fully the patient’s pulmonary function, with standard spirometry and quantitative ventilation and perfusion scans. This very important evaluation will determine whether a bronchoplastic procedure is the only option if anatomical findings are unfavorable at thoracotomy. I obtain these tests routinely for all patients if there is any question about their ability to withstand the alternative to sleeve lobectomy, i.e. pneumonectomy. Bronchoscopy should be performed by the operating surgeon. One should never rely on the observation of others to assess the suitability of a patient for a possible bronchoplastic procedure. The bronchoscopy should reveal the origin of the pathology, the extent of involvement, and the quality of the bronchial mucosa. The use of flexible bronchoscopes allows in almost every circumstance the evaluation of the bronchus distal to the pathology. Even neoplasms that protrude into the lumen of the main bronchus and seemingly occlude the entire bronchus can usually be passed by carefully insinuating the tip of the bronchoscope around the periphery of the neoplasm. I believe this is important to try to determine in every patient before thoracotomy. It can be sorted out at thoracotomy by bronchotomy, but this is not ideal and may compromise the procedure. It is important to assess the bronchial mucosa for inflammatory changes as well. One should not attempt bronchoplastic procedures through mucosa that is actively inflamed. The radiological assessment is very valuable in patients being considered for possible bronchoplastic procedures. Standard linear tomograms were quite useful in assessing bronchial pathology, but they have become virtually impossible to obtain. Computed axial tomograms (CT) and spiral CT scans have supplanted linear tomograms. Although not superior, they are satisfactory. They are superior, however, in determining extraluminal involvement and presence of enlarged lymph nodes. For malignant lesions, mediastinoscopy should be performed to assess involvement of mediastinal lymph nodes. Positive nodes may influence the choice of operation and the need for adjuvant therapy. I believe mediastinoscopy gives additional valuable information. Mediastinoscopy allows some assessment of the proximal mainstem bronchus as well as the main pulmonary artery. Combining these findings with bronchoscopic findings and pulmonary function tests is very valuable in determining the suitability of bronchoplasty. I prefer to perform mediastinoscopy at the time of thoracotomy or as close to it as possible. The resultant scarring that inevitably follows the procedure can compromise the mobility of the airway, dissection of the bronchus, and create some confusion as to what is scarring and what is neoplasm.

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Bronchoplasty in the presence of postintubation pneumonia Postobstructive pneumonia is common in patients with obstructing neoplasms [1]. It is preferable to try to resolve this before the bronchoplastic procedure. In addition to appropriate intravenous antibiotics and chest physiotherapy, aspiration bronchoscopy is invaluable. This may need to be repeated multiple times to achieve the desired effect. In some cases ‘core-out’ of the neoplasm should be done to open the obstruction. Balanced against this goal is the risk of hemorrhage from neoplasms such as carcinoids. In this situation multiple aspiration bronchoscopies may be preferable. Most other neoplasms can safely be ‘cored out’ with minimal risk of bleeding [2]. A few days spent relieving postobstructive pneumonia is time well spent. The general risk of sepsis is reduced, purulent secretions diminished and inflammation of the bronchial mucosa reduced. All of these diminish the risk of postoperative complications.

Anesthetic management It is important to perform these operations under optimal conditions. The management of the airway is critical to the safe conduct of the operation. I prefer the use of a double-lumen endotracheal tube whenever possible. Bronchial blockers are alternative solutions, but they do not provide as much protection of the opposite lung from spilled secretions and in general are only a consideration for left-sided bronchoplastic procedures. Placement of double-lumen tubes should be done with the aid of a flexible bronchoscope through the tube. This minimizes trauma to any neoplasm, reduces the risk of bleeding, and guarantees proper placement. The actual anesthetic should allow for extubation in the operating room at the conclusion of the operation. It is preferable not to have these patients intubated and mechanically ventilated. I routinely use epidural analgesia on all thoracotomy patients as many have difficulty clearing secretions. Maximal pain control helps enormously to allow vigorous coughing and thereby avoid complications from sputum retention.

Surgical technique Success depends upon precise attention to technical details, gentle handling of the tissues, preservation of blood supply and avoidance of tension on the anastomosis. The technical details are the same as for standard lobectomy until the bronchus is reached. Great care must be taken to avoid devascularization of the bronchus. Avoiding devascularization is important for bronchial healing. A balance must be achieved in lymph node dissection as well, because node dissection often interferes with bronchial blood supply. Sharp transection of the bronchus should be accomplished with minimal trauma to the remaining ends of the bronchus. To avoid confusion for the pathologist, it is best to submit a separate sliver of bronchus from each end for histological review. This practice minimizes sampling mistakes by the pathologist.

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Figure 5.1 (A) Depicted is a lateral view of the hilar structures. A U-shaped incision is seen beneath the inferior pulmonary vein. A dotted line depicts the extension of this incision to create a complete hilar release. (B) This depicts the mobility gained by a partial hilar release. (Reprinted from Grillo HC. Tracheal surgery. In: Atlas of General Thoracic Surgery. Ravitch M, Steichen T (eds), 1987, p. 315. With permission from Elsevier.)

Tension on any bronchial anastomosis must be avoided. When long segments of the main bronchus are included in the resection, it may be necessary to perform an inferior pericardial release. Release is accomplished by making a U-shaped incision in the pericardium beneath the inferior pulmonary vein (Figure 5.1). This incision gives enough mobility in all but extreme situations. An incision of the pericardium to completely encircle the hilar vessels can be used in this circumstance for maximal mobility. Two full-thickness traction sutures placed on the proximal and distal end of the bronchus to be reconstructed are quite helpful in reducing tension (Figure 5.2a). These sutures are usually 2–0 Vicryl sutures, and are placed in the same relative locations on the two ends of the bronchus. This helps to determine proper spacing of the individual anastomotic sutures. These sutures are placed 3–4 mm from the end of the bronchus and should always be around a cartilaginous ring rather than in the membranous wall. They are tied before the individual anastomotic sutures are tied and are left in place. Absorbable sutures eliminate the granuloma formation so common with non-absorbable sutures. Anastomotic sutures are carefully spaced and placed 3–4 mm from the cut end of the bronchus (Figure 5.2b). The sutures are 4–0 Vicryl. Each suture is clipped to the drapes and tied in reverse order of placement. The open technique allows precise placement of sutures and minimizes tension. There are size discrepancies usually between the proximal and distal ends of the bronchus. We avoid tailoring of either end in most circumstances and rely on

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Figure 5.2 (a) Traction sutures replaced in the mid-lateral position. They are placed full thickness around a cartilaginous ring about 2–4 mm from the cut end of the bronchus. They should be placed in the same relative position on the proximal and distal bronchus. (b) Individual anastomotic sutures are placed with the knots on the outside. An open technique is preferred to allow precise placement. The first suture is placed posteriorly at ‘6 o’clock’. The sutures are placed inside the preceding suture and sequentially clipped to the drapes to maintain the proper order. (c) The traction sutures have been tied (not seen in the diagram) first. The anastomotic sutures are tied in reverse order of initial placement. The completed anastomosis is seen.

proper spacing of sutures to make up for any size difference. Some telescoping inevitably occurs, but this has not been a problem in our experience. Occasionally, when the entire right main bronchus, upper lobe, middle lobe, and bronchus intermedius are removed, the size discrepancy is too great and the proximal bronchus must be narrowed. Narrowing of the bronchus inevitably creates a T intersection in the anastomosis. One must pay meticulous attention to detail to avoid creating a potential area for a fistula. Once all sutures have been placed, the traction sutures are tied bringing the two ends together. The individual anastomotic sutures are tied in reverse order of placement (Figure 5.2c). At the completion of the anastomosis, the operative field is flooded with saline and the lung ventilated. Any air leaks should be repaired even if it means taking the anastomosis down and redoing it. Air leaks from the anastomosis demand repair to avoid a fistula. Flexible bronchoscopy should be done at this point to be certain of proper alignment, patency of lobar and segmental bronchi, and that there are no loose anastomotic sutures. All of these problems are best identified and corrected at this point rather than identifying them in the recovery room. Once the integrity of the anastomosis has been

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confirmed, a pedicled flap of pleura or pericardial fat is developed and passed around the anastomosis. This may aid in healing, in sealing of small leaks that may develop, and in separating the bronchus from the nearby pulmonary artery. Special mention should be made of patients who are steroid dependent or who have had prior irradiation over 1 year before surgery. These circumstances influence bronchial healing and increase the risk of a bronchoplastic procedure and may preclude surgery. In those circumstances where bronchoplasty is elected, a pedicled intercostal muscle flap at the very least should be used to buttress the anastomosis. When wrapped circumferentially it should have the periosteum stripped to avoid a ring of bone that may constrict the bronchus. A pedicled omental flap passed through a substernal tunnel is probably even better protection than pedicled muscle. In those circumstances where postoperative irradiation is to be given, it is best to wait 4–6 weeks after surgery. A bronchoscopy should be done prior to initiation of radiation therapy to be certain adequate healing has taken place.

Management of complications The most common postoperative complication is sputum retention and atelectasis. Proper antibiotic selection, chest physiotherapy and pain control are very important to managing this problem. Beside aspiration, bronchoscopy with irrigation of the distal airway should be used liberally. Bronchoscopy should be done in the postoperative period to examine the anastomosis to ascertain whether or not normal healing is taking place. If the bronchial mucosa is ischemic but intact, a bronchoscopy should be done every few days to monitor the situation. If the anastomosis appears to remain intact, late stenosis may develop. This may take the form of a fibrotic stricture or exuberant granulations. Excessive granulation tissue may be debrided or lasered. A fibrotic stricture may be amenable to repeat dilations with either woven bougies through a rigid bronchoscope, pediatric rigid bronchoscopes, or balloon dilators. These procedures may need to be repeated to maintain patency and avoid postobstructive pneumonia or atelectasis of the lung. It is possible that a partial stenosis will result and be satisfactory. If recurrent infection, atelectasis or shortness of breath become troublesome, reoperation may be necessary. Sufficient time should be allowed for resolution of postoperative inflammation and fibrosis. A period of 3 months is ideal, but may not be feasible. Reoperation and redoing a bronchoplastic procedure may be impossible and completion pneumonectomy may be inevitable. The bronchial stump may be difficult because of rigidity or short length. A difficult bronchial stump of this nature should be reinforced with a pedicled muscle flap. Bronchial stents have limited application for stenosis following sleeve lobectomy because of the short length of distal bronchus available. A stent would be difficult to seat, maintain patency, and avoid granulation formation. If bronchoscopic inspection of the anastomosis reveals dehiscence, partial separation or frank necrosis, surgical intervention is mandatory. Completion

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pneumonectomy should be performed in most cases. Attempts to redo or repair the anastomosis are futile and very risky. If completion pneumonectomy is not an option because of certain respiratory insufficiency and the process is caught early enough, an attempted repair can be entertained. Conditions would have to be ideal: no gross infection, no involvement of the pulmonary artery, debridement of devitalized tissues, and no anastomotic tension. I would prefer to wrap this anastomosis with pedicled omentum to give the greatest chance of success and avoid fatal complications. Development of a bronchopleural fistula is a devastating postoperative complication and risks a bronchovascular fistula. If a bronchopleural fistula is suspected, a bronchoscopy should be done to evaluate the anastomosis. If the problem is identified and small, conservative management is possible. This includes proper antibiotics, adequate dependent drainage and possible irrigation to help evacuate infected material. A CT with contrast should be done to be certain that all infection is drained and no residual abscess remains. If any question exists, surgical exploration should be done to assess the problem more accurately. This may be the only way to avoid a fatal bronchovascular fistula. Long-term drainage may allow closure. If the fistula fails to close after adequate drainage and sufficient time (minimum 3 months), attempted repair could be entertained. Debridement, closure with absorbable sutures, and pedicled omental or muscle flap buttress should be done. The development of a bronchopleural fistula may result in late bronchial stenosis as well. This may influence the management of this problem and preclude local repair. The most dreaded complication following a bronchoplastic procedure is a bronchovascular fistula. This problem is clearly one that is best managed by avoiding the problem altogether. It is the reason I wrap every anastomosis with viable pedicled tissue of some sort. Most bronchovascular fistulas have a ‘herald bleed’ of a significant amount of blood. Any episode of hemoptysis after a bronchoplastic procedure should immediately be evaluated. Bronchoscopic findings may be subtle with only an area of granulation tissue or obvious with frank dehiscence. If suspicion of a bronchovascular fistula is confirmed, immediate surgical intervention is warranted. Delay may be fatal. It is unlikely that anything other than completion pneumonectomy is possible in this circumstance. It is essential to gain proximal control of the pulmonary artery before exposing the fistula. The mainstem bronchus may be difficult to close and should be buttressed with at least a pedicled muscle flap in every case. Because of the likelihood of contamination of the pleural space, copious irrigation with saline and an antibiotic solution should be done. If gross contamination of the pleural space exists, consideration should be given to postoperative antibiotic irrigation of the pleural space. Local recurrence of tumor is a complication of sleeve lobectomy. Because of the potential for this, I believe surveillance bronchoscopy twice a year is warranted in these patients. Early detection may afford an opportunity for resection in some cases.

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Results Bronchoplastic procedures carry an increased risk of mortality and morbidity compared with standard lobectomy and roughly equal results for pneumonectomy. We have had very few complications and an acceptable mortality in over 200 bronchoplastic procedures for benign and malignant disease [1,3]. The operative mortality in 100 patients with benign low-grade neoplasms was 2% and 4% for malignant neoplasms in 72 patients. The only mortality in the malignant neoplasm group occurred in patients with compromised pulmonary function. Early and late morbidity has been quite low in both groups of patients [1,3]. We have had no bronchovascular fistulas, one empyema, three bronchial stenoses (one partial stenosis asymptomatic, one requiring completion pneumonectomy, and one revised with reoperation), and one dehiscence requiring completion pneumonectomy (patient had failed bronchoplasty elsewhere). The most comprehensive review of complications and early mortality after bronchoplastic procedures was provided by Tedder and colleagues [4]. The mortality in 1915 patients was 7.5%. This is certainly comparable to that reported for pneumonectomy. The most common complication was atelectasis and pneumonia (Table 5.1). Stricture or stenosis occurred in 5.0%. Bronchopleural fistula, empyema, and bronchovascular fistula occurred between 2.6 and 3.5%. Most series of bronchoplastic procedures for benign or low-grade neoplasms report few if any local recurrences. Reported survival for malignant neoplasms ranges between 45 and 55%, similar to reported survival for pneumonectomies [3]. Bronchoplasty is a procedure about which all thoracic surgeons should be knowledgeable. Strict attention to patient selection, technical details, and postoperative care should allow the procedure to be done safely with low

Table 5.1 Complications and early mortality in 1915 patients after bronchoplastic procedures for malignancy. Complication

No. of patients

Incidence (%)

Local recurrence Thirty-day mortality Pneumonia Atelectasis Benign stricture/stenosis Bronchopleural fistula Empyema Bronchovascular fistula Pulmonary embolism

110/1064 143/1915 32/481 33/614 48/966 42/1186 17/599 16/615 13/672

10.3 7.5 6.7 5.4 5.0 3.5 2.8 2.6 1.9

Reprinted with permission from the Society of Thoracic Surgeons (Ann Thorac Surg 1992; 54: 387–391).

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operative morbidity and mortality. Early identification of potential complications should allow successful management of most and avoidance of fatal outcomes. Because of the excellent survival for low-grade malignancies (> 90%) and good survival for malignant neoplasms (50%) and the improved quality of life from preserved lung parenchyma, bronchoplastic procedures are the procedure of choice for anatomically suited neoplasms.

Tracheal resection and reconstruction The goals of tracheal surgery are to resect the diseased segment of trachea and perform an end-to-end reconstruction with a tension-free anastomosis [5]. Knowledge of tracheal anatomy, indications for surgery, surgical techniques, release maneuvers to reduce tension and airway management will improve the chance of success and minimize the risks of complications. Tracheal surgery is relatively uncommon, therefore thoracic surgeons need to be familiar with these issues to allow them to manage these problems successfully. Successful outcome will allow patency of the airway, preservation of voice and avoid the need for life-long tracheostomy. As with bronchoplastic procedures of the main bronchi, the best way to manage complications of tracheal surgery is to avoid them altogether by achieving a successful surgical outcome.

High-risk conditions Special mention should be made of certain high-risk situations. The burned trachea from inhalation is a very difficult situation to manage [6]. A long period of time should elapse before any consideration is given to attempted repair. The airway is best managed with a tracheostomy or T-tube. Patient selection and timing are critical. Patients that present on high-dose steroids must be weaned and a minimum of 4 weeks allowed for normal healing mechanisms to return. The combination of steroids and anastomotic tension is a prescription for disaster. Massively obese patients, patients at high risk for mechanical ventilation and patients with sleep apnea are relative contraindications for reconstruction. Quadriplegic patients are at high risk and must be carefully selected. A condition referred to as idiopathic tracheal stenosis requires careful patient selection and proper timing of repair. This condition is predominantly seen in women and usually presents in the subglottic area. If any degree of inflammation exists, surgical correction should be delayed until it has subsided. Dilation with a rigid bronchoscope provides temporary improvement.

Indications for surgery The most common indication for surgical resection remains tracheal stenosis following prolonged mechanical ventilation through an oral endotracheal tube or tracheostomy. Cuff injuries remain the most common problem despite the advent of ‘low-pressure cuffs’. Overinflated low-pressure cuffs can still lead to circumferential tracheal injury. It is very important to use the proper size endotracheal or tracheostomy tube. The cuff pressure should be kept as

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low as possible consistent with the needs for ventilation. The cuff pressure should be checked regularly and deflated periodically to reduce the chance of injury. Excessive traction on tracheostomy tubes is responsible for most stomal injuries leading to stenosis. Lightweight connecting tubing and constant nursing vigilance are required to reduce this injury. Neoplasms represent the next most common indication for tracheal resection. Other indications include post-traumatic, idiopathic, tracheoesophageal fistula, congenital stenosis, and failed primary repair.

Evaluation of tracheal pathology Thorough preoperative evaluation is invaluable to allow for optimal operative planning. Simple radiological studies will allow assessment of the extent of involvement of the airway. Soft tissue X-rays of the neck and linear tomograms will give excellent detail of the pathology. CT, spiral CT scans and magnetic resonance images are alternative exams, but are probably not superior to linear tomograms. The most important assessment is bronchoscopy. Bronchoscopy is best done in the operating room where emergency rigid bronchoscopy can be done to manage critical airway stenosis if it develops. Flexible bronchoscopy should be limited to inspection of the area proximal to the stenosis. Manipulation of the stenosis may lead to secretions, edema or bleeding which may precipitate critical airway stenosis. Formal bronchoscopic evaluation is best reserved for the time of definitive surgical correction. I believe it is best done with a rigid bronchoscope with telescopes for careful inspection. The length and location of involvement should be carefully measured. The total length of airway and amount of uninvolved airway should also be carefully measured. It is also important to assess the trachea for the presence of inflammation which is common in many conditions involving the trachea. Allowing the inflammation to subside may be helpful and allow resection and reconstruction to be achieved. It is thought that as much as half of the adult trachea can be resected and reconstructed, but this is dependent on many factors.

Airway management Perhaps nothing is more important than airway management. Failure to secure the airway may lead to a fatal outcome, inappropriate tracheostomy or trauma to the airway precluding future repair. Initial presentation of postintubation stenosis is rarely an emergency. Maintaining patients in the upright position and application of cool, humidified oxygen will often stabilize patients and allow airway assessment under optimal circumstances. The airway is best managed in the operating room with skilled anesthesiologists, an operating room team, pediatric and adult rigid bronchoscopes and tracheostomy kit available. Patients should be anesthetized with an agent that allows spontaneous ventilation. This technique requires patience to achieve the depth of anesthesia necessary to allow rigid bronchoscopy, but is clearly safer than any technique that utilizes paralysing agents. Once an adequate

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level of anesthesia has been achieved, an adult rigid bronchoscope is carefully inserted into the proximal airway to visualize the area of stenosis. A pediatric flexible bronchoscope can be inserted through the rigid bronchoscope to inspect the entire length of the stenosis. All strictures can be dilated by small woven bougies and then pediatric bronchoscopes (3.5–7 mm). This is done with gentle pressure under direct vision. It is almost always possible to dilate strictures to a 7-mm rigid bronchoscope. A sufficient lumen can be maintained in most patients for days to weeks following dilation. Tumors can be ‘cored out’ with a bronchoscope. If a tracheostomy is contemplated to manage the airway, it should be performed through the most damaged portion of the airway to preserve as much viable trachea as possible for future reconstruction.

Surgical technique The majority of tracheal resections can be performed through a cervical collar incision. A small partial upper sternotomy just beyond the angle of Louis gives additional exposure of the distal trachea. The important anatomical considerations are the recurrent laryngeal nerves located in the tracheo–esophageal groove, the esophagus posteriorly, and the segmental blood supply that enters the trachea in the mid-lateral position. Initial dissection is kept right on the tracheal wall. No attempt is made to identify the recurrent nerves as they are often embedded in scar and easily injured if there is an attempt to identify them. The trachea should be encircled just proximal or distal to the area of stenosis. This allows dissection in an area with minimal scarring which reduces the risk of injury to the esophagus. A tape is passed around the trachea to provide traction and elevation. We prefer to ventilate patients during resection with a sterile endotracheal tube on the operative field inserted into the distal airway connected to sterile tubing which is passed off the operative field to the anesthesiologists (Figure 5.3a). This allows the endotracheal tube to be removed allowing for careful inspection of the airway and precise placement of sutures. A conservation point of transection of the airway is determined and the trachea divided. Further dissection of the airway can be done by elevating the transected ends of the airway, again staying very close to the trachea at all times. If it appears that resection and reconstruction can be accomplished, the diseased segment is removed. Traction sutures (2–0 Vicryl) are placed in the proximal and distal ends of the trachea in the mid-lateral position (Figure 5.3a). They should be placed 3–4 mm from the cut ends and around a tracheal cartilage. Individual anastomotic sutures (4–0 Vicryl) are placed starting in the midline posteriorly (Figure 5.3a,b). The sutures are placed so the knots will be on the outside. Each suture is clipped to the drapes to maintain proper order. Once all of the sutures are placed, the neck is flexed and maintained by the anesthesiologist, the oral tube advanced across the anastomosis, and the traction sutures tied. With the traction sutures tied, each anastomotic suture is then tied in reverse order of placement (Figure 5.3c). This provides the least amount of tension on the anastomosis. The wound is then flooded with saline and the anastomosis checked for any air leaks. This is done by deflating the

Complications of tracheobronchial resection 103

Figure 5.3 (a) Traction sutures (2–0 Vicryl) are placed in the midlateral position of the proximal and distal airway. Individual anastomotic sutures are placed starting posteriorly. The oral endotracheal tube has been pulled back and a flexible endotracheal tube is inserted in the distal airway for ventilation. (b) Individual anastomotic sutures are placed circumferentially. (c) The traction sutures (not seen) are tied and each individual anastomotic suture is tied in reverse order of placement. The completed anastomosis is seen. (Reprinted from Grillo HC. Surgery of the trachea. Curr Probl Surg 1970: 7: 37. With permission from Elsevier.)

balloon of the endotracheal tube, occluding the nose and mouth, and ventilating to a pressure of 30–40 mmHg. Any air leaks should be repaired even if it means doing the entire anastomosis over again. If the anastomosis lies directly under the innominate artery, it is preferable to cover the anastomosis with a pedicled strap muscle. The previously divided thyroid isthmus is reapproximated and the wound closed in layers. A small drain should be placed to evacuate the wound. To secure the patient’s neck in a flexed position, a heavy suture is placed from just under the chin to the presternal skin. Patients are told before surgery to expect this. The patient is then extubated in the operating room. The chin stitch is divided on postoperative day 7.

Management of complications The most immediate problem one may encounter is a postoperative airway problem. If problems are anticipated, a protecting tracheostomy should be considered. If one is to be placed, it should be at least two tracheal rings below the anastomosis. A pedicled strap muscle based inferiorly should be placed over the anastomosis to separate the tracheostomy from the anastomosis. If a tracheostomy is not done, but concern exists, it is best to place the strap muscle and mark the spot of the proposed tracheostomy with a suture for future use. Immediate airway concerns can also be managed by intubating with a

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small uncuffed endotracheal tube. It can be left in for 48 h at which time the patient should be returned to the operating room and extubated under a light general anesthetic. Persistent airway problems necessitate placement of a tracheostomy. Airway problems that develop in the first 24–48 h may be related to edema. This should be managed with racemic epinephrine, 24 h of steroids, and diuresis. If the problem fails to respond, a small uncuffed endotracheal tube should be placed. This is best done with the aid of a flexible bronchoscope. Wound infections have been relatively uncommon (< 2%). Concern over infection is one reason to always try to cover the anastomosis with viable tissue (thyroid isthmus or strap muscle). I always cover the anastomosis with a strap muscle in diabetics or those patients where a tracheostomy stoma is present. These patients are at slightly greater risk. A superficial wound infection should be managed with dressing changes and antibiotics. Bronchoscopy should be done to check the integrity of the anastomosis. The presence of subcutaneous emphysema or an air leak through the wound drain usually means a small leak in the anastomosis. The patient should be returned to the operating room and the wound explored. If the leak can be identified, it should be repaired with a pedicled strap muscle. The anastomosis should be inspected as well. The presence of subcutaneous emphysema and respiratory distress usually heralds more serious problems with the anastomosis. Dehiscence and separation is a life-threatening problem. Great judgement is required to determine how best to manage this problem. If the separation is only partial, a tracheostomy or T-tube should be placed through the separation. Complete separation is a very serious situation. If enough length of the distal airway exists, it can be secured to the skin as an end-stoma. Insufficient length of the distal airway requires creative solutions to secure the airway. A tracheostomy tube should be placed and buttressed with muscle flaps to wall it off from surrounding vascular structures. The proximal airway should be closed or covered with a muscle flap. A T-tube can be used if the distance of separation is not too great. Muscle flaps should be utilized to buttress the T-tube. Late anastomotic stenosis is usually a result of exuberant granulations or stricture from ischemia or slow separation. Granulations are uncommon now that absorbable sutures are used. Mechanical debridement, lasering, and steroid ingestion may be utilized to manage the granulations with varying degrees of success. Early stricturing can be managed transiently with dilation. If dilation is unsuccessful, a tracheostomy or T-tube may be necessary. Whichever tube is chosen, it should be placed through the most damaged portion of the airway to insure as much viable trachea as possible for future reconstruction. If recurrent stenosis develops, reoperation is possible in highly selected patients. A period of at least 3 months should elapse before attempted resection and reconstruction. Paralysis of one vocal cord or performance of a suprahyoid laryngeal release predisposes patients to aspiration. This is usually a temporary problem.

Complications of tracheobronchial resection 105

Speech pathologists have been helpful in instructing patients about swallowing techniques that minimize aspiration. If these maneuvers fail, a temporary gastrostomy tube may be required until the patient no longer aspirates. Prolonged symptomatic vocal cord paralysis or bilateral cord paralysis may be amenable to otolaryngological techniques to lateralize a vocal cord to improve glottic opening or move a vocal cord to the midline if aspiration persists. One of the most dreaded postoperative complications is a tracheoinnominate artery fistula [7]. It is an uncommon problem (< 0.8%). It is best avoided by not directly dissecting the innominate artery itself and interposing a pedicled strap muscle as described previously. If a tracheoinnominate artery fistula develops, the patient should immediately be taken to the operation room. An endotracheal tube placed with the balloon inflated at the anastomosis should temporarily control the hemorrhage. A sternotomy should be done and proximal and distal control of the artery obtained. The artery should be divided and the two ends oversewn. The management of the airway depends upon the nature of the injury. If the tracheal defect is small, repair and buttressing with muscle or omentum may be possible. If there is circumferential injury to the anastomosis, placement of a tracheostomy through the damaged portion if preferable. We have tended to mobilize omentum or pass it substernally to bury the divided ends of the innominate artery and reinforce the tracheal repair.

Results Resection and reconstruction for neoplasms or postintubation stenosis has been successful in over 90% of patients (Table 5.2) [5]. However, complications do occur (Table 5.3). Proper patient selection, attention to technical detail and experience should minimize the incidence of complications (Tables 5.3, 5.4 and 5.5). When complications do occur, proper management can still lead to a favorable outcome [8,9,10]. Table 5.2 Results of primary reconstructions. Intubation

Good Satisfactory Failed/poor Death Lost to follow-up Total

Neoplasm

No.

%

No.

%

232* 27† 11 5 4 279

83.2 9.6 4.0 1.8 1.4

77‡ – 1 8 – 86

90 – 1 9 –

*7/232 required reoperation for stenosis. †2/27 required reoperation for stenosis. ‡6/77 required reoperation for stenosis.

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Table 5.3 Complications following tracheal resection and reconstruction in 365 patients. Complication

Intubation

Neoplasms

Fault

Granulations Separation

28 4

10 6

–

1

Non-absorbable sutures Excessive tension, devascularization – Granulation, separation

6 15 2

3 – 1

Tracheo–esophageal fistula Esophagocutaneous fistula Cord dysfuction Aspiration

1 – 5 1

– 1 3 –

Wound infection Laryngeal edema Respiratory failure Pneumonia Persistent stoma

6 1 – – 5

– – 2 2 –

Air leak only Stenosis (tension) Partial Complete Hemorrhage

Table 5.4 Effect of experience (postintubation lesions).

Case no.

Deaths Failures Complications

Innominate: incorrect dissection, injury Pulmonary a: no interposition – – Surgical injury Neurological deficit pre-op.; short trachea; laryngeal release

1–139

140–279

4 13 42

1 7 30

Table 5.5 Results of treatment of postoperative complications.

Granulations Separation Restenosis Malacia Hemorrhage Tracheo–esophageal fistula Cord dysfunction Aspiration Wound infection Edema

No.

Good

Satisfactory

Failed

Death

28 4 21 3 2 1 5 1 6 1

24 – 6 1 1 – – – 6 –

4 2 15 – – – 4 – – –

– – – 1 – – 1 1 – 1

– 2 – 1 1 1 – – – –

Complications of tracheobronchial resection 107

References 1 Bueno R, Wain JC, Wright CD et al. Bronchoplasty in the management of low grade airway malignancies and benign bronchial stenoses. Ann Thorac Surg 1996; 62: 824 –829. 2 Mathisen DJ, Grillo HC. Endoscopic relief of malignant airway obstruction. Ann Thorac Surg 1989; 48: 469– 475. 3 Gaissert HA, Mathisen DJ, Moncure AC et al. Survival and function after sleeve lobectomy for lung cancer. J Thorac Cardiovasc Surg 1996; 111: 948–953. 4 Tedder M, Anstadt MP, Tedder S et al. Current morbidity, mortality and survival after bronchoplastic procedures for malignancy. Ann Thorac Surg 1992; 54: 387–391. 5 Grillo HC, Donahue DM, Mathisen DJ et al. Postintubation tracheal stenosis: treatment and results. J Thorac Cardiovasc Surg 1995; 109: 486. 6 Muehrcke DD, Grillo HC, Mathisen DJ. Reconstructive airway surgery after irradiation. Ann Thorac Surg 1995; 59: 14. 7 Wright CD. Management of tracheoinnominate fistula. Chest Surg Clin N Am The Trachea 1996; 6: 865. 8 Mathisen DJ. Complications of tracheal surgery. Chest Surg Clin N Am. The Trachea 1996; 6: 853. 9 Grillo HC, Zannini P, Michelassi F. Complications of tracheal reconstruction. J Thorac Cardiovasc Surg 1986; 91: 322. 10 Grillo HC. Complications of tracheal operations. In: Complications of Intrathoracic. Surgery (eds AR Cordell, RG Ellison). Little, Brown Co, Boston, 1979: pp 287.

CHAPTER 6

Complications of lung volume reduction procedures Robert J Burnett, Douglas E Wood

Introduction Since the reintroduction by Cooper [1] of Brantigan’s [2–4] original concepts, surgical treatment other than transplantation has emerged as a viable option for patients with end-stage emphysema. Although there remains a great deal of controversy surrounding many aspects of this procedure, surgical reduction of hyperinflated emphysematous lungs improves symptoms and pulmonary function in selected patients. The excision of the most severely diseased portions of the lung that occupy space, but provide little or no gas exchange, allows improved function by decreasing small airway resistance and improving chest wall and diaphragmatic mechanics. Volume reduction procedures, or lung volume reduction surgery (LVRS), have been shown to benefit certain patients by improving the forced expiratory volume in 1 s (FEV1), timed walking distance, oxygen and steroid requirements and overall quality of life [1,5–8]. Additionally, LVRS can be an alternative or bridge to pulmonary transplantation in patients with end-stage emphysema. Many of the questions and controversies surrounding LVRS are currently being studied by the National Emphysema Treatment Trial (NETT). In the trial, patients are evaluated by strict criteria and initially undergo a period of pulmonary rehabilitation before being randomized to LVRS or continued medical therapy and rehabilitation. Overall survival and maximum exercise capacity are the primary outcomes being measured in the trial [9]. Survival is a clinically significant outcome, because patients with severe emphysema have a high mortality rate and there have been no studies that evaluate the effect of LVRS on overall survival. Standardized exercise testing is a way to evaluate improvements in cardiopulmonary and physical function in a qualitative and reproducible fashion. Secondary outcome parameters for the NETT include quality of life, utility, pulmonary function and gas exchange, radiographic changes, oxygen requirements, 6-min walk distances and other cardiovascular measurements. In addition to these primary and secondary outcome measurements, the trial will help to define the subgroups of patients with end-stage emphysema that may benefit from LVRS and which patients are at particularly high risk of complications. 108

Complications of lung volume reduction procedures 109

It is not the purpose of this chapter to discuss the controversies surrounding lung volume reduction procedures. The focus of this discussion is the prevention, identification, and treatment of complications associated with LVRS. Patients with end-stage emphysema have an unpredictable natural history. Most of these patients have a progressive course of their disease with exacerbations and hospitalizations accelerating the worsening of symptoms and quality of life. Mortality ranges from 10 to 30% per year and is higher in those patients who have required hospitalizations for complications of their emphysema. It is likely that any procedure performed routinely on patients with such severe emphysema is apt to produce significant and potentially lifethreatening complications. This becomes particularly true when the operation involves violation of the thorax and perturbation of respiratory mechanics. With an understanding of the lessons learned regarding this procedure and about the general intra- and postoperative care of this particular type of patient, many complications can be avoided and LVRS can be performed with acceptably low major morbidity and mortality.

Overview of mortality As pointed out by Cooper [10], there were several reasons why Brantigan’s work in the 1950s failed to gain popularity. In addition to the unsettling notion of removing lung tissue in a patient with existing respiratory dysfunction, there was a lack of objective evidence for the benefit of the operation and a 16% mortality that led to criticism and ultimate failure of acceptance. In 1995, Cooper [1] reported on his first 20 patients to undergo bilateral LVRS via median sternotomy in which there were no early or late deaths. In a later series reporting the first 150 consecutive patients in 1996, the same group had a mortality of 4% [5]. Similar mortality rates have been reported in other series as well [6–8,11–13]. Recently, Roberts et al. reviewed the mortality of patients after LVRS which ranged from 0 to 19%, with a weighted average of 6.8% [13]. Summarized at the bottom of Table 6.1 is the composite mortality from six recently published series, utilizing lung volume reduction via median sternotomy or unilateral or bilateral video-assisted thoracic surgery (VATS). The weighted mortality among this group of series is 4.6%. Although the best results and average mortality amongst published reports is approximately 5%, clearly there is a wide range of reported mortality to date, and unreported mortality rates may be even less favorable. Since LVRS is a palliative procedure directed primarily at the improvement in functional quality of life, it is critical that low mortality rates be maintained in order to sanction rationally its utilization for patients with end-stage emphysema. Death after LVRS can result from a variety of complications and can occur early or late in the postoperative period. Early deaths have been reported as a result of hemorrhage and myocardial infarction [5]. Respiratory failure can occur early as a result of profound CO2 retention or massive air leak, or late as a result of nosocomial respiratory tract infection, either of which can be fatal.

4

Other 34 50 68.0 2 4.0

6

1

1

NR

NR

3

NR

3

3

15

Naunheim [8] unilat,VATS N = 50

55 47 117.0‡ 4 8.5

5

NR

NR

NR

NR

NR

6

16

24

NR

Travaline [11] bilat, MS and VATS N = 47

10 26 38.5 1 3.8

1

NR

NR

NR

2

NR

3

3

1

2

Daniel [7] bilat, MS N = 26

111 129 86.0 0 0

2

2

NR

4

NR

NR

NR

1

5

77

Hazelrigg [12] bilat MS or staged unilat VATS N = 129

78 136 57.4‡ 12 8.8

19

5

NR

14

7

4

6

15

12

NR

Roberts [13] bilat MS or VATS N = 136

25

163 355 62 538 49 538 24 359 9 336 14 312 18 265 3 200 10 465 37 538 416 538

Sum*

4.6

77.3

6.9

2.2

1.5

6.8

4.5

2.7

6.7

9.1

11.5

45.9

Percent*

MS, Median sternotomy; VATS, video-assisted thoracic surgery; MI, myocardial infarction; GI, gastrointestinal; bilat, bilateral; unilat, unilateral; NR, not reported. *The sum of all patients reported with a given complication over the total reported and the associated percentage. †The total number of complications reported over the number of patients in the series. ‡Did not report prolonged air leak as complication.

128 150 85.3 6 4.0

2

GI perforation

Total number of complications Number of patients Percentage† Total number of deaths Mortality

2

MI

NR

5

Tracheostomy

Arrhythmia

2

Bleeding

11

Reintubation/ventilation

9

17

Respiratory tract infection

Reoperation

69

Prolonged air leak

Cooper [5] bilat, MS N = 150

Table 6.1 Morbidity and mortality in early LVRS series.

Complications of lung volume reduction procedures 111

Additional infections such as empyema and mediastinitis have been reported sources of mortality after LVRS, as have other generic postoperative problems such as pulmonary embolus and gastrointestinal perforation [13].

Overview of morbidity Despite a low mortality rate reported by different centres, LVRS is associated with significant morbidity. Because the incidence of prolonged air leak greater than 7 days is so high, complication rates reported range from 38 to 100% [5,7,8,11–13], including a report of the first 150 patients by Cooper et al. citing a complication rate of 85% [5]. Representative complication profiles are shown in Table 6.1. In a recent report comparing LVRS by sternotomy with bilateral VATS LVRS, the complication rate for all procedures, excluding prolonged air leak, was 57% [13]. This review of the published morbidity rates of LVRS performed at major centres emphasizes the fact that complications are an undeniable part of volume reduction surgery. Because of the generalized debilitated state of these patients preoperatively, any complication can become life-threatening. It is critical that these patients are managed with the utmost diligence so that complications are recognized early and treated aggressively to prevent further clinical deterioration. There is little room for error in this group of fragile patients. However, it also must be appreciated that the occurrence of a complication does not necessarily mean a poor outcome for the patient. As can be ascertained from the data presented, the vast majority of complications do not result in death, and despite complications, most patients will go on to appreciate some degree of overall benefit from the procedure.

Preoperative preparation Once a patient is deemed an appropriate candidate for LVRS, several things may be done to minimize the incidence and severity of postoperative complications. It has become standard practice to enroll patients preoperatively in aggressive pulmonary rehabilitation programs that are designed to optimize preoperative exercise endurance and pulmonary hygiene. Because these programs are time and energy consuming, they also serve to assure adequate patient motivation to get through a challenging postoperative regimen of early mobilization and pulmonary toilet. Assuring adequate preoperative nutritional status is also particularly important in this group of patients, often found to be chronically malnourished. Early and aggressive nutritional supplementation, often commensurate with pulmonary rehabilitation, should assure adequate postoperative immunological function and wound healing [14]. Weaning patients off of supplemental steroids or to the minimum amount tolerated is also a primary goal during this period. Patients who continue to require high doses of steroids in the absence of an acute exacerbating event are at prohibitively high risk for LVRS. Finally, treatment of acute bronchitis

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should be aggressive to maximize preoperative pulmonary toilet and minimize the risk of postoperative respiratory tract infection. Patients with large amounts of chronic sputum production or a history of frequent bacterial bronchitis have a relative contraindication to LVRS and should be considered carefully prior to undergoing surgery.

Complications of lung volume reduction procedures Air leak Prolonged air leak after LVRS is a major source of patient morbidity and resource expenditure. This is because the amount of time spent in the hospital after LVRS is predominately due to prolonged air leak and the associated hospitalization places patients at risk of complications. It is not uncommon to see patients doing well overall but subsequently developing a significant complication as they await the resolution of an air leak. For this reason, in addition to patient inconvenience and resource expenditure, every effort should be made to prevent and limit the occurrence of prolonged air leaks. As can be seen from the cited incidence, prevention is not all that simple. In several studies reviewed, air leak was so common as not to be considered a complication. The length of chest drainage was merely reported as a mean number of days. In the report by Roberts et al. [13] the mean chest drainage was 14.2 ± 14.5 for LVRS via sternotomy and 15.1 ± 19.3 for VATS LVRS. Six percent to 10% of patients were discharged from the hospital with chest drains and Heimlich valves in place. Although the overall incidence of air leak is not generally reported, air leaks lasting longer than 7 days are generally considered prolonged, and range from 8 to 60% [5,7,8,11–13]. There are a number of measures in and out of the operating room that can prevent or minimize the severity of air leak after lung volume reduction.

Intraoperative management The prevention and management of air leak begins in the operating room. Because of the characteristics of the emphysematous lung, significant air leaks can be created at any stage of the procedure. At the time of sternotomy the lungs are susceptible to injury given the significant amount of hyperinflation present. A generous skin incision should be used to assure adequate mobilization above the manubrium and below the xyphoid process. Cooper [1] recommends the placement of a rolled sponge on a clamp substernally to prevent inadvertent entry into the pleural space or pulmonary parenchyma. Avoiding pleural opening at sternotomy also has the benefit of keeping the ventilated lung out of the operative field during volume reduction of the contralateral side. In addition to the rolled sponge, a longer than usual period of exhalation should be allowed prior to sternotomy to provide for the prolonged expiratory time of emphysematous lungs. Similarly, problems may be encountered during video access for VATS LVRS, particularly if adhesions exist in the region of access. Care should be taken to gain access without parenchymal injury which

Complications of lung volume reduction procedures 113

may go unnoticed until the lung is re-expanded at the completion of the reduction, and be located in areas that are difficult to staple for complete aerostasis. The presence of some degree of visceral to parietal pleural adhesive disease is likely to be present, particularly in the apices. These adhesions are frequently the source of postoperative air leakage. Merely the weight of the unventilated lung against the adhesion may cause large parenchymal lacerations and air leaks. The anterior pleural surface should be examined prior to single lung ventilation. As the lung collapses, the lung should be supported while the adhesions are divided sharply or with cautery. Many consider the extent of adhesions to correlate with the amount of postoperative air leak and thus should be considered when evaluating patients preoperatively. Most authors list previous thoracotomy or pleurodesis as an exclusion criterion for LVRS [7,8]. Certainly one should be prepared for adhesions in any patient with end-stage emphysema; however, previous history of trauma, broken ribs or pneumothorax should alert the surgeon to an increased risk of pleural symphysis. Dense pleural space obliteration encountered at operation is a relative contraindication to proceeding with LVRS on that hemithorax due to the likelihood of serious air leak morbidity. Whether or not the inferior pulmonary ligament needs to be routinely divided when performing apical volume reduction is controversial, but it does not appear to be routinely necessary. When there is a space issue, or when performing basilar reduction, as is frequently the case in α1-antitrypsin deficiency patients, the division of the ligament is necessary. The potential to create air leaks with this maneuver is also significant, particularly on the left side where the heart makes access to the ligament difficult through a median sternotomy approach. Division of the ligament using video-assisted techniques is straightforward and poses less risk of inadvertent air leak than open techniques. The most treacherous time for the creation of air leaks is during the actual reduction. Hazelrigg et al. prospectively randomized patients undergoing unilateral VATS LVRS to receive either no buttressing of their staple lines or buttressing of all staple lines with bovine pericardial strips. The patients with buttressed staple lines had their chest drains removed, and were discharged from the hospital 2.5 days before the control group. The incidence of other complications and overall hospital charges were no different between the groups [15]. Despite the standard use of some form of staple line buttress, leaks often result from the staple lines and surrounding parenchyma. There are several potentially avoidable reasons for this. First, certain areas of the lung provide better surfaces to minimize tension. Such surfaces tend to be those with acute angles like the lung base and the anteroapical region (Figures 6.1 and 6.2). Resections in areas that incorporate larger amounts of lung parenchyma, such as broad lateral surfaces, create staple lines that are prone to high tension and leakage at the time of re-expansion. Second, the reduction is performed as sequential firings of a linear stapling device that ultimately forms a single buttressed staple line. The alignment of the lung tissue for division is critical

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Figure 6.1 Resection centred over the medial and apical edges of the upper lobes allows a large non-anatomical resection with a continuous staple line on a surface minimizing tension after re-expansion.

Figure 6.2 After division of the pulmonary ligament, a continuous staple line resection of the basilar segments can be performed, providing the least staple line tension after lung inflation.

Complications of lung volume reduction procedures 115

and often requires the use of multiple lung clamps. Every effort should be made to keep clamps off lung tissue that is not intended for resection. Retraction alone and stapler positioning have the potential to create air leaks in diseased lung near the staple lines and should be performed with extreme gentleness and caution. Third, as the staple line is advancing, it is often tempting to ‘roll in’ additional lung tissue in order to achieve adequate reduction or save an additional staple load. These areas of imbricated or ‘wrinkled’ lung also have the potential to create air leaks and should be avoided. Lastly, one of the areas of greatest potential for leakage is the apex of the evolving staple line. After a firing of the stapler, a ‘V’ is formed within the buttress material. While maneuvering the lung tissue for the next staple firing, it is very easy to place tension on this ‘V’, causing it to widen. As this occurs, the staples tear through the lung tissue creating sizable air leaks. If recognized, the next firing can be placed across the torn lung, at the expense of redirecting the entire staple line. If this is not recognized until after the staple line is completed, it can be quite difficult to deal with. Not all air leaks are created as a result of retraction-type injuries. The stapler itself can be the source of unwanted problems, particularly when there is axial rotation, or torque, applied to the stapler during or after firing. Once closed, any twisting of the stapler along the long axis, or lateral motion of the heel of the stapler, results in torn lung. This is particularly true after the stapler has been fired but not yet released. The multitude of staple posts act as tiny knives whenever tension or torsion is placed on the closed, fired stapler. This seems simple enough to avoid; however, when stapling through a particularly thick area of lung parenchyma or through several previous buttressed staple lines, the force required to fire the stapler can be significant. As the knife blade gives, it is easy to place undesirable forces on the device. Maximal stabilization should be maintained while firing the stapler. After the completion of the staple line it should be inspected carefully for areas that look suspicious for torn lung tissue. These areas are usually located at the junction between staple firings, but, as discussed, can occur anywhere along the staple line. A good time to attempt repair of these problem areas is before the re-expansion of the lung. An area of staple line in question may be gently held with a lung clamp while another application of buttressed staple line is placed slightly offset with the current staple line. This gives a crimping or plicating effect without the resection of much additional lung tissue. With this, problems can arise with the thickness of the staple line. If the initial resection was aggressive, in combination with one or more buttressed staple lines, the area can become too thick for the 3.5- or 3.8-mm staples or stapling device. If this is felt to be true, it may be adequately closed with a 4.8-mm stapler or alternatively an anatomic lobectomy may provide the most secure closure of central air leaks. The initial re-expansion of the lung is another time when significant lung damage can occur. As a result of the delicate nature of emphysematous lung tissue, injury at re-expansion can be inevitable, depending on the balance of

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the amount of lung resected, staple line location and integrity and strength of the tissue. After inspection of the staple line, the anesthesiologist is asked to hand ventilate the patient gently under direct vision, while keeping a watchful eye on peak inspiratory pressures. Because of the large amount of lung parenchyma drawn into the staple line, there is tremendous tension on both the staple line and adjacent lung tissue as the lung expands. It is very important for the surgeon and anesthesiologist to work very closely during this portion of the operation. The minimal pressures necessary to achieve modest re-expansion and acceptable gas exchange should be used initially. In open cases it may help to support the staple line manually to prevent rapid over-expansion. This also has the advantage of giving direct tactile feedback regarding lung tension that may not relate closely to airway pressures if there are secretions or a malpositioned double lumen tube. Once satisfactory ventilation has resumed, attention can turn to the contralateral lung. Some surgeons prefer the feedback of hand ventilation during this phase, but most important is close communication between the surgeon and the anesthesiologist, assuring adequate ventilation without air trapping and allowing two-lung ventilation temporarily as necessary to improve oxygenation without excessive airway pressures. At the completion of lung reduction, the hemithorax should be filled with warm saline solution and the lung should be inspected for areas of air leakage. Although the total absence of leak at this point is not uncommon, small leaks associated with the staple line may be present. This should be accepted and this type of leak usually seals within a few days. The goal is to detect large unsuspected leaks, that are often not associated with the staple line. Large blebs in areas of lung not resected are frequently the source of such leaks. The smell of anesthetic gases during the procedure is a clue to the presence of a large leak. An excellent way to handle these leaks, when easily accessible, is with additional stapling with buttressed staples. Suture plication with or without a pericardial pledgett can reduce the amount of leakage but will rarely make it stop completely. Another consideration is the use of fibrin glue. Until recently, its use was impractical due to the amount of time necessary to obtain the components from the blood bank. Currently, commercially available preparations have made the use of fibrin glue more practical by significantly decreasing the time to availability and eliminating the transfusion risk. This may prove to be beneficial and a decreased length of stay would certainly justify its expense. Recently, in a report by Macchiarini et al., an absorbable synthetic sealant was used after pulmonary resection in an animal study, significantly reducing the number of animals with postoperative air leak [16]. In addition to fibrin glue, the use of commercially available cyanoacrylate glue has been reported in the treatment of air leaks from other etiologies [17]. The authors have used fibrin glue successfully to control air leaks after cautery tumor excision or with anatomically difficult air leaks deep within a fissure. If these maneuvers are unsuccessful, if the area is not accessible or if anatomic resection is not appropriate, the leak should be accepted rather than risk worsening of the damage with continued efforts at exposure and repair.

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Maneuvers involving the pleura can be performed when significant air leak or space issues seem likely. Apical pleural tents can be performed with great ease and minimal morbidity or added operating time. They may shorten the time of leakage by eliminating the intrapleural space and allowing approximation of lung and suture line with pleura. Pleurectomy or pleural abrasion which can be performed to promote adhesions and leak closure would complicate performance of a subsequent lung transplant. Therefore, careful consideration should be given prior to using these procedures in patients that are current or potential transplant candidates.

Postoperative management It is not uncommon to detect an air leak either at the completion of the operative procedure or in the immediate postoperative period despite being apparently leak-free at the time of chest closure. This is probably due to continued expansion of the lung with increasing tension on the suture line. Management in the peri-extubation period is very important from an air leak standpoint. It is particularly difficult at this time, because arterial pCO2 levels can exceed 100 mmHg after combined single-lung ventilation and there will be some sense of urgency to reduce the CO2 level in preparation for extubation. At the completion of the procedure, neuromuscular blockade is reversed, the patient is allowed spontaneous respiration and is then extubated prior to the excitement phase and is supported with mask-assisted ventilation [18]. Vigorous coughing at this time is to be avoided as it will frequently cause or worsen an air leak. Adequate chest drainage is important in the management of postoperative air leak. We place two thoracic drains on each side, one anteroapical and one in the posterior diaphragmatic sulcus. The routine use of chest tube suction in this setting is controversial. Some recommend routine suction for 24–48 h, even in the absence of air leak or pneumothorax. Others advocate water seal, with suction applied only for a large pneumothorax or pneumothorax with respiratory distress. The use of suction for asymptomatic apical air spaces is also controversial. Some surgeons prefer to maximize lung expansion and subsequent pleural approximation as in other pulmonary surgery, while others prefer to avoid the potential deleterious effects of suction and accept small to moderate apical spaces. Although air leaks have not been shown to be eliminated more quickly without suction in a randomized trial, many thoracic surgeons firmly believe that less suction or no suction significantly decreases the magnitude and duration of postoperative air leak [19]. Regardless, small or moderate air leaks are expected to seal in the first 72–96 h if there is pleural to pleural apposition. Large air leaks, with continuous leakage throughout the respiratory cycle, are more difficult to manage. Using the minimum amount of suction that maintains lung expansion will also minimize the amount of air leak. Despite this, a significant percentage of the inspiratory volume can be lost to air leak. Occasionally, hypocapnea from this degree of air exchange results in a significant respiratory alkalosis. When profound, mechanical ventilatory

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support may be required to limit the inspiratory volume. Compensation by the prolongation of the inspiratory time usually results in adequate ventilation and oxygenation. Consideration may be given to reoperation in an effort to limit the volume of air leakage. The need for surgical re-exploration should be carefully assessed and only undertaken when all non-operative measures have failed to stabilize the situation. Surgical attempts to treat air leak in the postoperative period can be very gratifying if a discrete correctable cause of the leak is identified. However, further surgical manipulation of the lung can also result in significant exacerbation of the amount of leakage. Thoracic drains are removed 24 h after the cessation of air leak. When an air leak is present and the patient is stable, the tube(s) can be connected to a one-way valve to allow the patient to be discharged from hospital, with the tube later removed in an out-patient visit.

Respiratory tract infection The incidence of respiratory tract infection after LVRS is significant and can be life-threatening. Comparison of incidence is difficult because of different definitions used. Reports in the literature vary from 4 to 50% [5,7,8,11–13]. The higher numbers probably reflect the reporting of all respiratory infections including upper and lower respiratory tract infections. True bacterial pneumonia as reflected by purulent sputum, positive culture, fever, leukocytosis and infiltrate on radiograph occurs in approximately 4–15% of patients after LVRS. The consequences of pneumonia in this group of patients are severe, with Roberts reporting a mortality of 40% in patients who acquired a postoperative pneumonia [13]. It is our experience that even when patients survive postoperative pneumonia, they obtain subjectively less overall benefit from LVRS. Therefore, efforts to prevent respiratory infections are of paramount importance in producing favorable results and minimizing mortality. Prevention of postoperative respiratory infections begins with meticulous pain control in order to minimize the detrimental effects of sternotomy or thoracoscopy on respiratory mechanics and pulmonary toilet. This starts with the accurate, reliable preoperative placement of a thoracic epidural catheter. Even though a thoracic epidural does not completely block the pain of a median sternotomy, the amount of oral and parenteral analgesia required is significantly less when a functioning epidural catheter is utilized. The ability to minimize the amount of narcotic administration is so important that some recommend the placement of the catheter under fluoroscopic guidance to assure accurate placement at the T3–4 level [18]. Incomplete or unilateral blocks are unacceptable and require catheter adjustment or, if necessary, timely replacement. A few hours of inadequate pain relief, or high-dose systemic narcotics can be profoundly detrimental with regard to pulmonary toilet and overall oxygenation and ventilation. The complete support of an acute pain management team, available around the clock, is necessary to minimize the sequelae of poor pain control or narcotic over-sedation.

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Sympathetic blockade associated with epidural local anesthetic agents should be anticipated. Moderate hypotension may not require treatment, but in an effort to minimize fluid administration, α-agonists such as phenylephrine may be used. It is usually possible to wean the α-agonist over the first 12–24 h postoperatively. Ketorolac is a useful adjunct to postoperative pain management that helps to reduce the amount of narcotic required. In this setting, renal function should be followed closely given the relative hypovolemia and hypotension that many of these patients experience. To prevent renal or gastrointestinal complications, ketorolac should be written for 48–72 h courses with clinical re-assessment prior to renewal. If these measures do not adequately control postoperative pain, as determined by adequacy of pulmonary toilet and secretion clearance, some systemic narcotic may be required. Oral agents are avoided until the epidural has been removed, which usually coincides with the removal of the chest drains. When a prolonged air leak is present, the epidural may be removed safely after four or five postoperative days. Parenteral narcotics are best given as small doses of a short-acting agent to prevent respiratory depression. Narcotic use must be monitored very carefully to avoid over-sedation with subsequent CO2 retention and respiratory failure. A very low-dose patient-controlled analgesia (PCA) with continuous monitoring may optimize systemic analgesia. If there is any hypercapnia by blood gas analysis or the patient is too sedated to perform pulmonary toilet exercises, the narcotics are stopped and a reversal agent is used if necessary. Other measures are utilized to maximize pulmonary toilet and therefore minimize respiratory tract infections. Generous use of nebulized and metered dose β-agonists are used for both bronchodilation and to facilitate secretion mobilization. Incentive spirometry, early mobilization, and chest physiotherapy are routine. The patient is placed upright in a bedside chair postoperatively after arrival from the postanesthesia unit to the intensive care unit. Ambulation is expected on postoperative day 1, which often requires portable suction devices to maintain chest tube suction. Physical therapists that specialize in the care of these patients help to assure that they are mobilized safely and regularly despite the amount of associated equipment. When used aggressively in a motivated patient, these measures usually suffice for the management of pulmonary secretions. Occasionally, additional measures such as naso-tracheal suctioning, fiberoptic bronchoscopy or small-bore tracheotomy as a way to provide pulmonary toilet (Minitrach II; Portex, Keene, NH, USA) are required. Naso-tracheal suctioning is a profound motivational measure for some patients and is very effective for the patient who needs occasional assistance in clearing retained secretions. It is not ideal for patients who require frequent suctioning. If secretions are retained despite naso-tracheal suctioning, fiberoptic bronchoscopy is performed to obtain a sputum specimen as well as for directed pulmonary toilet. This may be required daily or even twice daily in some patients. If naso-tracheal suctioning or bronchoscopy are required

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more frequently than this, a small-bore tracheostomy, or ‘mini-trach’ can be performed at the bedside through the cricothyroid membrane under local anesthesia. Commercially prepared kits are available for this procedure which is quick and simple. This sheath provides access for diagnostic and therapeutic maneuvers with minimal patient discomfort or sequelae. When respiratory tract infections do occur, they must be treated early and aggressively. Classically, nosocomial pneumonias would be diagnosed only when multiple criteria were present including fever, purulent sputum, positive cultures from a tracheal aspirate or sputum specimen, leukocytosis and infiltrate on chest radiograph. In this patient population it may not be wise to wait for multiple criteria to be present. If any one of the clinical indicators above is present without an alternative explanation, it is prudent to obtain promptly a reliable sputum specimen for Gram stain and culture and sensitivity and begin broad-spectrum antibiotics with double coverage for Pseudomonas species. Antibiotics are then modified based upon the culture results and given for a full 10–14-day course. The mobilization and clearance of secretions remains an important adjunct to antibiotic treatment. Similar to pneumonia prevention strategies, adequate analgesia, patient mobilization and secretion management interventions should be maximized.

Respiratory failure The need for reintubation for respiratory failure after LVRS is a particularly concerning complication. It is uncommon that a patient dies after LVRS without first demonstrating respiratory failure. In the report of Cooper et al. of 150 patients, 11 (7%) required mechanical ventilation at some point during their postoperative course [5]. Of these, five went on to require tracheostomy and three ultimately died in hospital. Similarly, in the meta-analysis depicted in Table 6.1, 11.5% of patients required reintubation and ventilation, with an overall mortality of 4.6%. Thus, respiratory failure with reintubation, although not exceedingly common, carries an associated mortality of approximately 40%. Patients who require reintubation after reduction surgery can be categorized into one of three groups: those requiring early reintubation as a result of anesthetic or pain management difficulty, those requiring early reintubation for inadequate gas exchange, and those requiring late reintubation for respiratory failure secondary to respiratory tract infection. These distinctions are useful not only for prognostic reasons, but for treatment strategy as well. It is not uncommon for patients to demonstrate significant hypercapnia immediately after the completion of a reduction procedure, with arterial pCO2 levels > 80 mmHg. In an effort to minimize barotrauma, hand ventilation is used with caution and the patient is extubated in a deeper anesthetic stage to prevent harsh coughing or gagging. As a result of these maneuvers, gas exchange can be tenuous for a period after extubation. Reintubation may be required if somnolence, as a result of hypercapnia, results in worsening CO2

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retention with hemodynamic compromise. Similarly, patients with inadequate pain relief may experience worsening CO2 retention from hypoventilation. Intubation may be required if these conditions cannot be reversed prior to hemodynamic embarrassment. Over-sedation with resultant hypoventilation requiring reintubation may also be related to systemic narcotic administration. Given a certain component of somnolence from postoperative hypercapnia, even trivial amounts of systemic narcotic may result in early respiratory failure. With an experienced anesthesiologist these problems should rarely necessitate reintubation. When it is required, the causative factors may be addressed with expected successful extubation a few hours after reintubation. These events should not affect overall length of stay or outcome unless associated barotrauma has resulted in the development or exacerbation of air leakage. It is particularly worrisome when patients require reintubation for inadequate gas exchange in the absence of pain control or over-sedation issues. Oxygenation is rarely a problem after LVRS because of the ability to administer supplemental oxygen. Indeed, relative hyperoxemia at the completion of the procedure may contribute to respiratory depression in patients with chronic hypercapnia. Maintaining arterial oxygen levels close to baseline is a routine strategy at the time of extubation. Theoretical improvement in ventilation as a result of the reduction procedure, in the form of normalization of diaphragmatic function and improvement in functional airway obstruction, can be offset by the derangements in respiratory mechanics resulting from the surgical insult. This may not be tolerated by patients who are frequently tenuous even in the preoperative period. It may therefore be necessary to provide mechanical ventilatory support to assist in reducing CO2 from supraphysiological to normal levels. At this point, some patients will be capable of maintaining adequate ventilation allowing extubation. Meticulous pain control and pulmonary toilet are particularly important in keeping these fragile patients extubated. Some patients will not tolerate weaning of ventilatory support because of pCO2 retention. In these patients, the perturbations in respiratory mechanics as a result of the procedure are greater then the early improvements in ventilation. The duration of this is variable. Persistent CO2 retention despite the optimization of pain management and pulmonary toilet will usually require intermediate or long-term ventilatory support. As respiratory mechanics normalize over the ensuing days to weeks, there is hope for separation from mechanical assistance. It has been our experience that early tracheostomy is beneficial in the management of this group of patients. Tracheostomy helps with weaning and placement strategies, pulmonary secretion management, and patient comfort issues. We have not experienced problems associated with early tracheostomy after median sternotomy. Minimizing the number of patients that require chronic ventilator support after LVRS is one of the primary goals of the patient selection process. Although a discussion regarding the preoperative evaluation and screening process is not the focus of this chapter, a few comments as it relates to

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postoperative respiratory failure are warranted. There is controversy regarding the appropriateness of LVRS in patients with baseline CO2 retention. The range of resting arterial pCO2 for exclusion from most published series is between 45 and 55 mmHg [1,5,7,13]. Most agree that a resting pCO2 > 55 mmHg carries a prohibitive risk of postoperative respiratory failure leading to death or chronic ventilatory support. Likewise, most agree that a resting pCO2 < 45 mmHg correlates with a reasonably low risk of postoperative ventilatory insufficiency. There is controversy regarding the management of the significant number of patients that fall between 45 and 55 mmHg. In 1996, Szekely et al. published a report of preoperative predictors of operative morbidity and mortality after LVRS [20]. In this analysis, only two preoperative factors correlated with unacceptable postoperative outcome, as defined by death within 6 months or hospitalization ≥ 21 days. These factors were poor performance on a 6-min walk test and resting pCO2 > 45 mmHg, with the latter being a 10-fold negative predictor. Conversely, a European study published in 1998 reported on 80 patients undergoing LVRS, 22 of whom had resting hypercapnia > 45 mmHg [21]. Although the mortality in patients with hypercapnia was 9.1% vs. 5.2% in those with normal CO2 levels, this did not reach statistical significance. ICU stays and duration of chest drainage were similar, and improvement in FEV1 at 3 months favored the group with hypercapnia preoperatively. It appears that the group of patients with resting arterial pCO2 between 45 and 55 mmHg may gain significant benefit from LVRS but be at higher risk of postoperative respiratory failure. It may be wise to consider these patients at higher risk and counsel them accordingly. It also may be prudent to consider these patients only if there are no other extenuating circumstances, such as poor target areas for resection, high steroid dose, advanced age, significant sputum production or malnutrition. It is our general feeling that even when no single overt exclusionary criterion exists, one or more ‘borderline’ conditions in combination with marginal resting hypercapnia is a relative contraindication to LVRS. It is the intention of the NETT investigators to address these issues. Nosocomial pneumonia is the likely etiology in patients who experience late respiratory failure requiring reintubation and mechanical ventilation. Early and aggressive treatment of hospital-acquired respiratory tract infections is required for patient salvage. Despite these efforts, late nosocomial pneumonia resulting in respiratory failure carries a poor prognosis, often resulting in prolonged intubation, sepsis, multiorgan failure and death.

Hemorrhage Significant bleeding can occur during LVRS independent of operative approach. Although bleeding from sternotomy or VATS port sites can be troublesome, it is rarely significant enough to require transfusion or reoperation. Most bleeding of clinical significance originates at the buttressed staple line which can be life threatening on occasion. Hemorrhage can be intraparenchymal,

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intrapleural or both. Bleeding is frequently from major pulmonary arterial or venous branches and tends to occur when staple lines are too close to the hilum or major fissure or when staple lines are stressed by a large amount of parenchyma. Vascular injury can be a result of linear or rotational forces on the closed or closing stapler in a mechanism similar to that which results in air leakage, as previously discussed. When the bleeding is across the staple line into the pleural space, it can frequently be controlled with additional firings of the reinforced stapler, or by direct suture ligature. Similarly, when a parenchymal hematoma appears after stapling, attempts should be made to control the source of hemorrhage and thus limit the size and functional significance of the hematoma. These maneuvers may be difficult using video-assisted techniques and may require conversion to an open procedure to control the hemorrhage. Despite meticulous technique and careful inspection of staple lines, both reoperations and intraoperative mortalities have been described as a result of major hemorrhage. It is difficult to extrapolate the exact incidence of postoperative hemorrhage requiring transfusion, re-exploration or death. Studies that do report the complication in the form of re-operation generally show a 0–5% incidence with reported mortality < 1% [13].

Cardiac complications Patients who undergo LVRS are at risk of the same perioperative cardiac complications as other thoracic surgery patients. Most patients who are candidates for reduction surgery are also at high risk of cardiac disease based on age, sex, smoking and sedentary lifestyle. Unfortunately, because exercise tolerance in these patients is limited by pulmonary function, few patients present with a history of myocardial infarction (MI) or anginal symptoms. In one recent report, 10 (11%) of 90 patients had one or more perioperative cardiac events including atrial fibrillation (n = 3), supraventricular tachycardia (n = 3), congestive heart failure (n = 4), myocardial ischemia (n = 2), and premature ventricular beats (n = 1) [21]. The overall incidence of perioperative acute MI is low, reported between 0 and 2% [5,7,8,11–13]. The low incidence of MI and other cardiac events is attributed to the aggressive screening process that most centres employ prior to LVRS and the fact that patients with significant cardiac disease detected preoperatively are generally not offered surgical treatment options. On the other hand, self-selection may occur prior to presentation for possible LVRS due to the high baseline ‘stress’ of dyspneic patients, eliminating patients with concomitant coronary artery disease (CAD). In 1997, Thurnheer and associates reported on the incidence of CAD in patients being evaluated for LVRS [24]. Of 46 patients eligible for LVRS by other criteria, 44 underwent coronary angiography. All patients with a history of CAD and 15% of patients without a history of CAD demonstrated significant disease, emphasizing the prevalence of CAD in this patient population. Echocardiography with and without dobutamine stress has been used as a screening tool prior to LVRS [22]. Despite the hyperinflation of the lungs,

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images were obtained that satisfactorily assessed wall motion abnormalities, ejection fraction, valvular function and right heart abnormalities that might suggest pulmonary hypertension or cor pulmonale. Correlation between echocardiographic findings and catheterization results revealed that normal right heart findings on echocardiographic examination obviated the need for right heart catheterization. Correlation with results of coronary angiography were less reliable, however, with a sensitivity and specificity of 60 and 83%, respectively [22]. Although the authors concluded that all patients being evaluated for LVRS should be screened for cardiac disease using function and/or invasive studies, many centres reserve functional testing for patients with symptoms, signs, or ECG evidence of CAD. Patients should routinely undergo surface echocardiographic evaluation to identify right heart abnormalities and proceed to right heart catheterization if such abnormalities are discovered. Functional evaluation by dobutamine stress echocardiography or dipyridamole thallium-201 perfusion scintigraphy should be performed in selected patients, followed by coronary angiography when indicated. Only by such aggressive evaluation will it be possible to maintain such low perioperative cardiac morbidity in this high-risk population. When cardiac complications do occur, they are treated in a fashion similar to other thoracic surgical patients. Because of the risk of atrial fibrillation and supraventricular tachycardia, patients are monitored while in the ICU or on the ward. Myocardial ischemia or infarction should be suspected whenever a patient has hemodynamic instability that cannot be directly attributed to another factor. Chest pain that is different from the patients ‘usual’ sternotomy pain should be evaluated carefully any time in the postoperative period.

Gastrointestinal complications Gastrointestinal (GI) complications occur in patients after LVRS with an incidence similar to that of other postoperative patients. Both minor and major GI complications have been documented. Bleeding, reflux, with or without aspiration, adynamic ileus, obstipation and perforation have all been documented in LVRS patients. As a group, GI complications probably are underreported in the published series because several of these conditions may not impact patient outcome or hospitalization. In one report of over 100 patients, GI bleeding and perforation each occurred in five patients, giving a combined GI morbidity of 7% and were the only GI morbidities reported in that series [13]. In this same series, comparing LVRS by sternotomy with VATS LVRS, the five GI perforations all resulted in death and were responsible for five of the 11 deaths in the series. All of the GI perforations were in the sternotomy group. The patients in this group were significantly older than those undergoing VATS LVRS, but there was no significant difference in other measured parameters including non-steroidal anti-inflammatory drug use, narcotic use, steroids, duration of epidural, and duration of chest drainage. In several other series, GI perforation has been reported and may pose a particular problem in this

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patient population [5,8,12]. Postoperative pneumoperitoneum can be deceptive, as it is not uncommon for patients with air leaks and anterior chest drains to develop pneumoperitoneum from inadvertent placement of the tube through a small portion of peritoneum. When this is demonstrated on chest film, it is important to assess the patient clinically and document the absence of signs or symptoms of GI perforation as a source of the intraperitoneal air. Like any postoperative thoracic surgery patient, GI bleeding can develop. When GI bleeding does occur, it should be managed in the usual fashionafluid resuscitation, transfusion, H 2 blockers or proton-pump inhibitors, and endoscopy for diagnosis and/or therapeutic interventionawith surgery reserved for patients with bleeding refractory to medical therapy. Protection of the airway should be considered in any patient with significant bleeding and is particularly important in these patients.

Wound complications Sternal wound occurs after LVRS and can be particularly debilitating. Although the incidence of wound problems after LVRS does not appear to be any higher than after other operations utilizing median sternotomy, the perturbations in respiratory mechanics after sternal dehiscence can negate the benefits of the procedure. Appropriate perioperative antibiotics should be administered to prevent sternal infection and operative technique should be meticulous to prevent infection, dehiscence, or sternal non-union. Great care should be taken to assure that the sternotomy is midline, and retraction should avoid sternal fractures. Secure closure is paramount to withstand aggressive postoperative pulmonary toilet maneuvers. Should sternal instability occur postoperatively as a result of such maneuvers, the patient should be taken back to the operating room for sternal fixation. If sternal wound infection is the mechanism of dehiscence, early operative debridement and flap closure should be performed in a fashion that maximizes stability.

Pulmonary embolus The incidence of deep venous thrombosis (DVT) and pulmonary embolus in LVRS patients is unknown. Although this remains a theoretical and potential life-threatening complication, the lack of reports of pulmonary emboli as a significant source of morbidity and mortality probably reflects the early and aggressive mobilization policy employed by most centres performing LVRS. This in combination with routine prophylaxis should keep the incidence of DVT and pulmonary embolus low.

Psychiatric complications Patients who have end-stage emphysema are prone to develop emotional and anxiety-related issues. Many patients see LVRS as a hope to return to a more

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normal lifestyle and proceed with preoperative screening and rehabilitation with much expectation and enthusiasm. The operation itself, rather than the recovery, is often seen as the completion of the process. Combining the heightened anticipation of surgery with benefits that are often not appreciated for weeks to months after the procedure predisposes these patients to anxiety and depression that may alter outcome. Preoperative anxiety disorders or panic attacks have been associated with an increase in postoperative complications and mortality, and exacerbations in the postoperative period can complicate the assessment of physiological abnormalities, such as hypoxemia or pneumothorax [25]. Depression is common after any major surgery and can result in poor motivation and anorexia, easily leading to other complications, such as pneumonia and respiratory failure. These problems must be addressed and treated aggressively as they occur after surgery, including pharmacological intervention if necessary.

Summary A successful lung volume reduction program requires a multidisciplinary team approach that is committed to the significant amount of care that these patients require. If surgical options are to be available to patients with end-stage emphysema, it is imperative that LVRS centres focus on the minimization of perioperative morbidity and mortality, beginning with patient evaluation and selection. Intraoperative considerations by both surgeon and anesthesiologist significantly affect length of stay and ultimate outcome. Meticulous postoperative care with focus on the prevention and aggressive treatment of complications is the only way to achieve consistent success in this group of fragile patients.

References 1 Cooper JD, Trulock EP, Triantafillou AN et al. Bilateral pneumectomy (volume reduction) for chronic obstructive pulmonary disease. J Thorac Cardiovasc Surg 1995; 109: 106–119. 2 Brantigan OC, Mueller E. Surgical treatment of pulmonary emphysema. Am Surg 1957; 23: 789–804. 3 Brantigan OC, Mueller E, Kress MB. A surgical approach to pulmonary emphysema. Am Rev Respir Dis 1959; 80: 194 –202. 4 Brantigan OC, Kress MB, Mueller EA. The surgical approach to pulmonary emphysema. Dis Chest 1961; 39: 485–501. 5 Cooper JD, Patterson GA, Sundaresan RS et al. Results of 150 consecutive bilateral lung volume reduction procedures in patients with severe emphysema. J Thorac Cardiovasc Surg 1996; 112: 1319–1330. 6 Bingisser R, Zollinger A, Hauser M et al. Bilateral volume reduction surgery for diffuse pulmonary emphysema by video-assisted thoracoscopy. J Thorac Cardiovasc Surg 1996; 112: 875–882. 7 Daniel TM, Chan BB, Bhaskar V et al. Lung volume reduction surgery: case selection, operative technique and clinical results. Ann Surg 1996; 223: 526–533.

Complications of lung volume reduction procedures 127 8 Naunheim KS, Keller CA, Krucylak PE et al. Unilateral video-assisted thoracic surgical lung reduction. Ann Thorac Surg 1996; 61: 1092–1098. 9 The National Emphysema Treatment Trial Research Group. Rationale and design of the national emphysema treatment trial: a prospective randomized trial of lung volume reduction surgery. Personal communication, October 1998. 10 Cooper JD. The history of surgical procedures for emphysema. Ann Thorac Surg 1997; 63: 312–319. 11 Travaline JM, Furakawa S, Kusma AM et al. Bilateral apical vs nonapical stapling resection during lung volume reduction surgery. Chest 1998; 114: 981–987. 12 Hazelrigg SR, Boley TM, Magee MJ et al. Comparison of staged thoracoscopy and median sternotomy for lung volume reduction. Ann Thorac Surg 1998; 66: 1134 –1139. 13 Roberts JR, Bavaria JE, Wahl P et al. Comparison of open and thoracoscopic bilateral volume reduction surgery: complications analysis. Ann Thorac Surg 1998; 66: 1759–1765. 14 Mazolewski P, Turner JF, Baker M, Kurtz T, Little AG. The impact of nutritional status on the outcome of lung volume reduction surgery: a prospective study. Chest 1999; 116: 693–696. 15 Hazelrigg SR, Boley TM, Naunheim KS et al. Effect of bovine pericardial strips on air leak after stapled pulmonary resection. Ann Thorac Surg 1997; 63: 1573–1575. 16 Macchiarini P, Wain J, Almy S, Dartevelle P. Experimental and clinical evaluation of a new synthetic, absorbable sealant to reduce air leaks in thoracic patients. J Thorac Cardiovasc Surg 1999; 117: 751–758. 17 Horsley SW, Miller JI. Management of the uncontrollable pulmonary air leak with cyanoacrylate glue. Ann Thorac Surg 1997; 63: 1492–1493. 18 Triantafillou AN. Anesthetic management for bilateral volume reduction surgery. Sem Thorac Cardiovasc Surg 1996; 1: 94 –98. 19 Reynolds BR, Wood DE. A randomized prospective trial of suction versus water seal after lung volume reduction surgery. Personal communication, 1997. 20 Szekely LA, Oelberg DA, Wright C et al. Preoperative predictors of operative morbidity and mortality in COPD patients undergoing bilateral lung volume reduction surgery. Chest 1997; 111: 550–558. 21 Wiser W, Klepetko W, Senbaklavaci O et al. Chronic hypercapnia should not exclude patients from lung volume reduction surgery. Eur J Cardiothorac Surg 1998; 14: 107–112. 22 Bach DS, Curtis JL, Christensen PJ et al. Preoperative echocardiographic evaluation of patients referred for lung volume reduction surgery. Chest 1998; 114: 972–980. 23 Hogue CW, Stamos T, Winters KJ et al. Acute myocardial infarction during lung volume reduction surgery. Anesth Analg 1999; 88: 332–334. 24 Thurnheer R, Muntwyler J, Stammberger U et al. Coronary artery disease in patients undergoing lung volume reduction surgery for emphysema. Chest 1997; 112: 122–128. 25 Miller JI Jr, Lee RB, Mansour KA. Lung volume reduction surgery: lessons learned. Ann Thor Surg 1996; 61: 1464 –1468.

CHAPTER 7

Complications of lung transplantation Paul F Waters

Complications of thoracic surgery Lung transplantation This chapter will discuss the complications directly related to lung transplantation. The procedure may be performed through several standard thoracic incisions. Wound complications related to these will be discussed elsewhere in this volume. For purposes of discussion the complications will be divided into those that occur early and late in the postoperative period. Single lung transplantation is performed for patients with restrictive lung disease (e.g. pulmonary fibrosis), obstructive lung disease (e.g. emphysema) and pulmonary vascular disease such as primary pulmonary hypertension or in patients with pulmonary vascular disease secondary to congenital heart abnormalities [1]. It is generally performed through a standard posterolateral thoracotomy, although a median sternotomy has been used. Double lung transplant is generally performed for patients with septic lung disease such as cystic fibrosis or bronchiectasis of other etiologies. It is also sometimes done for pulmonary vascular disease or emphysema. The double sequential transplant procedure is usually carried out through a bilateral anterior 4th interspace thoracotomy, either transversely dividing the sternum or leaving it intact [2]. Depending on the diagnosis, a patient may expect a 1-year actuarial survival in the 75% range as reported by the International Society of Heart and Lung Transplantation Registry [3].

Early complications Early complications are related to the anastomoses, to the graft or to recipient problems. The standard implantation procedure involves a bronchial anastomosis, and two vascular connections of the pulmonary artery and left atrium. The left atrial anastomosis includes both the inferior and superior pulmonary veins. No reconstitution of the bronchial circulation is performed and consequently the implanted lung relies on the pulmonary circulation for both gas exchange and viability.

Air embolism Most single lung transplants are performed without cardiopulmonary bypass. Once the anastomoses are completed satisfactorily, the graft is reperfused and ventilated simultaneously. The pulmonary circulation of the transplanted 128

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lung contains residual preservation perfusate and air, both of which must be prevented from entering the left atrium. This is accomplished by several maneuvers. The patient is placed in the extreme Trendelenburg position so any inadvertent air in the left heart will avoid the cerebral circulation. With both the vascular anastomoses open, the atrial clamp is released, with the pulmonary artery (PA) clamp in place. This allows back bleeding through the lung and egress of unwanted material through the PA anastomosis. At this point the PA anastomosis is completed and the atrial clamp re-applied. The PA clamp is partially removed to allow anterograde flow, and venting through the still open atrial anastomosis. Care must be taken to avoid full PA flow without the open anastomosis. Once a suitable period has elapsed the atrial anastomosis is tied and the clamps removed simultaneously, and the lung re-ventilated. The anastomoses are examined for good flow, and hemostasis. The bronchial anastomosis is inspected for air leak, which if present is corrected with additional sutures where necessary.

Reperfusion response Most recipients will exhibit some degree of reperfusion response in the first 24–48 h after the transplant procedure. This may vary from being almost imperceptible to a fulminant reaction with serious and occasionally lethal results. The precise etiology of the process is unknown but its pathophysiology suggests a pulmonary capillary leak syndrome. It does not seem to be related to ischemic time, preservation technique or the precise method of reimplantation. Studies have failed to determine immunological phenomena as a basis. In the most common scenario the patient will exhibit a modest but manageable decline in oxygenation, a fluffy infiltrate of a varying degree with pleural effusion or some amount of increased chest tube fluid output. The problem is self-limiting and managed by judicious fluid balance, diuresis, ventilation with PEEP, nitric oxide and continued appropriate hemodynamic support [4]. The prophylactic use of inhaled nitric oxide appears to be a useful approach [5,6]. Vascular anastomosis abnormality, particularly a partial venous obstruction, should be searched for and ruled out. In the fulminant situation the situation can be more serious. The X-ray will demonstrate severe infiltrate or in some cases a complete ‘white-out’. Oxygenation may be difficult to maintain and hemodynamic instability is noted. In extreme cases extra-corporeal membrane oxygenator (ECMO) may be required to support the patient while the process runs its course [7,8]. The inflammatory response clearly produces vasoactive substances because hypotension, depressed myocardial function and peripheral profound vasodilatation can be observed. The patient may appear as if they are in septic shock. Many of these manifestations of ‘primary non-function’ can be mimicked by a problem with the vascular supply to the graft, bacterial infection and rejection eliminated as a cause. Most centres performing lung transplantation will have ECMO available if oxygenation and gas exchange become impossible in the severe case. Prolonged use of ECMO has resulted in poor results and high mortality but as a temporary strategy it has merit [9].

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Various techniques have been suggested for use prophylactically in attempts to prevent the development of reperfusion response. However, none has been predictably effective in its prevention [10–12].

Vascular anastomotic complications If care is not taken with the configuration and positioning of the vascular connections poor flow and occasionally thrombosis can occur. This is a disastrous complication that must be recognized promptly and treated with a return to the operating room and correction of the problem. Several methods are available for the evaluation of these. A simple bedside bronchoscopy may reveal a severely ischemic airway, suggesting a problem with its blood supply. Conversely, if the airway is obviously well vascularized it is unlikely that the PA has completely thrombosed. A portable quantitative perfusion scan can also be performed in the ICU setting. In general it should demonstrate preferential perfusion of the graft. If not, then usually rapid evaluation and reexploration are necessary. Transesophageal echocardiography with an experienced operator can demonstrate pulmonary arterial flow, on the transplanted side. The venous flow may be more difficult to demonstrate, but obviously if there is good PA flow then venous outflow is satisfactory. Angiography is seldom used at this stage since prompt correction of a suspected problem is necessary to prevent irreversible damage to the graft. Once again, if there is sufficient concern about the vascular anastomoses being patent then a prompt re-exploration is indicated. Problems with the anastomoses discovered at thoracotomy are usually due to redundant vessel or impingement with local tissue such as pericardium. The anastomosis is revised and thombectomy performed. Poor flow or lack of flow through the venous outflow tract can be a subtle diagnostic challenge. In the fulminant, thrombosed situation the patient will present with a pulmonary edema picture in the transplant and an abnormal transesophageal echocardiography (TEE). Technical misadventure with the anastomosis is usually the cause. In most cases where there is a complication with the anastomoses the diagnosis is readily apparent. However, on occasion because of the physiology and the residual native lung providing some support, it may not be obvious. I have personally seen a transplant patient, with emphysema, extubated and breathing spontaneously, albeit with high oxygen requirements, with complete thrombosis of the PA anastomosis following single lung transplant. For this reason it is mandatory to examine the vascular supply of the graft as a routine in the immediate transplant period using the tools described [13–15].

Bronchial anastomotic complications Complications with the bronchus do not usually occur in the first few days post transplant. Before the patient is transferred from the operating room the anastomosis is examined both at thoracotomy and bronchoscopically to ensure a satisfactory situation. Any problems should be diagnosed and corrected at that time. Later, problems with healing, usually on an ischemic

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basis, do not develop until necrosis of a portion of the donor bronchus occurs. This is frequently at the 10–14-day mark. Complete failure is decidedly uncommon and usually speaks of many other complications and an unsalvageable situation. The more common scenario will be the development of new mediastinal air or of a pneumothorax. A pneumothorax should be treated with the insertion of a chest tube. It does not always imply a bronchial anastomotic problem. In any case, a bedside fiberoptic bronchoscopy should be performed to examine and assess the status. A chest computed tomography (CT) scan is a very useful tool to determine the nature of the bronchus and the degree of contamination. Appropriate drainage, often done percutaneously under CT-guided control is necessary. With this and judicious antibiotics and pulmonary toilet the defect will heal satisfactorily. Sometimes such an occurrence in the early postoperative period will lead to subsequent stenosis or bronchomalacia.

Acute rejection Acute rejection in the early post-transplant period is a very common occurrence. Standard immunosuppression is based on cyclosporine or FK506 in combination with steroids and usually with the addition of mycophenilate mofetil or imuran. Cytolytic therapy with anti-lymphocyte globulin (ALG), anti-thymocyte globulin (ATG) or monoclonal anti-bodies is infrequently required. Acute rejection usually presents at about day 5–7 but can occur at any time. The patient will demonstrate deterioration in oxygenation, sometimes flu-like symptoms, a low-grade temperature and non-specific X-ray changes. These include a slight perihilar infiltrate or ‘flare’, a diffuse ground glass appearance or a small pleural effusion. There can also be no X-ray changes at all in the early stages. A moderate leukocytosis may also be observed. Infectious causes of this constellation of signs and symptoms are rapidly ruled out and the diagnosis of acute rejection made. Frequently a diagnostic and therapeutic dose of ‘pulse’ steroids will be given. If the problem is rejection, all of the abnormalities should subside within 8–12 h if the process is in its incipient stages. A more established process will take longer to reverse. Transbronchial biopsy at this point is appropriate but requires an experienced pathologist because of the changes associated with the inflammatory response to the ischemic period and reimplantation phenomena. Failure of the clinical diagnosis to respond promptly should trigger an immediate re-evaluation with transbronchial biopsies and if necessary, open lung biopsy to establish the diagnosis.

Late complications The complications that occur later are related to infection, rejection and airway problems.

Infection Because the graft always and forever remains exposed to the environment it is susceptible to opportunistic infection. These may be viral, fungal or bacterial.

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Cytomegalovirus infection Pneumonitis and generalized cytomegalovirus (CMV) disease are an ongoing problem in the long-term management of transplant patients. Logistically and practically very few programs perform donor to recipient matching with respect to CMV status. Donor CMV status at the time of organ retrieval is frequently unreliable. For this reason, many programs, including ours, have used an aggressive prophylaxis program against CMV. This involves high-dose ganciclovir, intravenously for the first 3 months post transplant when the level of immunosuppression is highest. CMV pneumonitis can mimic acute rejection, although it is often associated with a leukopenia. The diagnosis is made with transbronchial biopsy demonstrating the characteristic histological appearance and with the appropriate profile on serological testing. Treatment is with high-dose ganciclovir. Oral ganciclovir is available but is extremely poorly absorbed. Its efficacy is such that if the diagnosis is firm, intravenous therapy is required. Other viral infections seen include herpes and Epstein– Barr virus. Bacterial infection is common and should prompt a rapid response from the care giver. Appropriate antibiotics in appropriate doses should be begun promptly and tailored according to culture and sensitivity data. Once more, because of the chronic immunosuppression these infections can be fulminant. Infection with Pneumocystis carinii is uncommon, since all programs institute prophylaxis post transplant with twice weekly Septra or the like. Fungal infection or at least colonization is seen frequently. Aspergillus, Candida, and less commonly Nocardia and other pathogens are seen and should be looked for in unclear infectious scenarios. Bronchoscopic examination with cultures and biopsies, percutaneous needle biopsies or open lung biopsy may be necessary to establish the diagnosis. Oral antifungals are appropriate for colonization, whereas invasive infections are much more serious and often fatal.

Late airway complications Airway complications are either stenosis or bronchomalacia in the late postoperative period. Stenosis can be seen after a known airway problem in the earlier post-transplant period, such as a partial dehiscence. At other times the lesion can develop with no previous suggestion of trouble. It usually manifests with poor function and abnormal pulmonary function tests identifying airway obstruction. Bronchoscopy will make the diagnosis and treatment will be rigid bronchoscopy with dilation. Continued narrowing or recurrent problems can be managed with either silastic or expandable mesh wall stents. Both of these techniques have yielded satisfactory results for stenosis, although the disadvantage of the wall stents is that they can not usually be removed. Both types of stent can be problematic because of colonization with infectious organisms and because patients may have difficulty raising secretions through them. The more difficult problem to manage is that of bronchomalacia. These ‘floppy’ airways will lead to respiratory insufficiency because of their tendency to close

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during the respiratory cycle. Stenting is less successful since there is not a narrow area to grip the stent. Mesh stents seem to be the better choice in this situation.

Bronchiolitis obliterans and bronchiolitis obliterans syndrome As experience with isolated lung transplantation developed it became apparent that a percentage (probably 30–50%) of long-term survivors expressed a decline in pulmonary function, which was not due to acute rejection. This first manifested in a decline in objectively measured pulmonary functiona specifically a drop in forced expiratory volume in 1 s (FEV1). This decline can be expressed as a percentage of the best FEV1 obtained by the recipient in the post-transplant period. Transbronchial biopsies in such patients may not reveal the abnormality since the changes generally occur in the small airways. Sensitivity of transbronchial biopsy has been reported in wide ranges from 20 to 70%. Pathologically the lesion progresses from a lymphocytic bronchiolitis with epithelial damage to evidence of scarring in the submucosa, which is presumably permanent. It is this scarring which becomes obliterative to small airways, which leads to the decline in function measured both subjectively by the patient and objectively by pulmonary function tests. The so-called bronchiolitis obliterans syndrome (BOS) is now defined based on FEV1 determinations. This has been addressed in a working formulation to characterize and grade BOS [16]. The syndrome may remain stable but frequently can show a rapid downhill course and death by respiratory failure. Treatment strategies, none of which is reliably efficacious, include manipulation of immunosuppressive regimens, additional chemotherapeutic agents (e.g. methotrexate) and other approaches such as photopharesis. Multivariate analysis of large series of lung transplant recipients suggest that CMV infection, acute rejection, and lymphocytic bronchiolitis noted on lung biopsy are associated with an increased incidence of BOS. Therefore, management to avoid these, if possible, would make sense. If BOS patients do not stabilize, then consideration of retransplantation becomes inevitable. A multi-institutional report suggests that reasonable results of retransplantation can be expected in ambulatory, non-ventilated patients who are more than 2 years beyond their original transplant [17,18]. Certainly the experience with other organs in retransplantation would suggest that it is a reasonable tactic. In long-term follow-up this BOS accounts for most deaths and remains the Achilles’ heel of lung transplantation.

References 1 International guidelines for the selection of lung transplant candidates. The American Society for Transplant Physicians (ASTP)/American Thoracic Society (ATS)/European Respiratory Society (ERS)/International Society for Heart and Lung Transplantation (ISHLT). Am J Respir Crit Care Med 1998; 58: 335–339. 2 Meyers B, Sundaresan S, Cooper JD, Patterson GA. Bilateral sequential lung transplant without sternal division eliminates post transplant complications. J Thorac Cardiovasc Surg 1999; 117: 358–364.

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3 Trulock EP, Edwards LB, Taylor DO et al. The Registry of the International Society for Heart und Lung Transplantation: Twentieth Official Adult Lung and Heart-lung Transplant Report – 2003. J Heart Lung Transplant 2003; 22: 625 – 635. 4 Haydock DA, Trulock EP, Kaiser LR et al. Management of dysfunction in the transplanted lung: experience with 7 clinical cases. Ann Thorac Surg 1992; 53: 635–641. 5 Date H, Triantafillou A, Trulock E et al. Inhaled nitric oxide reduces human lung allograft dysfunction. J Thorac Cardiovasc Surg 1996; 111: 913–919. 6 Ardehali A, Laks H, Levine M et al. A prospective trial of inhaled nitric oxide in clinical lung transplantation. Transplantation 2001; 72: 112–115. 7 Zanati M, Pham SM, Keenan RJ, Griffith BP. Extracorporeal memberan oxygenation for lung transplant recipients with primary severe donor lung dysfunction. Transpl Int 1996; 9: 227–230. 8 Meyers BF, Sundt TM III, Henry S et al. Selective use of extracorporeal membrane oxygenation is warranted after lung transplantation. J Thorac Cardiovasc Surg 2000; 120: 20 –26. 9 Glassman LR, Keenan RJ, Fabrizio MC et al. Extracorporeal membrane oxygenation as an adjunct treatment for primary graft failure in adult lung transplant recipients. J Thorac Cardiovasc Surg 1995; 110: 723–726. 10 Struber M, Hohlfeld JM, Fraund S, Kim P, Warnecke G, Haverich A. Low-potassium dextran solution ameliorates perfusion injury of the lung and protects surfactant function. J Thorac Cardiovasc Surg 2000; 120: 566–572. 11 Suda T, Mora BN, Cooper JA et al. In vivo adenoviral-mediated endothelial nitric oxide synthase gene transfer ameliorates lung allograft ischemia reperfusion injury. J Thorac Cardiovasc Surg 2000; 119: 297–304. 12 Fujino S, Nagahiro I, Yamashita M et al. Preharvest nitroprusside flush improves posttransplant lung function. Ann Thor Surg 1997; 63: 1383–1390. 13 Cooper JD, Patterson GA, Trulock EP. Results of single and bilateral transplantation in 131 consecutive recipients. J Thorac Cardiovasc Surg 1994; 107: 460–471. 14 Waters PF. Lung transplant: postoperative management. In: Patterson GA, Courand L, eds. Current Topics in General Thoracic Surgery: an International Series, Vol. 3, Lung Transplant. Amsterdam: Elsevier, 1995; 260–261. 15 Weill D, Zamora MR. Postoperative care in lung transplantation. Semin Resp Crit Care Med 1996; 159–166. 16 Cooper JD, Billingham M, Egan TA. Working formulation for the standardiztion of nomenclature and for clinical staging of chronic dysfunction in lung allografts. J Heart Lung Transplant 1993; 12: 713–716. 17 Novick RJ, Andreassian B, Schafers H-J et al. Pulmonary retransplantation for obliterative bronchiolitis. J Thorac Cardiovasc Surg 1994; 107: 755–763. 18 Novick RJ, Stitt LW, Alkattan K et al. Pulmonary retransplantation: predictors of graft function and survival in 230 patients. Ann Thorac Surg 1998; 65: 227–234.

CHAPTER 8

Pleural space problems Sudish Murthy, Thomas W Rice

Introduction The pleura is a thin serous membrane that covers the lung and chest wall. It is divided into two anatomic layers, a visceral layer, which envelops the pulmonary parenchyma and includes interlobar fissures, and a parietal layer, which covers the ribs, diaphragm and mediastinum. The pleura also consists of two cellular layers: a mesothelial cell monolayer facing the pleural space and an underlying connective tissue matrix. The virtual cavity between visceral and parietal pleura is referred to as the pleural space. Under normal circumstances, the pleural surfaces are tightly coapted secondary to the negative pressure in the pleural space and the cavity contains only a small amount of fluid [1]. The pleura functions to mechanically couple the lung and chest wall, facilitating respiration [2]. Consequently, patients with disease processes affecting the pleura can present with exertional dyspnea and respiratory compromise. The most common pathological processes affecting the pleura include inflammatory disease, infection, trauma, and neoplasm.

Diagnosis Even though a complete physical examination and thorough medical history often suggest the nature of the disease, radiographic imaging is an important adjunct in the initial evaluation of patients with suspected pleural disease [3]. Conventional erect chest radiographs can demonstrate pneumothorax (Figure 8.1a), pleural-based fluid collections (Figure 8.1b), and pleural thickening (Figure 8.1c). The high-resolution axial imaging provided by chest computed tomography (CT) scans allows for detailed assessment of pleural-based disease (Figure 8.2) and is recommended for all patients with complex pleural space problems. Ultrasonography has a role in guiding percutaneous diagnostic maneuvers. Magnetic resonance imaging (MRI) is of use in the characterization of malignant mesothelioma to define resectability [4]. Blood tests are rarely useful in the diagnostic work-up of pleural disease. However, in the context of pleural-based pathology identified radiographically, an elevated leukocyte count or positive blood culture suggest pleural space infection. Hypoglycemia alerts the clinician to the possibility of a solitary fibrous tumor of the pleura. 135

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(a)

(c)

(b)

Figure 8.1 (a–c) Erect chest X-rays can demonstrate pleural disease. (a) Left-sided pneumothorax. (b) Bilateral complex pleural effusion. (c) Left-sided diffuse pleural thickening.

(a)

(b) Figure 8.2 (a,b) Chest computed tomography (CT) scans provide excellent anatomic detail of pleural-based disease. (a) From the same patient whose chest X-ray is shown in Figure 8.1b. (b) Circumferential pleural thickening characteristic of malignant mesothelioma and fibrothorax.

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Surgical evaluation of the pleural space Pleural effusion Pleural effusion is the most common clinical manifestation of pleural disease and the most frequently encountered indication for pleural-based surgery. The movement of fluid into and out of the pleural space is governed by local hydrostatic and colloid osmotic pressures. Derangement of these forces by various disease processes results in fluid accumulation. Pleural fluid collections are divided into transudates and exudates. Exudative effusions have a much higher protein content, with a pleural protein concentration to serum protein concentration of > 0.5, and a higher LDH concentration (pleural fluid LDH to serum LDH ratio > 0.6) [1]. Exudative effusions often require surgical intervention for both diagnosis and therapy. The etiologies of exudative pleural collections are infection (parapneumonic effusion or empyema), systemic inflammatory illness, and neoplasm [1,5]. With few exceptions, medical therapy is the mainstay for treatment of transudative effusions. The most common causes of transudative effusions include pulmonary embolus, heart failure and hepatic and renal dysfunction. Physical examination demonstrates diminished or vesicular breath sounds, decreased tactile fremitus, and less expansion of the affected hemithorax [3]. Chest X-ray usually reveals pleural effusions > 200 cm3. A lateral decubitus film will assess whether the effusion is free-flowing or loculated. A CT scan helps differentiate complex effusions from simple collections. Bulky pleural disease suggests a malignant process. A chest CT with an enhancing pleural rind is characteristic of empyema [6].

Thoracentesis Thoracentesis is easily performed in the out-patient clinic. Diagnostic yield approaches 75% [7]. Dependent effusions can usually be identified by percussion and safely aspirated with minimal morbidity. A lateral decubitis chest X-ray or chest ultrasound can be obtained for any question of loculation. Complications include a 3–20% incidence of pneumothorax [7], as well as hypovolemia, pleural infection, subcutaneous hematoma and hemothorax [8]. Many potential complications can be avoided by observing a few simple safeguards. There must actually be an effusion to tap. Consolidated lung secondary to pneumonia, tumor, or mucus impaction can radiographically mimic a pleural effusion (Figure 8.3). Thoracentesis for this may result in parenchymal injury. Ultrasound or chest CT scan is helpful to identify dependent fluid; bronchoscopy may be required for airway disimpaction. Bronchoscopy is only indicated in the work-up of an undiagnosed pleural effusion in the presence of lung consolidation or hemoptysis [9], as the diagnostic yield in the absence of either is only 4% [10]. All fluid collections should first be located with the same fine gauge needle used to deliver local anesthesia, prior to placement of a 16-G or larger drainage

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(a)

(b) Figure 8.3 Comparison of (a) plain chest X-ray and (b) chest computed tomography (CT) from a patient with opacification of the hemithorax. The CT scan demonstrates that the X-ray finding represents lung collapse, and not a large pleural effusion.

catheter for aspiration. Very rarely will lung puncture with the finer needle result in pneumothorax. Free-flowing effusions should be accessed in the posterior axillary line. This reduces the chance of intercostal pedicle disruption when more posterior attempts are made. One or two fingerbreadths below the scapular tip, while the patient is placed in a seated position and draped over a padded Mayo stand, will invariably place the catheter close to the dome of the diaphragm. Attempts at a lower access site can be complicated by liver or splenic puncture if done during exhalation. Loculated effusions usually require localization prior to thoracentesis. This can be done sonographically or by chest CT. Because of patient discomfort from pleural irritation, intractable cough, and the possibility of re-expansion pulmonary edema, seldom should more than 1500 ml be removed at one time. Serial procedures may be necessary for high-volume simple effusions.

Thoracoscopy Thoracoscopy, with or without video assistance, is an important adjunct in the management of pleural-based illness. The applicability of thoracoscopy has steadily increased since its inception 80 years ago [11]. Video assistance, first reported in 1991 [12], has facilitated the dissemination of technique. The most frequent application of thoracoscopy is evaluation of pleural effusion. For one-fifth of all pleural effusions, the etiology remains undetermined after thoracentesis and/or percutaneous pleural biopsy [13,14]. Thoracoscopy can supplant more invasive approaches and is frequently both diagnostic and therapeutic (Table 8.1). If unexpected lung, mediastinal, or pericardial pathology is found, the procedure is extended to include additional biopsies. The first thoracoscope was a hollow, open lighted endoscope introduced under local anesthesia [15]. Thoracoscopy performed under regional anesthetic techniques was introduced in 1987 [16]. Modern thoracoscopy, however,

Pleural space problems 139 Table 8.1 Common indications for thoracoscopy in the diagnosis and treatment of pleural disease. Indication

Goal of procedure

Pleural effusion of unclear etiology Suspicious pleural mass Pleurectomy for spontaneous pneumothorax Drainage/decortication of empyema Hemothorax Chylothorax

Diagnostic/therapeutic Diagnostic/therapeutic Therapeutic Diagnostic/therapeutic Diagnostic/therapeutic Diagnostic/therapeutic

Table 8.2 Differences between single-port thoracoscopy and percutaneous drainage in the management of pulmonary effusion of unclear etiology. Factor

Single-port thoracoscopy

Percutaneous drainage

Cost Diagnostic accuracy Hospital stay required Evaluation of pleura

> $4000* > 90% Yes Visual inspection of pleura Site-directed tissue biopsies Diagnostic and therapeutic Pain

< $500† < 80% No Primarily cytological

Goal of procedure Most frequent complication

Diagnostic Pneumothorax

*Estimate of Medicare reimbursement and co-payment for current procedural technology (CPT) 32650. †Estimate of Medicare reimbursement and co-payment for CPT 32000.

is conducted under general anesthesia and facilitated by lung isolation. Based on the complexity of the pleural disease, one of two surgical approaches is employed.

Single-port thoracoscopy Single-port thoracoscopy is a simple thoracic surgical technique. The differences between single-port thoracoscopy and thoracentesis are summarized in Table 8.2. For the former, a single incision (2 cm) is made in the mid or anterior axillary line of interspace 6 or 7 (Figure 8.4). Preoperative marking (ultrasound or CT) may be required for management of complex, loculated effusions. If possible, the ipsilateral lung is deflated. The pleural space is entered judiciously to prevent parenchymal, pericardial, or diaphragmatic injury. A mediastinoscope is then gently inserted through the interspace. The pleural space is evaluated under direct vision (a videoscope or a rigid optical forceps may be inserted through the thoracoscope if necessary). When bulky pleural disease is encountered (e.g. mesothelioma), the leading edge of the Wolf scope can be used to dissect the pleura from the endothoracic fascia to allow for a greater volume of tissue to be removed for diagnosis.

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Figure 8.4 Illustration of thoracoscopy; center, standard operative position, left, single-port thoracoscopy through anterior axillary line incision, right, multiport thoracoscopy with all ports placed in the same 180° viewing arc.

Multiport video thoracoscopy Multiport video thoracoscopy is reserved for more complex pleural operations. A variety of pleural applications have been described for this procedure. Central to all is the use of a standard 10-mm magnifying videoscope with either a zero or 30° lens. Commonly, three to four thoracoports are utilized (Figure 8.4), and two video towers are needed to allow both surgeon and assistant adequate visualization. The camera is usually introduced at interspace 6 or 7, in the mid or anterior axillary line, through a 10- or 12-mm port. Thoracoports placed in the same 180° arc reduce optical parallax problems (Figure 8.4). Ipsilateral lung isolation and thorough deflation are critical to the safety of the procedure. A digital survey of the chest cavity at the initial port site identifies lung adhesions and diaphragm. Once the videoscope is safely positioned in the pleural space, other ports can be strategically placed with video assistance.

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Appreciation of the complications associated with thoracoscopy facilitates the safe performance of the procedure [15,17–20]. Avoidable complications include improper patient selection, unfamiliarity with the technique, inadequate equipment, aberrant anatomy, and impatience. Complications are classified as local or regional. Local complications include hematoma, superficial infection, rib fracture, neuralgia, and tumor seeding. Standard sterile surgical techniques and gentle handling of chest wall tissues reduce local complications. An interspace large enough to allow passage of the scope or video port reduces soft tissue and rib trauma and decreases postoperative pain syndromes. The operating table may be slightly flexed and the patient buoyed off the table with pillows or a rigid beanbag placed under the contralateral flank (Figure 8.4). Intercostal spaces are wider anteriorly and, unless the pathology mandates a posterior approach, anterior interspaces should be reserved for large trocar or scope placement. The latissimus dorsi may be avoided by a more anterior port placement. The surgeon must also be mindful of excessive torque applied on the ribs at the access site. In this setting, creation of a second port, with a more favorable viewing angle, may decrease neuralgia and reduce postoperative pain. Smaller operating videoscopes (5 mm vs. 10 mm) result in smaller and less painful incisions. Wound infection rates, though poorly documented in most reviews, should be < 3%. In addition to tissue trauma and hematoma, it is possible that soilage of the incision with talc during pleurodesis (for a malignant effusion) increases the risk of port site infection. We thoroughly irrigate the port site prior to closure and occasionally tunnel the chest tube through a separate stab incision if the port site appears macerated. Tumor seeding of the thoracoscopy tract presents a more formidable challenge. Port site recurrence rates as high as 4% have been observed with mesothelioma [18,21], although this problem has seldom been encountered in cases of metastatic cancers to the pleura [15]. Resection of the biopsy tract is recommended if extra-pleura pneumonectomy is performed. Some surgeons advocate prophylactic radiotherapy (20 Gy) to each port following thoracoscopy for malignant mesothelioma [18]. There are also regional and systemic complications of thoracoscopy. Hemothorax and empyema complicate 1% of procedures [19]. Though considered to be a risk for empyema, thoracoscopy with talc poudrage has been used to treat recalcitrant pleural space infections [22]. Prolonged air leak and subcutaneous emphysema (2% incidence of each) are secondary to direct pulmonary parenchymal injury. This often occurs during port placement when adherent lung is present at the entry site. Careful review of the preoperative CT scan is essential. Incomplete decortication done thoracoscopically may injure lung, while not allowing proper lung re-expansion and chest wall apposition to promote parenchymal healing. If any concerns regarding lung entrapment or incomplete expansion remain after a thoracoscopic decortication, a utility incision should be made and the decortication finished. Esophageal, phrenic and recurrent nerve, diaphragmatic and cardiac injuries have been reported,

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and are attributable to the difficulty of appreciating anatomic boundaries in an operative field shrouded with blood, pus, or tumor. If any question of safety arises, it is advisable to convert to an open procedure. Multiport thoracoscopy with video assistance has four times the complication rate of conventional single-port thoracoscopy [17]. Most of the increased risk is secondary to the more complex nature of most video-assisted procedures. The surgeon must remember, however, that in direct single-port thoracoscopy, there is no optical dissociation between the operator and operative field to confuse matters. Lung isolation, mandatory for video thoracoscopy, is often accompanied by extreme changes in arterial blood gas values [23]. The decision to employ multiport video thoracoscopy vs. single port direct thoracoscopy must be tailored to the goals of the procedure, the fitness of the patient, and skill of the operator.

Thoracoscopy for the malignant pleural effusion Single-port thoracoscopy is ideally suited to management of malignant pleural effusion. Cost of the procedure is significantly greater than thoracentesis (Table 8.2); however, as a diagnostic and therapeutic intervention, it has no percutaneous equal. Talc poudrage through the thoracoscope is > 90% effective in controlling malignant effusions and appears to be 30–50% more efficacious than either tetracycline or bleomycin instilled at the bedside [24,25]. Over 50% of patients are febrile after talc pleurodesis [25]. Re-expansion pulmonary edema, acute respiratory distress syndrome, granulomatous pneumonitis, and cerebral microembolism have been reported as rare complications of talc insufflation [24,25]. We routinely instill 5 g of talc and often stage bilateral procedures to prevent such occurrences. If dense lung entrapment is noted at thoracoscopy, no attempt at talc insufflation is made, since lung expansion is a prerequisite for successful pleurodesis. This situation should be anticipated if a preoperative thoracentesis (> 1000 ml) results in minimal improvement in the patient’s respiratory status or if post-thoracentesis X-ray demonstrates incomplete lung expansion.

Thoracoscopy for empyema Early empyema can also be treated thoracoscopically. The algorithm of managing patients with suspected empyema usually begins with tube thoracostomy. An exudative effusion with a pH < 7.3, low glucose concentration, and preponderance of neutrophils is consistent with empyema. If evacuation of the pleural space is complete and the lung expands to fill the cavity, no further procedures are necessary. The chest tube may be converted to open drainage within a week. If, however, the effusion is incompletely drained or loculated, or if the lung is entrapped, additional therapy is required. Fibrinolytic therapy has been tried, but no randomized data support its efficacy and spontaneous hemothorax is an occasional complication of chemical fibrinolysis.

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Single-port or multiport thoracoscopy is an excellent option in this situation, and may prevent thoracotomy [26]. An early empyema can frequently be drained and the lung decorticated from its gelatinous peel through the thoracoscope. Large-bore chest tubes are then precisely placed under direct vision for optimum drainage in the postoperative period. If a more mature and complicated pleural space infection is found, video assistance facilitates complete drainage. In addition to the video port, two or three operating ports are placed under video guidance. Sharp dissection is frequently necessary to start the decortication, facilitated by endoscopic monopolar scissors. Thoracoscopic ring forceps and 5-mm gauze-tipped dissectors can then be used to develop the decortication plane. It is essential that the pleural space be completely visualized and the entire lung mobilized to prevent a residual undrained collection. The lung must completely fill the hemithorax at the conclusion of the procedure. Preoperative bronchoscopic toilet decreases the likelihood that muco-purulent impaction will cause poor pulmonary reexpansion after the decortication. A 20% conversion rate to thoracotomy has been reported [26]. It is not uncommon for patients to be septic after the operation. This is presumably attributable to cytotoxins liberated from the pleural space during surgery. Supportive care includes broad-spectrum antibiotics, early enteral nutrition, mechanical ventilation, and vasoactive medications. Postoperative fevers are most commonly associated with the septic syndrome, atelectasis, lower extremity venous thrombosis, or recurrent pneumonia. A chest CT scan may be needed to exclude an incompletely drained empyema. If a postoperative fluid collection is identified on the CT scan, percutaneous drainage is appropriate. Rarely should a repeat decortication be necessary if the initial procedure was done properly.

Thoracoscopy for hemothorax Though many of the same thoracoscopy principles apply in the operative management of hemothorax, a few additional guidelines should be followed. Thoracoscopic management of hemothorax should be considered only after large-bore chest tubes have failed adequately to drain the chest. Any acutely developing hemothorax with hemodynamic compromise mandates thoracotomy/sternotomy for control. Any coagulopathy must be corrected preoperatively. As with the management of empyema, drainage via single-port thoracoscopy is often sufficient. Single-port thoracoscopy is perhaps most useful to evacuate clot after an open heart procedure in which the hemithorax has been an innocent reservoir for mediastinal blood. In these instances, existing chest tubes may have become dysfunctional because of clot and they contaminate the space. Early thoracoscopic drainage reduces the incidence of empyema and fibrothorax. If an ongoing blood loss is suspected, this technique is likely to be inadequate. At a minimum, video assistance would be required to survey

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the chest cavity in an attempt to identify and control the bleeding source. Finally, in a post-traumatic hemothorax, all efforts should be made to avoid placing a port adjacent to a rib fracture as the injury may be worsened by scope trauma. In the absence of an obvious bleeding source, intercostal pedicle ligation at the sites of fractures should be considered to prophylax against a rebleed postoperatively. The lung may need to be decorticated if the hemothorax is subacute.

Thoracotomy for pleural disease With the advent of efficacious antituberculous therapy, a debilitating and painful thoracoplasty is seldom necessary. On the rare occasion that the pleural space needs to be reduced or collapsed, soft tissue transfer (e.g. rotational muscle flaps, omentum, etc.) is more effective, less painful and debilitating, and cosmetically more appealing. Thoracotomy for pleural disease is necessary for dense fibrothorax, mature empyema, and the primary neoplasm of the pleura, mesothelioma.

Thoracotomy for fibrothorax and mature empyema Fibrothorax and mature empyema are two common indications for thoracotomy. The procedure of choice for both conditions is pleurectomy/decortication. Since these are benign conditions, the durability of the surgery must be substantially longer than for malignant mesothelioma. Though many of the technical nuances are the same, a few points are worth noting. Fibrothorax is most often a sequela of an incompletely drained hemothorax. Medications have rarely been implicated in the genesis of the disease. An idiopathic variant, akin to mediastinal or retroperitoneal fibrosis, also exists [27]. The differential diagnosis includes desmoplastic malignant mesothelioma. Since reversible acute pleural inflammation may accompany a variety of conditions, surgery should be considered only if pleural disease persists for several weeks or months. Furthermore, the disease must be responsible for significant disability, and the patient must be a reasonable surgical candidate. Fibrothorax predominates in the lower chest. Frequently, the diaphragm is entrapped in the process. Parietal pleurectomy is as important as the decortication, since chest wall and diaphragmatic compliance are restored with the pleurectomy. When considering a patient for surgery, recognizing existing pulmonary hypertension alerts the surgeon to the risk of significant intraoperative blood loss. Mature or chronic empyema is an insidious disease that manifests with constitutional, rather than local, symptoms. Recent history of respiratory tract infection (2–6 months prior), low-grade fevers, night sweats, and fatigue characterize the disease. If accompanied by pleuritic chest pain and a complex fluid collection is found on chest X-ray, empyema becomes the most likely

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Figure 8.5 Chest computed tomography (CT) image demonstrating ring-enhancement of a loculated pleural fluid collection. This finding is consistent with empyema.

diagnosis. In these cases, a chest CT scan usually demonstrates a complex effusion with ring enhancement (Figure 8.5). When confronted with a mature empyema, it is prudent to proceed directly to thoracotomy. During the course of the decortication, peripheral parenchymal abscesses may be encountered. These should be widely debrided and, if small, can be left to drain into the pleural space. Visceral pleural defects should be suture ligated to prevent development of broncho-pleural fistulae. As a rule, fissures should be explored for entrapped fluid collections. Complete drainage of the pleural space must be achieved.

Surgery for mesothelioma Though much controversy remains, some clinicians consider mesothelioma a surgical disease. Often, the surgeon’s role in the management of the disease is restricted to tissue acquisition for diagnosis. Single-port thoracoscopy is the procedure of choice. A common clinical scenario is the patient with asbestos and tobacco exposures who presents with an effusion or diffuse pleural disease in the absence of a dominant pulmonary mass. Fine-needle aspiration is frequently non-diagnostic or yields a diagnosis of suspected epithelioid malignancy. Thoracoscopy allows evaluation of the pleural space, generous biopsy of the pleura (to allow differentiation of mesothelioma from metastatic adenocarcinoma), drainage of the effusion, and talc poudrage if necessary. Rarely, the procedure is extended to a mini-thoracotomy for tumors with a predominantly desmoplastic component, as much of the biopsy specimen is benign

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fibrous tissue. In these cases, it is critical that a diagnosis be made on frozen section prior to concluding the procedure.

Benign localized mesothelioma The prognosis for benign localized mesothelioma (pleural fibroma, solitary fibrous tumor of the pleura, fibrous mesothelioma) is favorable. Surgical therapy is generally straightforward. Preoperative chest CT scan usually demonstrates a well-circumscribed pleural-based mass with some degree of pulmonary collapse. The differential includes primary lung cancer, solitary pleural metastasis, primary sarcoma of the chest wall, bronchogenic cyst, neurogenic tumor, rounded atelectasis/pneumonia, loculated empyema, and diaphragmatic hernia. This tumor has no documented link to asbestos exposure. If the pleura appears diffusely involved, a malignant process is most likely. Curiously, unique extrathoracic manifestations (pulmonary osteoarthropathy, fever, hypoglycemia) are found in one-third of patients [3,28]. Unless resection is incomplete, surgery is curative. Surgical therapy includes en bloc resection of the pleural-based mass, which usually arises from the visceral pleura. Resection should include a small wedge of lung to insure that all involved visceral pleura is resected. If mediastinal or parietal pleura is the point of origin, generous margins of normal pleura should be included in the resection specimen. Bronchoscopy prior to extubation may be necessary to alleviate mucous impaction from chronically compressed lung, depending on the size of the tumor.

Malignant pleural mesothelioma Malignant pleural mesothelioma a rare malignancy, arises from the mesothelium that lines the pleural cavities. Usually found in patients with a history of asbestos exposure, the time from exposure to its clinical presentation is > 20 years. The disease manifests as progressive dyspnea or chest pain; malignant effusion develops in most patients. Advanced disease can present with cachexia, ascites and/or chest wall deformitiy [29]. Microscopically, these tumors exhibit epithelioid, sarcomatoid, or mixed differentiation patterns. Of the three, the more common epithelioid variants have the best prognosis; the least common, pure sarcomatoid tumors, have the poorest survival. Median survival of untreated malignant mesothelioma is approximately 1 year [30–33]. Three different surgical approaches should be considered for malignant mesothelioma: talc pleurodesis, pleurectomy/decortication, and extrapleural pneumonectomy. Choice of treatment plan depends on the fitness of the patient, histology type, stage of disease, and access to skilled radiation and medical oncologists. Contraindications for aggressive therapy because of the increased risk of postoperative complications are age > 70 years, compromised cardiac function (ejection fraction < 45% or ischemia), pulmonary hypertension, hypercarbia (PCO2 < 45 mmHg), hypoxemia (PO2 < 65 mmHg), or a postresection predicted forced expiratory volume in 1 s < 1 l [29]. N2 or

Pleural space problems 147

T3 – 4 disease and mixed or sarcomatoid histology should relegate the patient to drainage and pleurodesis if a symptomatic effusion exists.

Pleurectomy/decortication for mesothelioma Indications for pleurectomy/decortication in the management of malignant pleural mesothelioma are shrinking, as trimodality therapy with extrapleural pneumonectomy gains acceptance for appropriate candidates. Initial optimism to incorporate pleurectomy/decortication into multimodality protocols for mesothelioma has subsided, after recent trials revealed a 60% local failure rate [34,35]. Yet, in an otherwise fit patient considered unsuitable for extrapleural pneumonectomy, pleurectomy/decortication remains a reasonable option for severe lung entrapment. Incision is usually made through the 5th interspace. Though seldom necessary, resection of part of the 6th rib can be used to facilitate entrance into the endothoracic fascial plane. The parietal pleural is bluntly separated from the fascia and points of dense adherence usually connote reactive desmoplasia or periosteal and rib involvement. Cautery or sharp dissection can be used to disconnect the pleura in these regions. Intraoperative blood loss can be minimized by serially packing the chest with laparotomy pads as the parietal pleura is mobilized from various regions. Gradually, the parietal pleura is separated from the anterior, lateral and posterior chest wall. If intercostal pedicles are avulsed during the dissection, the plane is too deep. Sharp dissection is necessary to regain the proper plane. Difficulty is most frequently encountered in the apex, medially, and inferiorly. At the apex of the hemithorax, great care must be taken when detaching the pleura from the subclavian vessels. Antero-medially, careful dissection to avoid internal mammary artery injury is important as this is difficult to control if injured. Postero-medially, esophageal (right-side) or aortic (left-side) perforation is catastrophic. An injury to the phrenic pedicle anywhere along its course may negate the benefit of the procedure, as will diaphragmatic evulsion. A small amount of gross tumor left in these regions may be warranted to prevent an intraoperative calamity or postoperative disability. Some surgeons utilize ‘bunk-bed’ thoracotomies (a second intercostal entry at the 7th interspace) to simplify the dissection on the diaphragm. After the parietal pleura has been sufficiently mobilized, the tumor is incised sharply at a convenient location and the visceral pleura decorticated. Raw parenchyma can be exposed when visceral pleura is peeled away along with the tumor. As long as the lung injury remains superficial, this is of little concern. Bleeding from both parenchymal and chest wall sources is easily controlled with direct pressure, electrocautery, or argon beam coagulation. Care must be taken when decorticating the fissures as they can be inadvertently followed into the distal pulmonary artery. After the tumor peel is removed, the air leak may be imposing; however, as long as the lung inflates to fill the hemithorax, resolution of the air leak is surprisingly quick. Large parenchymal

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rents should be plicated to reduce healing time and shorten hospital stay. Two to three large-bore chest tubes are usually necessary to keep the hemithorax drained during the early recovery period. A preoperative epidural catheter is important for early ambulation and pulmonary toilet. Most patients are kept intubated and ventilated on the first postoperative night to promote lung expansion. If the air leak is manageable, chest tubes are placed on high suction to evacuate fluid from the pleural space. Positive end-expiratory pressure can be applied to tamponade parenchymal and chest wall bleeding. Currently, we do not advocate the routine use of adjuvant radiotherapy following pleurectomy/decortication. The amount of radiation that can be administered to the hemithorax is limited by the radiation intolerance of normal lung and, even when the radiation planning has been meticulous, significant radiation pneumonitis results [34]. Regardless, most patients recur within 1 year. Currently, no salvage therapy exists for recurrence.

Extrapleural pneumonectomy for mesothelioma The technical challenge of this resection is matched equally by the diligence and experience required to recover patients postoperatively. In 1976, the initial operative mortality was reported at 30% [36]; today, a 30-day mortality of > 5% would be considered excessive [37]. This procedure is not restricted to mesothelioma. Pleural sarcoma and advanced, refractory tuberculous disease may also require extrapleural pneumonectomy as therapy. Comprehensive reviews of clinical indications [38] and technique of extrapleural pneumonectomy [29] have been written. Since malignant mesothelioma is a locally aggressive disease, in theory the more complete the resection, the better the outcome should be expected. This may explain the markedly lower local recurrence rate after resection compared with pleurectomy/decortication [39]. Local control can be enhanced by aggressive adjuvant radiotherapy to the empty hemithorax. Patients who benefit most from resection have early-stage, node-negative, epithelioid tumors [38,40]. Extrapleural pneumonectomy for mesothelioma should be reserved for patients enrolled in a trimodality protocol. Extrapleural pneumonectomy entails resection of the pleural envelope with lung, diaphragm, pericardium and a complete lymphadenectomy. Difficulties encountered during the resection are identified in Figure 8.6. Resection of all gross disease is the goal, as benefit from the procedure has only been demonstrated with negative resection margins [40]. Involvement of the ribs, mediastinum, esophagus, aorta, or subclavian vessels contraindicates resection. This should be investigated preoperatively by MRI scanning [4]. If trans-pericardial or trans-diaphragmatic spread is found, the resection should be aborted. Limiting the number of intraoperative surprises facilitates a safe and beneficial outcome. As with pleurectomy, much of the dissection is done bluntly. Hemostasis is obtained by direct pressure. If the proper extrapleural plane is developed, the

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Figure 8.6 Depending upon the side of the malignant mesothelioma, several anatomic structures must be protected during extrapleural pneumonectomy. (a) Subclavian vessels. (b) Esophagus. (c) Aazygous vein. (d) Vagus nerve. (e) Left recurrent nerve. (f ) Aorta. (g) IVC. Injury to any of these structures will result in intraoperative difficulty and postoperative morbidity.

dissection proceeds smoothly. In the case of a frozen hemithorax, the 6th rib may be sacrificed to allow access to the endothoracic fascial plane, although rib resection makes chest closure significantly more difficult. Using a sponge-stick and sharp dissection, it should be possible to mobilize the superior sulcus, leaving subclavian vessels, stellate ganglia, esophagus and vagus nerve intact. A nasogastric tube permits intraoperative identification of the esophagus. In very early-stage disease, with low tumor burden, dissection is frequently more tedious; the pleura is not thickened and the plane is difficult to develop. In these cases, islands of normal-appearing, thin, parietal pleura often separate from the specimen and remain attached to the chest wall. A piecemeal approach must be adopted to finish the resection. Diaphragmatic and pericardial resections are undertaken only after it is certain that the resection can be completed. The diaphragm is mobilized bluntly, beginning from the costovertebral sulcus. Much of this dissection is done blindly, with fingers being interdigitated between slips of diaphragm muscle (a ‘bunk-bed’ thoracotomy may simplify this aspect). This sulcus is a difficult area to visualize and a common site for gross disease to be left behind. It is therefore typical to spend more time during this part of the resection than for mobilization of the rest of the pleura. Once the diaphragm has been partially disconnected, the specimen can be rolled into view, the lateral aspect of the diaphragm incised with cautery and bluntly separated from underlying peritoneum. As the diaphragm is resected, the peritoneum is frequently adherent to the underside of the central tendon and commonly avulsed. Any defects are oversewn to reduce the chance of ascites developing as the ipsilateral chest fills

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Figure 8.7 After the surgical specimen has been removed during extrapleural pneumonectomy, postoperative complications may result from improper reconstruction and closure. Specific sites include: (a) pericardial patch disruption leading to cardiac herniation or a tight patch resulting in tamponade; (b) IVC entrapment by either pericardial or diaphragm patches; (c) dehiscence of the diaphragm patch and abdominal herniation; (d) unsuspected hemorrhage below the reconstructed diaphragm. Bronchial stumps should be covered (the thymic fat pad is illustrated).

up with pleural fluid postoperatively. As the dissection proceeds posteromedially towards the crus, inferior phrenic pedicles need to be effectively controlled. For right-sided resections, disconnection of the diaphragm at the level of the inferior vena cava is best done after the pericardium has been opened anteriorly with continuation posterior to the cava. The specimen is removed when the posterior pericardium is cut, after the intrapericardial division of the pulmonary veins and pulmonary artery and stapling of the bronchus (some surgeons prefer vascular and bronchial disconnection prior to the diaphragmatic resection). It is surprisingly easy to tent the esophagus up into the field while detaching the specimen from the posterior pericardium. Attention to the position of the esophagus during this part of the procedure is prudent. Soft tissue coverage of the bronchial stump is recommended (Figure 8.7). The procedure is concluded with gortex patch reconstruction (Figure 8.7) of the diaphragm and pericardium for right-sided procedures [38].

Pleural space problems 151 Table 8.3 Observed postoperative complications following extrapleural pneumonectomy. Complication Hypotension Falling HCT Stable HCT

Hoarseness/weak cough Respiratory insufficiency

Ventricular arrhythmia

Dysphagia Incisional seroma Contralateral pleural effusion

Possible cause

Bleeding ± coagulopathy Epidural analgesia ± ipsilateral sympathetic chain injury Hypovolemia secondary to early fill-up Myocardial ischemia Atrial arrhythmia Right-sided Gortex patch compressing IVC Sepsis from occult esophageal injury Left recurrent nerve injury Post-pneumonectomy pulmonary edema Mediastinal shift from rapid fill-up Aspiration Myocardial ischemia Pericardial/diaphragm patch disruption and cardiac malrotation or entrapment Submucosal esophageal hematoma Vagal injury Improper chest closure and extravasation of fluid from chest Contralateral parietal pleura injury during the procedure

In a procedure of this magnitude, even small technical complications can be catastrophic. Table 8.3 summarizes complications observed after extrapleural pneumonectomy. Cognizance of the technical subtleties of the procedure promotes a more uneventful postoperative course. During the recovery period, pulmonary edema, mediastinal shift, atrial arrhythmia, vocal cord palsy, and pain all contribute to respiratory insufficiency. In addition to effective pain management and early ambulation, aggressive diuresis, balancing of the mediastinum and vocal cord injection (to restore a functional cough) may be necessary. Most diaphragmatic patch problems manifest within the first week, if not the first day, and mandate an immediate return to the operating room. A postoperative chest X-ray demonstrates a leftsided diaphragm patch dehiscence as the gastric air bubble (and other abdominal organs) ascend into the left chest. A right-sided diaphragm patch disruption may be more insidious. The liver is still partially fixed to the peritoneal cavity laterally and posteriorly after resection, and may not swiftly fill the cavity if the reconstruction fails. If the liver does herniate into the right chest, the chest X-ray may not change appreciably. Often, an ultrasound or chest CT is required to diagnose the problem. Dehiscence of the right-sided pericardial patch usually results in ventricular tachycardia followed promptly by fibrillatory arrest. When the heart herniates into the pneumonectomy space, venous return is severely compromised as both inferior and superior vena cavae become occluded. If this happens, the patient should be immediately

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placed in a left-lateral decubitus position, to drop the heart back into the pericardial cavity, and returned to the operating room. Cardiac compressions, if necessary, should be done open. If the pericardial patch is made too tight, a tamponade-like syndrome is created. It is important to reef or ‘pie-crust’ the pericardial patch to permit ample laxity (Figure 8.7). Chest closure in these cases is also critical. Compared with a standard pneumonectomy, the extrapleural dissection induces rapid filling of the hemithorax. Often, the fluid level is well above the carina on the first postoperative day, long before the thoracotomy has biologically sealed itself. Meticulous suture closure of the thoracotomy is important. If a rib was resected, serratus anterior mobilization and coverage may be required. The closure should be watertight to lessen the risk of a superficial seroma in free communication with the intrathoracic space. Should this occur, a compressive chest wrap can be employed at the expense of pulmonary restriction. The skin incision must be kept intact to prevent seeding of the chest cavity by skin flora. Regardless of mechanism, the development of empyema following extrapleural pneumonectomy is a challenging problem. Infection is complicated by patch material in the field and is not amenable to catheter-based, percutaneous, antibiotic irrigation protocols (even in the absence of a broncho-pleural fistula). As with a post-pneumonectomy empyema, patients are lethargic and fatigue easily. Low-grade fevers are common, but very little else localizes the infection to the chest. A sterile thoracentesis is reassuring but does not rule out the diagnosis. Open drainage after debridement of the chest cavity and removal of the patch material is recommended, particularly if a bronchial dehiscence is identified. The diaphragm can be reconstructed with vicryl mesh and allowed to granulate. For empyema following a right-sided resection, the pericardial patch may be replaced by bovine pericardium, autologous fascia lata [41], or ipsilateral parietal pleura [42], and the cavity managed with dressing changes. A more conservative approach of closed antibiotic irrigation can be considered in the absence of a bronchial stump problem. Removal of infected tissue and the patch(es) at re-thoracotomy is a prerequisite. Regardless, this postoperative complication usually prevents the patient from receiving adjuvant therapy, severely compromising the benefits of the surgery.

Conclusion Long gone are the days when the most frequently performed pleural procedure was the morbid and deforming thoracoplasty. The modern era of pleural surgery demands expertise in minimal access techniques as well as a thorough understanding of surgical anatomy. There must be no reluctance to abort a video-assisted procedure in favor of the standard open approach if circumstances dictate. Thorough preoperative assessment, meticulous attention to detail intraoperatively, and the recognition and treatment of postoperative complications facilitate the safe performance of pleural surgery.

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References 1 Andrews CO, Gora ML. Pleural effusions. Pathophysiol Manage Ann Pharmacother 1994; 28: 894–903. 2 LoCicero J. Benign and malignant disorders of the pleura. In: Baue AE, Geha AS, Hammond GL, Lak H, Naunheim KS, eds. Glenn’s Thoracic and Cardiovascular Surgery, 6th edn. Stanford, CT: Appleton and Glange, 1996; 537–555. 3 Deslauriers J, Carrier G, Beauchamp G. Diagnostic procedures. In: Pearson FG, Deslauriers J, Ginsberg RJ, Hiebert CA, McKneally MF, Urschel HC, Jr, eds. Thoracic Surgery. New York: Churchill Livingstone, 1995; 987–1001. 4 McLoud TC, Flower CDR. Imaging the pleura. Sonography, CT and MR imaging. AmJ Roentgenol 1991; 156: 1145–1153. 5 Idell S. Evaluation of perplexing pleural effusions. Contemp Intern Med 1994; 6: 31–39. 6 Im J-G. Imaging of the pleura. Opin Radiol 1991; 3: 387–393. 7 Collins TR, Sahn SA. Thoracentesis: clinical value, complications, technical problems and patient experience. Chest 1987; 91: 817–822. 8 Kennedy L, Sahn SA. Non-invasive evaluation of the patient with a pleural effusion. Chest Surg Clin N Am 1994; 4: 451–465. 9 Tomlinson JR, Sahn SA. Invasive procedures in the diagnosis of pleural disease. Semin Respir Med 1987; 9: 30–36. 10 Feinsilver SH, Barrows AA, Braman SS. Fiberoptic bronchoscopy and pleural effusions of unknown origin. Chest 1986; 90: 516–519. 11 Jacobæus HC. The practical importance of thoracoscopy in surgery of the chest. Surg Gynecol Obstet 1922; 34: 289–296. 12 Krasna M, Flowers JL. Diagnostic thoracoscopy in a patient with a pleural mass. Surg Laparosc Endosc Percutan Tech 1991; 1: 94 –97. 13 Kohmar LJ. Thoracoscopy for the evolution and treatment of pleural space disease. Chest Surg Clin N Am 1994; 4: 467– 478. 14 Boutin C, Astoul P, Seitz B. The role of thoracoscopy in the evaluation and management of pleural effusions. Lung 1990; 168 (Suppl.): 1113–1121. 15 Kohman LJ. Thoracoscopy for the evaluation of treatment of pleural space disease. Chest Surg Clin N Am 1994; 4: 467–479. 16 Rusch VW, Mountain C. Thoracoscopy under regional anesthesia for the diagnosis and management of pleural disease. Am J Surg 1987; 154: 274–278. 17 Inderbitzi RGC, Grillet MP. Risk and hazards of video-thoracoscopic surgery: a collective review. Eur J Cardiothorac Surg 1996; 10: 483–489. 18 Chrétien J, Bignon J, Hirsch A, eds. The Pleura in Health and Disease. New York: Marcel Dekker, 1985; 587–610. 19 Viskum A, Enk B. Complications of thoracoscopy. Poumon Coeur 1981; 37: 25–28. 20 Viskum K. Contraindications and complications of thoracoscopy. Pneumologie 1989; 43: 55–57. 21 Aelony Y, King R, Boutin C. Thoracoscopic talc poudrage pleurodesis for chronic recurrent pleural effusions. Ann Intern Med 1991; 115: 778–782. 22 Weissberg D, Ben-Zeev I. Talc pleurodesis. J Thorac Cardiovasc Surg 1993; 106: 689–695. 23 Zaugg M, Lucchinetti E, Zalunardo MP et al. Substantial changes in arterial blood gases during thoracoscopic surgery can be missed by conventional intermittent laboratory blood gas analysis. Anesth Analg 1998; 87: 647–653. 24 Yim APC, Liu H-P. Complications and failures of video-assisted thoracic surgery: experience from two centers in Asia. Ann Thorac Surg 1996; 61: 538–541.

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25 Walker-Renard PB, Vaughan LM, Sahn SA. Chemical pleurodesis for malignant pleural effusions. Ann Intern Med 1994; 120: 56–64. 26 Scherer LA, Battistella FD, Owings JT, Aguilar MN. Video-assisted thoracic surgery in the treatment of post-traumatic empyema. Arch Surg 1998; 133: 637–642. 27 Buchanan DR, Johnston ID, Kerr IH et al. Cryptogenic bilateral fibrosing pleuritis. Br J Dis Chest 1988; 82: 186–193. 28 Immerman SL, Sener SF, Khandekar JD. Causes and evaluation of tumor-induced hypoglycemia. Arch Surg 1982; 117: 905–908. 29 Sugarbaker DJ, Richards WG, Garcia JP. Extrapleural pneumonectomy for malignant mesothelioma. Adv Surg 1998; 31: 253–271. 30 Antman K, Pass HI, Recht A. Benign and malignant mesothelioma. In: DeVita VT Jr, Hellman S, Rosenberg SA, eds. Cancer: Principles and Practice of Oncology, 3rd edn. Philadelphia: JB Lippincott, 1989; 1399–1414. 31 Chahinian AP, Ambinder RM, Mandel EM et al. Evaluation of 63 patients with diffuse malignant mesothelioma. Proc Am Soc Clin Oncol 1980; 21: 360A. 32 Law MR, Hodson ME, Turner-Warwick M. Malignant mesothelioma of the pleura: clinical aspects and symptomatic treatment. Eur J Respir Dis 1984; 65: 162–168. 33 Ruffie P, Feld R, Minkin S et al. Diffuse malignant mesothelioma of the pleura in Ontario and Quebec: a retrospective study of 332 patients. J Clin Oncol 1989; 7: 1157–1168. 34 Mychalczak BR, Nori D, Armstrong JG et al. Results of treatment of malignant pleural mesothelioma with surgery, brachytherapy, and external beam irradiation. Endocurie Hypertherm Oncol 1989; 5: 245. 35 Rusch VW, Saltz L, Venkatraman E et al. A phase II trial of pleurectomy/decortication followed by intrapleural and systemic chemotherapy for malignant pleural mesothelioma. J Clin Oncol 1994; 12: 1156–1163. 36 Butchart EG, Ashcroft T, Barnsley WC et al. Pleuropneumonectomy in the management of diffuse malignant mesothelioma of the pleura. Thorax 1976; 31: 15–24. 37 Sugarbaker DJ, Garcia JP, Richards WG et al. Extrapleural pneumonectomy in the multimodality therapy of malignant pleural mesothelioma. Results in 120 consecutive patients. Ann Surg 1996; 224: 288–296. 38 Rusch VW. Indications for pneumonectomy: extrapleural pneumonectomy. Chest Surg Clin N Am 1999; 9: 327–338. 39 Rusch VW, Piantadosi S, Holmes EC. The role of exptrapleural pneumonectomy in malignant mesothelioma. A Lung Cancer Group Trial. J Thorac Cardiovasc Surg 1991; 102: 1–9. 40 Sugarbaker DJ, Flores RM, Jaklitsch MT et al. Resection margins, extrapleural node status, and cell type determine postoperative long-term survival in trimodality therapy of malignant pleural mesothelioma: results in 183 patients. J Thorac Cardiovasc Surg 1999; 117: 54–65. 41 Sollman M, Henze A, Peteffy A. Extended thoracic resection for lung cancer. Scand J Thorac Cardiovasc Surg 1987; 21: 69–72. 42 Kageyama T, Suzuki K, Matsushita K et al. Pericardial closure using fascia lata in patients undergoing pneumonectomy with pericardiectomy. Ann Thorac Surg 1998; 66: 586–587.

CHAPTER 9

Complications of chest wall reconstruction M Bulent Tirnaksiz, Claude Deschamps

Prevention of complications is the key. Selection of the appropriate procedure for a given patient, meticulous surgical technique and dedicated perioperative care are paramount to prevent complications after chest wall (CW) resection. Complications can occur in the early postoperative period or late, as long-term sequelae (Table 9.1). Considerations for reconstruction of CW defects depends on factors such as the location and size of the defect, full or partial thickness involvement, duration, conditions of the local tissue, general condition of the patient, life style, type of work and the vital prognosis [1]. In small defects the skeletal component can be ignored as it will not affect chest wall function and the defect closed with only soft tissues. If structural stability is required, however, either autogenous tissue, such as fascia lata or rib, or prosthetic material, such as the various meshes, metals, or soft tissue patches, may be used. Defects of the CW almost always occur as a result of surgery for neoplasm (primary or recurrent), radiation injury, infection, or trauma. CW defects produced by excision of most neoplasms results in loss of the skeleton and frequently the overlying soft tissues as well. Radiation injury, infection, and trauma produce partial or full-thickness defects depending upon their severity. Not uncommonly, various combinations of these afflictions occur in the same patient, and management of these problems often becomes problematic. The surgeon is anxious to obtain wide margins and rid the patient of all possible malignant, contaminated, or irradiated tissue while at the same time leaving a defect that can be closed in order to maintain life Table 9.1 Type of complications after chest wall resection and reconstructions. Early

Late

Acute infection Hemorrhage Seroma Flail chest wall Ischemia/necrosis of a flap Injury to vascular pedicle Respiratory failure

Recurrent/chronic infection Instability/flail Arm weakness/wing scapula Chest contour irregularity Local recurrence of malignancy Chronic pain Ventral hernia

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itself. A thorough knowledge of reconstructive techniques with a clear operative plan that includes a ‘secondary or fallback’ procedure, if possible, is most desirable. This dilemma is best managed by the combined efforts of both a thoracic and plastic surgeon [1–6]. Reconstruction of the bony CW is controversial. Differences of opinion exist about which patients should be reconstructed and what type of reconstruction should be done [7–14]. In general, all full-thickness skeletal defects that have the potential for allowing paradoxical chest wall motion should be reconstructed. The decision not to reconstruct the skeleton depends on the size and location of the defect. Defects < 5 cm in greatest diameter anywhere on the thorax are not usually reconstructed. Posterior defects < 10 cm, likewise, do not require reconstruction because the overlying scapula provides support unless they are located at the tip of the scapula where entrapment of the scapula can occur during movement of the arm. The choice of prosthetic material can be confusing. Numerous prostheses exists and all work reasonably well [13,15]. For the most part, choice is based on surgeon’s preference. We tend to use either Prolene® Mesh (PM) or GoreTex® Soft Tissue Patch (GT), although both materials are contraindicated in contaminated wounds unless the surgeon thinks that the patient cannot be extubated without this additional support. PM is more difficult than GT to stretch and suture without wrinkles and surface irregularities and does not achieve a watertight seal of the pleural space. GT, in contrast, is much easier to suture, stretch and mold into the wound and provides a barrier that prevents fluid and air from moving between the pleural and subcutaneous space. We secure the patch with heavy interrupted non-absorbable sutures, which are placed either through or around the ribs. GT, however, must be 2 mm thick as the 1 mm thickness does not hold sutures well at the tension needed to stabilize the CW. For these reasons GT became our prosthesis of choice in the mid 1980s. As experience was gained, we avoided placing a prosthesis in a contaminated wound, but we became confident in leaving the prosthesis in situ in a subsequent wound infection if the prosthesis was incorporated by granulation tissue at the level of insertion to the chest wall. Combining this approach with intensive wound debridement and frequent dressing changes, the prosthesis can be salvaged in most cases. Suction drains are more often used in conjunction with muscle flaps when dead space and raw surface are significant. They are left in place usually until daily drainage is < 25 cm3 per drain. Small seromas that do occur are best managed with observation as most eventually will resolve. When large or symptomatic, aspiration under strict aseptic conditions offers the best treatment option. Surgical obliteration of the seroma cavity is rarely necessary in our experience. Soft tissue reconstruction with local tissue, if possible, offers the simplest and most practical method of covering the prosthesis. If local tissue is not available, muscle transposition is the tissue of choice for coverage, with the omentum being reserved as back-up if muscle transposition has failed or if no

Complications of chest wall reconstruction 157

muscle is available [1–3]. Tension on a soft tissue flap should be avoided at all times, and on occasions a second and a third flap may be necessary to achieve proper closure of a defect. Ischemia of a flap can lead to varying degrees of tissue loss (including total necrosis of the flap) if not corrected immediately. Prevention of such circulatory embarrassment is one of the paramount goals of any reconstruction [16]. Skin grafts are utilized where appropriate. Several measures exist in addition to standard analgesia that may be used to decrease chest wall pain and respiratory complications in patients after CW reconstruction. These include liberal use of intercostal blocks and postoperative epidural analgesia [16]. Most patients in our experience can be extubated within 24 h of CW reconstruction. Long-term sequelae following chest wall resection are uncommon. These include recurrent/chronic infection, instability/flail, arm weakness/wing scapula, chest contour irregularity, local recurrence of malignancy, chronic pain and ventral hernia [17]. Surgical removal of the sternum and manubrium in conjunction with muscle flap repair is usually well tolerated and will result in minor changes in pulmonary function if any [18]. We recently reviewed our experience in patients undergoing prosthetic bony reconstruction after CW resection with the specific goal of analysing early and late morbidity and mortality [2]. From 1 January 1977 to 31 December 1992, 197 patients underwent CW resection and reconstruction with prosthetic material at the Mayo Clinic in Rochester, Minnesota. This review covers two time periods. Skeletal reconstruction was achieved with Prolene® Mesh (PM) (Ethicon, Inc., Somerville, NJ, USA) in 64 patients (32.5%) during the period from 1977 to 1984. Subsequently, a 2 mm thick Gore-Tex® Soft Tissue Patch (GT) (W.L. Gore and Associates, Inc., Flagstaff, AZ, USA) was utilized in 133 (67.5%) in the second period from 1984 to 1992. Soft tissue coverage was achieved with transposed muscle in 116 patients, local tissue only in 78, and omentum in three. Muscles transposed included latissimus dorsi in 45 patients, pectoralis major in 44, serratus anterior in 15, external oblique in six, rectus abdominis in four, trapezius in one and internal oblique in one. Postoperative complications occurred in 91 patients (46.2%) (Table 9.2). Wound seromas occurred in 10 patients with GT and in four with PM; none developed a wound infection. Twelve seromas were small and resolved, six spontaneously and six after repeated aspirations. The remaining two patients (both with GT) required wound explorations and obliteration of the cavity with eventual healing. Wound infections occurred in nine patients (five with PM and four with GT). The three patients who had a contaminated wound preoperatively developed a postoperative infection. All three patients had their CW reconstructed with PM, and in each the PM was later removed, but at that point (13–64 days) the underlying lung had adhered to the CW preventing open pneumothorax. Thus, no further skeletal reconstruction was done. In addition, two other patients with wound infections had the PM removed. In contrast, the wounds in the four patients with GT were opened, debrided and packed with gauze. All four wounds were closed by secondary intent and

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Chapter 9 Table 9.2 Complications in 197 patients undergoing prosthetic chest wall reconstruction. (Reprinted from [2], with permission from Elsevier.) Complication

Number

Percent

Respiratory Seroma Wound infection Arrhythmia Hemorrhage Myocardial infarction Prolonged air leak Other

48 14 9 5 4 3 2 6

24.4 7.1 4.6 2.5 2.0 1.5 1.0 3.0

all were healed by the time of hospital dismissal. There were eight operative deaths (mortality 4.1%). All occurred in patients who had concurrent pulmonary resection. Indications for lung resection were contiguous lung cancer in five patients, contiguous breast cancer in one, metastatic carcinoma to the CW in one, and malignant fibrous histiocytoma in one. Cause of death was myocardial infarction in three, respiratory failure in three, pulmonary embolus in one, and multiple organ failure in one. Median hospitalization for all 197 patients was 14 days and ranged from 2 to 76 days. Follow-up was complete in 179 operative survivors (94.7%) and ranged from 1 to 204 months (median 26 months). Sixty-six patients (36.9%) were alive at time of last follow-up. Cause of death in the remaining 113 patients was recurrent malignancy in 65, causes unrelated to the original CW condition in 15, and unknown in 33. At last follow-up or at the time of death, 127 patients (70.9%) had a well-healed, asymptomatic chest wall. An additional 43 patients (24.0%) initially also had a well-healed chest but subsequently developed a CW local cancer recurrence. The status of the wound was unknown in the remaining eight patients. The local cancer recurrence was breast carcinoma in 24 patients, chondrosarcoma in five, other sarcoma in seven, lung carcinoma in two, desmoid tumor in two, squamous cell carcinoma of the skin in one, malignant pleural mesothelioma in one, and metastatic hypernephroma in one. Six patients with local recurrence were re-operated a median of 18 months after the initial CW resection (range 8–21 months). The CW was again resected and a GT was used for reconstruction in all six patients. At follow-up, four of these patients reoperated for local recurrence developed a second local recurrence; the remaining two were asymptomatic with a well-healed CW. None of the nine patients who developed a postoperative wound infection had further evidence of infection. All had a healed wound without drainage. One other patient required reduction mammoplasty because of breast deformity attributed to the CW reconstruction. Factors affecting long-term outcome were analyzed. Neither preoperative chemo- and/or radiation therapy, oral corticosteroid, diabetes, smoking history,

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presence of chronic obstructive pulmonary disease, histological type, nor type of prosthesis significantly affected the incidence of seroma, wound infection, length of hospitalization, local cancer recurrence and other complications. Similarly, the extent of rib or sternal resection had no effect on postoperative morbidity and mortality. However, associated pulmonary resection had an adverse effect on operative mortality (P = 0.0002). This review demonstrated that CW resection and reconstruction with prosthetic material will yield satisfactory results in most patients and that little difference exists between skeletal reconstruction with Prolene® Mesh and Gore-Tex® Soft Tissue Patch. The decision of which prosthesis to use remains the surgeon’s choice. The goal of therapy after chest CW resection and reconstruction remains a healthy patient with a healed and functional chest wall with no evidence of infection or recurrent malignancy.

References 1 Pairolero PC, Arnold PG. Thoracic wall defects: surgical management of 205 consecutive patients. Mayo Clin Proc 1986; 61: 557–563. 2 Deschamps C, Tirnaksiz BM, Darbandi R et al. Early and long-term results of prosthetic chest wall reconstruction. J Thorac Cardiovasc Surg 1999; 117: 588–591. 3 Arnold PG, Pairolero PC. Chest-wall reconstruction. An account of 500 consecutive patients. Plast Reconst Surg 1996; 98: 804 –810. 4 Arnold PG, Pairolero PC. Reconstruction of the radiated-damaged chest wall. Surg Clin North Am 1989; 69: 1081–1089. 5 Arnold PG, Pairolero PC. Surgical management of the radiated chest wall. Plast Reconstr Surg 1986; 77: 605–612. 6 Arnold PG, Pairolero PC. Chest wall reconstruction: experience with 100 consecutive patients. Ann Surg 1984; 199: 725–732. 7 Soysal O, Walsh GL, Nesbitt JC et al. Resection of sternal tumors: extent, reconstruction and survival. Ann Thorac Surg 1995; 60: 1353–1359. 8 McCormack P, Bains MS, Beattie EJ Jr et al. New trends in skeletal reconstruction after resection of chest wall tumors. Ann Thorac Surg 1981; 31: 45–52. 9 Ryan MB, McMurtrey MJ, Roth JA. Current management of chest-wall tumors. Surg Clin North Am 1989; 69: 1061–1080. 10 McKenna RJ, McMurtrey MJ, Larson D et al. A perspective on chest wall resection in breast cancer patients. Ann Thorac Surg 1984; 38: 482– 486. 11 Kroll SS, Walsh G, Ryan B et al. Risks and benefits of using Marlex mesh in chest wall reconstruction. Ann Plast Surg 1993; 31: 303–306. 12 Economou SG, Southwick HW. The repair of thoracic wall defects with sliding rib grafts. J Thorac Surg 1958; 36: 112–116. 13 McCormack PM. Use of prosthetic materials in chest wall reconstruction: assets and liabilities. Surg Clin North Am 1989; 69: 965–976. 14 McKenna RJ Jr, Mountain CF, McMurtrey MJ et al. Current techniques for chest wall reconstruction: expanded possibilities for treatment. Ann Thorac Surg 1988; 46: 508–512. 15 Eschapasse H, Gaillard J, Henry E et al. Chest wall tumors: surgical management. In: Grillo HC, Eschapasse H, eds. International Trends in General Thoracic Surgery. Major Challenges. Philadelphia: W.B. Saunders Co., 1987; 2: 292–307.

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16 Graeber GM, Seyfer AE. Complications of chest wall resection and the management of flail chest. In: Waldhausen JA, Orringer MB, eds. Complications in Cardiothoracic Surgery. St Louis: Mosby Year Book, 1991; 39: 413–421. 17 Yuen JC, Zhou AT, Serafin D et al. Long-term sequelae following median sternotomy wound infection and flap reconstruction. Ann Plast Surg 1995; 35: 585–589. 18 Meadows JA III, Staats BA, Pairolero PC et al. Effect of resection of the sternum and manubrium in conjunction with muscle transposition on pulmonary function. Mayo Clin Proc 1985; 60: 604–609.

CHAPTER 10

Complications of esophageal resection Richard J Battafarano, Nasser K Altorki

Esophageal surgery is now commonly performed for both benign and malignant disorders of the esophagus. Hospital mortality for esophageal resection has dramatically decreased over the past two decades and is currently well below 10% in most esophageal centres. However, the procedure is still associated with substantial morbidity [1–3]. Because of the frequency and severity of complications associated with esophagectomy, surgeons must become familiar with each of the potential complications and take aggressive steps to anticipate and treat any problems that might arise in the postoperative period.

Hospital mortality Underscoring the importance of appropriate management of postoperative complications, operative mortality has been shown to be inversely related to surgeon experience [4,5]. In a retrospective review of esophagectomies performed for cancer, 42 patients were operated on by surgeons who performed six or more esophagectomies per year and 32 patients were operated on by surgeons who performed five or fewer esophagectomies per year. In the 42 patients operated on by frequent surgeons, there were three (7%) anastomotic leaks and no operative deaths. In 32 patients operated on by occasional surgeons, there were seven (22%) anastomotic leaks and seven (22%) operative deaths. The difference in anastomotic leak rates approached but did not quite reach statistical significance (7% vs. 22%, P < 0.07) and frequent surgeons had a significantly lower operative mortality (0% vs. 7%, P < 0.001) [5]. A retrospective study attempted to determine if increased hospital volume as well as surgeon frequency for selected surgical oncology procedures is associated with a decreased operative mortality. Over 5000 patients were identified in the Surveillance, Epidemiology, and End Results (SEER)-Medicare linked database who underwent esophagectomy, pneumonectomy, pancreatectomy, liver resection, or pelvic exenteration for cancers of the esophagus, lung, colon and rectum, and various genitourinary cancers diagnosed between 1984 and 1993. Higher hospital volume was linked with lower operative mortality for esophagectomy (P < 0.001), pancreatectomy (P = 0.004), liver resection (P = 0.04), or pelvic exenteration (P = 0.04), but not for pneumonectomy (P = 0.32). The most striking results were for esophagectomy in which the 161

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operative mortality was 17.3% in low-volume hospitals compared with 3.4% in high-volume hospitals [6].

Patient selection Although individual surgical expertise and familiarity of all hospital personnel with the management of patients after esophagectomy are important, the selection of patients who have adequate physiological reserves to withstand an extended operation and a potentially complicated postoperative course remains an important responsibility of the surgeon. In an attempt to define objective criteria that might help to identify those patients unable to tolerate esophagectomy, a three-phase study was undertaken [7]. In phase I, the records of 432 patients who underwent esophagectomy from 1982 to 1991 were retrospectively reviewed. From this analysis, four parameters were identified that correlated with morbidity and mortality after esophagectomy: (i) Karnofsky index < 80%, (ii) aminopyrine breath test < 0.4, (iii) vital capacity < 90%, and (iv) PaO2 < 70 mmHg. Using this information, they devised a composite risk score incorporating a multiplier factor based on the relative risk associated with each individual factor: general status × 4, cardiac function × 3, pulmonary function × 2, and hepatic function × 2 (Table 10.1). Summation of the results creates a single composite score ranging from 11 points in those patients without any risk factors to 33 points for a patient with the highest risk in all categories. Table 10.1 Classification of individual organ dysfunction.

General status Normal Compromised Severely impaired Cardiac function Normal Compromised Severely impaired Pulmonary function Normal Compromised Severely impaired Hepatic function Normal Compromised Severely impaired

Objective data

Score*

Karnofsky index > 80% and good cooperation Karnofsky index ≤ 80% or poor cooperation Karnofsky index ≤ 80% and poor cooperation

1 2 3

Normal risk for major surgical procedure Increased risk for major surgical procedure High risk for major surgical procedure

1 2 3

VC > 90% and PaO2 > 70 mmHg VC < 90% or PaO2 < 70 mmHg VC < 90% and PaG2 < 70 mmHg

1 2 3

Aminopyrine breath test > 0.4 Aminopyrine breath test < 0.4, no cirrhosis Cirrhosis

1 2 3

*A composite risk score was created by incorporating a multiplier factor based on the relative risk associated with each individual factor: general status × 4, cardiac function × 3, pulmonary function × 2, and hepatic function × 2. Summation of the results creates a single composite score ranging from 11 points in those patients without any risk factors and 33 points for a patient with the highest risk in all categories.

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In phase II, prospective evaluation of this composite scoring system in 121 consecutive patients undergoing esophagectomy for esophageal cancer confirmed the ability of the scoring system in predicting postoperative course. Postoperative mortality was 2% in 46 patients classified as low risk (11–15 points), 5% in 55 patients classified as moderate risk (16–21 points), and 25% in the 20 classified as high risk (22–33 points). Operative mortality was significantly higher in patients categorized as high risk compared with moderate risk (P < 0.05), and low risk (P < 0.01). Importantly, of the nine patients who died postoperatively, five had a score of 22 points or greater. In phase III of this study, the authors used the scoring system to determine how to manage these patients with esophageal cancer. Use of the two-stage esophageal reconstruction (resection and delayed reconstruction 4 weeks later) in moderate and high-risk patients or complete exclusion of these patients from esophageal resection resulted in a marked reduction in the 30-day postoperative mortality rate from 7.4% to 1.6% in 252 patients who underwent esophagectomy. Although rigid adherence to this system may exclude some patients from esophagectomy who might otherwise survive operation, it does provide an objective means to identify those patients at greatest risk of death after esophagectomy for whom palliative measures such as stenting and/or radiation therapy might be more appropriate.

General complications Cardiac complications The most common cardiac complications after esophagectomy are supraventricular tachydysrhythmia (SVT) and myocardial infarction. After obtaining a careful history identifying a patient’s functional capacity and risk factors for atherosclerotic cardiovascular disease, the need for further cardiovascular investigation is individualized based on the patient’s risk of developing perioperative cardiac events [8,9]. Identification of cardiac ischemia on preoperative stress electrocardiography or thallium studies mandates a complete evaluation prior to proceeding with esophagectomy. In an effort to identify the incidence of cardiac complications after esophagectomy, 100 consecutive patients who underwent transhiatal esophagectomy without a prior history of cardiac arrhythmias were prospectively studied. The postoperative incidence of SVT was 13% and the incidence of acute myocardial infarction was 1%. SVT was associated with hemodynamic compromise in nine (69%) of 13 patients and myocardial ischemia in four (31%) of 13. One patient required immediate cardioversion for a systolic arterial pressure < 70 mmHg. After controlling the ventricular rate with diltiazem, no patient had evidence of ongoing myocardial ischemia or infarction. The one myocardial infarction in the study resulted in the patient’s death [10]. Two episodes of SVT developed late in the postoperative period (days 10 and 28) and were associated with sepsis. The median time to development of SVT was 72 h (range 16–576), suggesting that availability of cardiac telemetry in the first 3–5 days of the postoperative period is advisable.

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Deep venous thrombosis/pulmonary embolus Deep venous thrombosis (DVT) and pulmonary embolism (PE) represent serious complications in surgical patients. Although the exact incidence is unknown in patients undergoing esophagectomy, the overall incidence of DVT and PE in general surgical patients has been calculated by pooling data from control patients in published trials examining the effectiveness of prophylactic methods [11]. The overall incidence of DVT using fibrinogen uptake tests and phlebography confirmation was 19%. In surgical patients with malignant disease, the incidence of DVT was 29%. In this analysis, the incidence of clinically recognized PE and fatal PE was 1.6% and 0.9%, respectively. Because patients undergoing esophagectomy are considered at highest risk of developing a DVT or fatal PE (major surgery in patients > 40 years plus malignant disease), all patients should receive preoperative prophylaxis. Successful preventive strategies include low-molecular-weight heparin, lowdose unfractionated heparin, intermittent pneumatic compression stockings, or oral anticoagulation. In a prospective randomized study of 2551 patients who had cardiac surgery, the combination of low-dose unfractionated heparin with intermittent pneumatic compression stockings resulted in a lower incidence of PE compared with patients receiving low-dose unfractionated heparin alone (1.5% vs. 4%, P < 0.001) [12]. Based on this information, all patients should have pneumatic compression stockings placed before the induction of anesthesia and used throughout the postoperative period until the patient is ambulating on his own. In addition, subcutaneous low-dose unfractionated heparin is given every 12 h until the time of discharge from the hospital.

Complications associated with esophageal resection Anastomotic leaks Anastomotic dehiscence is the most serious complication associated with esophageal resection. The rate of anastomotic leak and its associated morbidity and mortality vary depending on the location of the esophagogastric anastomosis. In a meta-analysis of the literature of the surgical treatment of patients with esophageal carcinoma by Muller [13], the anastomotic leak rate for intrathoracic anastomoses was significantly lower compared with cervical anastomoses (11 ± 6% vs. 19 ± 15%). However, the mortality associated with an intrathoracic leak was three times higher (69 ± 16% vs. 20 ± 11%). In contrast, a single group compared its experience with cervical anastomoses and thoracic anastomoses and found no statistical difference in anastomotic leak rate (4.3% vs. 3.7%) or mortality associated with anastomotic leak (40% vs. 36%) [14]. In a more recent review, Urschel categorized esophagogastric anastomotic leaks into four groups according to their clinical presentation and subsequent outcome [15]. Group 1 constitutes early fulminant leaks that present within the first 48 h and are usually caused by gastric (or colonic) necrosis. These patients

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present with purulent chest tube drainage and septic shock and require immediate thoracotomy, resection of non-viable portions of the stomach, cervical end esophagostomy, and abdominal gastrostomy. This complication occurs infrequently but is usually fatal even with prompt aggressive treatment. Group 2 includes clinically apparent but less catastrophic thoracic leaks. These leaks are often identified by the development of a pneumothorax or pleural effusion associated with septic deterioration. The three critical principles in the management of this problem are: (i) complete drainage of the pleural space, (ii) adequate control of the esophagogastric fistula, and (iii) reexpansion of the lung. Small anastomotic leaks will often heal if the lung is completely expanded because the visceral pleura functions to buttress the leak. Chest tube drainage alone, thoracoscopic drainage and repair, and reoperative thoracotomy with direct repair and muscle flap reinforcement of the leak can all be successfully used to treat this complication as long as adherence to the above principles is followed. Because the mortality associated with intrathoracic anastomotic dehiscence approaches 60% [13,16,17], an aggressive approach to this problem is required. The third group consists of clinically apparent cervical leaks. These patients often develop wound erythema and crepitus associated with fever and an elevated white blood cell count. Initial management requires reopening the wound at the bedside. In the majority of patients, the leak will be contained in the neck by the surrounding tissues and frequent dressing changes are all that is required. However, a small subset of patients with esophagogastric anastomoses constructed via a cervical approach will leak into the mediastinum or pleural space and will require the aggressive approach described above for clinically apparent thoracic leaks. The overall mortality associated with these clinically apparent leaks from cervical anastomoses has been reported to be 20% [13], indicating the importance of managing these patients appropriately. Clinically silent leaks are found incidentally during routine postoperative contrast studies in patients with no systemic signs of infection. The leak identified is contained by surrounding structures and often drains back into the lumen through the anastomotic defect. Management of these leaks is dictated by their location and the patient’s clinical course. In the absence of signs of infection, the patient is simply maintained on intravenous fluids and/or jejunostomy tube feedings until repeat radiological studies document anastomotic healing. Contained leaks close to the aorta and the trachea should be drained because of the risk of developing fistulas to these vital structures [18–20]. In addition, radiographic progression of the leak or clinical deterioration of the patient mandate immediate drainage of the leak.

Anastomotic stricture Dysphagia following esophageal resection as a result of narrowing at the anastomosis occurs frequently in the postoperative period. The need for anastomotic dilation ranges from 5% to 44%, but the incidence of true anastomotic stricture is much lower [21–24].

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Stricture formation in the immediate postoperative period is probably related to inflammatory changes associated with wound healing. In support of this hypothesis, the incidence of postoperative stricture has been shown to increase if there is a postoperative anastomotic leak [24]. The treatment of early strictures consists of dilation with either the mercury-tipped Maloney dilators (46–50 Fr) or with the Savory dilators (12–60 Fr) over a guide-wire under fluoroscopic control. Most anastomoses require only a single dilation, but up to 10% will persist and require repeated dilations. Delayed stricture formation most commonly is a result of either recurrent carcinoma or reflux esophagitis. An aggressive search for anastomotic recurrence including barium swallow, contrast-enhanced computed tomography imaging of the chest, and esophagoscopy with biopsy is necessary prior to initiating anastomotic dilation. In the absence of recurrent cancer, most strictures can be easily dilated. Persistent strictures can be resected and new cervicogastric anastomoses can be constructed.

Dumping syndrome Sweating, palpitations, tachycardia, nausea, and epigastric distension following meals in patients undergoing esophagogastrectomy represent symptoms of the dumping syndrome. These intestinal vasomotor symptoms are thought to occur because of the rapid transit of hyperosmolar gastric contents into the jejunum resulting in rapid hyperglycemia followed by reactive hypoglycemia. Although most patients will report some symptoms attributable to the dumping syndrome early in the postoperative period, dietary modifications including multiple small meals, avoidance of fluids during meals, avoidance of milk products and high carbohydrate meals and the occasional use of antidiarrheal medications allow the patient to overcome these symptoms within the first year after esophageal resection.

Delayed gastric emptying Delayed gastric emptying occurs in a minority of patients following esophagogastrectomy and has been attributed to any of a number of factors. Vagotomy, torsion of the stomach into the posterolateral gutter of the right chest, the size of the gastric conduit, the pressure gradient between the intrathoracic stomach and the abdominal duodenum, compression of the distal stomach at the level of the diaphragmatic hiatus, and the lack of a drainage procedure have all been associated with this complication. Those patients with delayed gastric emptying are at increased risk of aspiration pneumonia and ultimately impaired oral alimentation. Gastric outlet obstruction at the level of the pylorus should be addressed at the time of the original operation. One prospective, randomized trial studying the effect of pyloroplasty vs. no drainage in a group of patients undergoing Ivor-Lewis esophagogastrectomy found that pyloroplasty decreased the amount of nasogastric aspirate, the gastric emptying time by radioisotope study, and long-term symptoms of gastric outlet obstruction [25]. It would

Complications of esophageal resection 167

therefore seem reasonable to perform a pyloroplasty or a pyloromyotomy in all patients during reconstruction after esophagogastrectomy. In addition, the diaphragmatic hiatus should comfortably admit three or four fingers alongside the stomach at the completion of the operation to allow free flow of gastric contents into the duodenum. This may necessitate an incision in one or both pillars of the esophageal hiatus. Delayed gastric emptying early in the postoperative period is often caused by mucosal edema at the level of the pyloromyotomy or pyloroplasty and generally resolves within 10–14 days. During this interval it is important to keep the stomach decompressed to prevent aspiration and to decrease tension on the esophagogastric anastomosis. In those patients with persistent delayed gastric emptying after 14 days, erythromycin has been shown to improve emptying [26,27].

Respiratory complications Pulmonary complications including atelectasis, pneumonia, and respiratory insufficiency result in significant morbidity and mortality after esophagectomy regardless of technique used. The incidence of pulmonary complications ranges from 25% to 47%, and these complications are responsible for many of the deaths that occur after esophagectomy [1,2]. Cessation of smoking combined with an exercise program including the use of incentive spirometry for at least 2 weeks is an important part of the patient’s preoperative preparation. Adequate perioperative and postoperative analgesia using epidural catheters and patient-controlled analgesia has been shown to decrease the incidence of pulmonary complications especially in patients who underwent a transthoracic esophagectomy [28]. These should be routinely incorporated into the postoperative care of these patients so that they can cough and breath deeply, thus clearing secretions and maintaining bronchoalveolor expansion. The use of postoperative ventilatory assistance by keeping the patient on a ventilator the night of operation was used previously. However, extubation can safely be performed postoperatively as soon as the patient is awake, maintaining satisfactory ventilation and has a good gag reflex [29]. Prevention of aspiration and the control of pulmonary secretions are the two most important factors in decreasing the incidence of postoperative respiratory complications. Elevation of the head of the patient and decompression of the gastric tube or colon interposition graft using a nasogastric tube are required in the postoperative period until the return of gastrointestinal function. Ambulation and chest physiotherapy are initiated on the first postoperative day and continued until the time of discharge. In those patients with significant bronchorrhea after esophagectomy, daily therapeutic bronchoscopy at the bedside is performed until the patient is independently able to mobilize his secretions on his own. This is especially important in those patients who have sustained a recurrent laryngeal nerve injury.

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Chylothorax Chylothorax following esophagectomy has an incidence ranging from 0.4% to 2.7% [30,31]. However, this complication is poorly tolerated in nutritional depleted patients with esophageal cancer and mortality rates as high as 50% have been reported. Postoperative chylothorax presents as persistently elevated chest tube output that increases with the initiation of oral intake. As the patient’s oral or feeding tube diet is advanced to include a higher fat content, the chest tube output becomes milky white. Definitive diagnosis can be confirmed by determining the triglyceride content of the output, but this is often unnecessary. In equivocal cases, a triglyceride level in the pleural fluid of > 110 mg/dl is associated with a 99% chance of a chylous leak, whereas a triglyceride level of < 50 mg/dl has less than a 5% chance of a chylous effusion [32]. Prevention of unrecognized thoracic duct injuries and subsequent chylothorax requires careful dissection along the course of the thoracic duct during esophagectomy. The thoracic duct begins at the confluence of the cisterna chyli in the abdomen and enters the thorax through the aortic hiatus posterior to the aorta and anterior to the vertebral bodies of T10–L2. It then ascends just to the right of the anterior surface of the vertebral bodies between the aorta and the azygous vein in the right hemithorax. At the level of the T4 and T5 vertebral bodies, the duct crosses over to the left side of the spine and passes behind the aortic arch and into the neck. In the neck, the duct passes posteriorly to the carotid sheath and drains into the junction of the left jugular and subclavian veins. Any injury to the thoracic duct identified intraoperatively should be managed with ligation of all tissues lying between the azygous vein and the descending aorta. Careful inspection of the thorax along the course of the duct should be performed to identify chylous leaks prior to closure of the thorax. The management of chylothorax after esophagectomy remains controversial, with advocates of both conservative therapy and immediate surgical intervention. Conservative management usually includes total parenteral nutrition, alone, or in combination with medium-chain triglyceride enteral formulas. Surgical intervention is usually performed via a right thoracotomy with ligation of the thoracic duct as it enters the thorax. Early surgical ligation of the thoracic duct after recognition of a chylous leak effectively controls this complication [33], but requires either an open right thoracotomy or a videoassisted approach and anterior retraction of the gastric or colonic conduit in the early postoperative period. Conservative management of this complication results in closure of the chylous fistula in approximately 80% of patients within 14–35 days, but has associated nutritional and septic complications [34,35]. In an effort to identify those patients who will spontaneously seal their chylous fistula without surgical intervention, Dugue et al. [31] retrospectively examined their experience in 23 patients who developed chylothorax after Ivor-Lewis esophagectomy. Initial management included unilateral or bilateral chest drainage and total parenteral nutrition as soon as the diagnosis

Complications of esophageal resection 169

of chylothorax was established. Conservative treatment was continued for at least 12 days, after which reoperation through the previous right thoracotomy was attempted if daily chest tube output was > 500 mL/day or the lung was not reexpanded. Just prior to reoperation, a cream-rich diet was administered via the nasogastric tube or feeding enterostomy to facilitate identification of the chylous leak. Conservative management resulted in successful recovery in 14 (61%) of 23 patients. In these patients, chest drainage was stopped after a mean of 9 days (range 3–17) and initiation of enteral nutrition within 12 days (range 7–21) without the recurrence of the chylous effusion. Conservative therapy was complicated in one patient who developed sepsis from his central venous catheter. In nine patients, conservative therapy did not result in closure of the chylous leak. These patients underwent reoperation after a mean of 18 days (range 12–27). Reoperation with identification and ligation of the chylous fistula was successful in all nine patients. However, two patients died from sepsis associated with anastomotic dehiscence. Retrospective analysis of the data identified one variable that was reliable for differentiating those patients in whom conservative therapy succeeded from those who required operation. Chylous drainage from the chest tube on postoperative day 5 was < 10 ml/kg in 12 of 14 patients (mean 6.7 ± 5.5 ml/kg) who did not require reoperation and > 10 ml/kg in all patients (mean 23.5 ± 16.6 ml/kg) who underwent reoperation. Using this information, any patient with a chylous output of > 10 ml/kg on postoperative day 5 should be returned to the operating room for either an open or a video-assisted transthoracic ligation of the thoracic duct. Administration of heavy cream containing methylene blue via the feeding jejunostomy for 4 h prior to surgery facilitates identification of the leak and should be utilized in all patients. In addition to identification and ligation of the leak, supradiaphragmatic ligation of all tissues between the azygous vein and the aorta is performed during reoperation.

Recurrent laryngeal nerve injury Injury to the recurrent laryngeal nerve during esophagectomy results in significant postoperative morbidity. The recurrent laryngeal nerve supplies motor function to the intrinsic muscles of the larynx (except for the cricothyroid muscle which is supplied by the external laryngeal nerve) and supplies sensory fibers to the mucous membrane of the larynx below the vocal folds. Although hoarseness is often the initial presenting sign in patients with this injury, the risk of aspiration and the development of pneumonia represent its most serious consequences. Because recurrent laryngeal nerve injury results in inability to generate a vigorous cough, postoperative pulmonary toilet is severely compromised and the risk of postoperative pneumonia is increased. In addition, cricopharyngeal motor dysfunction and its associated dysphagia combined with an inability to completely appose the vocal cords markedly increase the risk of aspiration in these patients.

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The reported incidence of recurrent laryngeal nerve injury after esophagectomy ranges from 3% to 45% [1,24,36–38]. Higher vocal cord palsy rates have been reported in those series utilizing the extended radical esophagectomy technique; however, this is not a universal finding. Baba et al. and Nishimaki et al. reported vocal cord palsy rates of 33% and 45%, respectively, whereas Altorki et al. had only a 6% incidence. Although the majority of patients suffer only transient vocal cord paralysis, its impact on postoperative pulmonary care is significant. The injury to the recurrent nerve most commonly occurs in the neck; therefore, care must be taken in that location. It is important to keep the plane of dissection on the esophageal muscle when mobilizing the esophagus from the trachea to minimize the chances of injuring the nerve in the tracheo–esophageal groove. Additionally, avoiding the use of metal retractors against the medial cervical structures and the use of forceps in the area of the tracheo–esophageal groove will diminish the odds of traumatizing the nerve. Vocal cord paralysis may not become apparent until the third postoperative day or later when patients are noted to have difficulty generating a vigorous cough. This delay in presentation is thought to be caused by a gradual decrease in vocal cord edema in the postoperative period resulting in abduction of the paralyzed cord and an inability to generate pressure against a closed glottis. The diagnosis is often confirmed at the time of therapeutic bronchoscopy for retained secretions and bronchorrhea. Optimal management of these patients includes repeated therapeutic bronchoscopy and ultimately medialization of the paralyzed vocal cord prior to the initiation of oral intake.

References 1 Altorki NK, Girardi L, Skinner DB. En bloc esophagectomy improves survival for stage III esophageal cancer. J Thorac Cardiovasc Surg 1997; 114: 948–955. 2 Ferguson MK, Martin TR, Reeder LB et al. Mortality after esophagectomy: risk factor analysis. World J Surg 1997; 21: 599–603. 3 Kelsen DP, Ginsberg R, Pajak TF et al. Chemotherapy followed by surgery compared with surgery alone for localized esophageal cancer. N Engl J Med 1998; 339: 1979–1984. 4 Matthews HR, Powell DJ, McConkey CC. Effect of surgical experience on the results of resection for oesophageal carcinoma. Br J Surg 1986; 73: 621–623. 5 Miller JD, Jain MK, de Gara CJ et al. Effect of surgical experience on results of esophagectomy for esophageal carcinoma. J Surg Oncol 1997; 65: 20–21. 6 Begg CB, Cramer LD, Hoskins WJ et al. Impact of hospital volume on operative mortality for major cancer surgery. JAMA 1998; 280: 1747–1751. 7 Bartels H, Stein HJ, Siewert JR. Preoperative risk analysis and postoperative mortality of oesophagectomy for resectable oesophageal cancer. Br J Surg 1998; 85: 840–844. 8 Eagle KA, Brundage BH, Chaitman BR et al. Guidelines for perioperative cardiovascular evaluation for noncardiac surgery. Report of the American College of Cardiology/ American Heart Association Task Force on Practice Guidelines. Committee on Perioperative Cardiovascular Evaluation for Noncardiac Surgery. J Am Coll Cardiol 1996; 27: 910–948.

Complications of esophageal resection 171 9 Mangano DT, Goldman L. Preoperative assessment of patients with known or suspected coronary disease. N Engl J Med 1995; 333: 1750–1756. 10 Amar D, Burt ME, Bains MS et al. Symptomatic tachydysrhythmias after esophagectomy: incidence and outcome measures. Ann Thorac Surg 1996; 61: 1506–1509. 11 Clagett GP, Anderson FA Jr, Geerts W et al. Prevention of venous thromboembolism. Chest 1998; 114: 531S–560S. 12 Ramos R, Salem BI, De Pawlikowski MP et al. The efficacy of pneumatic compression stockings in the prevention of pulmonary embolism after cardiac surgery. Chest 1996; 109: 82–85. 13 Muller JM, Erasmi H, Stelzner M et al. Surgical therapy of oesophageal carcinoma. Br J Surg 1990; 77: 845–857. 14 Lam TC, Fok M, Cheng SW et al. Anastomotic complications after esophagectomy for cancer. A comparison of neck and chest anastomoses. J Thorac Cardiovasc Surg 1992; 104: 395–400. 15 Urschel JD. Esophagogastrostomy anastomotic leaks complicating esophagectomy: a review. Am J Surg 1995; 169: 634 –640. 16 Patil PK, Patel SG, Mistry RC et al. Cancer of the esophagus: esophagogastric anastomotic leakaa retrospective study of predisposing factors. J Surg Oncol 1992; 49: 163–167. 17 Tam PC, Fok M, Wong J. Reexploration for complications after esophagectomy for cancer. J Thorac Cardiovasc Surg 1989; 98: 1122–1127. 18 Marty-Ane CH, Prudhome M, Fabre JM et al. Tracheoesophagogastric anastomosis fistula: a rare complication of esophagectomy. Ann Thorac Surg 1995; 60: 690–693. 19 Bartels HE, Stein HJ, Siewert JR. Tracheobronchial lesions following oesophagectomy: prevalence, predisposing factors and outcome. Br J Surg 1998; 85: 403–406. 20 Matory YL, Burt M. Esophagogastrectomy: reoperation for complications. J Surg Oncol 1993; 54: 29–33. 21 Dewar L, Gelfand G, Finley RJ et al. Factors affecting cervical anastomotic leak and stricture formation following esophagogastrectomy and gastric tube interposition. Am J Surg 1992; 163: 484–489. 22 Mathisen DJ, Grillo HC, Wilkins EW Jr et al. Transthoracic esophagectomy: a safe approach to carcinoma of the esophagus. Ann Thorac Surg 1988; 45: 137–143. 23 Wong J, Cheung H, Lui R et al. Esophagogastric anastomosis performed with a stapler: the occurrence of leakage and stricture. Surgery 1987; 101: 408–415. 24 Orringer MB, Marshall B, Stirling MC. Transhiatal esophagectomy for benign and malignant disease. J Thorac Cardiovasc Surg 1993; 105: 265–276. 25 Fok M, Cheng SW, Wong J. Pyloroplasty versus no drainage in gastric replacement of the esophagus. Am J Surg 1991; 162: 447–452. 26 Burt M, Scott A, Williard WC et al. Erythromycin stimulates gastric emptying after esophagectomy with gastric replacement: a randomized clinical trial. J Thorac Cardiovasc Surg 1996; 111: 649–654. 27 Hill AD, Walsh TN, Hamilton D et al. Erythromycin improves emptying of the denervated stomach after oesophagectomy. Br J Surg 1993; 80: 879–981. 28 Tsui SL, Law S, Fok M et al. Postoperative analgesia reduces mortality and morbidity after esophagectomy. Am J Surg 1997; 173: 472–478. 29 Caldwell MT, Murphy PG, Page R et al. Timing of extubation after oesophagectomy. Br J Surg 1993; 80: 1537–1539. 30 Cerfolio RJ, Allen MS, Deschamps C et al. Postoperative chylothorax. J Thorac Cardiovasc Surg 1996; 112: 1361–1365.

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31 Dugue L, Sauvanet A, Farges O et al. Output of chyle as an indicator of treatment for chylothorax complicating oesophagectomy. Br J Surg 1998; 85: 1147–1149. 32 Staats BA, Ellefson RD, Budahn LL et al. The lipoprotein profile of chylous and nonchylous pleural effusions. Mayo Clin Proc 1980; 55: 700–704. 33 Orringer MB, Bluett M, Deeb GM. Aggressive treatment of chylothorax complicating transhiatal esophagectomy without thoracotomy. Surgery 1988; 104: 720–726. 34 Marts BC, Naunheim KS, Fiore AC et al. Conservative versus surgical management of chylothorax. Am J Surg 1992; 164: 532–534. 35 Bolger C, Walsh TN, Tanner WA et al. Chylothorax after oesophagectomy. Br J Surg 1991; 78: 587–588. 36 Baba M, Aikou T, Natsugoe S et al. Quality of life following esophagectomy with threefield lymphadenectomy for carcinoma, focusing on its relationship to vocal cord palsy. Dis Esoph 1998; 11: 28–34. 37 Gillinov AM, Heitmiller RF. Strategies to reduce pulmonary complications after transhiatal esophagectomy. Dis Esoph 1998; 11: 43–47. 38 Nishimaki T, Suzuki T, Suzuki S et al. Outcomes of extended radical esophagectomy for thoracic esophageal cancer. J Am Coll Surg 1998; 186: 306–312.

CHAPTER 11

Complications of esophageal reconstruction Alex G Little

Introduction Esophageal reconstruction obviously follows upon an esophageal resection. Discussion of avoidance and treatment of complications of esophagectomy per se are reviewed in another chapter, while this chapter focuses on the reconstruction issues. The length of replacement organ required is dependent upon the amount or length of the esophagus which is resected, which is in turn dependent, among other factors, on whether or not the primary esophageal disease is malignant or benign. Reconstruction can require replacement of the entire length of the thoracic esophagus with a proximal anastomosis in the neck or replacement of a shorter length of esophagus with a proximal anastomosis in the chest. For reconstruction, either the stomach, colon, or jejunum are alternatives and any of them might be utilized. Finally, the location of the reconstruction can be either in the native bed of the esophagus in the posterior mediastinum, in a substernal location, or even above the sternum in a subcutaneous location. It is also the case that reconstruction of the esophagus must restore both anatomic and functional continuity; failure or complications can take place from either or both perspectives.

Anatomic complications The principal anatomic issues related to complications of esophageal reconstruction are anastomotic leak, which is an early complication, and anastomotic stricture formation, which is typically identified weeks or months after the operation. These are really two sides of the same coin and will be discussed together as some of the causes of either one of these two complications are also implicated in the etiology of the other [1]. Further, anastomoses that leak are more likely to stricture than those that do not. This is because the intense local inflammation and the ultimate wound-healing process, with collagen deposition and wound contraction, which follow exposure of the local tissues to enteric contents and purulent material, inevitably result in constriction and narrowing of the anastomosis.

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Prevention Organ selection The choices for reconstruction are stomach, colon or jejunum. Each has advantages and disadvantages, but the stomach is usually preferred because of the reliability of the blood supply to the apex of the fundus [2]. In fact, regardless of the organ which is utilized, the arterial flow to and venous drainage from the part of the interposed organ most distal from the origin of its blood supply are probably the most important factors which influence the healing process and therefore the fate of the anastomosis. Stomach When stomach is used, the whole stomach can be utilized following division of the gastro–esophageal junction [2,3]. This division should be on the gastric side of the junction and not on the esophagus so that a remnant of squamous epithelium exposed to gastric contents is not retained. This can lead to irritation and even erosion of the squamous island which is situated in a continually acidic environment. Alternatively, the lesser curve of the stomach, to include the left gastric artery and its proximal branches with accompanying lymph nodes, can be resected so that a tubular configuration of the interposed stomach is achieved (Figure 11.1) [2,3]. Utilization of techniques which create socalled gastric tubes from either the lesser or greater curve, such as the Heimlich gastric tube, is not necessary and probably has less reliable vascularization of the distal end than either whole stomach or the tubularized stomach. Resecting the lesser curve is also beneficial from an oncological perspective for cancer patients, as it removes lymph nodes which frequently contain tumor metastases; however, the stomach is shortened by a few centimeters compared with the whole stomach. Even so, the stomach tubularized in this fashion will still routinely reach the neck through both the posterior mediastinum and the substernal route without an increase in either leak or stricture rates compared with the whole stomach. Stomach preparation for esophageal replacement requires division of the left gastric and short gastric arteries, leaving perfusion of the fundus dependent on flow from the right gastroepiploic and the right gastric arteries through the intramural vascular network. Gentle and minimal handling of the fundus during gastric mobilization is important for preservation of the small vessels in this intramural plexus. If they are traumatized by rough handling or a clamp, the anastomosis of the esophagus will be to relatively ischemic tissue, increasing the likelihood of poor healing and therefore both leak and stricture. Colon A variety of colon segments can be developed depending on which artery the segment is based upon. When choices are not restricted by intrinsic colon disease such as divertulosis or prior surgery, I prefer a colon segment based on the ascending branch of the left colic artery as shown in Figure 11.2 [4,5]. The shorter the length of colon which is utilized, the more reliable is both

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Figure 11.1 The technique for resecting the gastro–esophageal junction and the lesser curve of the stomach. This both removes the lymph node bearing left gastric artery arcade and tubularizes the stomach. The stomach is not significantly shortened by this maneuver.

the arterial supply and the venous drainage, and the better is the result, i.e. the less likely is anastomotic leak. Regardless of the length of the colon segment, meticulous attention to detail is essential. Gentle handling of the mesentery and the colon itself minimizes trauma to the arterioles and venules; loss of blood flow through these small vessels because of spasm or thrombosis can render ischemic the distal tip of the colon and either leak or stricture of the anastomosis to the esophagus is the result. Jejunum Because of the anatomy of its vascular arcades, the jejunum will not usually bridge a long gap such as the distance from the abdomen to the neck or even the upper chest. Therefore, absent a microvascular anastomosis of mesenteric vessels to neck or internal mammary arteries or veins to ‘supercharge’ the

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Figure 11.2 This schematic drawing shows a segment of the left colon (so-called because it is based on the left colic artery) prepared for interposition. The colonic segment will be oriented isoperistaltically.

jejunal segment, jejunum is not often used for esophageal replacement/reconstruction and therefore will not be further discussed.

Route of reconstruction When the posterior mediastinum is available, this location for the replacement conduit is preferable to the more anterior anatomic options. The posterior location, the normal bed of the esophagus, is the shortest distance between the neck and abdomen and is the only possible placement for intrathoracic reconstruction [6]. This places both the arterial supply to and the venous drainage from the part of the interposed organ most distal to the origin of the blood supply in the least stressful situation. Not surprisingly then, the anastomotic leak rate is greater when the interposed organ is routed anteriorly, either beneath or above the sternum, than when placed posteriorly.

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Figure 11.3 The appearance of the bony elements of the thoracic inlet after resection of the clavicular head, first rib and manubrium to decompress this space.

Location of the anastomosis The esophageal anastomosis to the interposed organ can be in the neck or in the posterior mediastinum via either the right or the left chest. Predictably, the incidence of leak is higher when the anastomosis is in the neck [6]. This, presumably, is because the arterial supply is increasingly challenged the further the anastomosis is from the abdomen. Also, for the stomach to some extent but particularly for the colon, the venous drainage can be compressed and obstructed by passage through the esophageal hiatus or the thoracic inlet. Either side of the hiatus can and should be incised to decompress the hiatal aperture if there is any concern at this level. If the interposition is positioned substernally, compression at the thoracic inlet by the bony protuberance posteriorly created by the union of the clavicular head and first rib with the manubrium can occur. As shown in Figure 11.3, resection of these offending bony structures opens up the thoracic inlet and decompresses the passageway. This is carried out by mobilizing the pectoralis muscle from the manubrium and clavicle and using the electrocautery to detach strap muscles from the sternum and clavicle. The substernal space is developed bluntly with a finger as for a median sternotomy. An oscillating saw is then used to resect half of the manubrium, the clavicular head and the first rib. This dramatically enlarges the thoracic outlet and minimizes compression on the interposed organ. A clinical conundrum, however, in choosing between the neck and the chest for the anastomotic site is posed by the observation that although the leak rate is higher in the neck, mortality and morbidity are greater if there is an anastomotic leak in the chest [7]. Currently, however, leak rates are so low in both locations that this is not as much of an issue as just a few years earlier [7].

Anastomotic technique No clear-cut advantage has been conclusively demonstrated for any particular anastomotic technique regarding either leak or stricture. As long as the standard principles of constructing an anastomosis are followed and the blood supply of the interposed organ is adequate, choice of suture material, whether a running

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Figure 11.4 In this representation of a cervical esophagogastrostomy, the patient’s head is to the right. The esophagus is lying on top of the stomach and a gastrointestinal anastomosing stapler has been fired, creating an anastomosis between the esophagus and stomach. The ‘hood’ of esophagus will be sutured to the gastrotomy to achieve final closure. (Reprinted from [8], with permission from Elsevier.)

or interrupted sewing technique is employed, and even whether the anastomoses is hand sewn or stapled, do not seem greatly to matter. I have, however, become convinced that the anastomotic technique of choice is that described by Orringer and illustrated in Figure 11.4. In my hands, this technique has proved to be technically straightforward, i.e. easy. In addition, Orringer’s experience suggests this technique has the potential nearly to eliminate both early leak and late stricture occurrence at least for cervical anastomoses [8].

Treatment Leak Prompt diagnosis of an anastomotic disruption is extremely important. The longer a leak is untended, the more tissue contamination occurs and the

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greater the likelihood of septic complications. Therefore, a high level of suspicion is paramount. When an untoward, but non-specific event such as an unexplained fever or tachycardia intrudes on a previously benign clinical course, anastomotic leak must be considered and a prompt barium swallow should be obtained. A normal radiological study causes no harm, while early detection of a leak may permit salvage of the reconstruction and the patient. If the leak is from a cervical anastomosis, initial treatment consists of fully opening all layers of the neck incision and providing local wound care with packing of the wound with saline-soaked gauze while supporting the patient either with, preferably, enteral feeding via a jejunostomy, or parenteral nutrition. Only if ischemic necrosis of the esophageal substitute is present is it necessary to intervene surgically. If this situation does occur, the nonviable portions of the interposed organ must be resected. If this precludes immediate reanastomosis, stomach is returned to the abdomen and a feeding gastrostomy tube placed. After the patient has recovered, an alternative reconstruction can be attempted. If colon is involved, usually all of it is necrotic and must be removed. If only the distal tip is lost and there is a significant viable portion which can be retained in the neck, after the patient has recovered the gap between colon and esophagus can be bridged by a free flap of jejunum.

Stricture When dysphagia is manifested in the very early postoperative period, within the first few weeks, the patient should be kept on a soft diet in the expectation of improvement as perianastomotic edema and inflammation subside. If resolution of the swallowing difficulty does not take place or if difficulty swallowing manifests after a few months have passed, anastomotic stricture formation is the likely cause. Intervention should be swift so that further nutritional depletion does not occur. Endoscopy should be performed to rule out the slim possibility that recurrent carcinoma is present. In addition, I prefer to initiate dilation with Savary dilators passed over a wire placed during the endoscopy. Subsequent dilations can utilize either Savary or Maloney dilators. I believe multiple, gradual dilations are safer and more effective than abrupt, aggressive dilations. The use of balloon dilators has been reported, but I fear that anastomotic strictures might rupture and a gradual rather than an abrupt stretching process seems preferable.

Functional complications Even if anatomic continuity is restored following esophagectomy, there is no benefit if the patient is not able to sustain a reasonable quality of life and eat and drink in a fashion approximating normal, i.e. the reconstruction must function properly. Achieving this goal requires identification of and attention to technical maneuvers during surgery that can reduce the incidence of dysfunction.

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Prevention Stomach The ways in which gastric function can go awry are the occurrence of iatrogenic reflux, delayed gastric emptying and its opposite, rapid gastric emptying which causes the dumping syndrome. When stomach is used, the questions are whether to use the whole or the tubularized version and whether to perform a gastric emptying procedure. There is an enormous experience with the use of stomach as an esophageal substitute following esophagectomy for cancer and the functional results are generally satisfactory. Although the reported data are somewhat conflicting, the tubularized stomach seems to provide somewhat superior function than the whole stomach [3]. Peristalsis is not an important contributor to function of the transposed stomach but the tubularized configuration is less frequently associated with delayed emptying, probably because the smaller tube results in a rapid increase in intragastric pressure as the stomach fills because of the lower compliance of the gastric wall. This rise in intragastric pressure is presumed to facilitate gastric emptying [9]. Although most patients have satisfactory gastric emptying following gastric interposition, up to 20% of patients have dysphagia and regurgitation caused by trapping of gastric contents because of pylorospasm caused by vagotomy. For this reason, a judicious gastric emptying procedure is recommended [10–12]. An excessively aggressive pyloroplasty can allow rapid emptying of solids into the duodenum and dumping-type symptoms. I have found that a short Heinike–Mikulz pyloroplasty or a pyloromyotomy that divides all pyloric muscles but requires only three sutures to close achieves a reasonable balance. Gastric emptying is expedited but does not occur with such rapidity that dumping sequelae ensue.

Colon In general, the shorter the length of the colon interposition, the better the function and the greater the patient’s satisfaction with their ability to eat [4]. When colon is utilized, avoidance of redundancy is important, as if the segment sags it loops on itself and these loops can act as food traps, delaying emptying causing dysphagia and permitting aspiration. To prevent this complication the surgeon should use an appropriate, and not excessive, length of colon. This requires that the surgeon take care intraoperatively to account for the tendency of the harvested colon to develop spasm. If this is not done, when the colon relaxes, the excess length will be redundant. Although the colon contracts only infrequently, and does not immediately respond to the arrival of a food bolus, it has a peristaltic orientation which should be respected, i.e. the interposed segment should be oriented peristaltically [12]. Placing a colon segment antiperistaltically and hoping that food, salmon-like, will find its way upstream against the peristaltic gradient is foolishly hopeful.

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Treatment Stomach When a gastric emptying procedure is not performed initially and/or gastric retention occurs postoperatively because of the failure of pyloric relaxation, a prokinetic agent such as metoclopramide or erythromycin can be tried. If this clinical trial does not succeed, endoscopic balloon dilation of the pylorus is safe and usually effective. Reoperation to perform a pyloroplasty can be difficult, as the pylorus may be near or in the hiatus, but fortunately is rarely necessary. Most symptoms of dumping secondary to overly rapid gastric emptying will resolve without specific treatment. Encouraging water intake with meals and having the patient eat frequent small meals rather than large ones reduces the frequency and severity of the problem. Over time, symptoms typically relent and the patient can resume a more normal eating pattern.

Colon Normally, colonic transit occurs in an intermittent fashion, not continuously. It is therefore predictable that an interposed segment of colon is relatively inefficient and empties by gravity assisted by intermittent mass peristalsis. Occasionally, however, a colon interposition simply does not function sufficiently and therefore retains food and empties mainly by gravity. Symptomatically, patients have dysphagia and frequent regurgitation and may aspirate. This is a trying situation both for the patient and the surgeon, but when it becomes clear that the problem is functional and not anatomic (e.g. an anastomotic stricture is not the problem) then the alternative, if the stomach is available, is resection of the colon segment and replacement with a gastric interposition.

References 1 Dewar L, Gelfand G, Finley R et al. Factors affecting cervical anastomotic leak and stricture formation following esophagogastrectomy and gastric tube interposition. Am J Surg 1992; 163: 484–490. 2 Akiyama H, Miyazono H, Tsurumaru M et al. Use of the stomach as an esophageal substitute. Ann Surg 1978; 188: 606–610. 3 Collard JM, Tinton N, Malaise J et al. Esophageal replacement: gastric tube or whole stomach? Ann Thorac Surg 1995; 60: 261–267. 4 Curet-Scott MJ, Ferguson MK, Little AG. Colon interposition for benign esophageal disease. Surgery 1987; 102: 568–574. 5 Little AG, Skinner DB. Colon interposition for esophageal replacement. In: Cohn LH, ed. Modern Techniques in Cardiothoracic Surgery: Installment XII. Mount Kisco, NY: Futura Publishing Co., 1985; 77-1–77-15. 6 Ngan SYK, Wong J. Lengths of different routes for esophageal replacement. J Thorac Cardiovasc Surg 1986; 91: 790–792. 7 Hulscher JBF, Tijssen JGP, Obertop H, vanLanschot JJB. Transthoracic vs transhiatal resection for carcinoma of the esophagus: a meta-analysis. Ann Thorac Surg 2001; 72: 306–313.

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8 Orringer MB, Marshal B, Iannettoni MD. Eliminating the cervical anastomotic leak with a side-to-side stapled anastomosis. J Thorac Cardiovasc Surg 2000; 119: 277–288. 9 Bemelman W, Taat C, Slors JFM et al. Delayed postoperative emptying after esophageal resection is dependent on the size of the gastric substitute. J Am College Surgeons 1995; 180: 461–464. 10 Cheung HC, Wong J. Is pyloroplasty necessary in esophageal replacement by stomach? A prospective, randomized controlled trial. Surgery 1987; 102: 19–24. 11 Fok M, Cheng S, Wong J. Pyloroplasty versus no drainage in gastric replacement of the esophagus. Am J Surg 1991; 162: 447– 452. 12 Law S, Cheung M, Fok M, Chu KM, Won J. Pyloroplasty and pyloromyotomy in gastric replacement of the esophagus after esophagectomy: a randomized controlled trial. J Am College Surgeons 1997; 184: 630–636. 13 Little AG, Scott WJ, Ferguson MK et al. Functional evaluation of organ interposition for esophageal replacement, In: Siewert JR, Holscher AH, eds. Diseases of the Esophagus. Berlin: Springer-Verlag, 1988; 1067–1092.

CHAPTER 12

Complications of antireflux surgery Riivo Ilves, Mark R Dylewski

Introduction There are multiple surgical approaches for the treatment of patients with symptomatic gastroesophageal reflux disease (GERD). For many years surgeons debated the most appropriate route and technique by which an antireflux operation should be conducted, general surgeons advocating an abdominal approach with thoracic surgeons supporting a transthoracic approach. Today, the laparoscopic approach has been established as the approach of choice for the great majority of patients. Several alternative procedures such as the posterior gastropexy described by Hill in 1959 can only be performed through the abdomen, whereas others, such as the modified Belsey Mark IV (1952), the Nissen fundoplication (1955), and the Collis modifications (1957), can be constructed from a thoracic or abdominal approach. The answer to which route and technique is utilized is often dependent on the surgeon’s formal training as well as various physiological principles of GERD, which are beyond the scope of this chapter. Independently of the approach utilized, opinions differ regarding the quality of the various antireflux procedures currently available to surgeons. Many criticisms have been reported for each technique, a number of which are the result of technical challenges involved in performing these operations and the incidence of early and late surgical complications reported in the literature. The results of antireflux surgery published since the mid 1980s reveal that overall patient satisfaction is good to excellent in 86% (range 73–97%) of patients, whereas a poor outcome was obtained in 14% (range 3–33%) of patients [1,2]. The factors responsible for a poor outcome following antireflux surgery are numerous and may result from erroneous preoperative evaluation or patient selection, intraoperative technical misjudgement, iatrogenic complications, in addition to degradation or breakdown of the initial repair. The purpose of this chapter is to identify the pre-, intra-, and postoperative pitfalls and perils of antireflux surgery that contribute to the acute and long-term unsatisfactory results, and outline methods to manage these complications.

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Preoperative pitfalls Preoperative evaluation Surgical therapy for GERD was once reserved for patients who failed to respond to maximum medical therapy or for those who developed complications of the disease. However, since the improvement in surgical results and the advent of laparoscopic techniques, this is no longer the belief of many physicians. Current antireflux medical therapy is very effective in controlling symptoms in most patients with reflux. When an individual presents with symptomatic reflux completely refractory to medical therapy, one should be suspicious that reflux is not the cause of symptoms. Atypical respiratory and extra-esophageal symptoms secondary to GERD have been shown to respond to medical treatment [3]. Therefore, a high index of suspicion is required to conduct the proper preoperative evaluation and accurately identify and select the patients who will benefit from surgery. The goals of preoperative evaluation are fivefold: (i) to diagnose GERD, (ii) to identify the anatomical and physiological defect predisposing the individual to reflux, (iii) to exclude other etiologies for the patient’s symptoms, (iv) to document objective measures of the severity of reflux, and (v) to define the anatomy for surgical planning. These objectives are accomplished by performing a history and physical examination. In addition, more objective data are obtained from upper gastrointestinal series, esophagoscopy, manometry, and 24-h pH monitoring. The performance of a thorough history and physical examination cannot be understated in this patient population. Particular attention should be paid to excluding other etiologies that may be the underlying cause of the patient’s symptom complex. The disease is generally idiopathic in origin, occurring more commonly as the population grows older. Symptoms are often associated with a variety of exogenous factors (i.e. alcohol, spicy food, smoking, obesity, etc.). These factors may exacerbate the disease, but are rarely the primary cause [4]. There are a variety of medical diseases, natural physiological states and surgical procedures that predispose patients to symptoms that mimic GERD and require an experienced clinician to differentiate them from classical GERD. Such conditions are often resistant to standard medical therapy and result in failure of surgical treatment when they go unrecognized [3]. The prototype condition is achalasia, in which there is insufficient relaxation of the lower esophageal sphincter and aperistalsis of the esophageal body predisposing the patients to retention esophagitis which can mimic heartburn. In order to avoid erroneous diagnoses or a misadventure in patients being considered for reflux surgery, the workup should follow a logical and systematic algorithm. An upper gastrointestinal series should be the initial study performed in patients being evaluated for GERD. The benefit of this study is that it defines the anatomy of the esophagus, the cardia and the relationship of the gastro–esophageal (GE) junction to the esophageal hiatus. The presence

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of a foreshortened esophagus becomes an important detail in patients requiring antireflux surgery. Ferguson et al. documented a success rate for Nissen fundoplication of 75% in patients requiring surgical treatment of a distal esophageal stricture without shortening and an 85% success rate when a Collis-gastroplasty was added to a fundoplication in the presence of a foreshortened esophagus [5,6]. Furthermore, a barium study may demonstrate spontaneous and inducible reflux of barium in a retrograde fashion. Such a finding on barium swallow has a high correlation with abnormal gastroesophageal reflux. It excludes things such as gastric outlet obstruction, particularly in previously operated patients. Endoscopy is an essential part of the preoperative evaluation for GERD. It is particularly useful to exclude those less obvious lesions not well visualized on barium swallow. Contrast-enhanced radiography is relatively insensitive in diagnosing esophagitis and/or Barrett’s mucosa with dysplastic changes and even early in situ carcinoma. Barrett’s esophagus is suggested when the squamocolumnar junction is very irregular, with tongues of columnar epithelium extending cephalad; however, the endoscopic diagnosis is not always reliable. Therefore, if Barrett’s mucosa is suspected, it is imperative that one obtains histological confirmation and excludes malignant disease prior to proceeding with antireflux surgery. Biopsies should be performed in all four quadrants at the squamocolumnar junction and at multiple levels within the Barrett’s mucosa to determine histology. Brushings are also done for cytology. The presence of an esophageal stricture should be suspected prior to endoscopy. When present, the surgeon should attempt to determine the underlying etiology (benign peptic vs. malignant). This requires multiple biopsies. On occasion the length and diameter of the stricture may be significantly long and narrow, making it difficult to advance the endoscope and obtain adequate biopsies. Aggressive attempts at dilating the stricture using the endoscope should be condemned. If better visualization of the distal GE junction and stomach is needed in such circumstances a guide-wire should be advanced via the endoscope through the stricture. Under fluoroscopy, serial dilatations of the stricture can be performed using Savory dilators. If the distal esophageal stricture is determined to be non-dilatable, primary antireflux surgery is unlikely to be successful. Esophageal manometry provides essential information about the function of the upper and lower esophageal sphincters as well as the body of the esophagus. A discussion of the diagnostic findings on manometry is beyond the scope of this chapter, but there are some important facts to remember when considering whether to perform the study. The manometric studies are usually performed following the clinical examination, barium and endoscopic studies. Although numerous authors have debated the utility of manometry, its principal value is to exclude motility disorders. Some authors argue that little benefit is received from additional studies beyond endoscopy when patients present with classical clinical finding of GERD. In such patients who have failed medical management, these authors suggest that one can proceed with

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antireflux surgery with confidence that a motility disorder does not exist [7]. In our experience, we strongly recommend performing both manometry and 24-h pH studies if the patient has symptoms that are not typical of GERD or if there is any significant dysphagia or abnormal findings on initial clinical studies. Monitoring 24-h pH remains the gold standard for documenting GERD and quantifying the episodes of reflux. Much like manometry, patients who present with classical findings suggestive of reflux disease and are refractory to medical therapy may not require such documentation. Twenty-four-hour pH testing is particularly valuable in documenting gastroesophageal reflux in patients who present with atypical manifestations that do not respond to medical treatment. Other studies that have been utilized to evaluate GERD such as esophageal transit and gastric emptying studies, endoscopic ultrasound, and computed tomography scan are reserved for specific indications to help establish the diagnosis or evaluate the surgical anatomy.

Misdiagnosis Achalasia The complication that surgeons who perform antireflux surgery hope to avoid is performing an inappropriate fundoplication in patients with a primary motility disorder. According to Jamieson, the reason for failure of antireflux surgery and need for reoperative surgery in 4–16% of patients is an undiagnosed motility disorder [2,8]. The most common undiagnosed motility disorder is achalasia. It is a rare condition with an incidence of one case per 100 000 population. Early achalasia may have symptoms similar to reflux disease, and without esophageal manometry is difficult to recognize. The patient who has erroneously undergone a fundoplication will represent with severe postoperative dysphagia. It is imperative that a thorough preoperative evaluation be conducted. The earliest symptom of achalasia is dysphagia, described in nearly all patients as a postprandial sticking sensation in the substernal area. Occasionally the sensation is referred to the pharyngoesophageal region. Regurgitation has been reported in more than 70% of patients with achalasia. In later stages it may be reported to occur at sleep and be associated with a nocturnal cough and perhaps aspiration in 10%. Odynophagia is recorded in as many as 30% of patients. The pain is often described as radiating from the substernal area to the mid-back or jaw [2]. Even to the most experienced surgeon all of these subjective clinical findings can be erroneously linked to GERD. If a definitive diagnosis of achalasia is made a total fundoplication is not the appropriate treatment.

Scleroderma Scleroderma is a progressive systemic sclerosis that is characterized by generalized inflammation, vasculitis, and fibrosis of multiple organ systems including: skin, gastrointestinal tract, heart, lungs, and kidneys. Esophageal disease,

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namely gastroesophageal reflux, because of involvement and weakening of the muscle of the distal esophagus and lower esophageal sphincter (LES), has been documented in 70–90% of patients diagnosed with scleroderma. An important associated finding present in nearly all patients with scleroderma involving the esophagus is the presence of Raynaud’s phenomenon [2]. Therefore, patients with atypical symptoms who are refractory to medical therapy or those who present with recurrent disease following antireflux surgery should be questioned about episodes of Raynaud’s. There is no specific therapy for systemic scleroderma. The treatment of gastroesophageal reflux associated with scleroderma is primarily medical. More aggressive therapy is reserved for the development of complications of GERD. Peptic stricture should be treated with repeated dilatation. The indication for esophageal surgery in scleroderma patients includes refractory disease: peptic stricture causing dysphagia, intractable esophagitis, and documented pulmonary complications. Orringer et al. argue that antireflux surgery is effective in scleroderma and the presence of such a systemic disease is not a contraindication to surgery and does not affect long-term results [3,9]. Because of decreased esophageal motility, others have advocated a loose total fundoplication or partial (i.e. Belsey Mark IV) technique, combined with a Collis gastroplasty and stricture dilatation in patients with peptic stricture [10–12]. However, it remains unclear how well scleroderma patients do in long-term follow-up because of the rarity of this condition. In patients with refractory disease, severe esophagitis or peptic stricture and significantly depressed esophageal motility, some authors have advocated total esophagectomy with gastric pull-up for primary treatment because of the high likelihood of dysphagia developing after a standard antireflux procedure [13]. Because of the multifocal and progressive nature of scleroderma, which often leads to an early mortality, a cavalier approach to surgical therapy should be avoided. In our experience early recognition and optimal medical treatment with close followup have been effective in reducing symptoms and avoiding the development of the severe complication of GERD.

Miscellaneous Other conditions or disease processes that are associated with gastroesophageal reflux and should be considered include: pregnancy, irritable bowel syndrome, other upper GI surgery (partial gastrectomy, gastrojejunostomya Billroth I or II, etc.) and states of hypersecretion of acid such as Zollinger– Ellison syndrome [3].

Selection of operation Following the completion of the preoperative evaluation and the establishment of the diagnosis of GERD, the next step is to select the most appropriate antireflux procedure. The majority of patients that present for surgical evaluation have classic GERD secondary to poor LES tone and have essentially normal esophageal motility. The most popular antireflux operationathe Nissen

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fundoplicationais appropriate in this patient population. The Nissen fundoplication has many potential advantages. It is simple, reproducible, and easily adaptable to laparoscopic techniques. Although both patient and surgeon have embraced the laparoscopic Nissen fundoplication, it is important to realize that no single operative procedure is suitable for all patients with GERD. Surgeons who operate on the esophagus for GERD must have a thorough understanding of esophageal pathophysiology and the expertise to recognize those individuals with atypical symptoms that would be harmed by performing a total fundoplication. Surgeons must have the ability to tailor an antireflux procedure to a particular patient who may have a foreshortened esophagus from a peptic stricture or abnormal esophageal motility. Surgeons in this field must have within their armamentarium the ability to perform both partial and total fundoplications as well as Collis gastroplastic modifications and an esophageal myotomy in the appropriate setting. An algorithm for the selection of an appropriate operation is difficult to devise, particularly for patients who are atypical and have abnormal esophageal motility. The selection of the operation is based on several factors, including: the anatomic or physiological defect, the training and experience of the surgeon, his/her comfort level with a transthoracic or transabdominal approach and the various operative techniques. To the apprentice this decision tree may appear complex. However, there are a few basic principles to remember. Patients with gastroesophageal reflux and abnormal motor function experience a high incidence of dysphagia with a total fundoplication. Therefore, a partial fundoplication (Toupet, Belsey IV, Thal, Hill gastropexy, etc.) should be performed in those patients. Patients with classical severe reflux disease will have greater success with a 360° Nissen fundoplication, which results in a higher resting tone at the level of the LES. In patients with a foreshortened esophagus, benefit has been demonstrated from increasing the distal esophageal length by performing a Collis gastroplasty [14]. This technique reestablishes the natural position of the GE junction. A laparoscopic abdominal approach can be utilized for most patients with normal esophageal contractility and length. For patients with a shortened esophagus or an associated hiatal hernia, extended mobilization of the intrathoracic esophagus may be required. Some authors prefer the thoracic approach in this circumstance. However, in our experience adequate mobilization can be achieved via the abdominal approach and the complications associated with a thoracotomy can be avoided. The transthoracic or thoracoabdominal approach is reserved for patients with a hostile abdomen from prior surgery, recurrent hiatal hernia, or recurrent GERD who may require extended esophageal mobilization and Collis gastroplasty.

Intraoperative pitfalls Antireflux surgery is associated with a low operative mortality and morbidity, which differ only slightly depending on the technique utilized. Adherence to

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basic principles of antireflux surgery and paying meticulous detail to operative technique will minimize the frequency of complications. These principles apply whether an open or minimally invasive approach is utilized. With the recent enthusiasm for laparoscopic techniques in antireflux surgery, performance of these operations by surgeons unfamiliar with the principles of standard fundoplication and who have not yet advanced beyond the laparoscopic learning curve leads to an initial increase in technical errors accounting for operative complications or failure of the antireflux operation. Surgery for gastroesophageal reflux is associated with an acceptable incidence of morbidity and mortality when performed by experienced personnel. Complications are appropriately separated into acute perioperative events occurring intraoperatively or in the immediate postoperative period, and those occurring in a delayed manner. A number of the perioperative events that can occur following major abdominal or thoracic gastrointestinal surgery are not unique to antireflux surgery but are common to most surgical procedures. The primary focus of this section is to define the complications unique to the surgical approach or type of antireflux operation. The following discussion will center on detailing the potential operative pitfalls and perioperative complications for a variety of antireflux operationsaNissen fundoplication, Hill posterior gastropexy, Belsey Mark IV repair and the Collis gastroplasty modification.

Acute perioperative complications Serious perioperative complications of antireflux surgery are uncommon, with studies in the literature reporting morbidity ranging from 2% to 17% and mortality typically < 1% in properly selected candidates [15,16]. It is difficult to determine the exact incidence of acute perioperative complications because of the scarcity of reports with thorough documentation. However, a variety of complications associated with antireflux surgery and their rate of occurrence have been compiled from various sources (Table 12.1). The majority of this comprehensive list of complications is not exclusive to antireflux surgery but may develop following any major abdominal or thoracic operation and is only mentioned for the sake of completeness. The purpose of this section is to discuss the perioperative complications that are unique to the various types of antireflux operations and the methods to avoid these pitfalls.

Bleeding—splenic, hepatic and vascular injuries The spleen is particularly susceptible to unintentional injury during antireflux surgery. Small lacerations or capsular tears causing postoperative bleeding have been reported to range from 1% to 7% in most series [15,17]. Splenic injuries requiring total splenectomy occur in < 1% of all antireflux operations [6]. Most iatrogenic splenic lacerations occur during division of the short gastric arteries and mobilization of the gastric cardia. In general, splenic

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Incidence

Acute gastroesophageal avulsion Aortic injury (iatrogenic) Bleeding (non-splenic) Postoperative bowel obstruction Cardiac Deep venous thrombosis Dehiscence of Collis gastroplasty Esophageal/gastric perforation Esophageal/gastric obstruction Gastro-aortic fistula Gastric necrosis Gastric ulceration Hiatal stenosis Liver laceration Mesenteric ischemia Paraesophageal hernia Pneumonia/atelectasis Pneumomediastinum Pneumo/hemothorax Pulmonary embolism Splenic capsular tear Sepsis (no visceral leak) Subphrenic abscess Vagal nerve injury Wound dehiscence Wound infection (open) Wound infection (laparoscopic)

NR NR 5% NR 1% < 1.0% 1–2% 0–4% 2% NR NR NR NR 2–5% NR 1% 1–4% NR 2–5% 1% 1–7% 1–3% NR NR 1–2% 3–10% 0–2%

NR, Not referenced.

injuries occur regardless of the type of operative approach utilized. However, the frequency of operative splenic bleeding appears to be less in minimally invasive procedures and more frequent in reoperative surgery. The use of the harmonic scalpel via a laparoscopic or open abdominal approach significantly reduces the amount of manipulation and traction placed on the splenic hilum, and facilitates safe division of the short gastric arteries. Orringer and Sloan have reported technical difficulty when dividing the short gastric arteries through the esophageal hiatus during the transthoracic construction of a Belsey type fundoplication [18]. However, the incidence of significant splenic injuries is not different from that reported for other techniques. The authors suggest that if the Belsey technique is utilized, sequential division of the short gastric arteries (SGA) be performed until sufficient fundus is mobilized. An attempt at delivering the entire cardia into the chest prior to dividing the SGA may result in splenic injury. During the mobilization of the stomach, complete mobilization of the gastric fundus and cardia is required.

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There is a well-known pitfall during this maneuver that all surgeons should be familiar with, when performing either a Belsey repair or a Nissen fundoplication through the chest. The upper end of the gastrohepatic and gastrocolic omentum requires division to deliver the proximal fundus and cardia into the chest cavity. An anastomotic vessel between the ascending branch of the left gastric artery and the inferior phrenic artery referred to as ‘Belsey’s artery’ requires careful division. If splenic capsular injuries occur, most lesions can be repaired with standard splenic salvage techniques without significantly increasing the perioperative morbidity. Subphrenic abscesses are uncommon following a splenic injury. However, the incidence increases when splenic bleeding is associated with iatrogenic injury to the esophagus or stomach with contamination of the left subdiaphragmatic space. In this situation drainage of the subdiaphragmatic space has proven to be ineffective but perioperative antibiotic coverage should be considered [19]. In case of reoperative antireflux surgery or a suspected hostile abdomen, a preoperative bowel preparation is prudent. Mobilization of the left lobe of the liver can be difficult in one-third of patients and is associated with complications in up to 2–5% undergoing open or laparoscopic antireflux surgery [6]. Bleeding, bile leaks and collateral injuries to the diaphragm and heart can occur as a result of mobilization or aggressive retraction of the liver. The incidence of vascular injuries to the aorta, mesenteric arteries and veins, diaphragmatic vessels, iliac vessels, inferior vena cava, and hepatic veins (left) has been reported and remain unusual. The celiac axis is at risk during median arcuate ligament dissection for the Hill gastroplasty repair. These complications are more commonly associated with port placement during laparoscopic procedures, operations performed by inexperienced surgeons, aberrant anatomy and gross obesity.

Iatrogenic complications to the esophagus or stomach Intraoperative injuries to the esophagus and stomach are an infrequent occurrence during antireflux surgery. The incidence of these iatrogenic complications has been reported to be between 0 and 4% in various studies [6]. The incidence of perforating injuries to the stomach or esophagus during antireflux surgery in experienced hands does not appear to be related to any particular type of operation. However, the true percentage is difficult to determine due to insufficient data. Perforation of the esophagus and stomach in addition to other visceral organs is a particular risk in minimally invasive antireflux surgery. Most laparoscopic series of antireflux surgery report approximately a 1% incidence of perforation in experienced hands [20]. Perforation of the posterior aspect of the esophagus occurs when dissection of the posterior hiatus is performed. To avoid this, proper traction and counter traction dissection techniques should be utilized. The backside of a blunt dissecting instrument is used to lift the esophagus anteriorly while the other dissector

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is used to perform the posterior dissection. Once the esophagus is mobilized circumferentially, the esophagus should be encircled with a tape or Penrose drain, stapled or sutured together anteriorly in order to utilize it for traction. This technique essentially avoids handling the esophagus directly. The anterior esophageal wall is at risk when a bougie is passed through the GE junction to calibrate the tightness of the fundoplication. This is avoided by careful placement of the bougie and continued observation during an open or laparoscopic approach. Improperly using instruments can cause gastric perforations from avulsion injuries of the gastric wall due to aggressive traction. When recognized intraoperatively esophageal-gastric injuries generally can be repaired either laparoscopically or via an open technique without significant morbidity. When repairing a minor full-thickness esophageal injury, it is recommended that the mucosa and muscular layers be closed in two layers and buttressed with the fundoplication wrap. Injuries to the stomach are closed in the standard single or two-layer fashion. In the unusual situation that a perforation becomes apparent in the postoperative period, and is contained, an attempt at conservative management with antibiotics, parenteral nutrition and no oral intake may be successful. Overt contamination of the abdominal or pleural cavities requires an aggressive surgical approach. The mortality associated with unrecognized visceral perforation during antireflux surgery is reported to range from 10% to 15% [21,22]. Injury to collateral viscera more commonly occurs in minimally invasive procedures and usually is a direct result of trocar placement or careless introduction of the operating instruments into the abdominal cavity. Perforation is less frequent with the open technique. Iatrogenic injuries are more likely to occur in reoperative antireflux surgery as well as during Collis gastroplastic procedures when the esophagus is foreshortened and may have a surrounding inflammatory reaction. One particular complication that we have witnessed is the complete avulsion of the GE junction secondary to aggressive traction on the stomach. Individuals that are elderly and reoperative candidates who may have poor tissue quality or those who have an inflamed, shortened esophagus are susceptible to an avulsion injury. Attention to detail and good communication with the surgical assistant will avoid this complication. Repair entails a neo-esophagogastric anastomosis.

Paraesophageal herniation Paraesophageal hernia or herniation of the fundoplication wrap through the hiatus usually presents in the late follow-up period. However, the acute development of hiatal hernia in the early postoperative period has been reported in up to 1% of patients undergoing antireflux surgery [6,23,24]. The occurrence of paraesophageal hernias is more common following laparoscopic fundoplications and in patients who have GERD with an associated large hiatal hernia. Early postoperative disruption of the hiatal crura can occur secondary to several mechanisms. The most common is failure to approximate adequately the

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Figure 12.1 Reherniation of an intact Nissen fundoplication into the chest.

right and left crural fibers. The hiatus must be closed sufficiently to prevent reherniation but not excessively as esophageal compression by an overzealously closed hiatus can result in dysphagia. Typically, two to four sutures in the hiatus are required for this closure. An additional factor that may result in dehiscence of the hiatal closure is the stripping of the abdominal peritoneum and the thin layer of diaphragmatic fascia off the crura during dissection. This simple technical detail may result in disruption of the hiatus because of tearing of the sutures through the crural fibers with any sudden increase in abdominal pressure. The development of an acute paraesophageal or wrap herniation in the perioperative period is usually associated with a constellation of symptoms, which may be difficult to differentiate from others etiologies. A sudden change in clinical status with complaints of new-onset dysphagia, early satiety and occasionally non-specific epigastric pain should prompt a diagnostic evaluation. The most appropriate diagnostic study is an esophageal swallow (Figure 12.1). If a hiatal disruption and herniation is discovered, immediate repair is indicated to avoid the potential risk of gastric strangulation. Reparative antireflux surgery can be accomplished via the same transabdominal or less commonly transthoracic approach with a low incidence of recurrence.

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Miscellaneous complications The discussion of pitfalls associated with antireflux surgery is not complete without mentioning a variety of rare complications that have been reported in the literature and others that have been witnessed during our experience with gastroesophageal reflux surgery. Cardiopulmonary complications such as perioperative pneumonia, atelectasis or cardiac events are not unique to antireflux surgery. However, there have been a number of reports in the literature documenting specific complications associated with laparoscopic fundoplications [6,15,23,25]. The development of deep venous thrombosis and subsequent perioperative acute pulmonary embolism, pneumothorax, pneumomediastinum, extensive subcutaneous emphysema, in addition to mesenteric arterial and venous thrombosis has all been linked to the use of intra-abdominal CO2 insufflation. The result of increased intraperitoneal pressure from the CO2 theoretically causes increased pressure on the pliable structures within the abdominal cavity. The intra-abdominal venous pressure rarely exceeds 15 mmHg. With the standard use of intraperitoneal insufflation pressures of 15 mmHg the venous structures may collapse and contribute to stasis and thrombosis. Hypovolemia and increased ventilator pressures predispose the patient to hypotension and low mesenteric arteriovenous flow that may aggravate the sequence of events. Presumably this mechanism may also function in small arterial beds, thus contributing to the occasional rare development of mesenteric ischemia associated with laparoscopic surgery. To avoid these complications we recommend the routine use of lower-limb compression devices, perioperative hydration, and limiting intraperitoneal CO2 pressure to below 15 mmHg. The development of emphysema within the subcutaneous layer or mediastinum is also secondary to high insufflation pressures. This commonly occurs in three circumstances: when the initial intraperitoneal insufflation is delivered into the tissues of the abdominal wall, setting the insufflation pressure above 15 mmHg, or when the anesthesia is inadequate and the intra-abdominal pressure intermittently increases as the patient begins to awaken. Pneumothorax occurs primarily as a result of excessively zealous mobilization of the esophagus resulting in penetration of the parietal pleura. The incidence of a pneumothorax occurring during laparoscopic antireflux surgery varies between 2% and 5% [6,25].

Postoperative complications The general postoperative complications of antireflux surgery are similar to those of other major upper abdominal or thoracic operations in a population which is typically middle aged or older, and often more obese than average. Thus, we will concentrate on problems specific to antireflux operations.

Gas bloat This is one of the commonest postoperative problems [6,26,27,28]. It is more common with the Nissen total fundoplication than with the other types of

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antireflux operations, although it occurs in all types. The causes are manifold. Many GERD patients are chronic air swallowers, having learned this habit to lessen symptoms. They continue this postoperatively, but the newly created antireflux barrier makes belching more difficult, leading to gaseous distension of the fundus and wrap. This produces symptoms of upper abdominal fullness, discomfort, and distension. A temporary reduction in gastric motility often occurs after antireflux surgery due to vagal nerve dysfunction or gastric atony. This worsens the gas-bloat problem. Management of gas bloat begins intraoperatively. Good surgical technique includes gentle handling of tissues, especially the stomach and vagus nerves. The vagi should be maintained on the esophagus to avoid handling and destruction of small perforating branches. In the Nissen fundoplication, the wrap should be made loose, or ‘floppy’ [6,27]. This requires the ligation and division of almost all of the short gastric vessels. It is my belief that the wrap should be so loose that a bougie of any size is unnecessary. It is possible to stretch a wrap tightly around the largest bougie and still produce problems. Nonetheless, a large dilator should be in place as the wrap is constructed to contribute to the likelihood of a loose fundoplication. The length of wrap also may contribute to increased gas bloat. The tendency over the years has been to shorten the wrap, with a few authors advocating only one stitch [28,29]. Our preference has been to use two horizontal mattress type sutures, for an overall length of 2.5 cm. Gas bloat syndrome improves with time. Gastro kinetic agents may help with the problem in the short term, and by 1 year only a few percent of patients remain troubled by it.

Flatulence This problem is similar to gas bloat, with air swallowers being the most affected. Because of the antireflux nature of the operation, belching is more difficult and most swallowed air ends up in the intestines. This creates distension, cramping and increased flatulence. Any vagal dysfunction may contribute to this increased gaseousness, as may spastic colon that is often clinically associated with reflux disease. Avoidance of gaseous foods, intestinal kinetics and time again are the therapy.

Dysphagia Control of reflux would be simple were it not necessary to preserve the ability to swallow normally. Thus, there is a fine balance between these two requirements in performing antireflux surgery. Early dysphagia can occur in up to 50% of patients [6,30]. It can occur for many reasons. There may be postoperative inflammation or edema at the operative site, improving with time. Occasionally a hematoma may develop in the gastric wall of the wrap due to suture injury of the submucosal vessels. Again, this improves spontaneously. As mentioned previously, the wrap may be too tight, or too long. There may be some spontaneous improvement from the former, as smooth muscle

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Figure 12.2 Slipped Nissen fundoplicationaarrow shows wrap around stomach.

adaptively relaxes. There may also be distal esophageal dysfunction, due to vagal injury, usually improving with time. A small percentage of patients have persistent dysphagia. This may be due to too tight a wrap, or a wrap created below the GE junction on the stomach wall, or a true ‘slipped Nissen’ (Figure 12.2). It may be due to too narrow or too long a neo-esophageal tube after a Collis gastroplasty. It may also be secondary to a narrow esophageal hiatus from over-tight approximation of the crurae. These problems can all be avoided in the operating room, and are much more difficult to manage postoperatively. It is worth attempting esophageal dilatation for some, but dilatation is unlikely to work for most and the need for reoperation to correct the underlying problem is likely. Patients with a stricture preoperatively need to be dilatated to an adequate size pre- and perioperatively. On occasion this may produce an esophageal rupture. This iatrogenic complication should be recognized promptly, and can be best dealt with by esophagectomy and cervical anastomosis, or short segment colon interposition. Patients with strictures successfully treated by antireflux surgery may require several dilatations until the inflammation and scarring settle down. The development of late dysphagia in patients with previous strictures, or Barrett’s esophagus, should alert the surgeon to consider the development of carcinoma, and lead to prompt endoscopy and biopsies.

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Bleeding Late intra-abdominal or intrathoracic bleeding is exceedingly rare. However, it can occur from the late rupture of a subcapsular splenic hematoma. Also, one author while in training saw two late exsanguinating hemorrhages from the aorta at the hiatus several weeks after operation. Two possible etiologies are periaortic infection and the most posterior crural closure stitch being placed too far posteriorly, and when tied was positioned similar to a ‘bowstring’ across the anterior aorta, eroding through the aortic wall over time. Intraluminal late bleeding has been reported to occur from the gastric wrap. This is most often if the wrap has been left in the chest or more commonly when there is reherniation of an intact wrap into the chest through the hiatus [31]. This is due to venous stasis, or ulceration, and can be occult or massive. It is inadvisable to have a wrap in the chest because of the many potential complications. To avoid this, a lengthening procedure should be performed. Wrap herniation can be minimized by mobilizing sufficient esophagus, lengthening procedures if there is too much tension, and also fixing the wrap to the median arcuate ligament of Hill when feasible. Also crural repair should be part of every antireflux procedure.

Complete obstruction Complete occlusion of the GE junction has been infrequently reported [32]. It may occur with an extremely tight wrap, and has happened more in the learning stages of laparoscopic fundoplication. It can also occur due to a slipped Nissen or a herniated wrap. Avoidance of too tight a wrap, particularly by mobilizing sufficient fundus, is important. The wrap should never be created on the stomach, and wrap stitches should incorporate sufficient esophageal wall to prevent wrap slippage. If this occurs, reoperation is almost always necessary.

Internal fistulization On occasion, a fistula will develop from the wrap to the esophagus (Figure 12.3). This is usually above the lower esophageal sphincter, and thus leads to intractable reflux symptoms. There may be several causes, depending on the operation. Stitches placed too deep in the gastric and esophageal wall, or sutures tied too tightly may cause strangulation and necrosis of tissue, leading to a fistula site. Infection at the stitch site may also be a cause. It has been reported that internal wrap to neo-esophagus fistulas have occurred in the uncut Collis–Nissen operation [33,34]. This occurs due to staple pull through. As always, avoidance by meticulous surgical detail is paramount. Fistulas have also been reported to pericardium and lung as well as other organs [35]. When discovered, surgical intervention is usually necessary. The wrap is taken down and the fistula closed. A redo antireflux procedure is then performed. If the area is felt to be beyond repair, then local resection with replacement of the distal esophagus with a short segment of colon, or esophagectomy with esophagogastric anastomosis in the neck is warranted.

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Figure 12.3 Esophagogastric fistula following Belsey Mark IV fundoplication (arrow).

External fistulization Anecdotal and case reports exist of leaks from either the esophagus, the stomach or the wrap itself. These can be relatively early postoperatively from unrecognized perforation at the time of surgery. However, they can occur at a later time. Delayed leaks can occur from a variety of causes. There may be damage to the stomach or esophagus from diathermy. Ties or clips placed on blood vessels, particularly the short gastric arteries, may catch full-thickness stomach wall leading to subsequent necrosis. I know of one Collis gastroplasty, which necrosed because the left gastric artery had been previously ligated. External fistulas have also been reported due to an ulcer perforation within the fundic wrap. Again, this has been most common in fundoplications left within the thoracic cavity, or those which have subsequently herniated into the chest. These situations, when found, usually involve a sick patient, one who is septic. The management is often complicated and individualized, requiring drainage, resuscitation and reconstruction as appropriate to the patient.

Bowel dysfunction Early postoperatively, this is a common complaint, as it is with any abdominal

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procedure. Long-term problems with diarrhea or dumping may occur with vagal nerve injury, or the use of pyloroplasty as is sometimes done with redo antireflux surgery. Most of these problems are self-limited and lend themselves to the conservative management of dumping syndrome.

Post-thoracotomy neuralgia The Belsey Mark IV procedure, as well as many of the combined Collis–Nissen, or Collis–Belsey operations, requires a thoracotomy or thoracoabdominal incision. Unique to this incision is the occasional development of long-term incisional pain. Thus, for benign disease, it is recommended that one avoid these incisions if at all possible. If not, the use of epidural analgesia intra- and postoperatively reduces the immediate postoperative pain and long-term neuralgia. Adequate intermediate pain control is also important. If pain persists, intercostal nerve block may be of short and even sometimes long-term benefit. Established post-thoracotomy neuralgia is difficult to treat, requiring analgesia, anti-inflammatory drugs, antidepressants, transcutaneous electrical nerve stimulation (TENS) apparatus, epidural steroids and even acupuncture in any combination.

Failure The commonest complication, particularly over time, is the failure of the operation to prevent gastroesophageal reflux. The incidence of this varies by type of operation, author, and length of follow-up. In the open era, the recurrence rate over the years has been reported between 5% and 20% [6,25,26]. In the laparoscopic era, the data are still in evolution. Much is made of the learning curve and the complications and poor outcomes associated early with the laparoscopic approach. Nonetheless, in series of sufficient numbers, the relatively early recurrence rates range from 1 to 10% [20]. It is hard to believe the long-term rates will be any better than for open procedures. Thus, there are and will be a significant number of patients presenting with recurrent reflux symptoms at some time following previous antireflux surgery. This has and will always be a particular challenging group of patients to manage. Their management will again involve the making of a precise diagnosis prior to any consideration of further surgical intervention. Treatment should once again be medical therapy at the onset. The indications for redo surgery must be even more stringent than for first-time operations. This is because the mortality and morbidity are higher, as is the likelihood of poorer long-term results [36]. This in fact remains one of the most frustrating and challenging areas in surgery.

Summary Complications of reflux surgery begin in the preoperative period, with erroneous diagnoses or choice of operation for the patient. Many intraoperative

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pitfalls exist, leading to immediate or delayed problems. Many of these can be avoided by a thorough preoperative evaluation, appropriate selection of patient and procedure and proper surgical technique and attention to detail.

References 1 Little AG. Failed antireflux operations: pathophysiology and treatment. Chest Clin N Am 1994; 4: 697–703. 2 Hinder RA, Klingler PJ, Perdikis G, Smith SL. Management of the failed antireflux operation. Surg Clin N Am 1997; 77: 1083–1097. 3 Day JD, Richter JE. Medical and surgical conditions predisposing to gastroesophageal reflux disease. Gastroenterol Clin N Am 1990; 19: 587–603. 4 Donahue PE. Basic considerations in gastroesophageal reflux disease. Surg Clin N Am 1997; 77: 1017–1040. 5 Ferguson MK. Medical and surgical management of peptic esophageal strictures. Chest Surg Clin N Am 1994; 4: 673. 6 Ferguson MK. Pitfalls and complications of antireflux surgeryaNissen techniques. Chest Surg Clin N Am 1997; 3: 489–511. 7 Jenkins AF, Cowan RJ, Richter JE. Gastroesophageal scintigraphy: is it a sensitive test for gastroesophageal reflux disease. J Clin Gastroenterol 1985; 7: 127–131. 8 Jamieson GG. The results of antireflux surgery and re-operative antireflux surgery. Gullet 1993; 3: 41–45. 9 Orringer MB. Surgical management of scleroderma reflux esophagitis. Surg Clin N Am 1983; 63: 859–867. 10 Henderson RD, Pearson FG. Surgical management of esophageal scleroderma. J Thorac Cardiovasc Surg 1973; 66: 686–692. 11 Pearson FG, Henderson RD. Experimental and clinical studies of gastroplasty in the management of acquired short esophagus. Surg Gynecol Obstet 1973; 136: 737–744. 12 Pearson FG, Langer B, Henderson RD. Gastroplasty and Belsey hiatal hernia repair: an operation for the management of peptic stricture with acquired short esophagus. J Thorac Cardiovasc Surg 1971; 61: 50–63. 13 Orringer MB, Orringer JS. Esophagectomy: definitive treatment for esophageal neuromotor dysfunction. Ann Thorac Surg 1982; 34: 237–248. 14 Stirling MC, Orringer MB. The combined Collis–Nissen operation for esophageal reflux strictures. Ann Thorac Surg 1988; 45: 148–157. 15 Urschel JD. Complications of antireflux surgery. Am J Surg 1993; 65: 68–70. 16 Nicholson DA, Nohl-Oser HC. Hiatus hernia. A comparison between two methods of fundoplication by evaluation of the long-term results. J Thorac Cardiovasc Surg 1976; 72: 938. 17 Rossetti ME, Lieberman-Meffert D. Nissen antireflux operation. In: Nyhus LM, Baker RJ, eds. Mastery of Surgery. Boston: Little, Brown & Co., 1992; 505–515. 18 Orringer MP, Sloan H. Complications and failings of the combined Collis–Belsey operation. J Thorac Cardiovasc Surg 1977; 74: 726–732. 19 Carmichael J, Thomas WO, Dillard D, Luterman A, Ferrara JJ. Indications for placement of drains in the splenic fossa. Am Surg 1990; 56: 313–318. 20 Collet D, Cadiere GB. Formation for the development of laparoscopic surgery for gastroesophageal reflux disease group: conversions and complications of laparoscopic treatment of gastroesophageal reflux disease. Am J Surg 1995; 169: 622.

Complications of antireflux surgery 201 21 Schauer PR, Meyers WC, Eubanks S, Norem RF, Franklin M, Pappas TN. Mechanisms of gastric and esophageal perforations during laparoscopic Nissen fundoplication. Ann Surg 1996; 223: 43. 22 Urschel FD. Gastroesophageal leaks after antireflux operations. Ann Thorac Surg 1994; 57: 1229. 23 Johansson B, Glise H, Hallerback B. Thoracic herniation and intrathoracic gastric perforation after laparoscopic fundoplication. Surg Endosc 1995; 9: 917. 24 Thayer JO Jr, Gibb SP, Ellis FH Jr. Gastroplasty and fundoplication for severe gastroesophageal reflux with esophageal shortening. Dis Esoph 1988; 1: 153. 25 Bittner HB, Meyers WC, Brazer SR, Pappas TN. Laparoscopic Nissen fundoplication: operative results and short-term follow-up. Am J Surg 1994; 167: 193–200. 26 Maddern GJ, Jamieson GG, Chatterton BE, Collins PJ. Is there an association between failed antireflux procedures and delayed gastric emptying? Ann Surg 1985; 202: 162–165. 27 Vassilakis JS, Xynos E, Kasapidis P et al. The effects of floppy Nissen fundoplication on esophageal and gastric motility in gastroesophageal reflux. Surg Gynecol Obstet 1993; 177: 608. 28 Lundell LR. Gas bloat syndrome. An avoidance outcome of antireflux surgery? Dis Esoph 1993; 6: 54. 29 Low DE, Mercer CD, James EC et al. Post-Nissen syndrome. Surg Gynecol Obstet 1988; 167: 1. 30 Ferguson MK. Open Nissen fundoplication. Chest Clin N Am 1995; 5: 379. 31 Buskin FL, Woodward ER, O’Leary JP. Occurrence of gastric ulcer after Nissen fundoplication. Am Surg 1967; 42: 821–826. 32 Hill LD, Ilves R, Stevenson JK, Pearson JM. Reoperation for disruption and recurrence after Nissen fundoplication. Arch Surg 1979; 114: 542–548. 33 Pearson FG. Complications and pitfalls: Belsey and Collis-Belsey Anti-reflux repairs. Chest Clin N Am 1997; 7: 513–531. 34 Pearson FG, Cooper JD, Patterson GAP et al. Gastroplasty and fundoplication for complex reflux problems. Ann Surg 1987; 206: 473–481. 35 Hill LD. The Esophagus: Medical and Surgical Management. Philadelpia: Saunders, 1988; 167–179. 36 Hinder RA, Klingler PJ, Perdikis G, Smith SL. Management of the failed antireflux operation. Surg Clin N Am 1997; 77: 1083–1099.

CHAPTER 13

Complications of esophageal instrumentation Donald E Low

Upper gastrointestinal endoscopy and esophageal dilatation Upper gastrointestinal endoscopy now ranks among the most common invasive procedures currently carried out in the USA. The vast majority are diagnostic. However, endoscopy serves as an avenue for a wide variety of therapeutic maneuvers, the most common of which is esophageal dilatation of webs, congenital rings, and a variety of strictures produced as the result of gastroesophageal reflux disease, corrosive ingestion, neoplastic disease, and as a result of surgical intervention. The most common complications seen in standard diagnostic endoscopy include medication reaction, aspiration, bleeding, and esophageal perforation. The problem most frequently confronted by the thoracic surgeon in association with diagnostic endoscopy is perforation of the esophagus, the incidence of which overall has decreased from 0.03% in 1976 to 0.008% in 1987 [1,2], and in association with dilatation of esophageal strictures is variously reported to be between 0.3% and 0.5% [3]. Perforations are much more common in the presence of abnormal anatomy, uncooperative patients, and pathological conditions including Zenker’s and pseudodiverticula, large hiatal hernia, and acute angulation associated with malignant and non-malignant strictures. The risks of perforation can be decreased by routinely intubating the esophagus under direct vision, avoiding examinations and dilatations under general anesthesia, and appropriate use of fluoroscopy and sequential dilatation techniques. There are a wide variety of dilators available for the management of both benign and malignant strictures. These include mercury-filled bougies, e.g. Maloney and Hegar bougies, the polyvinyl wire directed dilating systems [e.g. American ([CR Bard, Inc., Billerica, MA, USA), or Savary–Gillard [Wilson-Cook, Inc., Winston-Salem, NC, USA)] and the TTS (through-thescope) balloon dilating systems (see Figure 13.1). The mercury-filled bougies are best reserved for uncomplicated strictures with a residual luminal diameter of between 0.8 and 1 cm. The preprocedural identification of any irregularity proximal to the stricture should lead to these bougies being used with fluoroscopic guidance. The routine use of fluoroscopy with Maloney bougies is controversial, although one study has demonstrated an increase in the rate of achieving relief of dysphagia from 69% 202

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Figure 13.1 Examples of currently used esophageal dilating systems. From the top down: Maloney and Hegar mercury-filled bougies; an American and a Savary wiredirected dilating system, and the TTS (through-the-scope) dilator.

to 93% when fluoroscopy is used compared with blind passage of the dilator [4]. Long, complicated strictures, i.e. > 2.5 cm, especially those associated with pseudodiverticula, are most safely dilatated with wire-directed polyvinyl bougies, or the TTS balloons. The TTS balloons are reputed to be safer secondary to the fact that they work through ‘radial dilatation’ without the longitudinal shear forces required in other dilating systems [5]. However, the reliability of dilatation to a set size and the ability to maintain symptom improvement in the long term, has been more difficult to ensure with the TTS balloons [3,6,7]. In spite of the fact that randomized, controlled trials are limited, and the results comparing the wire-directed and TTS systems are mixed, both systems seem to be safe and effective in experienced hands [6–8]. The wire-directed bougies are so efficient that using ‘resistance’ as a hallmark for how much to dilatate can be misleading. It is best to assess the size of the stricture, either endoscopically or with a contrast study, before deciding at what size to initiate dilatation. Factors felt to be major contributors to the occurrence of perforation during esophageal dilatation include: (i) excessive force; (ii) dilating too much, too fast; and (iii) impaction of dilator tips or dilating wires in diverticula, ulcers, or angulations caused by large hiatal hernias or malignancies. As a general rule, when treating either benign or malignant strictures, dilatating more than 10–12 Fr gauge (3–4 mm) at a single session should be avoided. Initial dilatation should rarely be taken higher than 45 Fr, except in instances such as Schatzki’s rings when initial dilatation up to 54–60 Fr is recommended. Wire-directed dilatation should be done under fluoroscopic control, unless the wire can be placed in the antrum under direct endoscopic

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guidance [9]. Guide-wires should routinely be placed in the antrum, i.e. further than 60 cm from the incisors, and the wire position should be reconfirmed following each sequential dilatation. Kinks in the wires can act as lead points which have the potential for producing esophageal or gastric trauma. The experience of the operator is a major factor in the incidence of complications in general, and the occurrence of perforations in particular. Two large series of esophageal dilatations for a variety of pathological conditions demonstrated no major complications [10,11]. A major survey done by the American Society of Gastrointestinal Endoscopy in 1974 suggests that perforation will occur in one out of every 500 endoscopies with dilatations when all techniques are combined [12]. Whatever dilatation system is used, there should be no routine requirement for postprocedural chest X-rays or barium studies. However, dilatation should not be done with patients oversedated or under general anesthesia under normal circumstances, and patients should be closely monitored while maintaining a high level of suspicion for postprocedural symptoms of chest pain, dyspnea, voice changes, abdominal pain, or subcutaneous emphysema which may indicate the presence of a perforation. It should be noted, however, that transient chest pain is common following dilatation of tight malignant strictures [13].

Diagnosis and treatment of perforation following upper endoscopy and esophageal dilatation procedures Since the prompt diagnosis of perforations is essential to a good outcome, any suspicion of perforation should lead to further studies. Cervical, mediastinal, or subdiaphragmatic air, pneumothorax or pneumopericardium, pleural effusion and persistent and/or severe chest or epigastric pain are all suggestive of perforation. Non-contrast studies are negative in up to 33% of cases of esophageal perforation [14]. Contrast radiographic studies, with water-soluble contrast followed by thin barium when required, will demonstrate virtually all significant perforations. Water-soluble contrast should be used initially, but will miss some perforations [15]. When these initial studies are negative, a second examination with thin barium will identify more subtle perforations [15,16]. Water-soluble contrast examinations should not be done in patients who are significant aspiration risks. One of the most important aspects of these contrast studies in patients who may have esophageal perforation is the need to provide clinical information to the radiologist and having the surgeon present for the examination when possible. We have had situations in which patients have been transferred to our institution with equivocal, unclear, or even frankly misleading, outside studies. This can lead to inappropriate operative decisions which significantly impact the outcome in these patients. As a result, any studies that are unclear or that do not match the clinical situation should be repeated, especially if there is any question regarding whether perforation is present or its exact location (see Figure 13.2a,b).

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(a)

(b) Figure 13.2 (a) Chest radiograph demonstrating mediastinal and cervical free air in a 78-year-old man who has had a longstanding esophageal inlet stricture dilated with American wire-directed dilators to 52 Fr gauge. (b) Upper gastrointestinal contrast study of the same patient sent from another center reporting to demonstrate extravasated mediastinal contrast consistent with a mid-thoracic esophageal perforation. Repeat study confirmed a cervical perforation with contrast tracking along the esophagus into the mediastinum.

If contrast studies are negative but suspicion remains, endoscopy will help identify mucosal lacerations but cannot usually confirm transmural perforation unless subcutaneous and mediastinal emphysema is seen to increase during the examination. Chest computed tomography (CT) will demonstrate more subtle amounts of mediastinal air or fluid [17] but will not localize the perforation. CT’s greater role resides in following up patients managed conservatively or operatively who deteriorate or fail to improve [18]. The treatment approach for esophageal perforation depends on the extent of the perforation and nature of pre-existing pathology. Some patients can be initially treated non-operatively, as long as they fit the criteria proposed by Cameron et al. [19] These patients must demonstrate: (i) a contained perforation without evidence of free extravasation or distal obstruction; (ii) drainage of the perforation back into the esophagus; and (iii) no significant signs of clinical sepsis. Jones and Ginsberg [20] have suggested that non-operative therapy is best applied in cases of: (i) instrumental perforation, especially in the cervical esophagus; (ii) small perforations following dilatation of peptic strictures, achalasia, or following sclerotherapy where periesophageal fibrosis can limit contamination of the mediastinum; and (iii) esophageal perforation diagnosed

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several days following injury with minimal symptoms. Careful patient selection remains the hallmark for successful, non-operative therapy as mortality rates remain in the range of 22% in collected series [20]. Conservative management of esophageal perforation includes appropriate fluid resuscitation, broad-spectrum antibiotics, enteral (preferably nasojejunal) or parenteral nutrition, proton pump inhibitors, and prokinetic agents, especially in patients with pre-existing reflux disease. A baseline CT scan is used for comparison purposes in patients who deteriorate or fail to progress. This treatment strategy should always be associated with early surgical consultation. If initial studies demonstrate esophageal perforation that extravasates freely, or if there is evidence of systemic sepsis, then patients should always undergo immediate surgical management. In cases in which the esophagus is normal, surgical treatment will predominantly involve primary repair associated with chest and mediastinal drainage. Previous experience suggests that primary repair is less likely to succeed when a delay in diagnosis, i.e. > 24 h, has occurred [21]. This philosophy has been increasingly challenged recently [22–25]. I would agree that although early operative management is always preferable, primary repair is often appropriate even when a delay of several days has occurred prior to surgical intervention. I base the decision regarding the suitability of primary repair on endoscopic examination of the esophageal mucosa done either immediately before or at the time of surgery. If the esophageal mucosa is healthy, I carry out a primary repair utilizing intraoperative endoscopy to minimize mediastinal and esophageal dissection by directing the surgeon precisely to the actual site of perforation. Experience has shown that even when leaks occur following appropriate primary closure, they are usually small and self-limited [22,24]. I often use a pedicled intercostal muscle bundle with attached pleura to buttress the repair, especially when contamination is significant or the diagnosis has been delayed. Grillo and Wilkins have demonstrated that buttressing with thickened pleura alone is another viable option [26]. Much has been written regarding debridement of tissue during primary treatment of esophageal perforation. Devitalized tissue should be removed, although minimal dissection and debridement of the esophagus is preferable. The area of the perforation should be vigorously lavaged and thoroughly drained and lung decortication should be carried out when required. Mucosal and muscular planes should be closed in separate layers, the mucosal repair being of particular importance. Endoscopic guidance can be used to minimize the extent of esophageal muscular mobilization required to demonstrate the mucosal defect in its entirety. If esophageal perforation occurs in the presence of distal obstruction, mortality rates are significantly higher when treatment is limited to primary closure alone [27]. Distal obstruction can often be managed with intraoperative dilatation of a distal stricture. In the presence of extremely fixed or malignant obstructions, I often carry out a primary repair of the perforation over a Celestin tube which is fixed to the stomach with a chromic suture (see Figure 13.3). This

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Figure 13.3 Upper GI contrast study in a 64-year-old man following perforation with persistent distal obstruction. The patient was treated with primary closure around a surgically placed Celestin tube. Note the absence of leak on this study, although extraluminal contrast remains in the mediastinum (arrow) from a previous barium examination.

approach eliminates the distal obstruction and the Celestin tube can be removed endoscopically 4–6 weeks postoperatively. These patients must be treated as high aspiration risks postoperatively and kept with head upright more than 45° and on proton pump inhibitors until the Celestin tube is removed. If the perforation has occurred in association with a resectable neoplasm, a chronic or refractory stricture or previous history of lye injection, or if the esophagus demonstrates profound and extensive necrosis, the best initial approach is esophageal resection with esophagogastric anastomosis in the neck (see Figure 13.4a,b) [28,29]. Selecting the correct patients for esophagectomy at the time of initial operative intervention leads to improved shortand long-term functional results [30–32]. When surgical resection is not appropriate, patients can be successfully treated either non-surgically [33], or in selected cases palliated with endoscopically placed expandable, coated stents with chest and abdominal drainage as deemed appropriate (see Figure 13.5a,b) [33–36]. Much has been written regarding exclusion/diversion procedures for esophageal perforation. These procedures involve cervical esophagostomy,

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(a)

(b) Figure 13.4 (a) Endoscopic photograph demonstrating a stenosing distal esophageal adenocarcinoma prior to esophageal dilatation with a wire-directed American dilator to 48 Fr gauge. (b) Endoscopic photograph of the same tumor showing a large, full-thickness perforation of the tumor and exposed mediastinum. The patient underwent immediate esophagectomy and recovered uneventfully.

(a)

(b) Figure 13.5 (a) Endoscopic photograph demonstrating a perforation at the level of an esophagojejunal anastomosis following dilatation of a recurrent obstructing neoplasm. (b) Endoscopic photograph in the same patient following treatment of the perforation with an endoscopically placed Wallstent. This picture provides a good illustration of how the barbs associated with early model stents could increase the incidence of bolus obstruction and pose a risk to endoscopes during subsequent upper endoscopy. This problem can be minimized by passing a polyvinyl dilator to realign the barbs with the walls of the stent.

chest drainage, plus or minus primary repair, gastric isolation with esophageal stapling at the esophago–gastric (EG) junction and gastrostomy. This procedure has been advocated primarily in cases of delayed diagnosis when primary repair is considered inadvisable. I have never found this approach necessary, although I have had the opportunity subsequently to manage multiple patients

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sent to us following this procedure at other institutions. Patients with perforation can virtually always be treated initially by either primary repair with intercostal muscle buttressing, creation of a controlled fistula (see section on sclerotherapy), or esophagectomy, even leaving reconstruction for a second operation if the patient is unstable. All of the above approaches should be combined with placement of enteric feeding tubes, preferably a feeding jejunostomy which decreases the potential for esophageal reflux and leaves the stomach intact in case it is required as an esophageal replacement.

Pneumatic dilatation for achalasia Successful dilatation therapy for achalasia requires forceful stretching and disruption of the muscle layer of the EG junction to a diameter of ≥ 3 cm, thereby producing marked reduction in the lower esophageal sphincter pressure. The most commonly utilized device at the present time is the Rigiflex dilator (Microvasive, Inc., Natick, MA, USA), which consists of a double lumen catheter with a polyethylene low compliance 13.5 cm long radiolucent cylindric balloon. Radiopaque markers on the flexible shaft mark the two ends and the center of the balloon and the balloons come in three diameters of 30, 35, and 40 mm. Prior to dilatation, a complete upper endoscopy is carried out and the esophagus emptied of food and fluid. A guide-wire is passed into the stomach and the level of the EG junction noted fluoroscopically and measured from the incisors. The Rigiflex dilator is passed over the wire and positioned across the EG junction. Initial inflation is done with air to position the waist (area of narrowing in the balloon pertaining to the EG junction) in the center of the balloon. The balloon is fully inflated with air until waist obliteration occurs (usually between 48 and 103 kPa). This inflation is maintained for 60 s. During this period, patients often complain of chest discomfiture. After the 60 s is complete, the balloon is deflated and then immediately reinflated until waist obliteration is again noted. Pressure required for obliteration during this inflation is usually in the range of < 21 kPa. The balloon at this point is removed. It is often found to be streaked with blood. Chest pain usually does not persist for more than 15–20 min following dilatations. Patients should be observed for 3–6 h following the procedure and during this period of time an upper GI contrast study should be obtained. Good or excellent results can be expected after a single treatment in 70% of patients undergoing pneumatic dilatation [37]. However, there is debate as to whether this level of success extends into the long-term. Eckardt and colleagues demonstrated only 25% good outcomes at 5 years’ follow-up [38]. Treatments can be repeated with larger balloons, but success rate with subsequent treatments do not usually achieve the levels attained with primary dilatations [39]. There is no convincing evidence to date to suggest that larger balloons or longer inflations are more effective at relieving symptoms [40].

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Diagnosis and treatment of perforation following pneumatic dilatation The most significant complication requiring surgical management is perforation, the instance of which is reported between 0 and 22% of the time, with most series citing an incidence of 3–8% [37,41]. Patients historically thought to be at increased risk of perforation include those with massively dilatated, tortuous ‘sigmoid’ esophagus, epiphrenic diverticula, or those who have undergone previous myotomy. In fact, pneumatic dilatation can be carried out safely in any of these situations [40], although patients with massively dilatated tortuous esophagus should be considered for resection. The key to successful management of esophageal perforation requires maintaining a high level of suspicion and recognizing perforations when they occur. Any persistent pain should be considered highly suspicious and all contrast studies should utilize initially water-soluble contrast medium followed by dilute barium. Perforations can be intramural, contained extramural, or freely extravasating, and can involve the chest or abdominal cavities. Some carefully selected patients with perforation, especially those with non-transmural tears [42], can be managed non-operatively (see guidelines and special recommendations for non-operative therapy of perforations listed earlier in this chapter). This approach should always include early surgical consultation. All extramural perforations should be treated surgically. This can involve either a transthoracic or transabdominal approach. In the absence of significant chest involvement, I prefer the transabdominal approach to minimize contamination of the pleural space (see Figure 13.6). Intraoperative endoscopic guidance minimizes the need for additional dissection and esophageal muscle disruption. The mucosal and muscular layers are closed independently with monofilament absorbable suture. A myotomy is then carried out on the opposite side of the esophagus. I carry the myotomy down onto the surface of the stomach to completely disrupt the lower esophageal sphincter. This may necessitate the addition of a non-obstructive antireflux procedure to avoid postoperative gastroesophageal reflux disease without causing dysphagia. If the procedure is being done transabdominally, a Toupet procedure, or if transthoracically, a Belsey Mark IV, are excellent alternatives. Prompt diagnosis and surgical treatment of perforation in achalasia patients produces long-term results comparable to primary surgical treatment [43]. If perforation occurs in achalasia patients with hugely dilatated, tortuous end-stage esophagus, primary treatment should be esophageal resection and reconstruction with either stomach or colon. This approach not only provides immediate and effective treatment for the perforation, but also significantly increases the likelihood of good long-term results with respect to the ability to swallow and patient satisfaction [44].

Esophageal laser therapy The most common application for esophageal laser treatment is palliation of patients with obstructing malignant strictures. The most commonly used laser

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(a)

(b) Figure 13.6 (a) Chest radiograph showing a left pleural effusion in a 60-year-old woman following pneumatic dilatation for achalasia. (b) Lateral radiograph in the same patient showing extraluminal contrast and subdiaphragmatic air (see arrow). Following the insertion of a left chest tube, this patient was operated on transabdominally with primary repair of the perforation, esophageal myotomy, and Toupet repair. This patient went on to have an uneventful recovery.

is the Nd-Yag (wavelength 1060 nm) which can be applied with external beam or a contact tip. The laser’s clinical effect relies on localized tissue vaporization and thermal necrosis with subsequent tissue sloughing. Laser ablation is most effective when used in conjunction with prior dilatation and snare cautery debridement [45]. Tumors should be treated in retrograde fashion, i.e. bottomto-top. Laser therapy is particularly effective when used to treat overgrowth of tumor around stents, short segment, especially proximal tumors, and anastomotic recurrences. Laser treatment is not appropriate for tumors with severe extrinsic compression, submucosal tumors, tumors with large gastric components, and very long (> 8 cm) and angulated tumors. Treatments usually need to be repeated to be effective and the most important single factor regarding avoiding complications is the experience of the operator. Functional success in tumor palliation has been reported in 75–80% of cases [13,45] and laser therapy can be combined with treatment with photodynamic therapy, brachytherapy, or esophageal stents. Laser treatment is seeing less application following the introduction of the expandable coated metallic stents. Recent studies have suggested these stents are more successful than laser therapy alone for the palliation of malignant dysphagia [46].

Diagnosis and treatment of perforation following laser therapy Perforation is the most common complication requiring surgical attention. It

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is reported to occur in between 4% and 6% of cases [47–49], and is the single most common cause of mortality associated with laser treatment [48]. Since the majority of these patients are not surgical candidates, most of the patients who sustain perforations associated with laser therapy will be treated supportively [33], or with expandable coated wire mesh stents [50,51]. These stents are highly successful in providing the dual role of sealing the perforation and maintaining luminal patency. Occasionally, multiple stents are required [34] and separate decisions must be made regarding the requirement of surgical or radiological mediastinal or pleural drainage.

Esophageal sclerotherapy Sclerotherapy for esophageal varices secondary to portal hypertension has improved and simplified the treatment of these complex patients [52]. With the introduction of endoscopic variceal ligation, and transjugular intrahepatic portal systemic shunting (TIPS), it has seen somewhat less application over the last 4–5 years. Sclerotherapy works by injecting a sclerosing agent (e.g. sodium tetradecyl sulfate, sodium morrhuate, or ethanolamine) into or around the esophageal varices to promote an intense inflammatory reaction which results in variceal fibrosis and obliteration. Most injections are made in the distal one-third of the esophagus, more proximal varices being located below the muscularis mucosa, making injection more difficult and increasing the potential for complications. Sclerotherapy is usually not initiated prior to the onset of bleeding. When treatments are applied acutely at the time of hemorrhage, they are usually repeated three to six times until variceal obliteration. Meta-analysis of combined, randomized, controlled trials show significant benefit of sclerotherapy over medical treatment in controlling initial bleeding, and reducing early rebleeding rates, while suggesting the possibility of a decreased mortality [53].

Diagnosis and treatment of complications associated with variceal sclerotherapy Complication rates of 20–40% and procedure-related mortality rates of 1–5% following sclerotherapy are documented. These complications include esophageal ulceration, stenosis, intramural hematoma, and perforation. Perforation is the most devastating complication and the one most likely to come to the attention of thoracic surgeons. It is often associated with pre-existing esophageal ulceration and has been reported in up to 6.5% of patients undergoing sclerotherapy treatment. Some of the patients can be managed non-operatively; however, due to the fact that chest pain is often associated with sclerotherapy injections, it is not uncommon for the diagnosis of esophageal perforation in these patients to be delayed, resulting in the patients presenting with severe mediastinitis, abscess, empyema, or even esophagorespiratory fistula. Some of the most challenging perforations I have encountered have been in these otherwise medically compromised patients who present late with perforations following sclerotherapy. Many times, these patients are referred

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after treatment of an ‘atypical varix’, often in an unusual location. These patients can be septic due to widespread infection and at the time of surgery are sometimes found to have large esophageal defects where portions of the esophageal wall are dissolved or necrosed as a result of the sclerosing agent. Perforations in these patients should be managed by the same criteria presented earlier in this chapter; however, primary repair is often impossible due to the size of the defect. Esophagectomy is a daunting proposition in these patients, who usually have coexistent liver dysfunction, portal hypertension, malnutrition, and coagulopathy. Exclusion and diversion procedures are particularly unsuited in this situation. I have found two approaches useful in these difficult situations. One approach involves the creation of a controlled fistula with a 20 Fr gauge T-tube sewn into the esophageal defect (see Figure 13.7) [54,55]. The second option relies on stenting of the defect with an adult Celestin tube (sewn in place with a

(a)

(b)

Figure 13.7 (a) Contrast study through a no. 20 T-tube placed in a 64-year-old man presenting 3 days following an esophageal perforation resulting from variceal sclerotherapy. (b) Upper GI study following removal of the T-tube in the same patient showing a very tiny persistent controlled fistula to a chest drain which had been left immediately adjacent to the perforation at the time of surgery. (c) Final upper GI study after chest drain was removed sequentially over a 7–10-day period showing no evidence of persistent esophageal leak and only minor esophageal stricturing.

(c)

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Figure 13.8 Chest radiograph of a Linton tube which has been inflated within the esophagus. Fluoroscopy had not been used to ensure correct positioning of the balloon prior to inflation.

chromic suture) and closing the defect in the esophagus with a muscle flap either pedicled intracostal muscle with pleura or latissimus dorsi, depending on the location of the perforation. The muscle flap must not be sewn to the edge of the defect because further necrosis may occur. It should be fixed to the esophagus 5–10 mm away from the edge of the perforation. Both of these approaches also require extensive mediastinal and pleural drainage, appropriate antibiotic therapy, and attention to postoperative nutrition (preferably a feeding jejunostomy). Massive perforations can occur with inappropriate application of Linton or Sengstaken–Blakemore tubes for tamponade of bleeding varices (see Figure 13.8). Fortunately, with the introduction of sclerotherapy and TIPS, these devices are seeing less application. In instances when these devices are still used, a good working knowledge of the mechanics ‘prior to their acute application’ is essential. They should always be inserted with fluoroscopic guidance to verify the actual location of the balloon(s) during insertion. Mortality rates approaching 100% are associated with the inflation of gastric balloons in the esophagus due to the massive dimensions of the resultant perforation. An interesting complication of sclerotherapy is the appearance of an obstructing intramural hematoma (see Figure 13.9). Once recognized, usually requiring a CT scan, this problem is usually self-limited and resolves with supportive therapy [56,57].

(a)

Figure 13.9 (a) Upper gastrointestinal contrast study showing esophageal stenosis secondary to an extramucosal hematoma following variceal sclerotherapy. (b) Repeat contrast study 3 days later in the same patient demonstrating re-opening of the esophageal lumen following spontaneous evacuation of the hematoma. (Reprinted with permission, Am J Gastroenterol 1988; 83: 435–438.)

(b)

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Figure 13.10 Examples of conventional plastic prostheses: Atkinson tube (above), Wilson-Cook prosthesis (below).

Esophageal stents Various types of endoscopic, radiological, or surgically placed esophageal prostheses have been utilized for the palliation of obstructing esophageal malignancies, and more recently to treat malignant esophagorespiratory fistulas [50]. Endoscopically placed stents originally were limited to conventional plastic prostheses, such as the Wilson-Cook prosthesis (Wilson-Cook), the Atkinson tube (Key Med, Ltd, Southend, UK), or Celestin tube (Medoc, Ltd, Tetbury, UK) (see Figure 13.10). Recently, a new generation of expandable wire mesh stents, such as the Z-stent (Gianturco; Wilson-Cook, Winston Salem, NC), Wallstent (Schneider, Inc., Minneapolis, MN, USA), Esophacoil (InStent; Eden Prairie, MN, USA), and Nitinol Ultraflex (Microvasive, Inc., Natick, MA) has been introduced (see Figure 13.11). Most of the newer stents have a silastic coating to help impede tumor ingrowth and facilitate fistula occlusion. The exceptions are the Ultraflex I type stent, which is a tightly woven mesh stent, and the Esophacoil, which is made from a single flattened wire shaped into a tight coil. These newer, expandable stents are reputed to be smaller and easier to insert, and potentially more effective and safer to use. This statement may or may not be true and will be refuted or confirmed with more experience, additional comparative trials, and future technological advances. Conventional plastic stents can be successfully placed in over 90% of cases [50,58]. These stents usually require initial dilatation up to a range of 45–54 Fr gauge to facilitate insertion. Alternatively, the expandable stents are mounted on delivery systems as small as 18 Fr gauge, thereby requiring less preinsertional dilatation. Although a review in our institution suggests that conventional and expandable prostheses are comparable with respect to dysphagia relief, fistula occlusion, and instance of complications [50], two randomized,

Complications of esophageal instrumentation 217

Figure 13.11 Examples of wire mesh expandable prostheses. From top to bottom: Wallstent, Z stent, Esophacoil, and Ultraflex.

prospective, controlled clinical trials comparing treatment efficacy and safety of conventional vs. expandable prostheses do demonstrate that expandable stents are associated with fewer complications and fewer procedural-related deaths [59,60]. As a result, the vast majority of stents currently being inserted are the expandable, coated variety. This is the case in spite of a large cost differential favoring conventional prostheses [$100 (£63) vs. > $1000 (£626) per unit]. Well-documented early complications from conventional plastic prostheses include perforation 6%, bleeding 3.5%, aspiration 2%, tube migration 15%, and airway obstruction 1% [13]. Late complications include tube obstruction secondary to food impaction or tumor overgrowth, bleeding secondary to tube erosion, stricture due to gastroesophageal reflux disease, and tube migration. Results with the expandable stents have improved with the routine addition of silicon coating to decrease tumor ingrowth. Success rates with respect to insertion of the expandable stents are routinely > 90%; however, one specific situation in which expandable stents routinely fail involves the presence of significant extraluminal esophageal compression which will not enable the stents to deploy or will compress the stents despite postdeployment dilatation with TTS balloons. The possible exception to this is the Esophacoil, which has a much higher level of maximum radial force than its counterparts. However, in general terms, extraluminal esophageal compression may be better managed with a conventional plastic prosthesis, specifically, the Wilson-Cook tube. In spite of this limitation, multiple series have reported excellent results for the relief of dysphagia, ease and safety of insertion, and minimal associated complications with expandable stents [61–64]. The frequency of complications is directly related to the experience of the operators [63].

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(a)

(b) Figure 13.12 (a) Endoscopic photograph of a patient with two inappropriately deployed Wallstents placed proximally to an obstructing neoplasm. (b) Radiograph of same patient who has been successfully treated with the insertion of an Esophacoil stent through the previous two stents and the obstructing tumor.

Complications of esophageal instrumentation 219

Diagnosis and treatment of complications associated with expandable, coated esophageal stents Perforation The mortality rates of perforation associated with stent insertion are reported to be as high as 50% [61]. However, the incidence of perforation associated with these stents is reported to be as low as 0–2% [63–65]. This fairly low rate is attributed to the fact that expandable stents require significantly less preinsertional dilatation than the rigid devices. Since these stents are usually inserted in patients who, for a variety of reasons, are not considered appropriate surgical candidates, surgical decision making following perforation is usually limited to whether additional stents will be required to seal the perforation and a decision regarding the placement of thoracic and abdominal drains.

Stent misplacement Due to the ease of insertion of the wire mesh, expandable stents, larger components of the radiological, GI, and surgical specialties are utilizing these stents, in some cases with only limited experience of stent placement or patient selection. As a result, the incidence of inappropriate stent placement is variously reported between 5% and 13% [63,65]. With the exception of the Z-type stents, the vast majority of expandable stents will shorten between 20% and 50% when deployed. This must be taken into account when placing the prosthesis and choosing the appropriate length. Placement of these stents should always be under fluoroscopic guidance after exact definition of the proximal and distal tumor margins with either mucosal contrast injection or externally placed radiopaque markers. Once deployment has been initiated, only the Nitinol Ultraflex, Z stents, and the Wallstent can be repositioned. Most importantly, if inappropriately fully deployed or damaged, the majority of these stents cannot be safely removed endoscopically. Paradoxically, the situation is usually salvaged by the insertion of additional stents (see Figure 13.12) [34,66,67]. The Esophacoil stent has been presented as a design which can be removed when it is inappropriately placed or has migrated. We have had the same experience reported by Segalin [68] where these devices have produced major esophageal injuries when the coiled stents are removed by pulling one end of the coiled wire out of the patient’s mouth (see Figure 13.13). When removed endoscopically, these stents should be removed as a whole unit, preferably utilizing an overtube.

Stent migration The incidence of wire mesh, expandable stents migrating following insertion is in the range of 0–27% [19,50,63,65]. The incidence of this problem can be decreased by ensuring full deployment, which often requires inflating TTS balloons within the stent at the time of insertion. Particular care must be exhibited with stents placed across the EG junction. The majority of these stents must be placed within the tumor and the esophagus to minimize the potential for distal displacement. Recently, reports have suggested that the Ultraflex

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Figure 13.13 Endoscopic photograph demonstrating an extensive mucosal tear involving the entire length of the esophagus following attempted removal of a misplaced Esophacoil stent.

stent has the greatest tendency for incomplete deployment and the need for more complex interventions [69,70]. While conventional plastic prostheses could be left in the stomach when distal migration occurs, this is clearly not the case with the new expandable stents. Small-bowel obstruction and perforation have been reported [71]. These stents must be removed, either endoscopically or surgically. Safe endoscopic removal can often be facilitated with the use of an overtube (see foreign body extraction) (see Figure 13.14).

Tumor overgrowth Overgrowth of expandable stents with tumor was a much greater problem prior to the routine coating of many of these appliances with silicone. Although overgrowth is still noted in up to 36% of patients [70], it can usually be effectively managed with laser [13], snare electrocautery, photodynamic therapy (PDT) [72], or the insertion of additional stents (see Figure 13.15) [70].

Airway obstruction Obstruction of the tracheal or proximal bronchial airway can occasionally occur with stent deployment, the risk being especially high in very proximal tumors. This problem can be identified prior to stent deployment by initial

Complications of esophageal instrumentation 221

(a)

(b) Figure 13.14 (a) Radiograph demonstrating two Z stents following migration into the stomach. (b) Endoscopic photograph of removing a Z stent from the stomach with an endoscopic snare. The stent was pulled up into an overtube prior to removal.

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Figure 13.15 Endoscopic photograph showing a Z stent being fully deployed with a through-the-scope (TTS) balloon inside an Ultraflex stent which had become obstructed secondary to tumor ingrowth.

prolonged dilatation with a polyvinyl dilatator or a TTS balloon prior to stent deployment. If concern still exists, then one of the stents that can be subsequently removed, specifically the Ultraflex or Esophacoil, should be considered in these patients. Particular care must be exhibited when deploying stents near the upper esophageal sphincter because life-threatening airway compromise has been documented [73].

Pressure necrosis Pressure necrosis is a late complication of insertion of expandable stents and is often associated with acute angulation at the point of stenosis. The most common manifestation of pressure necrosis is chest pain. Bleeding is a common sequelae which can be massive, indicating erosion into a major vascular structure [65,66,74–77]. The frequency of reports of major exsanguinating hemorrhage with these new stents is worrisome. As a result, any indication of minor upper GI bleeding should be investigated endoscopically and if major ulceration or erosion is identified, every effort should be made to remove or modify the offending stent. Expandable stents have also been seen to erode into other major mediastinal structures, such as pericardium [78], and the tracheal-bronchial tree [79,80]. Pressure necrosis and significant bleeding may increase when patients undergo radiation or chemoradiation therapy following stent placement [81]. However, the risk of complications does not seem to be higher when stents are placed in patients who have completed radiation therapy or chemotherapy prior to stent placement [66,82].

Complications of esophageal instrumentation 223

Expandable wire mesh stents in benign disease The ease with which these stents can be inserted makes it tempting to apply this relatively new technology to patients with refractory dysphagia secondary to benign disease. An increasing number of anecdotal reports is appearing in the literature citing experience with expandable stents in situations other than end-stage esophageal malignancy. As discussed, the incidence of major complications with these stents is not insignificant. Major complications in patients with benign disease such as perforation and death are reported [83], with some series noting complication rates of 100% [84]. Utilization of these stents in patients with benign disease outside of an Institutional Review Board (IRB)-approved clinical trial is condemned.

Avoidance and treatment of complications associated with esophagogastric foreign body removal Presence of foreign bodies in the upper gastrointestinal tract is a very common problem involving a wide and sometimes unbelievable variety of items. Upper endoscopy is the primary tool of investigation and treatment. The majority of complications involve misadventure during attempted foreign body extraction. The most important initial decision involves which foreign bodies require removal and which are too large and dangerous to be removed endoscopically and therefore require an initial surgical approach. Approximately 70% of foreign bodies will pass through the GI tract spontaneously and only 1% will result in perforation. Evidence of perforation at the time of discovery of foreign bodies should be responded to with the decision profile outlined previously in this chapter. Patients who are prisoners, psychotic, or mentally retarded are at higher risk for having multiple foreign bodies. The reasons to remove a foreign body from the upper GI tract can be summarized as: (i) esophageal impaction (small and smooth objects impacted in the lower esophagus can undergo a short observation period of 12 h or less to see if they will spontaneously pass; however, no foreign body should remain impacted in the esophagus for greater than 24 h [85]); (ii) evidence of airway compromise; (iii) sharp or pointed objects (e.g. toothpicks, safety pins, and wires) even when they pass into the stomach; (iv) foreign bodies > 6 cm in children and 10 cm in adults [86,87]; (v) all button, disk, or regular batteries (disk batteries can result in esophageal perforation in a remarkably short period of time when impacted in the esophagus); and (vi) packets of cocaine in either condoms, balloons, or layers of tubular latex (these should be removed surgically because endoscopic rupture during extraction can be fatal). All patients experiencing esophageal bolus obstruction require upper endoscopy, even when the bolus is seen to spontaneously pass. This is due to the high incidence (70%) of underlying disease, i.e. peptic stricture, rings, etc. [88,89] which should be identified and appropriately treated. Up to 20–25 years ago, the routine approach to esophageal and gastric foreign bodies was removal with rigid esophagoscopy under general anesthesia.

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Figure 13.16 Examples of long (esophageal) and short (gastric) esophageal overtubes.

However, with the advent of flexible upper endoscopy which now provides better visibility, maneuverability, and safety, the requirement for rigid esophagoscopy has virtually disappeared. Success rates for endoscopic extraction of foreign bodies are reported to range between 84% and 99% [88,89]. An initial surgical approach is usually reserved for very large foreign bodies, cocaine packets, and patients presenting with complications at the time of foreign body diagnosis. The endoscopic approach to foreign body extraction usually involves a double lumen endoscope in association with an armamentarium of forceps, graspers, and snares. Some recent snares have even been fitted with a net to facilitate the removal of round or oval foreign bodies. The single most important piece of equipment for the removal of sharp or irregular objects is the esophageal overtube (see Figure 13.16). This flexible plastic tube fits over the endoscope and subsequently slides down the scope when it is in place in the esophagus or stomach. Sharp foreign bodies can be pulled up into the tube prior to removal. In addition, the tube can be left in place to facilitate the scope being passed repeatedly into the esophagus or stomach, thereby avoiding repetitive instrumentation of the pharynx and hypopharynx for piecemeal removal of meat boluses or removal of multiple foreign bodies [90]. If the foreign body is radiopaque, a plan for removal and the appropriate instrumentation should be assembled prior to beginning the endoscopy. Intravenous glucagon will often aid removal by decreasing gastroduodenal motility. Elongated foreign bodies should be removed by grasping one end and aligning the object with the long axis of the esophagus during removal. Sharp objects should be removed with the point trailing, or as with irregular or spiculated foreign bodies, e.g. stents (see Figure 13.14) can be removed with the aid of an overtube. Special care must be used in passing overtubes through

Complications of esophageal instrumentation 225

the cervical esophagus, especially in elderly patients with osteophytes, due to the increased risk of perforation. Blind attempts at pushing a meat bolus through a distal obstruction of unknown etiology carries an increased risk of perforation [88,91]. However, if the nature of the distal obstruction can be assessed endoscopically, meat boluses can often be broken up with snares and safely pushed into the stomach. Dissolving meat bolus obstruction with papain (meat tenderizer) has been used with success; however, papain produces an enzymatic action on the esophageal wall and deaths have been reported with this approach [92,93]. The incidence of perforations associated with foreign bodies and their extraction has been reported between 0 and 73% [88,89,94]. Extraction rates are lower and perforation rates higher (23%) in cases of deliberate ingestion [95]. Inability to extract a foreign body endoscopically will require a surgical approach. For objects that are sharp or irregular in configuration, and become impacted or impaled in the lower esophagus, a transabdominal approach with transgastric digital manipulation from below, gentle palpation from outside the esophagus, in conjunction with continued endoscopy will virtually always be successful. Careful subsequent inspection, both endoscopically and from the outside of the esophagus and stomach (often submerging the EG junction in saline with endoscopic air insufflation) to identify any occult site of perforation is important following foreign body removal. If perforation is identified, it should be managed with the principles previously outlined. Primary repair will almost always be feasible, keeping in mind that the etiology of the esophageal obstruction may alter the approach used in repairing the perforation.

References 1 Carey WD. Indications, contraindications and complications of upper gastrointestinal endoscopy. In: Sivak MV, ed. Gastroenterologic Endoscopy. Philadelphia: Saunders, 1987; 296–306. 2 Mandelstam P, Sugawa C, Silvis SE et al. Complications associated with esophagogastric duodenoscopy and with esophageal dilation. Gastrointest Endosc 1976; 23: 16–19. 3 Nostrant TT, Nandi PS. Esophageal dilation. The Gastroenterologist 1998; 6: 5–15. 4 McClave SA, Brady PG, Wright RA et al. Does fluoroscopic guidance for Maloney esophageal dilation impact on the clinical endpoint of therapy: relief of dysphagia and achievement of luminal patency. Gastrointest Endosc 1996; 43: 93–97. 5 McLean GK, LeVeen RF. Shear stress in the performance of esophageal dilation: comparison of balloon dilation and bougienage. Radiology 1989; 172: 983–986. 6 Cox JG, Winter RK, Maslin SC et al. Balloon or bougie for dilation of benign oesophageal stricture? Gut 1988; 29: 1741–1747. 7 Clouse RE. Complications of endoscopic gastrointestinal dilation techniques. Gastrointest Endosc Clin North Am 1996; 6: 323–341. 8 Saeed ZA, Winchester CB, Ferro PC et al. Prospective randomized comparison of polyvinyl bougies and through-the-scope balloons for dilation of peptic strictures of the esophagus. Gastrointest Endosc 1995; 41: 189–195.

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9 Mohandas KM, Santhi Swaroop V, Desai DC. Marked wire-guided esophageal dilation and the need for fluoroscopy (letter). Gastrointest Endosc 1992; 38: 634–635. 10 Marshall JB, Afridi SA, King PD et al. Esophageal dilation with polyvinyl (American) dilators over a marked guidewire: practice and safety at one center over a five-year period. Am G Gastroenterol 1996; 91: 1503–1506. 11 Kadakia SC, Parker A, Carrougher JB. Esophagal dilation with polyvinyl bougies using a marked guidewire without the aid of fluoroscopy: an update. Am J Gastroenterol 1996; 88: 1381–1386. 12 Silvis SE, Nebel O, Rogers G. Endoscopic complications. Results of the 1974 American Society for Gastrointestinal Endoscopy Survey. JAMA 1976; 235: 928–930. 13 Reed CE. Pitfalls and complications of esophageal prosthesis, laser therapy and dilation. Chest Surg Clin North Am 1997; 7: 623–636. 14 Wychulis AR, Fontana RS, Payne WS. Instrumental perforation of the esophagus. Chest 1969; 55: 184–189. 15 Foley MJ, Ghahremani GG, Rogers LF. Reappraisal of contrast media used to detect upper gastrointestinal perforation. Radiology 1982; 144: 231–237. 16 Phillips LG, Cumingham J. Esophageal perforation. Radiol Clin North Am 1984; 22: 1607–1613. 17 Backer CL, LoCicero J 3rd, Hartz RS et al. Computed tomography in patients with esophageal perforation. Chest 1990; 98: 1078–1080. 18 Endicott JN, Molony TB, Campbell G et al. Esophageal perforations: the role of computerized tomography in diagnosis and management decisions. Laryngoscope 1986; 96: 751–757. 19 Cameron JL, Kieffer RF, Hendrix TR et al. Selective nonoperative management of contained intrathoracic esophageal disruptions. Ann Thorac Surg 1979; 27: 404–408. 20 Jones WG, Ginsberg RJ. Esophageal perforation: a continuing challenge. Ann Thorac Surg 1992; 53: 534–543. 21 Nesbitt JC, Sawyers JL. Surgical management of esophageal perforation. Am Surg 1987; 53: 183–191. 22 Whyte RI, Iannettoni MD, Orringer MB. Intrathoracic esophageal perforation. J Thorac Cardiovasc Surg 1995; 109: 140–146. 23 Reeder LB, DeFilippi VJ, Ferguson MK. Current results of therapy for esophageal perforation. Am J Surg 1995; 169: 615–617. 24 Wang N, Razzouk AJ, Safavi A et al. Delayed primary repair of intrathoracic esophageal perforation: is it safe? J Thorac Cardiovasc Surg 1996; 111: 114 –122. 25 Gawrychowski J, Rokicki W, Dziedzic M. Observations related to causes and treatment of iatrogenic esophageal injury. Wiadomosci Lekarskie 1997; 1: 254 –258. 26 Grillo HC, Wilkins EW. Esophageal repair following late diagnosis of intrathoracic perforation. Ann Thorac Surg 1975; 20: 387–399. 27 Moghissi K, Pender D. Instrumental perforations of the esophagus and their management. Thorax 1988; 43: 642–646. 28 Matthews HR, Mitchell IM, McGuigan JA. Emergency subtotal oesophagectomy. Br J Surg 1989; 76: 918–920. 29 Yeo CJ, Lillemoe KD, Klein AS et al. Treatment of instrumental perforation of esophageal malignancy by transhiatal esophagectomy. Arch Surg 1988; 123: 1016–1018. 30 Iannettoni MD, Vlessis AA, Whyte RI et al. Functional outcome after surgical treatment of esophageal perforation. Ann Thorac Surg 1997; 64: 1606–1609. 31 Saabye J, Nielson HO, Anderson K. Long-term observation following perforation and rupture of the esophagus. Scand J Thorac Cardiovasc Surg 1988; 22: 79–80. 32 Salo JA, Isolauri JO, Heikkilä LJ et al. Management of delayed esophageal perforation with mediastinal sepsis. J Thorac Cardiovasc Surg 1993; 106: 1088–1091.

Complications of esophageal instrumentation 227 33 Bisgaard T, Wojdemann M, Heindorff H et al. Nonsurgical treatment of esophageal perforations after endoscopic palliation in advanced esophageal cancer. Endoscopy 1997; 29: 155–159. 34 Watkinson A, Ellul J, Entwisle K et al. Plastic-covered metallic endoprostheses in the management of oesophageal perforation in patients with oesophageal carcinoma. Clin Radiol 1995; 50: 304–309. 35 Bethge N, Kleist DV, Vakil N. Treatment of esophageal perforation with a covered expandable metal stent. Gastrointest Endosc 1996; 43: 161–163. 36 Nicholson AA, Royston CM, Wedgewood K et al. Palliation of malignant oesophageal perforation and proximal oesophageal malignant dysphagia with covered metal stents. Clin Radiol 1995; 50: 11–14. 37 Reynolds JC, Parkman HP. Achalasia. Gastroenterol Clin North Am 1989; 18: 233–255. 38 Eckardt VF, Aignherr C, Bernhard G. Predictors of outcome in patients with achalasia treated with pneumostatic dilation. Gastroenterology 1992; 103: 1732–1738. 39 Parkman HP, Reynolds JC, Ouyang A et al. Pneumatic dilation of esophagomyotomy treatment for idiopathic achalasia: clinical outcomes and cost analysis. Dig Dis Sci 1993; 38: 75–85. 40 Pasricha PJ, Huang RL, Rai R et al. Achalasia and other motor diseases. In: DiMarino AJ, Benjamin SB, eds. Gastrointestinal Disease: An Endoscopic Approach. Malden MA: Blackwell, 1997; 219–240. 41 Abid S, Champion G, Richter JE et al. Treatment of achalasia: the best of both worlds. Am J Gastroenterol 1994; 89: 979–985. 42 Molina EG, Stollman N, Grauer L et al. Conservative management of esophageal nontransmural tears after pneumatic dilation for achalasia. Am J Gastroenterol 1995; 91: 15–18. 43 Ferguson MK, Reeder LB, Olak J. Results of myotomy and partial fundoplication after pneumatic dilation for achalasia. Ann Thorac Surg 1996; 62: 327–330. 44 Peters JH, Kauer WK, Crookes PF. Esophageal resection with colon interposition for end-stage achalasia. Arch Surg 1995; 130: 632–636. 45 Low DE, Pagliero MK. Palliative treatment of carcinoma of the esophagus. In: Bauer AE, ed. Glenn’s Thoracic and Cardiovascular Surgery, 6th edn. Stamford CT: Appleton & Lange, 1996; 939–950. 46 Adam A, Ellul J, Watkinson AF et al. Palliation of inoperable esophageal carcinoma: a prospective randomized trial of laser therapy and stent placement. Radiology 1997; 202: 344–348. 47 Tyrrell MR, Trotter GA, Adam A et al. Incidence and management of laser-associated oesophageal perforation. Br J Surg 1995; 82: 1257–1258. 48 Ell C, Demling L. Laser therapy of tumor stenoses in the upper gastrointestinal tract: an international inquiry. Lasers Surg Med 1987; 7: 491–496. 49 Fleischer D. The Washington Symposium on Endoscopic Laser Therapy. Gastrointest Endosc 1985; 31: 387–400. 50 Low DE, Kozarek RA. Comparison of conventional and wire mesh expandable prostheses and surgical bypass in patients with malignant esophagorespiratory fistulas. Ann Thorac Surg 1998; 65: 919–923. 51 Weigert H, Neuhaus H, Rosch T et al. Treatment of esophagorespiratory fistulas with silicone-coated self-expanding metal stents. Gastrointest Endosc 1995; 41: 490–496. 52 Low DE, Kozarek RA, Ball TJ et al. Endoscopic vascular sclerotherapy as primary treatment for bleeding esophageal varices. J Clin Gastroenterol 1989; 11: 253–259. 53 Trudeau W, Kotrila W. Gastrointestinal manifestations of portal hypertension. In: Dimarino AJ, Benjamin SB, eds. Gastrointestinal Disease: An Endoscopic Approach. Malden, MA: Blackwell, 1997; 424–445.

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54 Andrade-Alegre R. T-tube intubation in the management of late traumatic esophageal perforations: case report. J Trauma 1994; 37: 131–132. 55 Naylor AR, Walker WS, Dark J. T tube intubation in the management of seriously ill patients with oesophagopleural fistulae. Br J Surg 1990; 77: 40–42. 56 Low DE, Patterson DJ. Complete esophageal obstruction secondary to dissecting intramural hematoma after endoscopic variceal sclerotherapy. Am J Gastroenterol 1988; 83: 435–438. 57 Benoit R, Legoux JL, Serve MP et al. Obstructive intramural hematoma of the esophagus after sclerotherapy. Presse Med 1996; 25: 1281–1284. 58 Spinelli P, Cerrai FG, Ciuffi M et al. Endoscopic stent placement for cancer of the lower esophagus and gastric cardia. Gastrointest Endosc 1994; 40: 455–457. 59 DePalma GD, DiMatteo E, Romano G et al. Plastic prostheses vs expandable metal stents for palliation of inoperable esophageal thoracic carcinoma. Gastrointest Endosc 1996; 43: 478–482. 60 Knyrim K, Wagner HJ, Bethge N et al. A controlled trial of an expansile metal stent for palliation of esophageal obstruction due to inoperable cancer. N Engl J Med 1993; 329: 1302–1307. 61 Fugger R, Niederle B, Jantsch H et al. Endoscopic tube implantation for the palliation of malignant esophageal stenosis. Endoscopy 1990; 22: 101–104. 62 Moores DW, Ilves R. Treatment of esophageal obstruction with covered, self-expanding esophageal Wallstents. Ann Thorac Surg 1996; 62: 963–967. 63 Ramirez FC, Dennert B, Zierer ST et al. Esophageal self-expandable metallic stentsaindications, practice, techniques, and complications: results of a national survey. Gastrointest Endosc 1997; 45: 360–364. 64 De Palma GD, Galloro G, Sivero L et al. Self-expanding metal stents for palliation of inoperable carcinoma of the esophagus and gastroesophageal junction. Am J Gastroenterol 1995; 90: 2140–2142. 65 Kozarek RA, Raltz S, Brugge WR et al. Prospective multicenter trial of esophageal Z-stent placement for malignant dysphagia and tracheoesophageal fistula. Gastrointest Endosc 1996; 44: 462–567. 66 Kozarek RA, Ball TJ, Brandabur JJ et al. Expandable versus conventional esophageal prostheses: easier insertion may not preclude subsequent stent-related problems. Gastrointest Endosc 1996; 43: 204 –208. 67 Trowers EA, Dar S, Hodges D. Tandem expandable stent technique for a fractured nitinol stent. Gastrointest Endosc 1997; 45: 217–218. 68 Segalin A, Bonavina L, Siardi C et al. Can the expandable esophageal metal Endocoil stent be safely removed? Endoscopy 1997; 29: 337–339. 69 Dorta G, Binek J, Blum AL et al. Comparison between esophageal Wallstent and Ultraflex stents in the treatment of malignant stenoses of the esophagus and cardia. Endoscopy 1997; 29: 145–154. 70 Acunas B, Rozanes I, Akpinar S et al. Palliation of malignant esophageal strictures with self-expanding nitinol stents: drawbacks and complications. Radiology 1996; 199: 648–652. 71 Henne TH, Schaeff B, Paolucci V. Small-bowel obstruction and perforation. A rare complication of an esophageal stent. Surg Endosc 1997; 11: 383–384. 72 Scheider DM, Siemens M, Cirocco M et al. Photodynamic therapy for the treatment of tumor ingrowth in expandable esophageal stents. Endoscopy 1997; 29: 271–274. 73 Shields SJ. Esophageal self-expandable metallic stents. Gastrointest Endosc 1997; 45: 439–411.

Complications of esophageal instrumentation 229 74 Demarquay JF, Conio M, Dumas R et al. Fatal complications after placement of an esophageal self-expanding metal stent. Am J Gastroenterol 1996; 91: 178–179. 75 Grundy A, Glees JP. Aorto-oesophageal fistula: a complication of oesophageal stenting. Br J Radiol 1997; 70: 846–849. 76 Allgaier HP, Schwacha H, Technau K et al. Fatal esophagoaortic fistula after placement of a self-expanding metal stent in a patient with esophageal carcinoma. N Engl J Med 1997; 337: 1778. 77 Siersema PD, Tan TG, Sutorius FF et al. Massive hemorrhage caused by a perforating Gianturco-Z stent resulting in an aortoesophageal fistula. Endoscopy 1997; 29: 416–420. 78 Dennert B, Ramirez FC, Sanowski RA. Pericardioesophageal fistula associated with metallic stent placement. Gastrointest Endosc 1997; 45: 82–84. 79 Hendra KP, Saukkonen JJ. Erosion of the right mainstem bronchus by an esophageal stent. Chest 1996; 110: 857–858. 80 Neustater BR, Goldberg RI. Tracheoesophageal fistula complicating placement of a selfexpanding metallic tracheal stent. Am J Gastroenterol 1995; 90: 1360–1361. 81 Song HY, Do YS, Han YM et al. Covered, expandable esophageal metallic stent tubes: experience in 119 patients. Radiology 1994; 193: 689–695. 82 Raijman I, Siddique I, Lynch P. Does chemoradiation therapy increase the incidence of complications with self-expanding coated stents in the management of malignant esophageal strictures? Am J Gastroenterol 1997; 92: 192–196. 83 Hramiec JE, O’Shea MA, Quinlan RM. Expandable metallic esophageal stents in benign disease: a cause for concern. Surg Laparosc Endosc 1998; 8: 40–43. 84 Song HY, Park SI, Do YS et al. Expandable metallic stent placement in patients with benign esophageal strictures: results of long-term follow-up. Radiology 1997; 203: 131–136. 85 Ginsberg GG. Management of ingested foreign objects and food bolus impactions. Gastrointest Endosc 1995; 41: 33–38. 86 Pellerin D, Fortier-Beaulieu M, Gueguen J. The fate of swallowed foreign bodies: experience of 1250 instances of subdiaphragmatic foreign bodies in children. Prog Pediatr Radiol 1969; 1: 286–302. 87 Murat J, Vuillard P, Petua J et al. 108 cases of foreign bodies swallowed in the alimentary tract with the exception of the esophagus. Lyon Chirurg 1969; 65: 880–888. 88 Vizcarrondo FJ, Brady PG, Nord HJ. Foreign bodies of the upper gastrointestinal tract. Gastrointest Endosc 1983; 29: 208–210. 89 Webb WA. Management of foreign bodies of the upper gastrointestinal tract. Gastroenterology 1988; 94: 204 –216. 90 Rogers BH, Kot C, Meiri S et al. An overtube for the flexible fiberoptic esophagogastroduodenoscope. Gastrointest Endosc 1982; 28: 256–257. 91 Webb WA. Management of foreign bodies of the upper gastrointestinal tract: update. Gastrointest Endosc 1995; 41: 39–51. 92 Anderson HA, Bermatz PE, Grindley JH. Perforation of the esophagus after use of a digestive agent: report of a case and experimental study. Ann Otol Rhinol Laryngol 1959; 68: 890–896. 93 Holsinger JW, Fuson RL, Seavy WC. Esophageal perforation following meat impaction and papain ingestion. JAMA 1968; 204: 188–189. 94 Classen M, Farthmann ER, Seifart E et al. Operative and therapeutic techniques in endoscopy. Clin Gastroenterol 1978; 7: 741–763. 95 Garcia C, Frey CR, Bodai BI. Diagnosis and management of ingested foreign bodies: a tenyear experience. Ann Emerg Med 1984; 13: 30–34.

CHAPTER 14

Complications of mediastinal surgery Thomas A D’Amico

The mediastinum The mediastinum is an anatomic region that is characterized by complex relationships involving components of the cardiovascular, gastrointestinal, respiratory, central nervous, and lymphatic systems. Both localized and systemic disorders can involve the mediastinum. A spectrum of diagnostic and therapeutic procedures is employed in the management of patients with diseases that involve the mediastinum. The complex anatomic relationships of the mediastinum must be considered during the conduct of these procedures and the management of the associated complications. Mediastinal tumors and cysts occur in characteristic locations, therefore the mediastinum has been subdivided for the convenience of localizing specific types of lesions. Some subdivide the mediastinum into four compartments asuperior, anterior, middle, and posterior; however, the frequency with which tumors occurring in the anterior or posterior mediastinum extend into the superior mediastinum has prompted the recommendation of three subdivisions: the anterior, middle, and posterior. The anterior compartment is defined as the region posterior to sternum, anterior to heart and great vessels, and contains thymus, mediastinal lymph nodes, and fat. The middle mediastinum contains the heart, pericardium, pulmonary artery and veins, ascending and transverse aorta, brachiocephalic vessels, vena cava, trachea, bronchi, and lymph nodes. The posterior mediastinal compartment is posterior to heart and trachea, anterior vertebral bodies, and contains esophagus, descending aorta, azygos veins, autonomic ganglia and nerves, thoracic duct, lymph nodes, and fat.

Mediastinal masses The natural history of mediastinal masses varies: some are asymptomatic; some grow slowly and cause minimal symptoms; some are aggressive, invasive neoplasms that are often widely metastatic. Mediastinal masses are most frequently located in the anterior mediastinum (56%), with the posterior (25%) and middle mediastinum (19%) being less frequently involved [1]. Although differences in the relative incidence of neoplasms and cysts exist in some series, the most common mediastinal masses are neurogenic tumors (20%), 230

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thymomas (19%), primary cysts (18%), lymphomas (13%), and germ cell tumors (10%) [1]. Malignant neoplasms represent approximately 40% of mediastinal masses. Lymphomas, thymomas, germ cell tumors, primary carcinomas, and neurogenic tumors are the most common. The relative frequency of malignancy varies with the anatomic site. Superior mediastinal masses are more likely malignant (59%), compared with middle mediastinal masses (29%) and posterior mediastinal masses (16%) [1]. Patients in the second through fourth decades of life have a greater proportion of malignant mediastinal masses. This period corresponds to the peak incidence of lymphomas and germ cell tumors. In contrast, in the first decade of life, a mediastinal mass is most probably benign [1].

Clinical features The clinical presentation varies from patients who are asymptomatic, to those with symptoms related to mechanical effects of invasion or compression, to those who have systemic symptoms. The most common symptoms are chest pain, fever, cough, and dyspnea. Symptoms related to compression or invasion of mediastinal structures, such as the superior vena caval syndrome, Horner’s syndrome, hoarseness, and severe pain, are more indicative of a malignant histological diagnosis, although patients with a benign lesion may present in this manner. Primary mediastinal masses may produce hormones or antibodies that cause systemic symptoms, which may characterize a specific syndrome. Examples of these syndromes include Cushing’s syndrome, caused by ectopic production of adrenocorticotropic hormone, most frequently by carcinoid tumors; thyrotoxicosis, which is caused by a mediastinal goiter; hypertension, which may be caused by pheochromocytoma; and hypercalcemia, which may be secondary to increased parathyroid hormone release from a mediastinal parathyroid adenoma.

Diagnosis The goal of the diagnostic evaluation in a patient with a mediastinal mass is a precise histological diagnosis so that optimal therapy can be performed. The preoperative evaluation of a patient with a mediastinal mass should achieve the following: differentiate a primary mediastinal mass from masses of other causes that have a similar radiographic appearance; recognize associated systemic manifestations that may affect the patient’s perioperative course; evaluate for possible compression by the mass of the tracheobronchial tree, pulmonary artery, or superior vena cava; ascertain whether the mass extends into the spinal column; determine if the mass is a non-seminomatous germ cell tumor; assess the likelihood of resectability; and identify significant factors of medical comorbidity and optimize overall medical condition. The initial diagnostic intervention is a careful history and physical examination. The recognition of associated systemic syndromes with many mediastinal

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neoplasms is necessary to avoid potentially serious intraoperative and postoperative complications. Although the majority of systemic syndromes are of little consequence regarding the planned surgical management, the association of myasthenia gravis, malignant hypertension, hypogammaglobulinemia, hypercalcemia, and thyrotoxicosis with mediastinal neoplasms may significantly affect the operative course and postoperative management. The posteroanterior and lateral chest films provide important information concerning anatomic location and size of the tumor. Computed tomography (CT) scanning with contrast medium enhancement should be obtained routinely in patients with a mediastinal mass. Magnetic resonance imaging (MRI) may be more useful than CT in patients with posterior mediastinal masses, in evaluating involvement with the spinal canal, in patients with a contraindication to the use of contrast dye, or in patients with surgical clips in the anatomic region of interest. Additionally, MRI may provide information regarding involvement of major vascular structures and help identify a vascular abnormality. Serologic evaluation is indicated in certain patients. Male patients with an anterior mediastinal mass in the second through fifth decades should have alpha-fetoprotein (α-FP) and beta-human chorionic gonadotropin (β-hCG) serologies obtained. A positive serology is indicative of a non-seminomatous germ cell tumor. Patients with a mediastinal mass and a history of significant hypertension or hypermetabolism should have measurement of urinary excretion of vanillylmandelic acid and catecholamines. This enables the initiation of appropriate perioperative adrenergic blockers in patients with hormonally active intrathoracic pheochromocytoma, paraganglioma, and neuroblastoma, limiting perioperative complications secondary to episodic catecholamine release. Nuclear scans using metaiodobenzylguanidine are useful in tumor location and in identifying sites of metastatic disease, particularly when located in the middle mediastinum. Percutaneous needle biopsy may be performed in order to obtain histological diagnosis, especially in patients with anterior mediastinal masses. However, poorly differentiated malignant tumors of the anterior mediastinum, particularly thymomas, lymphomas, germ cell tumors, and primary carcinomas, can have remarkably similar cytological and morphological appearances. In addition to light microscopy using special staining techniques, immunostaining techniques and electron microscopy of multiple sections of the tumor may be necessary to establish an accurate diagnosis. Monoclonal antibodies for surface antigens specific to a cell line of origin and for tumorsecretory products can be useful in establishing a precise diagnosis. When needle biopsy techniques are contraindicated or do not produce sufficient tissue for the histological diagnosis, more invasive procedures are often required, such as mediastinoscopy, anterior mediastinotomy, thoracoscopy, thoracotomy, or median sternotomy. Mediastinoscopy is a useful technique to evaluate and biopsy lesions of the middle mediastinum. Lesions

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in the superior mediastinum, hilar, or paratracheal regions can be sampled using thoracoscopy. Unresectable posterior mediastinal masses may be biopsied thoracoscopically or through a limited posterolateral thoracotomy. A representative section of the tissue obtained should be submitted for immediate frozen section to establish adequacy of the biopsy before closing. Lesions that appear resectable should be completely excised. Median sternotomy and anterolateral thoracotomy provide optimal exposure for lesions in the anterior mediastinum. Middle and posterior mediastinal masses are usually excised through a posterolateral thoracotomy. Thoracoscopic procedures have been used to sample and resect mediastinal lesions in carefully selected patients [2]. Although most patients undergo surgical procedures safely, patients with large anterior or middle mediastinal masses, particularly children, have an increased risk of developing severe cardiorespiratory complications during general anesthesia. Patients with posture-related dyspnea and superior vena caval syndrome are at increased risk. In patients with airway compression or superior vena caval obstruction, the risk of general anesthesia is markedly increased and attempts to obtain a histological diagnosis should be limited to needle biopsies or open procedures done with local anesthesia. The majority of these lesions are malignant and unresectable.

Cervical mediastinoscopy Cervical mediastinoscopy with biopsy is applicable in the evaluation of mediastinal adenopathy associated with numerous malignant conditions, including lung cancer, lymphoma, esophageal cancer, head and neck cancer, breast cancer, melanoma, colorectal cancer, renal cell carcinoma, and mesothelioma. In addition, cervical mediastinoscopy may be used to characterize benign pathological conditions of the mediastinum, including sarcoidosis, histoplasmosis, and tuberculosis. Mediastinoscopy may be used to biopsy primary mediastinal masses, such as thymomas, germ cell tumors, lymphomas, and mediastinal cysts. General anesthesia is used in all patients. Because placement of the mediastinoscope under the innominate artery may limit flow in the right carotid artery, a catheter is placed in the radial artery to monitor dampening of blood pressure, in order to avoid prolonged limitation of cerebral blood flow. Similarly, insertion of the scope over the aortic arch during extended cervical mediastinoscopy may compress the left carotid and subclavian arteries, and a pulse oximeter placed on the left upper extremity is a surrogate to monitor left carotid blood flow. Sterile preparation and draping must allow for the possibility of an urgent median sternotomy or right anterolateral thoracotomy. A 2–3-cm incision is made in the suprasternal notch, the platysma is incised, and the cervical strap muscles are reflected bilaterally. There are two clearly defined mediastinal planes for the assessment of mediastinal structures: the retrovascular pretracheal

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plane and the prevascular substernal plane. Cervical mediastinoscopy is performed by entry into the pretracheal space, digital dissection in the cervicomediastinal plane and placement of the mediastinoscope in this plane [3]. After visual inspection of the pretracheal mediastinal structures, biopsy of paratracheal (levels 2 and 4) and subcarinal (level 7) lymph nodes is performed (Figure 14.1). Extended cervical mediastinoscopy, designed to assess the prevascular lymph nodes not accessible by cervical mediastinoscopy, utilizes the same cervical incision; however, digital dissection is performed anterior to the innominate vein and aortic arch [4]. The mediastinoscope is then guided into this plane for assessment and biopsy of aortopulmonary window lymph nodes (level 5) and preaortic lymph nodes (level 6) (Figure 14.2). Contraindications to mediastinoscopy include severe cervical arthritis limiting neck extension, a patient with size limitations that prevent insertion of the mediastinoscope, the presence of a tracheostomy, extensive atherosclerosis of the aortic arch or innominate artery, and severe fibrosing mediastinitis [5]. Avoiding mediastinoscopy in these rare conditions minimizes the complications of this procedure. Previous mediastinoscopy is not a contraindication, but does increase the difficulty of the dissection and may be considered to increase the risk of the procedure.

(a) Figure 14.1 Regional lymph node classification for lung cancer staging. (a) Superior mediastinal lymph nodes.

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(b) Figure 14.1 (cont’d) (b) Inferior mediastinal lymph nodes. (From Mountain CF, Dresler CM. Regional lymph node classification for lung cancer staging. Chest 1997; 111: 1718–1723, with permission.)

Figure 14.2 Extended cervical mediastinoscopy. (From CTSNet, with permission.)

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Complications of mediastinoscopy The morbidity and mortality associated with mediastinoscopy are low, with most series reporting complications in approximately 0.5–4% of patients and a morality of < 0.5% [5–10]. In a series of 1000 cases at the University of Toronto, complications were reported in 2.3% of patients, with no deaths [7]. In this series, only three complications were considered major, including two cases of hemorrhage and one tracheal injury. In a series of 2137 patients from Washington University, there were 12 complications (0.6%) and four deaths; of the four deaths, the authors attributed only one (0.05%) to mediastinoscopy [6]. The complication rate is higher in cases of repeat mediastinoscopy (approximately 7%) [11]. The most important common complication is hemorrhage. Minor bleeding is frequently encountered with routine dissection, especially in the subcarinal station, which is supplied by bronchial arteries. Minor bleeding from small vessels is usually controlled by direct pressure, applied with gauze packing, or precise electrocoagulation, taking care to avoid cautery in the left paratracheal station, which may endanger the left recurrent laryngeal nerve. Major bleeding, defined as hemorrhage that obscures the vision through the mediastinoscope, may originate from the azygos vein, innominate artery, aorta, pulmonary artery, or left atrium. The most common source is the azygos vein, which may be injured with vigorous dissection in the right paratracheal space or inadvertent biopsy. Biopsy-associated injury is preventable by ascertaining lymph node identity through either careful dissection or needle aspiration. Small tears in the azygos vein may be controlled with gauze packing; more extensive injuries must be addressed at thoracoscopy or thoracotomy. Rarely, an azygos vein injury may be controlled with a thoracoscopic clip applier through the mediastinoscope. If the bleeding is temporarily controlled with packing, the cervical incision is closed and the patient turned to the left lateral decubitus position for right thoracoscopy or thoracotomy. For patients with a resectable right-sided lung cancer, the pulmonary resection is completed at the same time. If the bleeding can not be temporized through the mediastinoscopy incision, a right anterolateral thoracotomy is urgently performed for repair of the azygos vein; however, access to the azygos vein, a posterior mediastinal structure, is limited through this incision. Caudal retraction of the upper and middle lobes is required to visualize the site of hemorrhage; this maneuver may be facilitated by temporarily interrupting ventilation. Injury to the innominate artery or aorta may occur when biopsy of firm, fibrous masses that encase the vessels is attempted. Such injuries should be completely preventable by limiting the traction placed on the biopsy forceps when firm, fibrous masses are encountered. Torrential bleeding ensues with injury to the innominate artery or aorta. Rather than attempting to pack such injuries, the surgeon should immediately remove the mediastinoscope and apply digital pressure to the injury while preparing for emergent median sternotomy [12]. It may be possible to repair injuries to the innominate artery

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or aorta without cardiopulmonary bypass. However, injuries to the posterior aorta, especially in the setting of extensive tumor, may be difficult to visualize without inducing severe prolonged hypotension. Cardiopulmonary bypass should therefore be made available as soon as the decision to perform median sternotomy is made. Systemic anticoagulation is achieved when it has been ascertained that cardiopulmonary bypass is required to repair the injury; delay in anticoagulation may cause disseminated intravascular coagulation if cardiopulmonary bypass is instituted prematurely. The site of the aortic cannulation site should be chosen carefully, to minimize the risk of compression of the arterial inflow line during manipulation of the aorta during repair. Extensive posterior aortic injuries may even require circulatory arrest in order to accomplish repair. Biopsy of paraaortic lymph nodes may be performed at the completion of successful repair of the innominate artery or aorta; however, no attempt to address a primary pulmonary tumor for resection should be made in this setting. The right pulmonary artery crosses anterior to the trachea. Injury to the pulmonary artery may occur with inadvertent biopsy, but this complication should be completely avoidable if precise dissection is performed under adequate visualization prior to biopsy. Injury to the pulmonary artery must be addressed emergently by median sternotomy and may require cardiopulmonary bypass. After median sternotomy, the right pulmonary artery is encircled in the pericardial recess between the vena cava and the aortic arch. If the injury can not be controlled with tamponade, direct suture or patched repair is attempted. Pneumonectomy must be performed if the pulmonary artery can not be successfully repaired. Prevention of this potentially devastating injury during mediastinoscopy is paramount. The left recurrent laryngeal nerve is at the left tracheobronchial angle and injury may occur as a result of vigorous dissection in attempting to biopsy the left paratracheal lymph nodes. When the nerve is visible, careful dissection and avoidance during biopsy should minimize the chance of injury. When the nerve is not visible, awareness of its presence in dissection and biopsy is essential. Laryngeal nerve injury results in vocal cord paralysis and hoarseness. Laryngeal nerve palsy may be palliated by supporting the vocal cord with injected gelfoam or Teflon, or medialization with a cartilaginous splint or silicone elastomer [13,14]. Stroke may occur after mediastinoscopy, although rarely. The mechanisms include atherosclerotic embolization from the aortic arch [15] or cerebral ischemia, secondary to compression of the innominate artery [9]. Preventative measures include arterial monitoring of the right upper extremity and palpation of the arterial structures to detect severe atherosclerotic disease prior to placement of the mediastinoscope. Extensive atherosclerotic disease in the aortic arch is a relative contraindication to proceeding with lymph node biopsy. Medical management of cerebrovascular accident is instituted as soon as possible. Prompt postoperative recognition of this complication is important.

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Esophageal perforation may occur during vigorous dissection of the subcarinal lymph nodes. Unlike other complications of mediastinoscopy, esophageal injury may not be apparent at surgery or in the immediate postoperative period. Dissection of the subcarinal space may be associated with bleeding that obscures visibility. It is inadvisable to continue to attempt to biopsy lymph nodes under these circumstances. Occult esophageal injury should be suspected in any patient with fever, leukocytosis, pleural effusion, or cardiac arrhythmia after mediastinoscopy. Perforation of the esophagus is confirmed by barium esophagogram, and immediate repair performed through right thoracotomy. Primary repair is achieved by identifying the complete extent of the mucosal injury and closing the mucosa precisely with interrupted absorbable suture [16]. The muscular layers should then be reapproximated as well. Reinforcement of the repair with an intercostal muscle pedicle is advisable, but optional. Gastrostomy or feeding jejunostomy should be considered after repair of the esophageal injury, depending on the extent of the injury. When extensive tumor fibrosis is present, especially after induction therapy or in repeated mediastinoscopy, dissection and biopsy may lacerate the trachea or bronchus. This injury is manifested immediately by a large air leak, easily recognized at mediastinoscopy. Repair is accomplished through a cervical incision, if the injury is proximal, or right thoracotomy, if the injury is more distal. If pulmonary resection is performed at the time of thoracotomy, the injury may be repaired by its incorporation in the bronchial stump suture line [17]. Prevention of this injury, in the setting of fibrosis, may be accomplished by using a thoracoscopic approach for paratracheal lymph node biopsy, rather than cervical mediastinoscopy. Pneumothorax may occur after mediastinoscopy, usually secondary to pleural entry. If recognized at surgery, the pleural space may be evacuated prior to closure using the mediastinoscope and the suction-dissector. If a small pneumothorax is present postoperatively, observation is appropriate. If the lung was biopsied or traumatized, tube thoracostomy may be required. The development of incisional metastases after mediastinoscopy has been reported [18]. Direct implantation of malignant cells in the surgical field during may be a plausible mechanism; however, it does not necessarily explain the appearance of incisional metastases arising after negative mediastinoscopy. Other possible explanations include lymphatic dissemination and hematogenous spread followed by implantation in the hyperemic wound in the early stages of healing [18]. In the absence of metastatic disease, the tumor implant may be locally excised and radiation therapy employed.

Thymectomy for myasthenia gravis Resection of anterior mediastinal masses is routinely performed using median sternotomy; however, thymectomy for myasthenia gravis can also be

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accomplished using median sternotomy [19], partial upper sternotomy [20], transcervical approach [21], and thoracoscopic approach, both right-sided [22] and left-sided [23]. The utility of thymectomy for myasthenia gravis is still debated, but most surgeons and neurologists support this strategy in operable patients [24]. A non-randomized study performed at the Mayo Clinic demonstrated a significant benefit in patients who underwent thymectomy, compared with patients who received medical management only [25]. The role of thymectomy in the treatment of myasthenia gravis was analyzed in 400 patients affected with generalized myasthenia [26]. There was a gradual, progressive increase of cumulative remission over time, that could be ascribed both to a delayed effect of thymectomy as well as the natural history of myasthenia gravis itself, characterized by an increasing probability of spontaneous remission with time. Patients without thymoma who did not require additional immunosuppressive therapy had the highest remission rate. In another study, 375 patients with myasthenia gravis (286 non-thymomatous and 89 thymomatous) who had extended thymectomies were reviewed by Masaoka and colleagues [27]. Remission rates of the non-thymomatous patients were 15.2% (3 months), 15.9% (6 months), 22.4% (1 year), 36.9% (3 years), 45.8% (5 years), 55.7% (10 years), 67.2% (15 years), and 50.0% (20 years). Remission rates in the thymomatous patients were 13.6% (3 months), 17.5% (6 months), 27.5% (1 year), 32.4% (3 years), 23.0% (5 years), 30.0% (10 years), 31.8% (15 years), and 37.5% (20 years). Absence of thymoma, younger age, and short duration of the disease were favorable prognostic factors [27].

Complications of thymectomy The ability to perform a complete thymectomy is considered essential to the strategy of thymectomy to improve the symptoms associated with myasthenia gravis, and the most important complication associated with this operation is incomplete resection [19,28]. Proponents of median sternotomy for maximal thymectomy claim that this procedure uniquely allows the complete removal of the thymus gland and all extraglandular thymic tissue [19,27]. Nevertheless, surgeons who employ the transcervical approach claim equivalent remission rates [21,29]. Comparison of recent series of thymectomy for myasthenia gravis using various surgical approaches demonstrates similar complete remission rates (40–52%) and partial response rates (87–95%) [19,21,29,30]. To add to the debate, thoracoscopic approaches are now being employed for thymectomy for myasthenia gravis [22,23]. Advocates of the right thoracoscopic approach maintain that it allows greater maneuverability of instruments in the wider right pleural cavity and easier identification of the left innominate vein because the superior vena cava serves as a landmark [22]. The advantages of the left thoracoscopic approach include the ability to remove the perithymic tissue in the left pericardiophrenic angle and in the aortopulmonary window [23]. At this point, complete removal of the thymus should be considered the goal of the procedure, and the approach should be at the

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discretion of the surgeon, provided equivalent remission rates have been documented. In the perioperative period following thymectomy for myasthenia gravis, the most important significant complication is considered to be respiratory failure, which occurs in 0–4% of patients [19,23,27,31,32]. Pulmonary function has been found to be significantly better after thoracoscopic thymectomy compared with sternotomy [33]. Adequate preoperative medical management, including plasmapheresis when appropriate, avoiding paralytic agents intraoperatively, and aggressive postoperative pulmonary physiotherapy contribute to minimizing the potential for postoperative respiratory therapy. Plasmapheresis involves filtering the plasma of specific proteins, including the acetylcholinesterase antibody. Plasmapheresis produces a rapid, transient clinical improvement in patients with myasthenia gravis and should be considered in every patient preoperatively. Plasmapheresis may be performed every other day for four to six cycles, up to 48 h prior to surgery. The clinical improvement associated with plasmapheresis minimizes the risk of postoperative weakness and respiratory failure and avoids the use of anticholinesterase agents perioperatively. The choice of agents to induce anesthesia is dependent on the degree of weakness that the patient demonstrates at the time of surgery. A patient with good muscle strength may be induced with an agent of choice (propofol, a barbiturate, or etomidate) followed by a fractional dose of a neuromuscular blockade agent. A weaker patient will require a more careful induction with a smaller dose of an induction agent and no neuromuscular blockade agent. Maintenance of anesthesia may be accomplished with propofol infusion or inhalational agent; muscle relaxation is not necessary after successful intubation. With minimization of anesthetic agents, such as narcotics and barbiturates and avoidance of benzodiazepines, the majority of patients can be successfully extubated in the operating room. Postoperative recovery in an intensive care unit is considered routine, but with excellent analgesia (including placement of an epidural catheter), most patients may be observed overnight on a step-down unit. The patient must be observed closely throughout the recovery period for signs of weakness, which may occur several days after thymectomy. In addition to monitoring for signs of weakness, attention must be given to aggressive pulmonary physiotherapy, in order to minimize the risk of postoperative atelectasis and pneumonia. Prolonged ventilator dependence may be treated with additional anticholinesterase agents, reversal of narcosis, intravenous immunoglobulin, or plasmapheresis to clear circulating antiacetylcholine receptor antibodies [24]. Tracheostomy is occasionally beneficial to facilitate pulmonary performance. Technical complications related to the conduct of thymectomy for myasthenia gravis should be rare in the absence of thymoma. Complications such as vascular or nerve injury, which are important considerations during the resection of anterior mediastinal masses, are completely avoidable. Injury to the recurrent laryngeal nerve or the phrenic nerve after thymectomy for

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myasthenia gravis has been reported, but should be extremely rare [34]. Postoperative mediastinitis has been reported [35]; the accepted precautions to avoid this devastating complication should be strictly observed [36]. Many complications primarily associated with the underlying myasthenia gravis may occur in the perioperative period after thymectomy [24]. Readmission secondary to weakness may be related to cessation of medications in the perioperative period, and reinstitution of anticholinesterase therapy, corticosteroids, or plasmapheresis may be required.

Resection of anterior mediastinal masses Thymoma Thymoma is the most common neoplasm of the anterior mediastinum and the second most common mediastinal mass. It may appear on radiographs as a small, well-circumscribed mass (Figure 14.3) or a bulky lobulated mass confluent with adjacent mediastinal structures. Patients are usually symptomatic at presentation. Symptoms may be related to local mass effects causing chest pain, dyspnea, hemoptysis, cough, and the superior vena caval syndrome. Furthermore, thymomas are often associated with systemic syndromes caused by immunological mechanisms. Although the most common syndrome is myasthenia gravis, many other syndromes have been associated with thymomas, including red cell aplasia, white cell aplasia, aplastic anaemia, Cushing’s syndrome, hypogammaglobulinemia and hypergammaglobulinemia, dermatomyositis, systemic lupus erythematosus, progressive systemic sclerosis, hypercoagulopathy with thrombosis, rheumatoid arthritis, megaesophagus, and granulomatous myocarditis [24]. Unlike myasthenia gravis,

Figure 14.3 Well circumscribed thymoma.

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Figure 14.4 Anatomy of the thymus. This illustration represents what is now generally accepted as the surgical anatomy of the thymus [42]. The frequencies (percent occurrence) of the variations are noted. Black, thymus; gray, fat that may contain islands of thymus and microscopic thymus. A-P window, Aorto-pulmonary window. (From: Neurology 1997; 48 (Suppl. 5): S52–S63.)

the other systemic syndromes often do not improve after successful control of the thymoma. The majority of patients with myasthenia gravis do not have thymoma; the incidence is 10–42%, depending on the reporting medical center. Approximately 15% of patients with thymoma have myasthenia gravis [1]. Whereas red cell aplasia occurs in only 5% of patients with thymoma, 33–50% of adults with red cell aplasia have a thymoma [1]. Whenever possible, the therapy for thymoma is surgical excision without removing or injuring vital structures (Figure 14.4). Even with well-encapsulated thymomas, extended thymectomy with eradication of all accessible mediastinal fatty areolar tissue should be performed to ensure removal of all ectopic thymic tissue. This approach lowers the number of tumor recurrences. The best operative exposure is obtained using a median sternotomy [19,28,30,37]. Because many thymomas are radiosensitive, the placement of surgical clips to outline the anatomic extent of disease aids in the determination of optimal radiation portals. The most commonly used staging system for thymomas was described by Masaoka and colleagues [27]. Stage I tumors are macroscopically completely

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encapsulated, with no microscopical capsular invasion; stage II tumors demonstrate microscopic invasion into surrounding fatty tissue, mediastinal pleura or capsule; stage III tumors have macroscopic invasion into adjacent mediastinal structures; stage IVa disease is characterized by pleural or pericardial dissemination; and IVb disease is defined by lymphogenous or hematogenous metastasis. Complete surgical resection for stage I thymoma is sufficient treatment. The adjunctive use of radiation therapy is the recommended treatment for stage II and III disease [37]. Tumors > 5 cm, locally invasive tumors, unresectable tumors, and metastatic tumors should be treated by protocols that include chemotherapy, followed by surgical exploration with the goal of complete resection and postoperative radiation. The best results are seen with cisplatinbased regimens with overall response rates of 70–100% [38]. An aggressive surgical approach is recommended for invasive thymomas including radical resection and vascular reconstruction of the superior vena cava or its branches when invaded. Utilizing this aggressive approach to obtain complete resections a significant difference in 5-year survival is seen in patients with stage III thymomas (94%) compared with those with incomplete resections (35%) [37]. Thymomas frequently show recurrence and reoperation for recurrent disease has been recommended. Since thymomas have been reported to have late recurrence, cure rates should be based on 10-year followup data.

Germ cell tumors Germ cell tumors are benign and malignant neoplasms thought to originate from primordial germ cells that fail to complete the migration from the urogenital ridge. These lesions are identical histologically to germ cell tumors originating in the gonads, but are not metastatic. The current recommendations for evaluating the testes of a patient with mediastinal germ cell tumor are careful physical examination and ultrasonography. Biopsy is reserved for positive findings. Teratomas are neoplasms composed of multiple tissue elements derived from the three primitive embryonic layers foreign to the area in which they occur. These tumors are located most commonly in the anterior mediastinum, although they are sometimes found in the posterior mediastinum (Figure 14.5). Symptoms are related to mechanical effects and include chest pain, cough, dyspnea, or symptoms related to recurrent pneumonitis. CT findings of a predominantly fatty mass with a denser dependent portion containing globular calcifications, bone, or teeth and a solid protuberance into a cystic cavity are considered specific. Malignant tumors are identified by the presence of embryonic tissue or by the presence of malignant components. Diagnosis and therapy rely on surgical excision. For those benign tumors of such large size or with involvement of adjacent mediastinal structures such that complete resection is impossible, partial resection has led to resolution of symptoms, frequently without relapse. For malignant teratomas,

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Figure 14.5 Large teratoma in the anterior mediastinum.

chemotherapy and radiation combined with surgical excision is individualized for the type of malignant components contained in the tumors. Serological measurements of α-FP and β-hCG are useful for differentiating seminomas from non-seminomas, quantitatively assessing response to therapy in hormonally active tumors, and diagnosing relapse or failure of therapy before changes that can be observed in gross disease. Seminomas rarely produce β-hCG and never produce α-FP; in contrast, over 90% of non-seminomas secrete one or both of these hormones. This differentiation is important because of the marked radiosensitivity of seminomas and the relative radioinsensitivity of non-seminomas. Unlike other malignant germ cell tumors, seminomas usually remain intrathoracic with local extension to adjacent mediastinal and pulmonary structures (Figure 14.6). Although metastatic spread occurs first through lymphatics, hematogenous spread with extrathoracic involvement may develop late in the course of disease. Bone and lung are the most common sites of metastatic spread. Patients are usually symptomatic owing to the mechanical effects of the tumor on adjacent structures. Therapy for seminomas is determined by the stage of the disease. Excision is recommended when possible. When complete resection is possible, the use of adjuvant therapy is unnecessary. However, careful follow-up with serial CT examinations is required to diagnose recurrences. When excision is not possible, a biopsy sample of sufficient size to establish the diagnosis should be obtained. Owing to the radio- and chemosensitivity of this tumor, cytoreductive resection before chemotherapy or radiotherapy is unnecessary and is contraindicated when vital structures are involved or when the procedure is technically difficult. Radiation therapy can be used for localized disease. Any residual disease should be surgically resected after chemotherapy.

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Figure 14.6 Seminoma in the anterior mediastinum.

Malignant non-seminoma tumors include choriocarcinomas, embryonal cell carcinomas, immature teratomas, teratomas with malignant components, and endodermal cell (yolk sac) tumors. The non-seminomas differ from seminomas in several aspects: (i) they are more aggressive tumors that are frequently disseminated at the time of diagnosis; (ii) they are rarely radiosensitive; and (iii) over 90% produce either β-hCG or α-FP. All patients with choriocarcinoma and some patients with embryonal cell tumors have elevated levels of β-hCG; α-FP is most commonly elevated in patients with embryonal cell carcinomas and yolk sac tumors. The presence of a significantly elevated titer of β-hCG or an elevated titer of α-FP is indicative of a non-seminomatous germ cell component. These tumors follow the natural history of a non-seminoma. The majority of patients with these neoplasms are symptomatic with chest pain, dyspnea, weight loss, cough, hemoptysis, fever, and chills and the superior vena caval syndrome. Chest films usually reveal a large anterior mediastinal mass with frequent extension into lung parenchyma and adjacent mediastinal structures. Frequent sites of metastatic disease include brain, lung, liver, bones, and the lymphatic system, particularly the supraclavicular nodes. Chest wall involvement is common. The local invasiveness of these tumors and frequent metastases usually preclude surgical resection of all disease at the time of diagnosis. Initially, operative intervention is necessary only to establish the histological diagnosis in patients without elevations in serum α-FP or β-hCG. Treatment of nonseminomatous tumors is by multiagent chemotherapy containing cisplatin followed by surgical resection of residual masses. Serum markers, α-FP and

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β-hCG are followed to assess response to treatment, and when these markers normalize the patient is taken to the operating room and removal of as much of the remaining tumors as possible is performed. The presence of residual disease after chemotherapy portends a poor prognosis and the need for additional chemotherapy. If the tumor markers do not normalize, a second course of chemotherapy is begun with new agents. Resection of tumors of the anterior mediastinum is usually performed through median sternotomy. Dissection of thymic malignancies and germ cell tumors requires the development of planes between the tumor and the phrenic nerves, the recurrent laryngeal nerve, the thoracic duct, the great vessels, the trachea, the pericardium, the sternum, and the lungs. Resection of locally advanced malignancies may require resection of involved structures; vascular reconstruction may be required in some circumstances.

Complications related to resection of anterior mediastinal masses Injury to one or both phrenic nerves may occur during resection. Prior to surgery, the function of the phrenic nerves may be assessed by evaluating the position of the diaphragms on the preoperative chest radiograph or by fluoroscopy. The phrenic nerves should be assessed intraoperatively in terms of their relationship to the tumor. If one phrenic nerve is non-functional due to tumor involvement, it is resected with the tumor, and every effort is made to preserve the contralateral nerve. The left phrenic nerve lies in a more anterior position than the right phrenic nerve in relation to the pulmonary hilum and is more likely to be in jeopardy during dissection. Unilateral phrenic nerve injury is tolerated by most patients, and no specific therapy is required. Plication of the diaphragm may be performed subsequently in patients who develop prominent diaphragmatic eventration or paradoxical motion. Bilateral phrenic nerve injury is poorly tolerated; patients with bilateral diaphragmatic dysfunction may require bilateral plication or tracheostomy and mechanical ventilation [39]. Tumors of the anterior mediastinum near the aortopulmonary window may involve the left recurrent laryngeal nerve. Complete resection of the tumor is the primary goal, and resection of the recurrent nerve is required if it is involved. Postoperatively, the resulting vocal cord palsy may be treated with Teflon or gelfoam injection or with vocal cord medialization [13,14]. Chylothorax may result after resection of mediastinal masses, although it is more commonly associated with esophagectomy or pneumonectomy. Injury to the thoracic duct during dissection of anterior mediastinal masses occurs at the level of the aortic arch, where the thoracic duct passes behind the left carotid artery, or at the insertion into the left subclavian vein. If the thoracic duct is involved with the tumor or is in jeopardy from the dissection, it should be intentionally ligated, rather than risk postoperative leak. If the injury is not recognized at surgery, the development of an early postoperative effusion or persistent pleural drainage, especially if the fluid is milky

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in appearance, suggests trauma to the thoracic duct. The diagnosis of chylothorax is confirmed if triglyceride level in the pleural fluid is > 110 mg/dl [40]. Prolonged drainage of chyle causes malnutrition if not recognized and managed aggressively. Non-operative management includes pleural drainage and enteral or parenteral nutritional support. Enteral support, using a formula based on medium chain triglycerides, is infrequently successful. Pleural sclerosis may be used to expedite closure of the injured thoracic duct [41]. The most successful approach is early reoperation and surgical closure of the thoracic duct [42]. Preoperative lymphoscintigraphy to identify the site of injury is unnecessary. Ligation of the thoracic duct in the right chest at the level of the diaphragm (using thoracotomy or thoracoscopy) is successful in a majority of cases. For patients who have undergone extensive mediastinal dissection for anterior mediastinal masses, direct ligation at the site of injury may be preferred. Intraoperative localization of the injury is improved if a substantial amount of lipid (such as cream or vegetable oil) is administered prior to surgery via nasogastric tube. Cerfolio and colleagues reported the Mayo Clinic experience with postoperative chylothorax [41]. Of the 47 patients in this series with postoperative chylothorax, six had undergone resection of mediastinal mass. In this series, conservative management was associated with failure, and the authors recommend early operative intervention. Resection of complex anterior mediastinal masses, especially stage III thymomas after induction chemotherapy, requires careful dissection of vascular structures, in order to avoid intraoperative hemorrhage and sacrifice of essential vessels. Most anterior mediastinal masses have a close relationship to the brachiocephalic vein; if the tumor is directly invasive or if the vessel is obliterated, the brachiocephalic vein may be resected en bloc with the tumor. Reconstruction is optional if the superior vena cava is patent; if both the brachiocephalic vein and the superior vena cava are involved, reconstitution of at least one cavoatrial connection is recommended to avoid severe cerebral edema [43]. Bacha and colleagues reported their results after extended radical resection in 89 patients with primary mediastinal tumors invading adjacent structures [43]. In this series, there were 35 invasive thymomas, 12 thymic carcinomas, 17 germ cell tumors, 16 lymphomas, three neurogenic tumors, three thyroid carcinomas, two radiation-induced sarcomas, and one mediastinal mesothelioma. Adjacent resected structures included 38 phrenic nerves, 21 superior venae cavae, 16 upper lobes, and 13 innominate veins, and in five patients a pneumonectomy was required. The complication rate was 17% and the mortality rate 6% [43]. A heterogeneous group of tumors, both benign and malignant, involve the thoracic inlet and adjacent structures, including superior sulcus tumors, primary neurogenic tumors arising in autonomic and somatic nerves around the spine or brachial plexus, soft-tissue neoplasms, and metastases from a variety of primary sites. Complete resection requires careful dissection, and

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may require the resection of major vascular, neural or skeletal structures. Although primary or metastatic tumors infrequently arise in or involve the thoracic outlet, they represent a major surgical challenge because of their tendency to encapsulate outlet structures. The antero-superior approach to tumors in the thoracic inlet has been described [39,44–46]. This approach uses an L-shaped cervical incision extended into the deltopectoral groove, resection of the internal half of the clavicle, and, in the case of tumor involvement, resection of the jugular and subclavian veins, phrenic nerve, subclavian artery, brachial plexus, and ribs. Revascularization of both the subclavian vein by an end-to-end anastomosis and the subclavian artery by a ringed polytetrafluoroethylene graft may be performed simultaneously. Neurological impairment secondary to resection of neural elements involved with the tumor will result. The anterior approach provides superior visualization of the brachial plexus, minimizing unnecessary collateral damage during dissection. Division of the subclavian vein without revascularization may lead to transient upper extremity edema. Revascularization of the subclavian artery is essential to avoid ischemic and potentially fatal complications [44–46].

Resection of posterior mediastinal masses Neurogenic tumors are the most common mediastinal neoplasm, constituting 20% of all primary tumors and cysts [1]. These tumors are usually located in the posterior mediastinum and originate from the sympathetic ganglia (ganglioma, ganglioneuroblastoma, and neuroblastoma), the intercostal nerves (neurofibroma, neurilemoma, and neurosarcoma), and the paraganglia cells (paraganglioma) (Figure 14.7). Only rarely are these tumors located in the

Figure 14.7 Neurofibroma in the posterior mediastinum.

Complications of mediastinal surgery 249

anterosuperior mediastinum. Although the peak incidence occurs in adults, neurogenic tumors comprise a proportionally greater percentage of mediastinal masses in children. Whereas the majority of neurogenic tumors in adults are benign, a greater percentage of neurogenic tumors are malignant in children. Many of these tumors are found in asymptomatic patients on routine chest films. When present, symptoms are usually caused by mechanical factors such as chest and back pain due to compression or invasion of intercostal nerve, bone, and chest wall; cough and dyspnea due to compression of the tracheobronchial tree; Pancoast’s syndrome; and Horner’s syndrome due to involvement of the brachial and the cervical sympathetic chain. Symptoms may be systemic and related to production of neurohormonal agents. Thoracoscopy has played an increasing role both in diagnosis and treatment of neurogenic tumors. Benign neurogenic tumors are particularly amenable to thoracoscopic removal, and more rapid postoperative recovery is seen with thoracoscopic removal compared with open excision [2]. For malignant tumors, the standard of care remains thoracotomy. The complications associated with resection of posterior mediastinal masses are similar to those following resection of anterior mediastinal masses. However, posterior masses uniquely may involve the vertebral bodies or spinal cord. Approximately 10% of neurogenic tumors have extensions into the spinal column [1]. These are termed dumbbell tumors because of their characteristic shape with relatively large paraspinal and intraspinal portions connected by a narrow isthmus of tissue traversing the intervertebral foramen. Although the majority of patients with a dumbbell tumor have neurological symptoms related to spinal cord compression, the significant proportion of patients without symptoms underscores the importance of evaluating all patients with a posterior mediastinal mass for possible intraspinal extension with a MRI. The recommended surgical approach to dumbbell tumors is a one-stage excision of the intraspinal component before resecting the thoracic component to minimize any spinal column hematoma. The incision used for the posterior laminectomy is extended into the appropriate interspace to allow resection of the mediastinal component. Anterior video-assisted thoracoscopy for removal of the intrathoracic component of the tumor is combined with a posterior laminectomy for microneurosurgical removal of the spinal component [47].

Thoracoscopic sympathectomy The thoracoscopic approach is the most commonly used approach for surgical sympathectomy of the upper extremities. Thoracoscopic sympathectomy is used in the treatment of palmar and axillary hyperhidrosis [48], reflex sympathetic dystrophy [49], atherosclerotic peripheral vascular disease [50], and Raynaud’s disease [51]. Usually, the sympathetic ganglia are removed from T2–T4, although some surgeons prefer a more limited dissection, at T2 only [48].

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Death after thoracoscopic sympathectomy has been reported, secondary to cerebral edema, when CO2 insufflation has been employed [52]. Another patient in this series sustained severe neurological dysfunction, secondary to cerebral edema. The development of cerebral edema after thoracoscopic sympathectomy is attributable to gas insufflation, which is not required and should be avoided. Major vascular injury during thoracoscopic sympathectomy has also been reported, and this complication should be completely avoidable [52]. Chylothorax after sympathectomy has also been described and is related to division of accessory ducts rather than injury to the thoracic duct [53,54]. In these cases, treatment with chest tube drainage was successful and reoperation was not required. The most common complications of sympathectomy are related to manipulation of the autonomic nervous system [55]. Injury to the brachial plexus has been described [56]. Inadvertent injury of the stellate ganglion will produce ipsilateral Horner’s syndrome, either total or partial (without meiosis). Injury to the stellate ganglion is caused by mechanical or thermal damage to T1 during dissection. In order to prevent this injury, precise identification of ribs 1–4 is required prior to dissection of the sympathetic ganglion at T2; no dissection is performed above this level. Furthermore, excessive nerve traction is avoided during dissection. Finally, the use of bipolar cautery or ultrasonic dissection will prevent current diffusion to the stellate ganglion. Neuralgia along the ulnar aspect of the upper limb may occur after sympathectomy, which usually resolves within 6 weeks [55]. Compensatory sweating may occur after upper extremity sympathectomy, in various areas, including the axillary, inguinal, and truncal regions. This complication is unpredictable and there are no techniques to avoid its occurrence. Gustatory sweating (facial perspiration provoked by the taste of food) can also occur [57].

Medical complications of mediastinal surgery In patients undergoing thoracic surgery, the incidence of atrial arrhythmias is 15–40% [58]. In addition to extent of resection, the risk factors for the development of atrial fibrillation include age, presence of coronary artery disease, history of congestive heart failure, and the use of theophylline. Proposed mechanisms for the development of atrial fibrillation include right ventricular dilatation, elevated catecholamine levels, and atrial conduction delay resulting in reentrant circuits, secondary to pulmonary vein manipulation and surgical dissection. Atrial arrhythmias most commonly present on postoperative days 2–4, related to the increased adrenergic activity in the postsurgical state. A treatment algorithm for postoperative atrial fibrillation includes the following: 1 Correction of hypoxia. 2 Correction of acid/base abnormalities. 3 Correction of hypokalemia, hypomagnesemia.

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4 Limitation of β-adrenergic agents and theophylline. 5 Rate control with diltiazem, if hemodynamically stable; β-adrenergic blockade may be used in patients with low risk of congestive heart failure and bronchospasm [58].. 6 Medical cardioversion with amiodarone, sotalol, propafenone, or procaineamide may be attempted in patients who do not spontaneously return to sinus rhythm. 7 Synchronized electrical cardioversion may be used in selective patients, including those who are hemodynamically unstable. 8 Anticoagulation may be required in patients who remain in atrial fibrillation. In patients with no history of cardiac disease, the incidence of myocardial infarction (MI) after thoracic surgery is < 0.5%. In patients with a previous MI, the incidence of postoperative MI is 3–15%, with an associated mortality of 25–50% [59]. If MI is suspected in the postoperative period, the diagnosis is confirmed with electrocardiography and serum isoenzymes, including troponin. If the patient is hemodynamically stable, optimal medical management should be instituted, including continuous electrocardiographic surveillance monitoring for at least 48 h, supplemental oxygen, heparin (unless contraindicated by surgical issues), β-blockade, control of hypertension, and close attention to acid/base and fluid/electrolyte balance. Thrombolytic administration and interventional procedures are usually not indicated in the stable postoperative patient. For patients who deteriorate despite medical management, more intensive therapy must be considered. If ventricular failure is a component of the presentation, pulmonary artery catheterization is performed for measurement of right and left heart pressures, more accurate assessment of volume status, and monitoring for the administration of inotropic and vasodilatory agents. Transesophageal echocardiography may be required for patients to determine the degree of mitral valvular insufficiency. Cardiac catheterization for angioplasty and stenting must be considered in the presence of ongoing ischemia. Intraaortic balloon pumping may also be used in patients with refractory ischemia, particularly in those with malignant ischemic arrhythmias. Atelectasis is a common postoperative complication, with several manifestations, including the creation of a pulmonary shunt and resulting hypoxia, decreased immune response and associated pneumonia, and potential permanent functional loss. Pathogenic factors that predispose to atelectasis include postoperative pain, general anesthesia, diaphragmatic dysfunction, chest wall alteration, partial pneumothorax, pleural effusion, abdominal distension, chronic obstructive pulmonary disease, and active smoking. The diagnosis of atelectasis is both radiographic and clinical. It may be difficult to distinguish from active pneumonia in the early postoperative period. The treatment of atelectasis includes adequate analgesia, chest physiotherapy, patient education regarding coughing, deep breathing, and incentive spirometry (preferably performed preoperatively), mucolytics, bronchoscopy, and tracheostomy (rarely).

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Analgesic regimen A comprehensive analgesic strategy should be made for every patient prior to thoracic surgery. Epidural analgesia, paravertebral blocks, extrapleural catheters, and intercostal blocks are all effective means of optimizing pain control that are superior to the practice of supplying analgesia in the postoperative period exclusively. Adequate pain control is essential to optimizing pain control and pulmonary toilet, to prevent pulmonary complications, and may help to limit catecholamine flux and the associated cardiac complications.

References 1 Davis RD, Oldham HN, Sabiston DC. Primary cysts and neoplasms of the mediastinum: recent changes in clinical presentation, methods of diagnosis, management, and results. Ann Thorac Surg 1987; 44: 229–237. 2 Demmy TL, Krasna MJ, Detterbeck FC et al. Multicenter VATS experience with mediastinal tumors. Ann Thorac Surg 1998; 66: 187–192. 3 Pearson FG. Mediastinoscopy. A method of biopsy in the superior mediastinum. J Thorac Cardiovasc Surg 1965; 49: 11–15. 4 Ginsberg RJ, Rice TW, Goldberg M et al. Extended cervical mediastinoscopy. A single staging procedure for bronchogenic carcinoma of the left upper lobe. J Thorac Cardiovasc Surg 1987; 94: 673–678. 5 Foster ED, Munro DD, Dobell AR. Mediastinoscopy. A review of anatomical relationships and complications. Ann Thorac Surg 1972; 13: 273–286. 6 Hammoud ZT, Anderson RC, Meyers BF et al. The current role of mediastinoscopy in the evaluation of thoracic disease. J Thorac Cardiovasc Surg 1999; 118: 894 –899. 7 Luke WP, Pearson FG, Todd TR et al. Prospective evaluation of mediastinoscopy for assessment of carcinoma of the lung. J Thorac Cardiovasc Surg 1986; 91: 53–56. 8 Puhakka H. Complications of mediastinoscopy. J Laryngol Otol 1989; 103: 312. 9 Trinkle JK, Bryant LR, Hiller AJ et al. Mediastinoscopyaexperience with 300 consecutive cases. J Thorac Cardiovasc Surg 1970; 60: 297–300. 10 Vallieres E, Page A, Verdant A. Ambulatory mediastinoscopy and anterior mediastinotomy. Ann Thorac Surg 1991; 52: 1122–1126. 11 Meersschaut D, Vermassen F, Brutel de la Riviere A et al. Repeat mediastinoscopy in the assessment of new and recurrent lung neoplasm. Ann Throrac Surg 1992; 53: 120–122. 12 Kirschner PA. Cervical mediastinoscopy. Surg Clin North Am 1996; 6: 1–19. 13 Kraus DH, Ali MK, Ginsberg RJ et al. Vocal cord medialization for unilateral paralysis associated with intrathoracic malignancies. J Thorac Cardiovasc Surg 1996; 111: 334 –341. 14 Mom T, Filaire M, Advenier D et al. Concomitant type I thyroplasty and thoracic operations for lung cancer: preventing respiratory complications associated with vagus or recurrent laryngeal nerve injury. J Thorac Cardiovasc Surg 2001; 121: 642–648. 15 Urschel JD, Vretenar DF, Dickout WJ et al. Cerebrovascular accident complicating cervical mediastinoscopy. Ann Thorac Surg 1994; 57: 740–741. 16 Whyte RI, Iannettoni MD, Orringer MB. Intrathoracic esophageal perforation. The merit of primary repair. J Thorac Cardiovasc Surg 1995; 109: 140–146. 17 Schubach SL, Landreneau RJ. Mediastinoscopic injury to the bronchus: use of incontinuity bronchial flap repair. Ann Thorac Surg 1992; 53: 1100–1103. 18 Al-Sofyani M, Maziak DE, Shamji FM. Cervical mediastinoscopy incisional metastasis. Ann Thorac Surg 2000; 69: 1255–1257.

Complications of mediastinal surgery 253 19 Jaretzki A, Penn AS, Younger DS et al. ‘Maximal’ thymectomy for myasthenia gravis. Results. J Thorac Cardiovasc Surg 1988; 95: 747–757. 20 Wilkins EW, Grillo HC, Scannell JG et al. Role of staging in prognosis and management of thymoma. Ann Thorac Surg 1991; 51: 888–892. 21 Cooper JD, Al-Jilaihawa AN, Pearson FG et al. An improved technique to facilitate transcervical thymectomy for myasthenia gravis. Ann Thorac Surg 1988; 45: 242–247. 22 Yim APC, Kay RLC, Ho JKS. Video-assisted thoracoscopic thymectomy for myasthenia gravis. Chest 1995; 108: 1440–1443. 23 Mineo TC, Pompeo E, Lerut TE et al. Thoracoscopic thymectomy in autoimmune myasthenia: results of left-sided approach. Ann Thorac Surg 2000; 69: 1537–1541. 24 Drachman DB. Myasthenia gravis. N Engl J Med 1994; 330: 1797–1810. 25 Buckingham JM, Howard FM, Bernatz PE et al. The value of thymectomy in myasthenia gravis: a computer-assisted matched study. Ann Surg 1976; 184: 453–456. 26 Durelli L, Maggi G, Casadio C et al. Actuarial analysis of the occurrence of remission following thymectomy for myasthenia gravis in 400 patients. J Neurol Neurosurg Psychiatry 1991; 54: 406–411. 27 Masaoka A, Yamakawa Y, Niwa H et al. Extended thymectomy for myasthenia gravis patients: a 20-year review. Ann Thorac Surg 1996; 62: 853–859. 28 Jaretzki A, Barohn RJ, Ernstoff RM et al. Myasthenia gravis: recommendations for clinical research standards. Ann Thorac Surg 2000; 70: 327–334. 29 Bril V, Kojic J, Ilse WK et al. Long-term clinical outcome after transcervical thymectomy for myasthenia gravis. Ann Thorac Surg 1998; 65: 1520–1522. 30 Mulder DG, Graves M, Hermann C. Thymectomy for myasthenia gravis: recent observations and comparisons with past experience. Ann Thorac Surg 1989; 48: 551–555. 31 Detterbeck FC, Scott WW, Howard JF Jr et al. One hundred consecutive thymectomies for myasthenia gravis. Ann Thorac Surg 1996; 62: 242–245. 32 Mack MJ, Landreneau RJ, Yim AP et al. Results of video-assisted thymectomy in patients with myasthenia gravis. J Thorac Cardiovasc Surg 1996; 112: 1352–1360. 33 Bulkley GB, Bass KN, Stephenson GR et al. Extended cervicomediastinal thymectomy in the integrated management of myasthenia gravis. Ann Surg 1997; 226: 3243–34. 34 Goldman L, Caldera D, Nussbaum S et al. Multifactorial index of cardiac risk in noncardiac surgical procedures. N Engl J Med 1977; 297: 845–850. 35 Rückert JC, Walter M, Müller JM. Pulmonary function after thoracoscopic thymectomy versus median sternotomy for myasthenia gravis. Ann Thorac Surg 2000; 70: 1656–1661. 36 Nieto IP, Robledo JPP, Pajuelo MC et al. Prognostic factors for myasthenia gravis treated by thymectomy: review of 61 cases. Ann Thorac Surg 1999; 67: 1568–1571. 37 Baskett RJF, MacDougall CE, Ross DB. Is mediastinitis a preventable complication? A 10-year review. Ann Thorac Surg 1999; 67: 462–465. 38 Masaoka A, Monden Y, Nakahara K, Tanioka T. Follow-up study of thymomas with special reference to their clinical stages. Cancer 1981; 48: 2485–2492. 39 Thomas CR, Wright CD, Loehrer PJ. Thymoma. State of the art. J Clin Oncol 1999; 17: 2280–2289. 40 de Leeuw M, Williams JM, Freedom RM et al. Impact of diaphragmatic paralysis after cardiothoracic surgery in children. J Thorac Cardiovasc Surg 1999; 118: 510–517. 41 Staats RA, Ellefson RD, Budahn LL et al. The lipoprotein profile of chylous and unchylous pleural effusions. Mayo Clinic Proc 1980; 55: 700–704. 42 Cerfolio RJ, Allen MS, Deschamps C et al. Postoperative chylothorax. J Thorac Cardiovasc Surg 1996; 112: 1361–1366. 43 Fahimi H, Casselman FP, Mariani MA et al. Current management of postoperative chylothorax. Ann Thorac Surg 2001; 71: 448–450.

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44 Bacha EA, Chapelier AR, Macchiarini P et al. Surgery for invasive primary mediastinal tumors. Ann Thorac Surg 1998; 66: 234 –239. 45 Dartevelle P, Chapelier A, Macchiarini P et al. Anterior transcervical-thoracic approach for radical resection of lung tumors invading the thoracic inlet. J Thorac Cardiovasc Surg 1993; 105: 1025–1034. 46 Macchiarini P, Dartevelle P, Chapelier A et al. Technique for resecting primary and metastatic nonbronchogenic tumors of the thoracic outlet. Ann Thorac Surg 1993; 55: 611–618. 47 Vanakesa T, Goldstraw P. Antero-superior approaches in the practice of thoracic surgery. Eur J Cardiothorac Surg 1999; 15: 774 –780. 48 Heltzer JM, Krasna MJ, Aldrich F et al. Thoracoscopic excision of a posterior mediastinal ‘dumbbell’ tumor using a combined approach. Ann Thorac Surg 1995; 60: 431–433. 49 Hsu C, Chen C, Lin C et al. Video-assisted thoracoscopic T2 sympathectomy for hyperhydrosis palmaris. J Am Coll Surg 1994; 179: 59–61. 50 Hazelrigg SR, Mack MJ. Surgery for autonomic disorders. In: Kaiser LR, Daniel TM, eds. Thoracoscopic Surgery. Boston: Little Brown, 1993; 89. 51 Daniel TM. Thoracoscopic sympathectomy. Chest Surg Clin North Am 1996; 6: 69–83. 52 Nicholson ML, Hopkinson DR, Dennis MJ. Endoscopic transthoracic sympathectomy: successful in hyperhidrosis but can the indications be extended? Ann R Coll Surg Engl 1994; 76: 311–314. 53 Cameron AE. Complications of endoscopic sympathectomy. Eur J Surg 1998; 164: 33–35. 54 Cheng W, Chang C, Lin T. Chylothorax after endoscopic sympathectomy: case report. Neurosurgery 1994; 35: 330–331. 55 Gossot D. Chylothorax after thoracoscopic sympathectomy. Surg Endosc 1996; 10: 949. 56 Gossot D, Kabiri H, Caliandro R et al. Early complications of thoracic endoscopic sympathectomy: a prospective study of 940 procedures. Ann Thorac Surg 2001; 71: 1116–1119. 57 Lange JF. Inferior brachial plexus injury during thoracoscopic sympathectomy. Surg Endosc 1995; 68: 1177–1181. 58 Nesathurai S, Harvey DT, Schatz SW. Gustatory facial sweating subsequent to upper thoracic sympathectomy. Arch Phys Med Rehabil 1995; 76: 104 –107. 59 Amar D. Cardiac arrhythmias. Chest Surg Clin North Am 1998; 8: 479– 493.

PART III

Cardiac surgery

CHAPTER 15

Complications of coronary artery bypass surgery Nader Moazami, Hendrick Barner

Improvements in surgical technique, anesthesia, and postoperative care have had a significant positive impact on results obtained with coronary artery bypass grafting (CABG) in the last two decades. Increasing and aggressive percutaneous interventions, use of new stents and potent platelet inhibitors have created a group of patients with an increasingly complicated risk profile that pose a challenge to all cardiac surgeons. Despite these factors, operative mortality from isolated CABG has steadily declined in the last decade to under 3% (STS Database 2000 results) with postoperative length of stay of about 6 days. Preoperative assessment clearly plays an important role in selecting patients for operative intervention. Risk factors associated with all cardiac surgical interventions include advancing age, obesity (wt > 1.5 × ideal), diabetes, chronic obstructive pulmonary disease, New York Heart Association (NYHA) functional class, peripheral vascular disease, previous history of cerebrovascular accidents, and renal failure. Furthermore emergency operations, presence of cardiogenic shock, recent myocardial infarction (MI), and reoperations are all factors that incrementally increase risk of morbidity and mortality after cardiac operations. The majority of these topics have been discussed in detail elsewhere and in major textbooks [1]. In this chapter, we will focus on decision-making and technical factors that effect the short-term outcome of CABG. Specifically, we will discuss how to avoid complications and how to correct mistakes during the operation. A short description of early postoperative complications is also given.

Preoperative assessment A complete history, physical, and review of available tests are important in assessing any patient prior to cardiac surgery. Several important elements are central in this evaluation.

Predisposition to bleeding Preoperative blood dyscrasias that may predispose to bleeding are infrequent but a key element in the history. Renal insufficiency can predispose to bleeding [2] but more commonly, bleeding problems arise from preoperative treatment 257

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with thrombolytic therapy or long-acting antiplatelet agents. Aspirin taken within 1 week may increase bleeding time but infrequently causes postoperative blood loss [3]. On the other hand, platelet inhibitors given during percutaneous interventions can have a profound effect on clotting. Urgent CABG can be safely performed on these patients and the effect can be reversed with platelet transfusion. Operative plan should include platelet transfusion for CABG after discontinuation of cardiopulmonary bypass only if persistent non-surgical bleeding is present [4].

Central neurological complications Stroke following CABG has been estimated to occur in 6% of operations with permanent neurological deficits occurring in about 3% [5]. Although the literature suggests that carotid stenosis is not a risk factor for patients without history of neurological symptoms [6], we are very aggressive in performing screening for carotid disease with color flow duplex ultrasound. We prefer carotid endarterectomy in all asymptomatic patients with critical stenosis (> 75%). In patients with symptomatic carotid stenosis carotid endarterectomy is performed before CABG or concomitantly. Although stroke after cardiac surgery is multifactorial, one of the most probable causes is atheroembolization from the ascending aorta or arch. Calcified aorta on chest X-ray is a particularly ominous sign. A non-contrast computed tomography scan can more accurately determine the extent of calcification. If cannulation of the ascending aorta is not possible and an on-pump operation is planned, axillary artery cannulation for antegrade flow during cardiopulmonary bypass (CPB) offers an excellent option [7]. Intraoperative epiaortic ultrasound is another option to ascertain the degree of disease prior to manipulation of the aorta [8].

Coronary angiogram Careful preoperative review of the coronary angiogram is of critical importance in developing a strategy for revascularization. Critical to this evaluation is selection of appropriate targets, size of the recipient vessel, and degree of proximal stenosis. We typically aim for complete revascularization in all cases, and if appropriate, an all arterial grafting strategy. The recipient vessel should be at least 1.5 mm in size and extend out from the A-V groove with a good run off. In cases where the degree of proximal stenosis is judged to be 70% we hesitate to use an all-arterial grafting practice because of concern for detrimental effect of competitive flow to overall graft patency, particularly when the radial artery is used. It should be noted that although the coronary angiogram is currently the best modality available for assessing anatomy, it frequently underestimates the degree of atherosclerotic involvement of the coronaries, and extent of calcification. This is of particular concern in diabetics and renal failure patients. In selecting an appropriate target it is important to view the vessel from different projections to ensure that the segment is suitable for grafting. Calcification is often best appreciated on the frames immediately prior to injection of dye.

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Selection of conduits We prefer an all-arterial revascularization strategy when feasible [8]. Recent data on patency support strategies to maximize the number of arterial anastomoses by T-grafting or Y-grafting techniques [9–11]. The radial artery or the right internal mammary artery (IMA) is taken off the left IMA for complete revascularization, using multiple sequential grafting. Early patency for these constructs has been excellent with freedom from reintervention of > 90% at 5 years. We emphasize that for low-grade stenoses of 70%, because of concerns regarding competitive flow and graft failure, we have moved away from using the radial artery (RA) as a conduit. Despite a resurgence of interest in the radial artery, use of vein grafts is always an excellent strategy. Saphenous vein grafts are free of atherosclerotic disease, have rarely been damaged by indwelling lines (as is the case with radial arteries), can be harvested quickly, and most importantly are reliable because they are not prone to spasm.

Harvesting techniques Radial artery Prior to harvesting, collateral circulation to the hand must be assessed. We have used only the Allen test, which requires occlusion of the radial and ulnar arteries at the wrist, closing of the hand totally for 20 s, followed by release of the ulnar artery. Capillary refilling of the palm and digits requires 2–10 s; if it takes longer than 10 s, the test is considered positive and the RA is not harvested. If the palmar skin is heavily pigmented so that capillary filling cannot be visualized, a digital pulse oximeter can be used to assess return of capillary flow. In 528 patients studied, 4.4% had a bilaterally positive test and 11.9% had a unilaterally positive test. The RA from the non-dominant arm is usually harvested. Hypoperfusion of the hand or claudication has not been noted in the current era of RA use. Sensory disturbance related to the lateral antebrachial cutaneous nerve or superficial branch of the radial nerve has occurred in 5–10%, but has not been a debilitating or persistent problem. Others have recommended that a more sophisticated and objective evaluation of collateral circulation to the hand be used. Non-invasive assessment has included pulse volume recording, oximetric plethysmography with calculation of a perfusion index, and pulsed Doppler scanning [12]. Measurement of flow velocity in the ulnar artery, in the palmar branch of the radial artery, and in the artery of the thumb is performed with and without radial artery occlusion at the wrist. With the latter technique, 5.9% (11/185) of non-dominant RAs were excluded from use. When the former methodology was used in 224 patients (448 extremities), 17 patients had bilaterally positive tests (7.6%) and 16 had unilaterally positive tests (7.1%) [12].

Harvesting technique The incision is made over the course of the RA with a central medial curve along the border of the brachioradialis muscle, which will reflect the antebrachial cutaneous nerve lying in the deep subcutaneous tissue in the lateral

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flap. Electrocautery is used to divide the subcutaneous tissue, but is limited to the deep fascia in the proximal half of the incision because distally the RA is close to the fascia. The brachioradialis muscle is reflected laterally to expose the RA beneath its medial edge. The RA is dissected as a pedicle, with its venae comitantes and associated fatty areolar tissue, beginning in its midportion and using blunt and sharp technique. A tape or vessel loop can be placed around the pedicle to facilitate exposure of the dorsally placed branches, which are divided between small clips. The dissection continues proximally to the origin of the artery, which is confirmed by identifying the ulnar artery. Division of the radial recurrent artery may add more length to the RA, depending on the level of origin of this branch. Division of the radial veins will expose the origin of the RA. Distal dissection continues to the major wrist crease, and the length of the artery is measured in situ as this information may be helpful in planning the operation. The superficial radial nerve runs lateral and parallel to the radial artery as far as the distal forearm, where it passes dorsally to the distal forearm. It is usually not seen in dissection of the RA unless dissection strays on the lateral side of the artery. The artery is ligated or clipped at both ends and removed. Some like to observe the distal pulse (with proximal occlusion) as evidence of adequate collateral flow before dividing the artery. We have not used this maneuver but have relied on the results of the Allen test. The incision is closed in layers with absorbable suture after achieving hemostasis, and the arm can be left on the arm board or tucked at the patient’s side. Drains are not used.

Internal thoracic artery We continue to harvest the left internal thoracic artery (ITA) as a pedicle graft with approximately 0.5 cm fascia on either side of the artery along with the accompanying mammary veins. Harvesting is performed with the hemisternum elevated and under direct vision with good lighting and magnification. Removal of the peri-pleural fat pad from underneath the sternum will aid in visualization of the course of the artery. A plane can be developed medial and parallel to the artery by dividing the endothoracic fascia and sternocostalis muscle which is then used as a handle for gentle traction. Excessive downward traction anywhere along the artery can lead to avulsion injury of the small perforating branches that may lead either to dissection of the vessel or persistent bleeding. If bleeding from one of the torn branches occurs, we prefer to mobilize the vessel off the chest wall to allow adequate access and visualization of the vessel. Blind repairs lead to unacceptable narrowing of the ITA. Harvesting is done with the cautery on a low setting. The cautery tip should be protected with a rubber-covered or insulated blade bent at 45–60°. Cautery should be used at short bursts at the branching sites with most of the dissection carried out bluntly with gentle strokes. Electrocautery injuries can lead to early graft failure or induce vasospasm. Branch arteries are generally controlled with small clips. It is important that the clip applier not ‘scissor’ during application, otherwise avulsion may occur leading to possible dissection.

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Mobilization of the ITA pedicle is carried from the level of the innominate vein to its bifurcation into the two subdivisions of this vessel (the musculophrenic and superior epigastric arteries). During the proximal dissection, care must be taken to identify clearly the phrenic nerve and avoid injury. Bleeding encountered in this area must be controlled under direct vision. By holding ventilation, the left lung will be out of the field allowing coagulation or clipping of the culprit vessel. The distal extent of the dissection should also be limited to immediately past the bifurcation. After this point the caliber of the vessel is small. In addition, preservation of collateral flow to the lower aspect of the incision may be important to avoid wound infection and necrosis of the lower sternum and subxiphoid area [13]. If additional length is needed and the superior epigastric artery is of good quality then it may be used, although some believe this segment to be associated with lower patency rates [14].

Skeletonization of the ITA Some prefer to harvest the ITA without associated tissue and without the venae comitantes. The ITA is exposed by incising the overlying endothoracic fascia and sternocostalis muscle with scissors, or the dissection can be initiated medially with cautery. Blunt dissection with the cold cautery tip is used to ease the artery from its bed. Electrocautery can injure the skeletonized ITA; branches must be divided between small clips. With magnification it is possible to see the anatomy of arterial branches and place clips to maximally preserve collateral sternal blood flow by dividing sternal/perforating and sternal/intercostal branches upstream to their division without injuring the ITA. Those who utilize the skeletonized ITA believe that there is less reduction in sternal blood flow, less mediastinal wound infection, longer length of the ITA, easier construction of sequential anastomoses, and easier recognition of persistent spasm or harvesting-related ITA injury [15]. Although preservation of collateral sternal blood flow is theoretically possible based on anatomic studies, this benefit has not been proved. Sequential grafting is facilitated by a skeletonized ITA because pedicle tissue may interfere with construction of a side-to-side anastomosis. Spasm and injury are recognized more easily, but the harvest technique is more difficult, and the potential for damage is greater. Skeletonization also requires twice the time needed for pedicle mobilization. Ultrasonic dissection can also be used for skeletonization. Division of the fascia, muscle and branches can be achieved with division of branches 2 mm from the ITA without injury to the ITA and preservation of distal branching to provide collateral flow [16]. Patency at 1 year is excellent [17].

Vein harvesting Superficial wound complications arising from the vein harvest site are common, especially in diabetic patients. In one study, impaired wound healing defined as mild inflammation, drainage, or erythema occurred in 24% of patients undergoing CABG [18]. Recent advances in endoscopic vein harvesting

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suggest that atraumatic dissection can be performed with a limited number of skin incisions. Because most of the dissection is done in a subcutaneous tunnel, risk of infection may be diminished [19]. Although endoscopic vein harvesting yields suitable conduits, and the incisions are more cosmetically appealing, large prospective studies are needed to show a reduced rate of infection. At our institution, we still use standard techniques for harvesting the vein and minimize skin incisions by creating ‘bridges’ of skin. A key factor in performing vein harvest, using any technique available, is to avoid excessive traction on the vein. Disruption of the endothelium can lead to early graft thrombosis. A suitable vein is 3–5 mm in diameter. Varicosed and aneurysmal vein graft should never be used unless they are focal and can be fixed. We refrain from using the lesser saphenous graft unless absolutely no conduits are available, usually in re-do operations.

Sternotomy We generally perform the incision down to the level of the sternum with the knife to avoid excessive damage caused by electrocautery. Extensive cautery application to the skin edges or the avascular subcutaneous fat leads to necrosis and postoperative infection. Closing the vessel shut using forceps and briefly applying cautery can control focal areas of bleeding without the need to apply cautery indiscriminately. We generally avoid marking the sternum in the middle with electrocautery to define the line of sternotomy. This devascularizes the sternum by burning the periosteum. If during sternotomy the line is not exactly followed, then areas of avascularized bone will remain and may act as a nidus for infection. Once the sternum is open, we try to avoid use of foreign bodies on the marrow, particularly bone wax. If bleeding is low grade, tamponade with pads will suffice. If bleeding is more brisk, then we generally rub Gelfoam (± thrombin) on the marrow (Pharmacia, Kalamazoo, MI, USA). This has excellent hemostatic properties. After harvesting the ITA, heparin is administered, clamped and the ITA is sharply divided. We measure flow visually and as long as the stream of blood projects 7.5–10 cm beyond the distal end, we consider it adequate. Green has suggested that the flow should be measured with the minimal acceptable flow being 50 ml/min [20]. Once satisfied with the conduit, papaverine (2 mg/ml) is sprayed on the pedicle, which is then wrapped in a Papaverine-soaked sponge and placed in the left chest. Alternatively, heparinized blood containing papaverine solution (2 mg/ml) can be injected directly into the lumen with a 1–2-mm blunt plastic or metallic olive-tip cannula. The ITA should not be occluded proximally during injection. We routinely combine papaverine with blood to utilize the buffering capacity of blood for the normally acidic pH of papaverine (pH 2–3). This preparation has a more physiological pH (7.3) and may cause less perturbation of the endothelial milieu. The cannula for injection must be inserted gently with adequate visualization of the lumen, otherwise the vessel may dissect. If a short dissection flap is created, then the vessel can be cut back to the point where normal lumen is present. We absolutely refrain

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from directly instrumenting the ITA with probes or dilators to avoid potential damage, which will jeopardize overall patency.

T-grafting with the RA or right ITA In cases where we have decided on complete revascularization with the radial artery or the right skeletonized ITA, we perform the proximal anastomosis first utilizing a T graft or Y configuration. Overall patency is reported as > 90% [9–11, 21,22]. In this configuration, the free right ITA is anastomosed to the dorsal (smooth or pleural surface) side of the left ITA pedicle at the level of the left atrial appendage (or where the left ITA crosses the edge of the incised pericardium), which has been cut across the pulmonic valve into the ‘bare area’ of the pericardium to the phrenic nerve and then parallel to the phrenic nerve 1–2 cm. It is helpful to harvest the left ITA with a pedicle to facilitate the T anastomosis. Two stay sutures are placed in the ITA pedicle at the site of the intended anastomosis to elevate the pedicle from the superior mediastinum and avoid motion transmitted from the heart and lungs (it may be necessary to pack the left upper lobe away from the operative area with a single laparotomy pad). After systemic heparinization (300 U/kg), the left ITA is bled distally to fill it with heparinized blood, and a vascular bulldog clamp (soft/Fibra, 6 mm; Applied Medical Resources, Laguna Hills, CA, USA) is applied proximally. A 4- to 5-mm incision is made in the left ITA, and the right ITA or RA is spatulated 2–3 mm. A Y-shaped anastomosis is performed with continuous 7–0 or 8–0 polypropylene suture which may lie at a right angle depending on the ultimate position of the anastomosis and its limbs. The pedicles of the two conduits are attached with two sutures of 6–0 polypropylene to relieve anastomotic stress. The bulldog clamp is released, and each conduit is then filled with heparinized blood containing papaverine (2 mg/ml), via 1- or 2-mm olive-tipped cannula. The conduits are allowed to dilatate while cannulation for cardiopulmonary bypass is completed. The conduits are then checked visually and by palpation for satisfactory dilatation. It not suitable, they are refilled with papaverine, and bypass is not initiated until the surgeon is satisfied with the conduits. The T and Y configuration grafts are technically complex and demanding for the surgeon. The elements involved in this procedure are best learned in a step-wise fashion, with mastery and confidence gained with each step before proceeding to another. Because all inflow is from a single source, there is the potential for hypoperfusion, which is greater than that from use of individual arterial conduits for each coronary artery. A faulty T anastomosis can jeopardize the entire arterial reconstruction.

Cannulation The pericardium is opened to the level of the pericardial reflection on the aorta. Complete exposure and visualization of the innominate vein is not necessary

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and may make future reoperation easier. The thymic fat pad can be ligated to avoid problems with bleeding. If a large amount of fatty tissue remains after ligation it should be resected as a devascularized segment can act as a nidus for infection. Inferiorly the pericardium is T’ed off to the right and left pleural reflections with approximately 1 cm of pericardial edge remaining on the diaphragm, again to avoid bleeding problems from diaphragmatic vessels. Initial palpation of the aorta will give a general sense of suitability of the aorta for cannulation. Palpation is a very gross assessment with a falsenegative rate of 55–60%. In patients with severe vasculopathy, age > 65 years, previous history of stroke or significant atherosclerotic disease in the descending aorta as assessed by transesophageal echocardiography (TEE), we routinely perform an epiaortic echocardiogram. This technique allows a better appreciation of the severity of intraluminal, non-palpable disease and for selection of proximal anastomotic sites [23]. If the aorta is judged not suitable for cannulation then an alternate site (femoral or subclavian artery) can be chosen, an off-pump procedure may be elected or hypothermic fibrillatory arrest with left ventricular venting is appropriate.

Cardioplegia delivery We acknowledge that there are many strategies for cardioplegia delivery and myocardial protection. We routinely use both antegrade and retrograde blood cardioplegia. We use a retrograde cannula with a soft tip self-inflating balloon that is inserted after arterial and venous cannulation. If during maneuvers for proper placement the patient becomes hypotensive, we generally go on bypass and position the cannula with the heart full, gently lifting the heart to visualize the coronary sinus. Excessive force for placing cannula can lead to rupture of the coronary sinus. If this happens the sinus can be repaired preferably with a pericardial patch. If repair is not possible then it can be ligated with pledgeted suture. The antegrade needle is generally placed while on bypass to avoid the risk of aortic dissection as the needle is introduced.

Distal anastomosis Selection of target site With the heart in its normal beating state, the distal targets can be visualized and palpated to select an area for anastomosis. Ideally the anastomosis is made to an area that is minimally diseased and has a diameter of 1.5–2 mm. Vessels that are 1 mm have very poor patency rates and should not be bypassed. On the right, the coronary artery in the A-V groove is frequently severely diseased, but not always, and may be used for distal anastomosis when the posterior descending artery or the posterior ventricular branch are not suitable for bypass. After application of the aortic cross clamp and cardiac arrest with combined antegrade and retrograde cardioplegia, the heart should be positioned to

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achieve easy access and visualization of the anastomotic site. The epicardium is then gently dissected with a rounded blade exposing the artery. Arteriotomy can be performed by multiple gentle strokes with a sharp Beaver blade or with a single upward movement of the blade after partially inserting the tip in the coronary artery at a 45° angle. Running retrograde cardioplegia during this maneuver will distend the vessel and help prevent damaging the posterior wall of the artery. If the posterior wall is damaged through the adventitia it must be repaired from the inside with fine 7–0 or 8–0 Prolene suture placed as a mattress suture and tied on the outside. Bleeding into the myocardium can cause significant myocardial dysfunction. The arteriotomy is extended in either direction. Care is taken to remain in the middle of the artery. Oblique arteriotomy incisions will distort the toe or heel of the anastomosis. Attempting to correct an oblique arteriotomy may lead to creation of a bivid-shaped arteriotomy that is difficult to sew to. The size of the arteriotomy incision should be approximately twice the diameter of the coronary or about 3–5 mm in length. Vein grafts can typically be transected at right angles to the long axis. If the vein is small it can either be beveled or ‘fish-mouthed’. The compliance of the vein allows it to stretch over the arteriotomy site. Arterial grafts are generally spatulated to create a hood about 1–2 mm longer than the arteriotomy because these grafts do not safely stretch over an arteriotomy that is longer than the graft opening. A mismatch can put the fragile coronary under tension and cause a tear. Occasionally after the arteriotomy is created a tight lesion is encountered at the toe of the anastomosis. This will lead to early graft failure unless the arteriotomy is extended further distally across the plaque as a patch angioplasty. This will create a longer anastomosis but reduce the likelihood of graft closure. If the area involved with stenosis is too long then a second separate distal anastomosis should be created. We frequently even consider a sequential anastomosis to the same artery with one graft to maximize the revascularization of the coronary artery bed in terms of proximal and distal perfusion. Occasionally, the diseased coronary vessel has an intramyocardial course and is difficult to identify. The course of the other coronary arteries, if visible, provide a road map to the general location of the target vessel. If branches are visible, they can be traced back to their origin to identify the main trunk. Alternatively, the distal end can be identified and traced back with electrocautery set at a very low level to divide muscle bridges. If none of these maneuvers allows identification of the vessel, the side branch can be chosen as the site of anastomosis provided that it is of sufficient caliber and has no proximal stenosis. This is especially useful when the left anterior descending artery can not be identified. In this case, the diagonal artery can be used if appropriate. When dissecting the submuscular left anterior descending (LAD), the right ventricle is occasionally entered, particularly if the LAD has a course just under the endocardium of the right ventricle. Historically, this has been repaired by placing sutures from the epicardium under the LAD and through

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the opposite epicardium. These are large, gross bites and can compromise septal branches. A preferable technique is that of closing the right ventricle endocardium with 6–0 polypropylene and then closing the epicardium over this repair. The anastomosis is done away from this area.

Anastomotic techniques End-to-side anastomosis The most critical parts of the anastomosis are the heel and the toe; narrowing at either location will comprise blood flow. We start most of our anastomoses at the heel taking bites that are approximately 1 mm from the edge and 1 mm apart from each other. Care should be taken to minimize handling of the graft for exposure. Gentle traction of the adventitia should provide adequate exposure. Instrumentation of the lumen should be avoided. Usually five sutures are placed around the heel before parachuting the graft onto the coronary artery as the suture line is tightened. The anastomosis is then continued on the side wall until the toe. At the toe, again small close bites are taken. If the bites on the coronary side are too deep a dimpling effect will occur at the distal site. In addition, this ensures that a purse-string effect would not narrow the lumen when the suture is tied. Minimizing leeks at the heel or toe is important because a repair at these locations can compromise the lumen. Once the toe sutures are placed, the suture is placed under tension and the lumen is gently probed with an undersized 1-mm probe to ensure proximal and distal patency. Excessive force or blindly passing the probe without noticing the course of the coronary artery can lead to intimal dissection or full thickness tear. This maneuver should be avoided if a large posterior plaque is present or the artery is severely diseased. Once patency is assured, the anastomosis is completed. Prior to tying the suture, the graft is flushed to de-air. Gentle pressure is maintained to minimize purse stringing as the suture is tied down. In case of the ITA graft, blood flow is re-established to accomplish this. The ITA graft is tacked down to the epicardium with 6–0 prolene near the anastomosis site. This prevents the pedicle from twisting or angulating along its axis.

Order of distals The order of performing distals depends on the conduits used, degree of disease in the native vessels, and planned strategy for cardiac protection. As described before, we routinely employ antegrade and retrograde cardioplegia for myocardial protection during CABG surgery. If vein grafts are used, cardioplegia is delivered down the grafts as each anastomosis is completed. Concerns for protection of the right heart with retrograde cardioplegia may prompt us to construct the distal right bypass first. On the other hand, if the circumflex territory has a very critical stenosis, we may proceed with branches of the circumflex system first. We almost routinely perform LAD anastomosis last because traction on the heart during access to the posterior vessels may damage the anastomosis.

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Figure 15.1 Side-to-side anastomoses with arterial conduits are always made in parallel. (A) Incisions are twice the diameter of the artery and usually 3–4 mm in length. The suture begins at the heel or proximal apex of the anastomosis. (B) The far side is completed in parachute fashion. (C) The suture line is tightened, and the near side is completed using one or both ends of the suture. (D) The pedicle, or adventitia of the skeletonized conduit, is tacked to the epicardium proximal and distal to the anastomosis when a marginal or posterolateral artery is involved. For a pedicled conduit to the diagonal artery, a tacking suture is placed at the heel and on the lateral side of the anastomosis to prevent the pedicle from catching the pericardial edge.

Side-to-side anastomoses Two types of side-to-side anastomoses are usually performed: parallel and diamond anastomoses. Technically the parallel anastomosis is easier to construct because the length of the incisions in the two vessels can be easily matched. In addition, parallel anastomoses are sewn in the same conventional manner as end-to-side anastomoses and have a better patency (by about 10%) over diamond anastomoses (Figure 15.1). The critical step in the construction of sequential anastomoses is judging the location of arteriotomy on the two

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Figure 15.2 Techniques of side-to-side vein-to-coronary artery anastomoses are illustrated. (A) Incisions are at least twice the diameter of the coronary artery, and the suture line begins at the heel or proximal part of the anastomosis and continues distally on the far side in parachute fashion. (B) After suture bites are placed around the toe, the suture line is pulled tight. (C) The near side is completed usually with the suture from the heel. (D) When the anastomosis crosses, the coronary incision is the same as in A, but the vein must be large enough for a similar incision. Again, the suture line starts at the heel and continues on the far side in parachute fashion until the toe is completed. The suture line is pulled tight, and the anastomosis is completed. (E) If the diameter of the vein is adequate, the anastomosis will be satisfactory. (F) If the vein is small, the vein will be flattened at the anastomotic site (seagull deformity). A better anastomosis for this situation is illustrated in G. The incision is made parallel to the long axis of the vein rather than transversely. (H) The completed anastomosis is shown. (I) No seagull deformity develops because the longitudinal incision in the vein adds tissue to the anastomosis.

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coronaries and the exact length between the two areas on the conduit. Long lengths can cause kinking, short lengths will cause excessive tension. For vein conduits it is important gently to distend the vein to judge the proper distance. Arterial grafts should also be distended by providing inflow. The graft should lay on the epicardium to allow the distal anastomoses to be created on good target areas without torsion or angulation. Either the proximal or distal anastomosis can be done first. Having one end of the conduit free allows for better visualization of the anastomosis since the free end can be moved back and forth. For vein grafts we typically construct the distal anastomosis first. For arterial grafts if the proximal is taken as a Y- or T-graft, we construct the more proximal coronary anastomosis first. If the arterial graft is taken off the aorta, we perform the distal sequential anastomosis first. The diamond side-to-side anastomosis is more difficult to construct (Figure 15.2). The incisions on the vein and artery should be the same length. We use the ‘parachute’ technique for full visualization and start taking one bite from the proximal apex of the coronary and one bite from the middle of the conduit. The suture line is continued using the parachute technique to the near arterial apex, at which point the suture line is tightened. Precise suture placement is important to avoid jeopardizing a graft that may supply more than one critical territory.

Endarterectomy Indications Coronary endarterectomy was used early in the history of direct myocardial revascularization, but enthusiasm for it has varied through the intervening 30 years. Some surgeons commonly utilize this technique, while others rarely do so. Endarterectomy is usually undertaken when there is diffuse, severe disease within a coronary artery so that no suitable site to anastomose is available without endarterectomy. Some surgeons undertake endarterectomy only if total occlusion is present to minimize the small risk of perioperative occlusion due to an intimal flap and/or acute thrombosis of the endarterectomized segment. This philosophy assumes that reocclusion will not cause infarction, but this is not entirely true, since extensive thrombosis can produce infarction despite good collateral flow. We prefer to avoid endarterectomy and achieve revascularization by one of several alternatives. Anastomoses can be placed distally, where disease is less or absent, if the lumen is 1.5 mm in diameter. Frequently a diffusely diseased vessel has small areas where the anterior wall is normal or relatively so with a reasonable lumen. One, two, or three anastomoses may be placed to a single coronary artery to provide flow into segments separated by severe stenoses alternating with intervening healthier areas. Finally, relatively healthy branches of adequate size (1.5 mm), such as diagonal arteries, can be grafted. These anastomoses provide retrograde perfusion of the primary trunk and secondary branches and distal perfusion of the grafted artery. Thus use of

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endarterectomy is based on practice, experience, and a philosophy that weighs risk, long-term success, and alternatives.

Technique There are two basic techniques for endarterectomy. In the closed method (Figure 15.3), a relatively short incision is made at the site where the graft anastomosis is anticipated. For the right coronary artery, this is in the distal third

Figure 15.3 A closed right coronary endarterectomy is most common and is illustrated. (A) A 5–10-mm incision is made in the distal right coronary proximal to the bifurcation. (B) A dissection plane is established in the outer third of the media to encircle the atherosclerotic core. (C) The core is completely divided, and the distal core is grasped with forceps while a microspatula dissects the medial plane. (D) Traction and dissection continue until the core breaks free. The specimen is inspected for tapered distal ends, and if an end is fractured, a second incision is made at the site of fracture to continue the endarterectomy. The arteriotomy is closed with a graft.

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just proximal to the bifurcation. After making a 5–10-mm incision, a dissection plane is developed in the outer third of the media and carried around the vessel. The core is elevated and divided. Using a variety of instruments including wire loop, microspatula, or a tonsil spatula, the endarterectomy plane is developed in both directions by placing gentle traction on the plaque as the dissection proceeds. At some point the plaque is fully dissected and is extracted from the coronary artery. Occasionally, firm traction must be applied to the core while countertraction is applied to the heart in the distribution of the involved artery to separate the plaque. The tip of the plaque is inspected to determine whether or not the plaque is tapered and has separated cleanly. If the plaque has fractured, a ledge is left that may produce an intimal flap. If the core is fractured, the vessel should be opened (unless too small, i.e. < 1.5 mm) at the site of fracture to extend the endarterectomy or to tack the intimal flap down with fine polypropylene. This can be difficult in a vessel less than 2.5 mm in diameter. The distal arteriotomy also can be used for graft anastomosis with closure of the proximal arteriotomy or use for a second anastomosis. A proximal (to the coronary arteriotomy) endarterectomy is safe in the right coronary system if the right coronary artery is occluded to its origin. However, if flow is antegrade to right ventricular branches, proximal endarterectomy should not be undertaken because it could disrupt flow into important right ventricular or collateral branches to the left ventricle. Proximal endarterectomy is not recommended for the left coronary arterial system. The bypass graft can be vein or artery and is anastomosed in standard fashion. The anastomosis may be longer than for a non-endarterectomized vessel because of the longer incision for the endarterectomy. Open endarterectomy is applied most commonly to the left anterior descending coronary artery, but can be applied to any coronary artery. The incision extends the length of the segment to be endarterectomized, but if the distal vessel becomes small (< 1.5 mm) and the disease extends beyond, a closed distal endarterectomy is performed. The dissection plane is developed circumferentially in the proximal or middle segment, and the plaque is divided. With gentle traction, the plaque is dissected in the outer third of the media, and large branches are identified. Care is taken to carry the dissection plane into branches so that the entire plaque is removed to achieve tapered endings if possible. Proximal dissection ends at the end of the arteriotomy where the plaque is sharply transected. Blind proximal endarterectomy, particularly on the left side, may disrupt flow into major proximal branches, including the circumflex artery, a ramus artery, or septal branches. It is possible to close the artery directly if the coronary artery is large, but usually a patch of vein or artery is used. Patch closure can be a free vein patch with subsequent incision of the patch for anastomosis of the bypass graft. Alternatively, the bypass graft, whether artery or vein, can be spatulated the length of the arteriotomy to create an end-to-side anastomosis with a long tongue. A third technique has been described for saphenous vein in which two circumferentially equidistant longitudinal incisions one-half the length of the

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arteriotomy are made in the vein to create two venous flaps with the body of the vein placed in the center to create a T anastomosis.

Anastomotic bleeding After each anastomosis is created it is important to check for bleeding and fix the leak on the non-beating heart. We run antegrade cardioplegia at 30– 40 mmHg down the graft spraying saline on the site to assess bleeding. If a major leak is identified, a 7–0 prolene suture on a small needle is used for repair as the vessel is gently distended. Blind suture placement in a collapsed vessel jeopardizes the integrity of the anastomosis. Large repair bites can distort the anastomosis.

Construction of the proximal anastomosis We use a single clamp technique to perform proximal anastomoses on the aorta. We avoid partial cross clamping because of the risk of embolization with repeated manipulation of the aorta. The disadvantage of this technique is that cross clamp time is prolonged. However, with current cardioplegia antegrade and retrograde protection seem to support this strategy. Recent increase in the use of Y-grafting has eliminated the need for this as the proximals have been already constructed prior to application of the cross clamp. For constructing proximals on the aorta it is important to create a visual estimate of where these grafts should lie while the heart is beating prior to application of the cross clamp. With the heart arrested one can then estimate the location of the proximals that would allow the grafts to lie well. It is important to orient the grafts along the longitudinal axis to avoid a twist which can sometimes be difficult to recognize. If the anastomosis is completed before a twist is recognized, the proximal should either be re-done or the vein can be divided and a venovenotomy created. We recommend the former. In order to measure the length of the graft the heart must be filled, all pericardial tacking sutures that elevate the heart should be released, and the conduit should be gently distended. These maneuvers help avoid the problem with having a short or long graft. The conduit is then cut obliquely at an angle leaving approximately 0.5 cm of extra length from the point of desired anastomosis to the aorta. The vein is spatulated for 5–7 mm to allow the creation of a ‘cobra-hood’ anastomosis. Using an 11-blade, 3–4-mm incisions are made in the aorta and a 4- or 5-mm aortic punch is used to remove circular segments of the aortic wall. A parachute technique is used to sew the graft with the needle traversing the aorta from inside to outside. Full intimal bites are important to avoid the dreadful possibility of aortic dissection once the heart resumes ejection. If a soft accessible plaque is encountered it should be removed. If removal is not technically possible then suturing must be done in such a way as to ensure the plaque is tacked to the aortic wall. Sometime the aortic wall may be diseased with only a limited area for proximal anastomosis. In this case a second vein graft can be taken off from the hood of the first vein graft by making a 5-mm incision on the hood. For free arterial grafts, we prefer this

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technique as opposed to taking them directly off the aorta. Occasionally after the initial punch it is apparent that the aortic wall is too diseased for a satisfactory anastomosis. One solution is to enlarge the aortotomy and cover the defect with a pericardial patch. The proximal anastomosis can then be made to the patch. If the aorta is extensively diseased, then ascending aortic replacement with a Dacron graft may be necessary. The conduits can be placed to the Dacron graft.

Flow capacity In contrast to the saphenous vein, ITA flow capacity is limited and relates to the diameter (2 vs. 5 mm) or cross-sectional area of the conduit. This obvious difference raises concern as to whether or not the ITA can supply adequate flow, particularly at times of increased need (i.e. after cross-clamp release or during exercise). Intraoperative measurements with an electromagnetic flowmeter or more recently with a transit-time flowmeter demonstrate that basal flows are comparable for the ITA and saphenous vein but that reactive hyperemic flows or those induced by intracoronary papaverine are significantly greater for saphenous vein [24]. In other reports, ITA flow is less than for saphenous vein, probably because of competitive flow in the native coronary artery [25]. Clinical studies [26] and earlier observations that ITA grafts enlarge over time in accordance with flow demand indicate that ITA grafts have the capacity to grow to meet physiological demands of the myocardium. Nevertheless, there may be perioperative situations or times of stress in the postoperative interval when myocardial flow requirements are not met by an ITA graft. A well-documented instance occurs during reoperative coronary bypass. If a diseased but patent vein graft to an occluded left anterior descending coronary artery is ligated and replaced with an ITA graft, the new graft may not immediately provide adequate perfusion of affected myocardium [27].

Solutions to problems during CABG Aortic tear Aortic tears may result from application of non-padded clamps to the ascending aorta. Tears vary from a limited transmural lesion to aortic dissection. Local tears are usually repaired with a 4–0 polypropylene running horizontal mattress suture without additional supporting tissue. If the aorta is fragile, two strips of pericardium are added. Alternatively, interrupted horizontal mattress sutures of 4–0 polypropylene with felt pledgets or with strips of felt are used to close the tear. Pericardium is easier to work with than Dacron for suturing to the aorta or vein graft. However, because long-term data on pericardial patches apply only to small patches, and because of concern about aneurysm formation, Dacron is used for large aortic patch repairs. If the injury is related to the aortic cannula, the cannula may have to be moved to the femoral artery to allow satisfactory repair of a tear or localized

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dissection. The aorta should not be repaired under arterial pressure as the tear will extend and the aorta will rupture. If a partial exclusion clamp or cross clamp does not give clear access to the injury, profound hypothermia with circulatory arrest may be necessary to repair the aorta. In this setting, direct suture may be inadequate, and a pericardial or Dacron patch or tube graft may be needed. Similarly, if the dissection has propagated beyond the local area, hypothermic circulatory arrest is necessary for inspection of the tear, evaluation of the arch and aortic replacement with a tube graft.

Root dissection When aortic root dissection occurs, the ascending aorta must be resected. This requires cardiopulmonary bypass with femoral artery cannulation and provision for profound hypothermia (18 °C or less) and an open distal anastomosis. Usually the aortic valve can be resuspended. Vein grafts are attached to the Dacron graft after it has been placed. If vein grafts were anastomosed to the aorta before the dissection occurred and are not involved in the dissection, an island patch can be placed in the anterior wall of the Dacron tube graft.

De-airing of aortic root Once the anastomoses are near completion, the heart is filled to allow for passive de-airing of the aortic root before the last suture is placed and tied. Administration of warm retrograde blood, with gentle suction on the aortic root vent, would allow for active de-airing of the root. If visible air remains in the vein grafts, a soft clamp can be placed on the vein and air removed with a small stab using a 27-G needle. The goal of all these maneuvers is to prevent air embolization to the coronaries, a frequent cause of myocardial dysfunction and arrhythmias, particularly ventricular fibrillation. If air appears to have embolized or wide QRS complexes are seen, increasing the mean arterial pressure to 90–100 mmHg may help in ‘washing out’ the air. Defibrillation of the heart should be attempted with the heart empty and non-ejecting. Lidocaine, calcium, and magnesium administration will help in cardioversion. If it appears that the ventricular fibrillation is refractory, amiodarone bolus at a dose of 150 mg followed by electrical cardioversion is usually successful. Restoration of a rhythm and contractility are important elements to prevent the non-beating perfused heart from becoming edematous. Myocardial edema leads to postoperative ventricular dysfunction and the need for inotropic support, which can further deplete the cardiac energy stores and also predispose to postoperative arrhythmias.

Reperfusion of the heart During the period of reperfusion and myocardial recovery all anastomoses should be checked for bleeding. Small needle stick bleeders should not be fixed. There are now many topical hemostatic agents available that can be used if bleeding continues after heparin reversal with protamine. Epicardial pacemaker wires are also placed in all cases to facilitate separation from CPB. The

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ability to control heart rate in the postoperative period can assist in managing blood pressure and cardiac output without the need to add pharmacological support. The wires should be positioned on the ventricle and atria in a fashion that the bare wires would not contact each other and short out. Finally, careful attention to the placement of the wires with respect to the position of the grafts is essential. If the wires are placed crossing under the grafts, at the time of wire removal a graft may be inadvertently avulsed or a side branch may be torn. During the reperfusion period we also study the flow through the conduits with a Doppler flow probe.

Failure to separate from cardiopulmonary bypass Separation from cardiopulmonary bypass may be directed by the anesthesiologist or the surgeon, but even if the former, the surgeon must have an intimate knowledge of the process and its physiology. During and after separation from CPB we routinely evaluate the heart by transesophageal endocardiography. Presence of new functional abnormalities in the coronary territory revascularized or new mitral regurgitation should raise suspicion regarding the adequacy of the target and patency of the graft. Vascular spasm, specifically in arterial conduits, can manifest as such. The ITA has less spasm than other arterial conduits, presumably because it contains less smooth muscle in the media. Spasm can be treated with a variety of drugs applied topically or systemically. We generally apply papaverine (2 mg/ml) mixed with heparinized blood topically on the conduits. Systemic nitroglycerin, nitroprusside, or one of the calcium channel blockers can also be administered. In addition, axial orientation of the conduits should be checked again. If a graft is too long and kinks, then a gentle curve should be given to the graft to remove kinking. The conduit can be tucked in that position by epicardial to adventitial suturing. Failure to separate from CPB with reasonable hemodynamics, low cardiac index (CI), poor ventricular function (specifically if regional and associated with poor graft flow) should prompt revascularization of that territory with a vein graft. If the surgeon is familiar with off-pump techniques then repeat cross clamping is not necessary and this is ideal. Currently available stabilizers are excellent in providing a stable platform for beating heart coronary bypass surgery. If the surgeon is not familiar with techniques of off-pump CABG then it is necessary to reclamp, arrest the heart and perform the distal anastomosis. The aortic clamp can then be removed and the proximal taken off from a previously vein graft to minimize the period of arrest. If after the new graft is placed, CI remains low or regional abnormalities persist, consideration should be given to placement of intra-aortic balloon pump (IABP). The mortality associated with postcardiotomy shock following CABG is high. If after inotropic support and IABP the CI still remains low, immediate consideration should be given to biventricular mechanical support. In these situations the problem may be secondary to poor myocardial preservation with global myocardial

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stunning or MI. Isolated left ventricular support is rarely the solution and consideration should be given to biventricular support and decompression of the heart to ‘rest’ the myocardium. Low flows should be maintained through the heart to prevent thrombosis. Patients should then be transferred to centres with transplant and device expertise.

Postoperative complications Early conduit failure The incidence of perioperative MI is between 3 and 7% in most series [28,29], but with better cardioplegia techniques these numbers are probably lower. Early graft failure may manifest in the ICU with arrhythmias, low output state, increase in pulmonary artery pressure, or ECG changes. Some conduits fail because of unrecognized harvest injury or injury sustained during graft preparation (instrumentation, excessive dilatation). Technical errors include large bites, deep bites, back walling, trauma to ITA during handling, and stenosis caused by linear tension or pursestring effect on a small anastomosis. Perioperative MI increases the risk of additional mortality and morbidity 2.5 times compared with patients who do not have infarction [29]. An aggressive approach in this setting is warranted. Immediate echocardiography can define wall motion abnormalities. Emergency angiography can identify conduit spasm which can be treated with direct intravascular injection of nitrates or calcium channel blockers. In addition, percutaneous interventions or surgical interventions could be promptly instituted depending on the findings on angiography [28]. We generally continue nitroglycerin in the perioperative period because of concerns with spasm, particularly with the radial artery. Aspirin is given soon after arrival to the ICU either via nasogastric tube or as a suppository. In patients who have had endarterectomy, Plavix 75 mg is given as soon as it is ascertained that there is no bleeding.

Pericardial tamponade Early pericardial tamponade typically occurs as a result of ongoing mediastinal bleeding. Increase in central venous pressure (CVP), or pulmonary artery pressure in the setting of low cardiac output is generally indicative of cardiac tamponade. Although the classical teaching is that the CVP and pulmonary artery pressures ‘equalize’, this clinical scenario may not necessarily be present after an open procedure. Localized clot may cause compression in one area sufficiently to compromise venous return but not cause pressure equalization [30]. The typical scenario is a patient who bleeds postoperatively receives blood products and has a sudden decrease in chest tube drainage with associated decreased cardiac output. Chest X-ray may or may not demonstrate a widened madisterium. Echocardiography is helpful but often delays intervention and does not provide adequate windows for evaluation. If the clinical diagnosis of tamponade is even a remote possibility, emergent return to the operating room and re-exploration is mandatory. This is particularly true with

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primary CABG patients who have excessive bleeding. In this case our threshold for re-exploration is even lower. Delay in treatment can be fatal. In the operating room the surgeon should be scrubbed and ready to open chest with the prep being carried out by others. It is very common that upon induction of anesthesia, with removal of the sympathetic tone, the blood pressure would precipitously fall resulting in cardiac arrest. If the patient remains stable, draping is done as to only expose the skin incision with wires and chest tubes out of the area to minimize contamination. Upon entering the chest all clots should be carefully removed without jeopardizing the grafts that may be buried under. Warm saline irrigation can help in cleaning the mediastinum. We typically pack the chest and initiate a search for the bleeder by removing the packs sequentially and looking in a systematic way in each area. Aortic, venous, and cardioplegia cannulation sites should be inspected. The conduits should be checked for branch site bleeding. The mediastinum, thymic remnant, ITA harvest site and sternal wire areas should all be inspected. Once the patient is hemodynamically stable, the distal anastomoses can be checked. Gently placing packs behind the heart, traction sutures on the pericardium to lift the heart, and rotation of the operating table can aid in visualization without hemodynamic instability. Placing the patient in Trendelenburg can also assist with higher blood pressure as the heart is lifted. Most bleeding should be controllable with gentle compression using topical hemostatic agents. Once bleeding is controlled the chest must be irrigated with copious amounts of warm saline. The chest tubes must be cleared and the sternum closed primarily. Delayed cardiac tamponade generally occurs after 1 week. The etiology is unclear but may be related to anticoagulation, persistent postperioperative mediastinal drainage, or post-pericardiotomy syndrome. Diagnosis is usually established by echocardiography and the treatment is drainage by surgical subxiphoid pericardial window. Percutaneous techniques in this setting are usually unsuccessful because the effusion is thick and loculated.

Arrhythmias Postoperative supraventricular arrhythmias are common after heart operations. The arrhythmia chapter deals with this matter in detail. In general, we favor an aggressive approach to treatment of postoperative atrial fibrillation which includes pharmacological treatment and electric cardioversion prior to considering anticoagulation. Of particular interest is a history of non-sustained ventricular tachycardia or perioperative ventricular tachycardia. In patients with low ejection fraction or previous MI, an electrophysiological study is indicated to search for inducible ventricular tachycardia. If found, placement of an automatic internal cardioverter defibrillator should be considered.

Wound complications Sternal wound complications are of particular concern in diabetics and patients with bilateral ITA harvest. The incidence of deep wound infections

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ranges from 0.4 to 5% [31]. Risk factors include re-exploration, obesity, prolonged ventilatory support, immunosuppression and renal insufficiency. Early aggressive drainage and debridement of the infected sternum are necessary. Areas of bone necrosis must be resected and necrotic tissue must be debrided and the mediastinum irrigated with antibiotic-containing solution. If the bone appears viable, primary closure can be attempted with chest tubes and Jackson–Pratt tubes left in the mediastinum for irrigation and drainage as needed. If the bone is not viable a complete sternectomy followed by omental or muscular flap coverage is necessary.

Conclusion The high-risk profile of patients requiring CABG continues to challenge surgeons daily. Meticulous attention to the preoperative selection and intraoperative technical details should minimize the morbidity and mortality of CABG. Every step can lead to a poor outcome unless care is taken to avoid complications and be prepared to fix problems as they arise.

Acknowledgments We thank Beverly Wolff for her assistance in preparing this manuscript.

References 1 Utley JR, Leyland SA, Edmunds HL. Preoperative evaluation. In: Edmunds, ed. Cardiac Surgery in the Adult. New York: McGraw-Hill, 1997. 2 Rawitcher RE, Jones JW, McCoy TA et al. A prospective study of aspirin’s effect on red blood cell loss in cardiac surgery. J Cardiovasc Surg 1991; 32: 1. 3 Anderson RJ, O’Brien M, MaWhinney S et al. Renal failure predisposes patients to adverse outcome after coronary artery bypass surgery. VA cooperative study #5. Kidney Int 1999; 55: 1057–1062. 4 Lemmer JH Jr. Clinical experience in coronary bypass surgery for abciximab-treated patients. Ann Thorac Surg 2000; 1986; 70 (2 Suppl.): 533–537. 5 Roach GW, Kanchuger M, Mora-Mangano C et al. Adverse cerebral outcomes after coronary bypass surgery. N Engl J Med 1996; 335: 1857–1863. 6 Smith PL, Treasure T, Newman SP et al. Cerebral consequences of cardiopulmonary bypass. Lancet 1986; 1: 823 – 825. 7 Gillinov AM, Sabik JF, Lytle BW, Cosgrove DM. Axillary artery cannulation. J Thorac Cardiovasc Surg 1999; 118: 1153. 8 Lytle BW, Blackstone EH, Loop FD et al. Two internal thoracic artery grafts are better than one. J Thoracic Cardiovasc Surg 1999; 117: 855–872. 9 Tector AJ, McDonald ML, Kress DC et al. Purely internal thoracic artery grafts: outcomes. Ann Thorac Surg 2001; 72: 450–455. 10 Sundt TM, Barner HB, Camillo CJ, Gay WA, Jr. Total arterial revascularization with an internal thoracic artery and radial artery T graft. Ann Thorac Surg 1999; 68: 399 – 404. 11 Calafiore AM, Teodori G, DiGiammarco G et al. Multiple arterial conduits without cardiopulmonary bypass: early angiographic results. Ann Thorac Surg 1999; 67: 450–456.

Complications of coronary artery bypass surgery 279 12 Broadman RF, Frame R, Camacho M et al. Routine use of unilateral and bilateral radial arteries for coronary artery bypass graft surgery. J Am Coll Cardiol 1996; 28: 959–963. 13 Francel TJ, DuFresne CR, Baumgartner WA. Anatomic and clinical consideration of an internal mammary artery harvest. Arch Surg 1992; 127: 1107. 14 Morin JE, Hedderich G, Poirier NL et al. Coronary artery bypass using internal mammary artery branches. Ann Thorac Surg 1992; 54: 911. 15 Cunningham JM, Gharavi MA, Fardin R. Consideration in the skeletonization technique of internal thoracic artery dissection. Ann Thorac Surg 1992; 54: 947. 16 Higami T, Mauro A, Yareashita T et al. Histologic and physiologic evaluation of skeletonized internal thoracic artery harvesting with an ultrasonic scalpel. J Thorac Cardiovasc Surg 2000; 120: 1142–1147. 17 Higami T, Yamashita T, Nohara H et al. Early results of coronary grafting using ultrasonically skeletonized internal thoracic arteries. Ann Thorac Surg 2001; 71: 1224–1228. 18 Utley JR, Thomason ME, Wallace DJ et al. Preoperative correlates of impaired wound healing after saphenous vein excision. J Thorac Cariovasc Surg 1989; 98: 147–149. 19 Isgro F, Weisse U, Voss B et al. Minimally invasive vein harvesting: is there an improvement of the results with the endoscopic approach? Eur J Cardiothorac Surg 1999; 16 (Suppl. 2): S58–60. 20 Green GE. Internal mammary artery-to-coronary anastomosis: three year experience with 165 patients. Ann Thorac Surg 1972; 42: 260. 21 Iaco AL, Teodori G, DiGiammarco G et al. Radial artery for myocardial revascularization: long-term clinical and angiographic results. Ann Thorac Surg 2001; 70: 1378–1383. 22 Calafiore AM, DiMauro M, D’Alessandro S et al. Revascularization of the lateral wall: long-term angiographic and clinical results of radial artery versus right internal thoracic artery grafting. J Thorac Cardiovasc Surg 2002; 123: 225–231. 23 Davila-Roman VG, Barzilai B, Wereing TH et al. Intra-operative ultrasonographic evaluation of the ascending aorta in 100 consecutive patients undergoing cardiac surgery. Circulation 1991; 84 (Suppl. 5): 47–53. 24 Barner HB. Blood flow in the internal mammary artery. Am Heart J 1973; 86: 575. 25 Navia D, Cosgrove DM, Lytle BW et al. Is the internal thoracic artery the conduit of choice to replace a stenotic vein graft? Ann Thorac Surg 1994; 57: 40. 26 Gurne O, Chenu P, Polidori C et al. Functional evaluation of internal mammary artery bypass grafts in the early and late postoperative periods. J Am Coll Cardiol 1995; 25: 1120. 27 Louagie YAG, Hayhe J-P, Buche M et al. Intraoperative electromagnetic flow meter measurements in coronary artery bypass grafts. Ann Thorac Surg 1994; 57: 357. 28 Baur HR, Peterson TA, Arnar O et al. Predictors of perioperative myocardial infarction in coronary artery operation. Ann Thorac Surg 1981; 31: 36. 29 Force T, Hibberd P, Weeks G et al. Perioperative myocardial infarction after coronary bypass surgery. Clinical significance and approach to risk stratification. Circulation 1990; 82: 903. 30 D’Cruz IA, Overton DH, Pai GM. Pericardial complications of cardiac surgery: Emphasis on the diagnostic role of echocardiography. J Card Surg 1992; 7: 257. 31 Blanchard A, Hurni M, Ruchat P et al. Incidence of deep and superficial sternal infection after open heart surgery: a ten years retrospective study from 1981 to 1991. Eur J Cardiothoracic Surg 1995; 9: 153.

CHAPTER 16

Complications of cardiopulmonary bypass and cardioplegia Lawrence L Creswell

Introduction Although cardiopulmonary bypass (CPB) and the use of cardioplegia for myocardial protection are used routinely today in the practice of cardiovascular surgery, these are both relatively new techniques. The potential utility of extracorporeal circulation was recognized in 1813, when Le Gallois wrote: ‘But if the place of the heart could be supplied by injecting and if, with a regular continuance of this injection, there could be furnished a quantity of arterial blood, whether naturally or artificially formed, supposing such a function possible, then life might be indefinitely maintained in any portion.’ [1] Bruchonenko was the first to suggest that extracorporeal circulation might be useful clinically. Using a circuit with a roller pump and excised canine lungs for oxygenation, he was able to support the arrested canine heart for several hours. A pump circuit of this design was later used for successful valvular heart surgery in animal models in the 1930s and early 1940s. Credit for the first successful clinical use of a pump-oxygenator, the forerunner of today’s modern CPB machine, goes to John H. Gibbon Jr, MD. His vision for this device dates to 1930 when he was caring for a patient who died of massive pulmonary embolism. At that time, he wrote: ‘During the 17 h by this patient’s side, the thought constantly recurred that the patient’s hazardous condition could be improved if some of the blue blood in the patient’s distended veins could be continuously withdrawn into an apparatus where the blood could pick up oxygen and discharge carbon dioxide and then pump this blood back into the patient’s arteries.’ [1] Gibbon also recognized the importance of heparin, which became available in sufficient quantities only in the late 1930s. Development of his pump oxygenator continued during the 1940s in laboratory animals. Even at this early stage, the potential complications associated with CPB were recognized by Gibbon and he made refinements related to the problems of hemolysis, air embolism, and the unwanted effects of a blood–surface boundary. The first 280

Complications of cardiopulmonary bypass and cardioplegia 281

clinical use of his pump oxygenator took place in 1952 in an infant with suspected atrial septal defect. The attempted use of the pump oxygenator in this patient and two other early patients was unsuccessful. The first successful operation using the pump oxygenator took place on 6 May 1953, when an atrial septal defect was repaired using a 26-min period of extracorporeal support [2]. As more complex cardiac operations became possible with the use of the pump oxygenator, it became apparent that there were still limitations imposed by the beating heart and the return of bronchial blood into the operating field. The technique of intentional cardiac arrest imposed by the injection of potassium chloride solution dates to animal studies from the early 1900s [1]. Melrose was the first to report in 1955 the technique of induced cardioplegic arrest of the heart during heart surgery, using injection of potassium citrate solution, or cardioplegia, directly into the aortic root after cross-clamping of the aorta [3]. The alternative technique of retrograde, or coronary sinus cardioplegia was introduced by Lillihei who reported its use during an aortic valve replacement in 1956 [4]. Both of these techniques have come into widespread clinical usage. The development and clinical application of CPB and modern techniques of myocardial protection have allowed a wide array of cardiopulmonary operations that would not otherwise be possible. These techniques, however, are associated with a variety of complications and pathophysiological consequences that affect nearly every patient in whom they are applied. This chapter focuses on the complications associated with the clinical use of CPB and myocardial protection, which are presented in five sections: (i) the mechanics of CPB and related complications; (ii) monitoring for CPB and related complications; (iii) anticoagulation for CPB and related complications; (iv) the pathophysiological consequences of CPB; and (v) the complications of cardioplegia. Many of these complications may also be covered in other chapters of this book that focus on specific organ systems (e.g. pulmonary, renal, neurological) or the complications related to specific cardiac operations (e.g. coronary artery bypass surgery, aortic surgery, valvular heart surgery). This discussion is necessarily a summary of the most important aspects of CPB and the related complications. The reader is referred to other, excellent texts on cardiac surgery in adults [5], the techniques of cardiopulmonary bypass [6–8], and cardiothoracic anesthesia [9,10] for additional information.

Mechanics of cardiopulmonary bypass and related complications Components of the cardiopulmonary bypass circuit and related complications CPB is used to facilitate many cardiac operations today. Although the features of the cardiopulmonary bypass circuit and the conduct of CPB will vary from institution to institution, and may vary with the special requirements dictated

Figure 16.1 A typical cardiopulmonary bypass circuit. (From Hessel EA, Hill AG. Circuitry and cannulation techniques. In: Gravlee GP, Davis RF, Kurusz M, Utley JR, eds. Cardiopulmonary Bypass: Principles and Practice. Philadelphia: Lippincott, Williams & Wilkins, 2000; 70, with permission.)

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by a particular operative procedure, many features are common to all applications [11]. A typical cardiopulmonary bypass circuit is presented in Figure 16.1. Many of the mechanical complications associated with the use of cardiopulmonary bypass are related to the individual components of the circuit.

Venous cannulas Venous cannulas are available in a variety of designs, materials, and sizes and are often categorized as either 1-stage (atrial) or 2-stage (cavo-atrial). The venous cannulas may be wire-wound or made from hard synthetic materials to prevent kinking. Thin metal, rather than thicker plastic, tips may increase the effective size of a given cannula. The simplest method for atrial cannulation is with a single venous cannula (either 1-stage or 2-stage). For most operations in which the right side of the heart is entered, however, bi-caval cannulation is required. With bi-caval cannulation, caval occlusion, often with umbilical tape secured around the cannulas, provides a clear operative field for operations on or through the right side of the heart.

Venous cannulation During venous cannulation, atrial arrhythmias or untoward hemodynamic effects may be caused by manipulation of the heart. This is particularly true if the heart must be retracted leftward and superiorly for placement of inferior vena cava (IVC) cannulation sutures. These hemodynamic effects are usually transient, but electrical cardioversion for atrial arrhythmias may be necessary and the appropriate equipment should be available during cannulation. The potential for arrhythmias may be increased if the systemic temperature is allowed to drift too low during opening and cannulation. In situations in which bi-caval cannulation will be used, IVC purse-string sutures can be placed and cannulation can be performed after CPB is initiated (i.e. with only superior vena cava (SVC) cannulation) to help avoid hemodynamic difficulties. Incisions in the atrium or vena cavae should be made carefully to prevent inadvertent extension of these incisions and unwanted bleeding. The fingers should be used to confirm the correct position of the venous cannulas during insertion. Without proper care, venous cannulas may be placed inadvertently in a variety of locations, including the innominate vein, the hepatic veins, the coronary sinus, or even through a septal defect to the left side of the heart. Caval tapes should be used carefully because they may tear or lacerate the atrium or vena cavae, particularly with retraction (i.e. as for mitral valve operations). After the termination of CPB, cannulation incisions in the SVC should be closed carefully to prevent narrowing of the SVC [12]. This problem can be avoided in many situations by inserting the SVC cannula through a purse-string in the right atrial appendage. Inadvertent narrowing of the cannulation incision is usually not a problem for incisions in the right atrium. Pre-existing central venous or pulmonary artery catheters may be displaced or dislodged during cannulation. The surgeon must be aware of this

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possibility and the anesthesiologist must monitor for this type of complication. On rare occasions, purse-string sutures may entrap or injure one of these catheters and may necessitate reoperation for removal of the affected catheter [13,14]. Transesophageal echocardiography (TEE) may sometimes be useful to identify these problems [14]. With the use of caval occlusion tapes, monitoring lines caught between the tape and the venous cannula may be rendered useless temporarily or even damaged permanently. In practice, it may be helpful to ‘pull back’ the pulmonary artery catheter before caval tapes are tightened and then advance the catheter once again when the caval tapes are released. During venous cannulation, it is important for the surgeon to be aware of the possibility of a persistent left superior vena cava (LSVC). This anomaly is present in approximately 0.5% of the general population, but it is more common in patients undergoing cardiac surgical procedures, and particularly those with congenital heart disease. When a 2-stage venous cannula is used, the presence of a persistent LSVC is not usually a problem. When the right heart must be entered and bi-caval cannulation is used, the extra return of blood through the coronary sinus may pose difficulties, however. If the innominate vein is normal in size, the persistent LSVC may simply be occluded during CPB. If the innominate vein is small or absent, occlusion of the persistent LSVC during CPB may produce venous hypertension and possibly neurological injury. Alternative approaches in this situation include the use of a cardiotomy suction device placed in the orifice of the coronary sinus through the open right atrium or direct (retrograde) cannulation of the persistent LSVC and the use of an occlusion tape around this vessel. Venous air embolism may occur during insertion of venous cannulas [15]. If an intracardiac shunt is present, this situation may potentially result in systemic air embolism. Before CPB is initiated, the presence of venous cannulas in the right atrium may obstruct the ordinary venous return to the heart and interfere with proper hemodynamics. This unwanted side-effect is most pronounced with bi-caval cannulation. If obstruction to proper venous flow produces persistent hemodynamic instability, CPB should be initiated immediately. Peripheral venous cannulation (rather than direct atrial cannulation) may be useful in circumstances such as cardiopulmonary arrest outside of the operating room, during redo operations before the repeat sternotomy, and in certain aortic surgery procedures. In these circumstances, the use of as large a venous cannula as possible will help to facilitate adequate CPB. When possible, a peripheral venous cannula should be advanced into the right atrium, using either palpation, measurement of the length of the cannula, or TEE to guide proper placement. A variety of commercially available thin-walled cannulas, often with guide-wire or other introducer systems, are available for use in this situation. When peripheral vessels are cannulated under direct vision using a cutdown approach, special care should be used after decannulation to close the venotomy without narrowing the vessel.

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Venous reservoir and drainage When a membrane oxygenator is used, the venous reservoir is placed in the circuit immediately before the pump. This device also serves as a gross bubble trap for all blood that returns to the perfusion circuit from the venous line and from cardiotomy suction lines. The venous reservoir may be constructed of heavy plastic or a collapsible plastic bag. Advantages of the heavy plastic variety include: ease of measuring blood volume in the reservoir, ease of priming, and the ability to attach a vacuum suction for assisted venous drainage, if desired. The collapsible type may be advantageous because it eliminates some of the blood–air interface and may help to prevent inadvertent air embolism. The collapsible type is more susceptible to damage (i.e. tearing), however. Regardless of the type of venous reservoir, this device provides the perfusionist with a ready source for volume infusion into the patient and also a safety margin if the venous return is interrupted during CPB. In most applications of CPB, the venous drainage is accomplished simply by siphon effect (due to gravity) to the venous reservoir which is placed below the level of the patient. The amount of venous drainage is affected by: (i) the height of the patient above the venous reservoir, (ii) the central venous pressure, and (iii) the resistance of the venous cannulas and circuitry. The relationship between the central venous pressure and these factors is given by: Pvsys = f [(Q, viscosity)/(cannula size, venous line size, venous line suction)], where Pvsys is the mean systemic venous pressure and Q is the systemic blood flow [16]. The goal during CPB is to maintain the systemic venous pressure as low as possible. Inadequate venous drainage will limit the ability of the perfusionist to maintain an adequate flow rate and can be due to one or more related factors. The venous drainage can be improved by: (i) elevating the patient in relation to the venous reservoir; (ii) increasing the venous cannula size (the sum of the cross-sectional areas of all venous cannulas in use); (iii) increasing the diameter of the venous line; or (iv) the use of venous line suction (augmented venous drainage).

Augmented venous drainage The technique of augmented venous drainage may be useful in a variety of clinical situations, but is particularly useful when long, relatively narrow venous cannulas are needed (e.g. for minimal access procedures). Two general techniques are available. In the first technique, either a roller or a centrifugal pump is placed in the venous line between the patient and the venous reservoir. When a roller pump is used, the perfusionist must be careful to monitor the pump speed continuously to prevent the build-up of excessive negative pressure that may cause the right atrium or great veins to collapse around the cannula. The use of a centrifugal pump may decrease this risk. In either case, a ‘shunt’ placed around the pump may reduce the risk of excessive negative pressure. The venous line pressure should be measured near the pump and kept < – 60 to – 100 mmHg [17]. The second general technique involves the application of a vacuum directly to the venous reservoir. This approach is

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simpler and avoids the use of a second pump. Application of 20–60 mmHg vacuum to the venous reservoir is usually adequate and safe. Although augmented venous drainage may facilitate operative procedures that would otherwise be more difficult, there are several potential risks. The most obvious problem relates to the increased risk of air entry into the venous circuit from holes in the heart or around the venous cannulas. Air may also enter the heart through central venous catheters or introducer sheaths that may be in place [18]. In most circumstances a small amount of air in the venous side of the circuit will be well tolerated, but large amounts of air that accumulate at the venous reservoir may predispose to systemic air embolization. In addition, if a second pump is used in the venous circuit, the perfusionist must be vigilant to keep the venous drainage and systemic flow balanced. If not, dramatic changes in the patient’s intravascular volume may occur very quickly. Lastly, hemolysis may result from excessive negative pressures in the venous line [19,20].

Arterial cannulas A wide variety of arterial cannulas are available for clinical use. Differences in their materials and design facilitate their use in different arteries, both central and peripheral, during cannulation. The arterial cannula is typically the narrowest portion of the perfusion circuit. As a result, the arterial cannula is subject to relatively large pressure gradients across the cannula. As a general rule, the shorter the narrow segment of the arterial cannula, the lower the pressure gradient will be. As an example, a long, uniformly narrow cannula will be highly resistant to flow and there are few examples of this type of design. Ordinarily, arterial cannulas narrow only at or near their tip to minimize this problem. At the tip, the use of hard plastic or metal may be used to increase the inside diameter (ID) to outside diameter (OD) ratio and minimize the pressure gradient. Hemolysis and protein denaturation may occur with pressure gradients of > 100 mmHg [21]. Regardless of the design of the arterial cannula, high-velocity jets of blood exiting the cannula and entering the cannulated artery may produce localized damage such as tearing, dislodgement of calcific plaque (producing circulating emboli), or arterial dissection. Devices such as the EMBOL-X Intraaortic Filtration System (EMBOL-X Inc., Mountain View, CA, USA) have shown promise in the extraction of particulate debris at the arterial cannula tip, but the clinical utility of these devices is yet to be proved [22]. These devices are promising since cerebral macroembolism is thought to be a major determinant of neurological injury after CPB [23–25].

Arterial cannulation Arterial cannulation for cardiac surgery can be accomplished through a variety of arteries. In adult cardiac surgical procedures, the aorta is the most common site for arterial cannulation, but other arteries such as the femoral artery or axillary artery may also be used.

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Aortic cannulation The aorta is easily exposed through the standard median sternotomy incision and is a relatively safe site for cannulation. Dislodgement and circulation of emboli from calcific plaque from the aorta is thought to be responsible for many of the neurological complications associated with cardiac surgery [23–25]. Embolization can be due to either direct manipulation of the aorta during cannulation or due to the effects of a high-velocity jet of blood striking the inner surface of the diseased aorta. Embolism of very small particles may produce no symptoms at all in many patients, but these small particles may be responsible for some of the neurocognitive changes encountered postoperatively in some patients [26–31]. Aortic cannulas with side holes, instead of end holes, near the tip may help to disperse blood as it enters the aorta and help to limit embolic injury [32]. Several techniques are available to help prevent inadvertent embolization. The surgeon should use manual palpation of the ascending aorta and exposed portion of the aortic arch and proximal great vessels to evaluate for the presence of calcific plaque. It is important to be sure that the planned sites for arterial cannulation, cardioplegia cannulation, aortic cross-clamping, and proximal anastomoses are free from significant disease. Unfortunately, manual palpation alone can underestimate the extent of atherosclerotic disease in these vessels [33–37]. With the introduction and increasingly widespread use of TEE during cardiac surgical procedures, this is another technique that can be used to assess the extent of atherosclerosis in the ascending aorta. Although TEE may not be able to image the mid-portion of the aortic arch completely, this technique can be used to assess the ascending and descending portions of the aorta [36–38]. More recently, epiaortic ultrasound has become the most sensitive method for the detection of significant atherosclerotic disease in the ascending aorta before cannulation [36,37]. With this technique, an ultrasound probe in a sterile sheath is passed into the operative field. The pericardium is filled with saline and the probe is placed directly on the aorta to create crosssectional or longitudinal images. When significant disease is discovered, the operative plan can be changed in response to the findings: (i) an alternative site for arterial cannulation such as the axillary artery or femoral artery may be selected; (ii) sites that are free of disease can be selected for cannulation, aortic cross-clamping, and siting of proximal anastomoses; (iii) for patients requiring only CABG, an off-pump approach might be selected; and (iv) a decision can be made in certain cases to replace the ascending aorta in addition to the originally planned procedure. When aortic cannulation is performed, most surgeons place a single or two concentric purse-string sutures directly in the anterior surface of the ascending aorta. Often, the adventitia is cleared within the purse-string suture(s) before cannulation. The systemic blood pressure should be kept in the low normal range during aortic cannulation to help prevent the complications of aortic tear or dissection. Intraluminal placement of the cannula is suggested by backbleeding into the cannula and the presence of a pulsatile blood pressure in the arterial line. Back-bleeding into the cannula may also facilitate removal of

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small particulate debris dislodged at the cannulation site as well as small amounts of entrained air. The tip of the aortic cannula should be directed toward the central portion of the aortic arch. A variety of complications are possible during or due to aortic cannulation. First, it may not be possible to introduce the cannula properly. This may be due to too small an opening, to fibrosis of the aortic wall, or to calcific plaque at the site of cannulation. It may be possible to insert the cannula tip into an intramural location; in this case, an improper cannulation may not be noticed until there is obstruction to blood flow and a high perfusion pressure is noted by the perfusionist when CPB is initiated. Too vigorous an introduction of the cannula may result in tearing at the cannulation site or to injury to the back wall of the aorta. Poor positioning of the tip of the cannula may result in ‘retrograde’ cannulation, with the tip pointing toward (or even through) the aortic valve. Other undesirable locations for the cannula tip include the head vessels or in a position firmly against the aortic wall itself; these positions may be suggested by high line pressures when CPB is initiated. Intramural hematoma may occur at the site of cannulation and is treated by prompt incision of the adventitia. Antegrade aortic dissection during cannulation occurs in < 0.1% of cases and is suggested by a sudden enlargement and bluish discoloration of the aorta, sudden bleeding from cannulation sites, and difficulties with venous return and arterial inflow [38–41]. Although this complication can be treated occasionally by suture plication of the ascending aorta, more often CPB must be reestablished via an alternative route (e.g. femoral artery) to facilitate repair or replacement of the ascending aorta. Immediately after decannulation, any bleeding at the aortic cannulation site can usually be controlled by placement of additional sutures. Late complications after aortic cannulation may include recurrent hemorrhage or the development of a pseudoaneurysm [42]. Femoral artery cannulation Femoral artery cannulation is used when the ascending aorta is not available for arterial cannulation (e.g. aneurysm or dissection of the ascending aorta, minimal access surgery with poor exposure of the ascending aorta). Although femoral cannulation can be accomplished percutaneously, more often the femoral artery is exposed surgically, necessitating an additional surgical incision. Complications related to femoral cannulation include: direct injury to the femoral vessel, bleeding, dissection, formation of a pseudoaneurysm, formation of a lymphocele, nerve injury, retrograde dissection of the aorta [43,44], and embolism (either air or calcific debris) to the distal extremity. During CPB with femoral cannulation, the distal extremity may become ischemic. With prolonged ischemia, tissue necrosis and the development of compartment syndrome in either the calf or thigh may occur [45]. As an alternative to direct cannulation, a graft (e.g. PTFE, Dacron) can be sutured end-to-side to the femoral artery to allow introduction of the arterial cannula while maintaining distal perfusion. Alternatively, a second, smaller caliber

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perfusion cannula can be placed in the femoral artery distal to the site of cannulation to provide distal perfusion to the extremity. Femoral cannulation and subsequent ‘retrograde’ perfusion may result in ‘retrograde’ embolism if any calcific debris is dislodged from the femoral, iliac, or descending aortic vessels. TEE can be used to screen for the presence of atherosclerosis in the descending aorta and if there is severe disease (and especially, for cases in which there is loose or ‘hanging’ debris), an alternative site for cannulation (e.g. axillary artery) should be selected. Axillary artery cannulation The axillary artery has recently been advocated for situations in which cannulation of the aorta or the femoral artery is not possible or desired [46,47]. The right axillary artery is typically favored over the left. The axillary artery is less likely than either the aorta or femoral artery to be heavily involved with atherosclerosis. In addition, there is good collateralization around this artery, and if a separate incision is used for cannulation, wound healing is often better than for a groin incision. The axillary artery can be cannulated directly or through a small caliber graft that is attached to the axillary artery in end-to-side fashion.

Pump oxygenator The two basic types of oxygenators in use today are the membrane oxygenator and the bubble oxygenator [48]. The membrane oxygenator is used almost universally worldwide, however. The ‘oxygenator’ is responsible for both oxygenation and ventilation (e.g. CO2 removal). For the typical microporous membranes (usually hollow fiber), there is direct contact between the blood and the membrane only at the outset of CPB. A thin protein coating then forms on the membrane quickly after the initiation of CPB and prevents direct contact between the blood and the membrane thereafter. Ventilation is controlled by the rate of gas flow and oxygenation is controlled by adjusting the oxygen fraction in the gas supplied to the oxygenator. There is a relatively high resistance to flow across the membrane, so blood must be pumped across the membrane before returning to the patient via the arterial line. Compared with bubble oxygenators, the use of a membrane oxygenator is associated with less hemolysis [49]. Studies have shown that, regardless of the type of oxygenator, there is reduced red blood cell survival after CPB [50]. The membrane oxygenator may also be associated with reduced complement activation, granulocyte activation, and platelet activation [49,51–53]. Some, but not all, studies have also shown less cerebral microembolism with membrane than with bubble oxygenators [54,55]. When an arterial filter is used, these differences are less pronounced, however. Recently, heparin-coated oxygenators have become available and have been advocated because of potential reductions in the subsequent systemic inflammatory response [56,57].

Bypass pump A pump is placed in the perfusion circuit to provide forward flow of blood

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through the circuit and back to the patient. Two general types are available: roller pumps and centrifugal pumps [58]. Each has relative advantages and disadvantages as well as its own set of potential complications. Even if a centrifugal pump is used as the primary pump, roller pumps are typically used for delivery of cardioplegia and the operation of any cardiotomy or vent suction lines. With the roller pump, a length of tubing is placed in a curved ‘raceway’ which is adjacent to a set of rollers. Forward flow is generated as the rollers spin, compressing the tubing in the raceway. For a given pump and tubing type, the flow rate that is generated is proportional to the pump speed (in rev/min). The degree of occlusiveness of the rollers against the tubing is important. Too much compression may promote hemolysis and too little compression may reduce the effective forward flow rate. The ideal degree of compression may occur when the rollers are adjusted to be just barely nonocclusive [19]. Other complications that are specific to the use of roller pumps include miscalibration [59] and the potential for fracture of the pump tubing. The roller pump is particularly susceptible to pumping large amounts of air into the arterial line if the venous reservoir is not monitored carefully and empties inadvertently. Spallation, the fragmentation and detachment of tubing particles, may also occur and an arterial line filter will limit subsequent embolization [60–62]. If there is inadvertent obstruction to outflow in the arterial line (e.g. from a clamp), pressure will build up in the arterial line until the tubing separates at a connector or the tubing ruptures. The centrifugal pump has an impeller design and is totally non-occlusive. The resulting flow rate with a centrifugal pump is not only determined by the rotational rate of the pump, but is affected by the afterload in both the circuit and the patient. When the pump is not rotating, blood can flow backward (e.g. from the patient) and exsanguination may occur if the arterial line is not clamped [63]. By the same mechanism, it is possible to draw air into the arterial side of the perfusion circuit at the cannulation site. In the event that the arterial line becomes occluded the centrifugal pump, unlike the roller pump, will not generate high pressures and it is unlikely that the tubing would rupture. One purported benefit of the centrifugal pump over the roller pump is a reduced likelihood of air embolism. Although it is true that a large amount of air will ‘de-prime’ the centrifugal pump (stopping it), smaller amounts of air may easily be pumped into the arterial line.

Heat exchanger One or more heat exchangers may be placed in the perfusion circuit to warm or cool the patient’s blood. The main heat exchanger is generally placed before the oxygenator to prevent any release of microbubbles because of warming blood that has just been oxygenated. The hot or cold water source may come from the hospital’s supply line or be part of a stand-alone unit. Malfunction of the heater-cooler during CPB will result in an inability to control the temperature of the patient’s blood properly [64].

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Cardiotomy suction The use of cardiotomy suction during cardiac surgical procedures allows for even large amounts of blood to be evacuated from the operative field during the procedure [65]. This blood is typically returned to the perfusion circuit at the cardiotomy or venous reservoir by way of a defoaming chamber and a microfilter. These suction lines are typically regulated by a roller pump. The perfusionist must constantly monitor the speed of the roller pump because if the line or suction tip becomes occluded, high negative pressures may build up and promote hemolysis. The use of cardiotomy and vent suction lines may result in hemolysis, gaseous or fat or other particulate microemboli, activation of coagulation and fibrinolysis, cellular aggregation, and platelet dysfunction [66–76]. Room air can be entrained into these suction lines and contribute to the formation of gaseous emboli and can produce additional shear stress that is detrimental to the blood elements. The detrimental effect of cardiotomy suction on the platelets is proportional to the amount of cardiotomy suction and the amount of entrained air [75,76]. Hemolysis is due to negative pressure at the cardiotomy suction tip and the entrainment of air and is minimized if the largest possible cardiotomy suction tip is used with the minimum necessary suction, and then, only when needed [77,78].

Cell saver The cell saver can be used in addition, or instead of, cardiotomy suction to scavenge blood from the operative field. With this technique, the scavenged cells are washed with saline and separated from the plasma by centrifugation. The cells can then be returned to the patient either intravenously or into the pump. In contrast to cardiotomy suction, the cell saver can be used, then, to filter out any particulates such as fat, air, and tissue before the blood is returned to the patient. The relative disadvantage is that there is loss of coagulation factors, platelets, and other plasma proteins that are lost during the centrifugation process. From a practical standpoint, the cell saver can be used instead of cardiotomy suction in operations in which there is little blood loss to the operative field (e.g. CABG). For operations in which larger volumes of bleeding are expected (e.g. redo operations, aortic surgery) and when venting is required, cell saver suction alone may not be practical. The cell saver can also be used at the conclusion of CPB to process any remaining blood in the venous reservoir before returning it to the patient.

Venting of the left heart Suction lines, or ‘vents’, can be used to decompress the left side of the heart during cardiac surgical procedures [65,79]. Even during cardioplegic arrest, there will be return of bronchial, Thebesian vein, and coronary sinus blood flow to the right side of the heart that will, unless vented, make its way to the left side of the heart. In addition, aortic insufficiency may lead to filling of the left ventricle (through an incompetent aortic valve) during administration of

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antegrade cardioplegia. On the basis of experimental as well as clinical studies, venting this blood prevents distension of the ventricle that might increase myocardial oxygen demand and reduce subendocardial perfusion [80–82]. In addition, venting of the left side of the heart may help to prevent unwanted rewarming of the heart during cardioplegic arrest and facilitate the operative exposure. Nonetheless, there remains considerable variation in clinical practice and debate about the true benefits of routine venting of the left heart [83,84]. Distension of the left side of the heart can be recognized visually, but the presence of cold saline or slush in the pericardium as well as the posterior location of the left ventricle may make recognition of left ventricular distension difficult. TEE can be used to monitor for distension of the left atrium and ventricle. An increase in the left atrial or pulmonary artery pressure (monitored by the pulmonary artery catheter) can also be an indication of left ventricular distension. Several methods are available for left heart venting. An antegrade cardioplegia cannula inserted into the ascending aorta provides an opportunity for aortic root venting. Venting is not possible during administration of cardioplegia, however. In addition, if aortic insufficiency is present it may be necessary to administer the antegrade cardioplegia intermittently to prevent left ventricular distension. Complications associated with the use of aortic root venting include potential injury to the aorta at the cannulation site (and even early or late aortic dissection) and introduction of air into the aorta if over-zealous suction is applied to the root vent. A second option for left heart venting is direct venting of the left ventricle, with insertion of a vent catheter directly through the apex into the left ventricle. This technique is seldom used today because of the risk of bleeding, myocardial injury, and even late pseudoaneurysm formation. Insertion of vent catheters directly into the left atrium or into the pulmonary artery may have applications [80], but these methods may not be completely effective for venting the left ventricle (LV). The most common method for LV venting is indirect, with insertion of a vent catheter through a pulmonary vein (usually the right superior) into the left atrium, and through the mitral valve into the LV. Several complications have been associated with left heart venting [85]. Air can be introduced into the left side of the heart, either during insertion or removal of the vent catheter. The likelihood of this complication can be reduced if the heart is allowed to fill, at least partially, during insertion and removal of the LV vent catheter. It may also be useful to remove the LV vent catheter while the pericardium is filled with saline (or blood) and the lungs are inflated to prevent aspiration of air into the left atrium. Excessive suction on the LV vent may cause introduction of air into the left heart around the purse-string suture or through open coronary arteries during the operative procedure [86]. It is important for the perfusionist to be vigilant for entrapment of the vent catheter tip and to prevent excessive suction. Mishaps with the LV vent line, in which positive pressure was applied to this line, have been

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reported. A 1-way valve in the LV vent line will prevent the introduction of air. Whenever LV venting is used, there should be meticulous efforts for de-airing to avoid subsequent embolization of air that is entrapped in the pulmonary veins, left atrium, or left ventricle. TEE can be used to evaluate the effectiveness of de-airing maneuvers [87]. More recently, many surgeons have adopted the practice of ‘flooding’ the field with CO2, particularly during portions of an operation when the left side of the heart is open. When this technique is used, excessive CO2 absorption may lead to hypercarbia and metabolic acidosis in rare cases [88]. Because it is more soluble, residual CO2 in the heart is much less likely to cause difficulties with embolization.

Mechanical complications during cardiopulmonary bypass Electrical failure A variety of electrical mishaps may occur during CPB, but these problems rarely cause significant harm to the patient [89]. A total power failure will affect the CPB pump as well as its monitors. All perfusion pumps should have a hand crank available so that manual operation of the CPB pump can continue despite an electrical power failure. Many hospitals in the USA are equipped with emergency power generators in the event of a power failure, but it may take several minutes for a back-up generator to come on line. More recently, operating rooms have been equipped with isolated electrical systems with a local back-up power supply in the event that the main hospital power fails. Newer perfusion machines are often equipped with battery back-up power units as a component. With all of these systems and safeguards, however, it is important to have regular safety checks and periodic review of emergency procedures.

Massive air embolism Massive air embolism is a rare complication, occurring in < 0.2% of cases, but the impact of this complication can be devastating [89]. Nearly 50% of affected patients die or suffer permanent neurological damage [90]. In general, this term refers to embolism to the systemic, rather than the pulmonary circulation. Because of the ‘open’ nature of the perfusion circuit, there are many potential sites for introduction of air, including the operative field, the perfusion circuit itself, or introduction of air inadvertently or iatrogenically through intravenous lines [91]. At the operative field, air can be introduced during the surgical procedure at a variety of stages. Before an aortic cross clamp is applied, small amounts of air may be introduced inadvertently during aortic cannulation or insertion of antegrade cardioplegia delivery cannulas. Back-bleeding into the cannulas during these cannulations may help to prevent the introduction of air. If the left side of the heart is opened during the procedure, there is an obvious opportunity for air to be introduced and entrapped. The left atrium, left ventricle, and pulmonary veins are all sites where air can become entrapped. Rigorous de-airing maneuvers at the conclusion of the operative procedure are

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warranted and TEE can be used to evaluate the success of these maneuvers. Even when the left side of the heart is not opened (e.g. during CABG operations), air can be drawn in through openings in the coronary arteries if there is excessive venting at the aortic root or through a superior pulmonary vein. There are many opportunities for introduction of air in the perfusion circuit [92]. Inadvertent emptying of the venous reservoir and pumping of air into the arterial side of the circuit may be the most common cause of massive air embolism [93,94]. Modern perfusion set-ups typically include monitors and alarms to indicate a low level in the venous reservoir, but attention to this potential situation on the part of the perfusionist is probably the most important safeguard. When a roller pump is used as the primary pump, fracture of the tubing at the roller head may cause the introduction of air. In addition, any break in the arterial side of the circuit (e.g. fracture, open stopcock) may predispose to the introduction of air. Another potential source for introduction of air is cavitation that can occur at sites of high-velocity flow through restricted diameter tubing (e.g. at kinks, at sites of clamping). Air embolism can be recognized at several stages during operation. Perhaps the most common stage where air embolism is suspected is during weaning from CPB. Introduction of air antegrade into the coronary arteries can produce temporary myocardial dysfunction that is recognized by regional ECG changes or regional changes in myocardial function by TEE. Raising the aortic root pressure, either pharmacologically or by partial manual occlusion of the distal aorta, may help to force air through the coronary arteries into the venous circulation. As an alternative, with the cross clamp still applied, a large syringe can be used to inject blood under pressure directly into the aortic root to help pass intracoronary air into the venous circulation [95]. In addition, the administration of retrograde cardioplegia may help to force air from the coronary arteries into the aortic root, where it can be removed with an aortic root vent catheter [96]. The patient can be supported by continued CPB and this problem should resolve in several minutes. If massive air embolism is recognized during operation, the source of the air must be determined quickly. CPB should be stopped immediately if the source of air is from the arterial side of the perfusion circuit. In this situation, the venous line should be clamped to prevent exsanguination. Air in the arterial line should be removed either by aspiration or by filling before CPB is reinitiated. A variety of techniques are available to remove unwanted air from the other components of the perfusion circuit, such as the oxygenator, centrifugal pump, and arterial filter [89]. Some authorities have recommended placing the patient in Trendelenberg position to allow air to flow back into the ascending aorta (for possible aspiration), but recent animal experiments have called this practice into question [97,98]. If a large volume of air is suspected to have entered the arterial circulation, the use of a period of retrograde cerebral perfusion and profound systemic hypothermia may limit permanent neurological injury [99–103]. Pharmacological therapy may be useful during an episode of massive air embolism, but there are few clinical data to guide

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the surgeon. Corticosteroids, anticonvulsants, barbiturates, and diuretics may be used to help limit neurological injury or the symptoms of that injury. One useful algorithm for the postoperative treatment of patients with massive air embolism is presented in Figure 16.2. When the operation is completed and the patient is sufficiently stable for transfer to a suitable facility, consideration should be given to additional treatment in a hyperbaric chamber [104–106].

Monitoring for cardiopulmonary bypass and related complications The level of monitoring for an individual patient undergoing a cardiac surgical procedure will depend not only on the patient’s characteristics (e.g. cardiac function, type of operation, other medical conditions), but also on institutional factors (e.g. availability of resources, technical expertise, program objectives, etc.). Typical monitoring may include arterial catheters, central venous catheters, pulmonary artery catheters, and TEE. Each of these monitoring techniques carries a small risk of complications.

Arterial catheters Placement of an arterial catheter allows for continuous blood pressure monitoring and facilitates blood sampling for arterial blood gas determinations both during and after CPB. The radial artery is the most common site of cannulation, but the femoral and other arteries may also be used [107]. Before sterile insertion of the radial artery catheter, the overlying skin should be cleansed thoroughly. Injury to the artery can be avoided by a gentle insertion technique; the catheter should not be advanced forcefully. Selection of the contralateral radial artery for cannulation may be preferable to repeated cannulation attempts at the same site. The use of a topical antibiotic at the insertion site is controversial, but a sterile dressing should be applied. If a stopcock and extension tubing set are used, care should be taken to ensure that excess pressure is not placed on the stopcock against the patient’s arm or hand because this may cause discomfort and skin necrosis. Complications of radial artery cannulation may include infection, embolization, ischemia, and hematoma formation [108–110]. Cellulitis at the site of cannulation may occur in as many as 10% of patients, but documented bacteremia is rare [111]. Ischemic complications are also uncommon. The Allen’s test is often used to evaluate the integrity of the ulnar artery and palmar arch before radial artery cannulation, but this test is not completely reliable for predicting ischemic complications. Distal embolization may produce evidence of ischemia at the fingertips and thrombosis of the radial artery may occur in 1–2% of patients. Serious sequelae are uncommon because of collateral blood supply [111,112]. Patients with poor peripheral blood flow, particularly in the setting of high-dose vasopressor therapy, are more prone to this complication. Removing the catheter is the treatment and the catheter should be removed as soon as an ischemic complication is suspected. Hematoma formation usually

Figure 16.2 An algorithm for postoperative treatment of patients with air embolism. (Reprinted with permission from the Society of Thoracic Surgeons (Ann Thorac Surg 1995; 60: 1138–1142).)

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occurs with inadequate compression after a failed cannulation attempt or removal of a radial artery catheter, particularly in the setting of systemic anticoagulation. Other uncommon complications include necrosis of the skin overlying the insertion site, formation of an arteriovenous fistula or pseudoaneurysm, and median nerve neuropathy. Femoral arterial cannulation is often used when the radial arteries are not available (e.g. used for bypass conduits) [113]. Sterile technique should be used and a longer catheter may help to prevent inadvertent dislodgement. The femoral arterial catheter should be sutured to the skin and a sterile dressing should be applied. Potential complications include infection at the cannulation site, bacteremia, distal embolization, pseudoaneurysm, the formation of an arteriovenous fistula, and injury to the femoral nerve. Femoral arterial catheters or introducer sheaths (often placed at the time of cardiac catheterization) should be removed as early as possible to prevent complications and promote early mobilization of the patient [114,115].

Central venous catheters Central venous catheterization can be used for: (i) intravenous access for the administration of medications, fluids, or blood products, (ii) monitoring the central venous pressure, and (iii) subsequent cannulation of the pulmonary artery with a Swan–Ganz catheter. The internal (or external jugular) and subclavian veins are used most commonly, but the femoral vein may also be used. The most common immediate complications of central venous catheterization include: (i) inadvertent injury to the nearby artery, (ii) misplacement of the catheter, and (iii) pneumothorax [116–122]. Arterial puncture can often be recognized by the return of pulsatile blood when the syringe is removed from the large-bore introducer needle. If this occurs, the needle should be removed immediately. In the case of jugular insertion, the frequency of carotid arterial puncture is approximately 4%. If the jugular or femoral route is being used, pressure should be held at the cannulation site to help prevent hematoma formation. The usefulness of manual pressure to the subclavian artery and vein is controversial. Occasionally, arterial cannulation will not be recognized until after the catheter has been inserted. Arterial catheterization may be indicated by i.v. fluids that do not flow freely into the catheter, an arterial pressure tracing, or an ‘arterial’ course of the catheter on a subsequent chest radiograph (CXR). Once arterial catheterization has been discovered, the catheter should be removed and pressure should be held over the cannulation site. Unexplained blood loss or hemodynamic instability during a cardiac operation should prompt consideration of vascular injury from central venous catheterization and the ipsilateral pleural space should be inspected. For catheters placed by the jugular or subclavian routes, the catheter tip should lie at the junction between the superior vena cava and the right atrium. A CXR immediately after operation should be used to document the correct position of the catheter tip and to evaluate for any unexpected hematoma or

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pleural effusion [123]. A variety of incorrect positions are possible: ‘doubled back’ into the contralateral neck, distally in the subclavian vein, in the internal mammary vein, looped or coiled in the right atrium, in the IVC, across the chest into the contralateral subclavian vein, or abutting the SVC wall [124]. A mispositioned catheter may not necessarily be harmful to the patient, but we recommend removal and replacement of all mispositioned catheters. If the guide-wire is inadvertently ‘lost’ into the central circulation, urgent retrieval is indicated. In many cases, these guide-wires can be retrieved by an interventional radiologist using an intravascular snare. Depending on the route of central venous catheterization, pneumothorax occurs in approximately 1–4% of cases [116–118,125]. Tension pneumothorax may be manifested by cardiopulmonary compromise or increasing airway pressures and can be treated by introduction of a large-bore needle or catheter through the 2nd intercostal space, anteriorly. Pneumothorax is occasionally recognized after opening the chest and visualizing the air in the pleural space; an opening in the pleura serves to decompress the pneumothorax. Late complications of central venous catheterization may not manifest until after the operation and, sometimes, not for hours to days. Venous thrombosis may occur, particularly in patients with large-bore, multilumen catheters that are left in place for long periods of time. This condition may manifest with unilateral upper extremity or neck swelling and discomfort. The diagnosis can be confirmed by ultrasound or venography. The catheter should be removed and consideration should be given to systemic anticoagulation. Catheter-related infection may be suggested by erythema or drainage at the insertion site, fever, leukocytosis, and documented bacteremia. When infection is suggested, the catheter should be removed and replaced at another site, if needed. Some authorities have recommended routine replacement of central venous catheters after several days to help prevent catheter-related infection, but there is no consensus [116,126]. Air embolism may occur if a port or stopcock is left open or if a catheter is removed with the patient in the upright position [127]. As little as 5–10 cm3 of air may cause cardiac arrest. If air embolism occurs, the patient should be placed on the left side and the catheter should be aspirated to remove any air. Thoracotomy is occasionally indicated for removal of air directly from the pulmonary artery. In some centres, multiple central venous catheters are used for monitoring in patients undergoing cardiac surgical procedures. By report, this practice is associated with little additional risk of complication compared with single venous catheterization [128].

Pulmonary artery catheters A pulmonary artery (e.g. Swan–Ganz) catheter is used to provide information about the central venous, pulmonary artery, and pulmonary artery wedge pressures and to allow continuous or ‘on-demand’ measurement of the cardiac output and mixed venous oxygen saturation. Postoperatively, the pulmonary artery catheter can be used to provide information about the patient’s intravascular volume status, aid in the treatment of heart failure, and facilitate

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temporary pacemaking (through a pacing port). Because the pulmonary artery catheter is typically placed through an introducer sheath in a central vein, pulmonary artery catheterization is associated with many of the same complications as central venous catheterization (see above). Serious complications related to the use of a pulmonary artery catheter for cardiac surgery are uncommon [129]. During insertion of the pulmonary artery catheter, transient or sustained arrhythmias may occur and should be treated by prompt advancement or withdrawal of the catheter. During any withdrawal of the catheter, the balloon should be deflated to prevent injury to the pulmonary or tricuspid valves. Persistent arrhythmias should prompt consideration of the administration of an antiarrhythmic medication such as lidocaine, but arrhythmias due to mechanical irritation of the catheter may be resistant to these medications [130]. Heart block may develop or may worsen, especially for patients with pre-existing fascicular block. Perforation or injury to the tricuspid valve [131], pulmonary valve [132], or ventricle during insertion is rare. A pulmonary artery catheter that becomes knotted can usually be removed non-surgically, often by the interventional radiologist [133]. Rupture of the pulmonary artery is the most serious complication of pulmonary artery catheterization and carries a substantial mortality rate [129,134–142]. Proper care of the pulmonary catheter aimed at preventing this complication requires frequent checking to make certain that the catheter tip does not remain in the ‘wedged’ position. Movement during the cardiac surgical procedure is common and the anesthesiologist should be vigilant for this possibility. Pulmonary artery rupture is a potentially life-threatening complication that may produce localized or uncontrolled hemorrhage and quick deterioration of the hemodynamic and respiratory status. If hemoptysis suggests pulmonary artery rupture before the cardiac surgical procedure has begun, several measures may help temporize the situation. First, medications that affect clotting (e.g. heparin, Coumadin, aspirin) should be stopped, if possible, and alterations in the patient’s clotting profile should be corrected with administration of vitamin K or fresh frozen plasma. Intubation and mechanical ventilation may be required. A thoracostomy tube should be inserted to drain any blood from the affected pleural space. Bronchoscopy may be helpful to determine an exact site of bleeding and can be used to insert a balloontipped catheter to isolate the affected pulmonary segment. Persistent bleeding should prompt exploration, either through a thoracotomy or median sternotomy approach. A segmentectomy or lobectomy is used to control the bleeding. In this circumstance, cardiac operation is deferred, if possible. Pulmonary rupture may manifest during the cardiac operation, usually at the conclusion of CPB, or later in the ICU. The principles of treatment outlined above apply in these situations as well.

Transesophageal echocardiography (TEE) Transesophageal echocardiography is a common diagnostic procedure outside of the operating room and is thought to carry little risk to the patient. In large series of TEE in the general cardiology population, the frequency of

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serious complications is < 0.2% [143,144]. The ultrasound probe and unit should be well maintained to prevent thermal or electrical injury to the patient and the probe should be cleaned properly to prevent disease transmission between patients. Intraoperative TEE is used commonly today as a monitoring tool in cardiac surgery, particularly in those patients undergoing valve procedures, aortic procedures, and correction of congenital defects. Intraoperative TEE provides information about the cardiac anatomy and function that can help to determine the most appropriate surgical procedure (e.g. valve repair vs. replacement), facilitate weaning from CPB, and assess the immediate results of operation. In a large series of intraoperative TEE, the morbidity rate was 0.2% and the reported mortality rate attributable to TEE was 0% [145]. The most frequent complication of intraoperative TEE is transient odynophagia [145]. Swallowing dysfunction has been reported in up to 4% of patients after operations in which intraoperative TEE was used [146]. Proper care should be exercised during insertion of the TEE probe to prevent dental injury or dislodgement of the endotracheal tube [145]. Upper gastrointestinal bleeding may occur after intraoperative TEE, but this may be due not only to mechanical irritation by the TEE probe but also to pre-existing conditions of the esophagus or stomach [145]. The most serious complication associated with intraoperative TEE is gastrointestinal perforation. This may occur in the oropharynx [147], hypopharynx [148], esophagus [145,149,150], or stomach. Some authorities have suggested that a preoperative history of dysphagia is a risk factor for perforation [148]. The treatment of patients with gastrointestinal perforation should focus on localization of the site of perforation, administration of antibiotics, and, in many cases, operative repair. This complication is associated with substantial morbidity and mortality risk for the patient [145,149,150].

Anticoagulation for cardiopulmonary bypass and related complications Anticoagulation for cardiopulmonary bypass Some degree of anticoagulation is required during CPB to prevent coagulation within the pump circuit and its components. Although heparin is the most common agent used for anticoagulation in conjunction with CPB, other anticoagulants may be useful in special circumstances. The surgeon, perfusionist, and anesthesiologist should be aware of the potentially adverse effects that are associated with each of these anticoagulants. Heparin is the most common anticoagulant used for CPB because this agent is effective, reversible, well tolerated, and inexpensive [151]. Unfractionated heparin is a mixture of mast cell polysaccharides (1000–50 000 d) that produces its anticoagulant effect by potentiating the activity of antithrombin III (ATIII) and inhibiting thrombin directly by binding to cofactor II. There is substantial interpatient variability in the clinical effects of a fixed dose of heparin, how-

Complications of cardiopulmonary bypass and cardioplegia 301

ever. In addition, acute reactions such as anaphylaxis, pulmonary edema, and disseminated intravascular coagulation (DIC) may occur rarely after administration of heparin. For clinical applications other than anticoagulation for CPB, the most common complication following heparin administration is bleeding. In the setting of CPB, however, anticoagulation is essential regardless of the risk of any potential excess bleeding. During cardiac surgery, bleeding into the operative field does not usually pose a problem because of the availability of cell saver or cardiotomy suction. Excess administration of heparin, however, may produce fibrinolysis and unwanted platelet activation. Insufficient anticoagulation during CPB may result in consumption of coagulation factors. Historically, heparin administration in preparation for CPB was guided empirically. Today, the appropriate dose of heparin can be monitored before and during CPB. The initial dosage is usually 200–400 U/kg, with maintenance doses (administered intermittently during CPB) of 50–100 U/kg. In addition, 10 000–20 000 U are typically placed in the bypass pump before the institution of CPB.

Heparin resistance Heparin resistance refers to the circumstance in which a patient receives the standard dose of heparin before CPB but does not become fully anticoagulated. Several etiologies are possible, including: congenital ATIII deficiency, acquired ATIII deficiency, thrombocytosis, pregnancy, sepsis, hypercoagulable states, and coagulopathic processes [152–156]. A deficiency of ATIII is the most common cause and can be treated with administration of fresh frozen plasma or recombinant ATIII [155].

Heparin-induced thrombocytopenia Heparin-induced thrombocytopenia (HIT) occurs in up to 10% of patients treated with heparin [157–161] and has been documented in 1–5% of surgical patients [157]. This condition may manifest after exposure to either unfractionated or low-molecular-weight heparin preparations. The relatively high incidence of HIT in surgical patients has been attributed, in part, to the widespread use of heparin for a variety of indications and a high prevalence of heparin-associated antibodies in patients who are referred for cardiac surgery [157]. Two forms of HIT have been described [158]. Type I HIT is due to platelet aggregation and is associated with mild thrombocytopenia (never less than 100 × 109/l) [158]. For patients with type I HIT, the thrombocytopenia develops within a few days of heparin exposure but resolves without specific treatment. Patients are often asymptomatic and the risk of serious associated morbidity is low. Type II HIT is immunologically mediated, with development of heparin-associated antiplatelet antibodies that promote platelet activation [158,159]. The IgG, IgA, or IgM antibodies are directed against the complex of heparin and platelet factor 4 (H–PF4) [159]. For patients with type

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II HIT, the thrombocytopenia often develops 5–14 days after heparin exposure and the platelet count is often well below 100 × 109/l [158]. The more serious condition of heparin-induced thrombocytopenia and thrombosis (HITT) occurs in a subset of patients with HIT, and in 10% of these individuals there is significant end-organ injury due to thrombosis [157]. A variety of vascular complications may occur, including cerebral infarction, mesenteric infarction, myocardial infarction, bypass graft occlusion, and limb ischemia. Amputation may be needed in as many as 25% of patients with affected limbs. The mortality rate approaches 30% [157]. There should be a high index of suspicion for the diagnoses of HIT and HITT. The diagnosis of HIT is suggested by a fall in the platelet count of > 50% or an absolute platelet count < 100 × 109/l [157]. When this diagnosis is suspected, heparin should be withheld in all of its forms, the platelet count should be measured daily, and the patient should be monitored closely for the development of thrombotic complications. A variety of laboratory tests are available to establish the diagnosis of HIT, including platelet aggregometry, the serotonin release assay (SRA), flow cytometric assays, and enzyme-linked immunosorbent assay (ELISA) to measure anti-H–PF4 antibody titres [159]. Each of these tests has relative advantages and disadvantages and may not be available in all institutions. Because of slow turnaround time for these tests, treatment should be instituted promptly while awaiting the results of the laboratory test(s). The primary treatment for patients with HIT is withdrawal of heparin and anticoagulation with another agent that reduces thrombin generation [160]. Agents that may be useful in this situation include danaparoid, ancrod, recombinant hirudin, and argatroban. Arterial thrombotic complications should be treated expeditiously.

Alternatives to heparin Alternatives to heparin for anticoagulation may be useful for patients with a known heparin allergy, protamine allergy, or history of HIT [161]. For patients with a history of HIT, a delay in surgery may allow time for antiplatelet antibodies to fall to an unmeasurable level. Unfortunately, this does not necessarily preclude the development of recurrent HIT [161]. Another useful strategy may be preoperative plasmapheresis to remove circulating antiplatelet antibodies [162]. A variety of anticoagulants may be useful alternatives to heparin in certain circumstances: warfarin, low-molecular-weight dextran, low-molecular-weight heparin, heparanoids (e.g. orgaran), ancrod, antithrombin agents (e.g. hirudin, argatroban), and prostacyclins [161,163–165].

Monitoring of anticoagulation for cardiopulmonary bypass Historically, heparin dosing was accomplished empirically, with a fixed dosage based on the patient’s weight. In most centers today, however, an initial dose of heparin is administered and then the activated clotting time (ACT) or heparin levels are monitored periodically to: (i) ensure adequate

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anticoagulation before the institution of CPB, (ii) assess for the need for additional doses of heparin during CPB, and (iii) assess the effectiveness of reversal of heparinization after CPB.

Reversal of anticoagulation At the conclusion of CPB, the effects of heparin are typically reversed with administration of protamine. Calculation of an appropriate dose of protamine is important because incomplete reversal of the heparin results from too little protamine and excessive protamine administration may lead to increased platelet dysfunction, increased postoperative bleeding, and increased transfusion requirements [151]. Individual patient factors (e.g. sensitivity to protamine, metabolism of heparin) as well as operation-related factors (e.g. degree and duration of hypothermia) will influence the appropriate dose of protamine for a given patient [166]. Several techniques are available to calculate the appropriate dose of protamine. In the simplest technique, a fixed dose of protamine can be administered per amount of heparin that is administered. This calculation can be based either on the initial heparin dose or on the total amount of heparin administered during the operation [167]. A variety of approaches have been described, with administration of as little as 1 mg to as much as 5 mg of protamine for every 1 mg of heparin administered. A second method of calculating the appropriate protamine dose is by use of heparin dose–response curves that are based on the ACT before and during CPB [168]. This curve can be used at the conclusion of CPB to estimate an appropriate dose of protamine. This approach has been reported to reduce the amount of protamine used compared with the fixed-dose approach [167,169]. There are potential disadvantages to the heparin dose–response method, however. In particular, the heparin dose–response curve is actually non-linear and this results in inaccuracies at either very low or very high levels of anticoagulation [167,170–172]. The last method for calculation of the appropriate protamine dose is based on measurement of heparin concentrations directly [166,173–175]. Protamine titration using measured heparin concentrations may reduce the amount of protamine used by as much as 30–40% compared with the heparin dose– response curve method [151,170]. Serious adverse reactions may occur with protamine administration [176,177]. Risk factors include pulmonary hypertension, previous exposure to protamine or protamine-containing insulin preparations, previous vasectomy, and fish allergies [178]. Some authorities have advocated administration of protamine on the left side of the circulation (e.g. into the aorta) to prevent pulmonary exposure to heparin–protamine complexes and to reduce the chance of pulmonary histamine release, but the results from clinical studies have been conflicting [179,180]. Protamine reactions are usually described in three categories: type I, with transient hypotension; type II, with anaphylaxis; and type III, with pulmonary vasoconstriction [181,182]. The type I protamine reaction is mediated by

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release of histamine from mast cells and basophils. This effect is more pronounced with rapid injection, so it is recommended that protamine be administered over 5–10 min, or longer [178,183,184]. Pretreatment with histamine receptor antagonists may reduce the effect but not eliminate the possibility of a type I reaction [185]. Histamine release produces reductions in the systemic arterial pressure and the central venous pressures. There will often be a reduction in the cardiac output, but this may be due simply to decreased preload [186,187]. Animal studies have suggested a direct negative effect of protamine on myocardial contractility, but the evidence is not convincing in humans [187–189]. The classic type II protamine reaction is mediated by IgE on the surface of mast cells which interacts with protamine and causes degranulation. The symptoms may include rash, bronchospasm, edema, stridor, hypotension, and cardiovascular collapse. Patients at increased risk of this type of reaction include those with previous exposure to protamine or protamine-containing insulin preparations (e.g. NPH or protamine-zinc insulin), previous vasectomy, or fish allergies. Several tests are available to evaluate the patient for potential protamine allergy, including: intradermal skin testing [178,190]; in vitro whole blood leukocyte histamine release [180,191]; and radioallergosorbent testing for serum antiprotamine IgE [178,191,192]. For most patients undergoing cardiac surgical procedures, however, these tests are not practical. Less commonly, type II anaphylactoid reactions are mediated by the classic complement pathway, in which protamine–heparin complexes cause release of C3a, C5a, and other vasoactive mediators, producing anaphylaxis [193,194]. In the type III protamine reaction, patients develop acute pulmonary hypertension, decreased left atrial pressure, right ventricular failure, and systemic hypotension [177,178]. It is not clear whether the rate of protamine administration affects the likelihood of a type III reaction [181,195]. The reaction may be transient or prolonged and may necessitate re-institution of CPB. Re-administration of protamine in a given patient may or may not result in the same reaction again. Although the mechanism of the type III reaction is not completely understood, it is probably mediated by complement when protamine–heparin complexes result in release of vasoactive substances (e.g. oxygen free radicals, thromboxane A2) [196–200]. There are several alternatives to protamine for the reversal of the effects of heparin, but none enjoys much clinical use. Hexadimethrine neutralizes heparin with the same mechanism as protamine and with less effect on the systemic hemodynamics [201,202]. Unfortunately, this agent also produces direct lung injury and can cause a clinical syndrome of non-cardiogenic pulmonary edema [203]. Moreover, this agent may produce platelet aggregation and renal failure [204,205]. Because of these side-effects, this agent is not currently clinically available. A second alternative is the use of a cellulose filter that contains immobilized protamine [206–208]. This filter can be placed in the arterial line just before the termination of CPB. Several passes of blood through the circuit

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may be needed for effective neutralization of heparin, however, and this may result in fibrin-clot deposition at the filter. A third alternative to protamine is heparinase [209,210]. In animal studies, a heparinase-bonded filter has been shown to neutralize heparin effectively with two to three passes of the blood through the filter. A fourth alternative to protamine is platelet factor 4, a protein released from platelets with a highly specific heparin-neutralizing property [211–215]. In animal models, platelet factor 4 has been shown to neutralize heparin effectively, with no effect on the platelet count, leukocyte count, or complement levels. Residual circulating heparin may be present even after protamine administration if an insufficient amount of protamine is used or if there is subsequent release of heparin from heparin–protamine complexes, heparin-binding proteins, or from other sites [151]. The term ‘heparin rebound’ is used to describe the situation in which there is recurrent heparin activity after complete neutralization of heparin. Persistent circulating heparin, regardless of the cause, may lead to an increase in bleeding after CPB [151].

CPB and bleeding Cardiac surgical patients are particularly susceptible to postoperative mediastinal bleeding. The incidence of severe bleeding after CPB depends on the definition, but as many as 5–7% of patients may experience bleeding of > 2 l during the first 24 h after operation [216]. In recently reported large series of adult cardiac surgery patients, as many as 3–5% of patients require reexploration of the chest because of excessive postoperative bleeding [217,218]. The need for re-exploration of the chest after a cardiac surgical procedure is associated with substantial morbidity and mortality [219]. In one large series, re-exploration was associated with a twofold increase in operative mortality as well as a significantly increased incidence of renal failure, adult respiratory distress syndrome (ARDS), prolonged mechanical ventilation, sepsis, and atrial arrhythmias [217]. In addition, the transfusion of blood products because of excessive bleeding is associated with a variety of potentially adverse events, including blood-borne disease transmission (e.g. hepatitis, HIV), increased incidence of wound infection, and transfusion reactions [219].

Aprotinin and Amicar Fibrinolysis ordinarily prevents or limits propagation of intravascular thrombosis. Although the mechanism is not entirely clear, there is typically increased fibrinolytic activity during cardiac surgery [220]. Three antifibrinolytic agents are currently available to help limit fibrinolytic activity during CPB and to help reduce postoperative bleeding: tranexamic acid, epsilon-aminocaproic acid (EACA, Amicar), and aprotinin (Trasylol) [221]. Of these agents, epsilon-aminocaproic acid and aprotinin have both been shown to reduce antifibrinolytic activity during CPB and to reduce postoperative bleeding and transfusion requirements, particularly among patients undergoing ‘redo’ operations [220].

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A variety of complications have been described in association with antifibrinolytic therapy, particularly with the administration of aprotinin. In particular, there were early concerns that antifibrinolytic therapy might increase the possibility of a thrombotic complication. Although the data have been conflicting, the majority of reports have not found an increase in perioperative myocardial infarction or early bypass graft occlusion [220]. Many authorities have suggested that intraoperative thrombosis associated with aprotinin may be due to inadequate anticoagulation and have suggested a minimum (celite) ACT of 750 s [220]. Another potential complication is the development of renal failure after aprotinin therapy, particularly when used in conjunction with hypothermic circulatory arrest [222]. Prospective trials have failed to demonstrate an association between aprotinin therapy and postoperative renal insufficiency, however, [223]. Lastly, the overall incidence of anaphylactoid reaction to aprotinin is reported by the manufacturer to be approximately 0.5%, but this risk may increase to as much as 6–9% following re-exposure [220,224].

Blood conservation techniques Although blood product transfusion is generally safe, transfusion can be associated with viral or bacterial transmission [225] (Table 16.1), isoimmunization, potentially increased incidence of postoperative wound infection [226–228], and increased cost. Because of these potential risks as well as a limited supply of banked blood products, there is considerable impetus to avoid transfusion whenever possible, and today transfusion can be avoided in many cardiac surgery patients. A variety of techniques that can be applied before, during, and after operation can be used to help avoid blood product transfusion in patients undergoing cardiac surgery procedures (Table 16.2).

Preoperative techniques Although the technique may be available to only a minority of cardiac surgery patients, autologous red blood cell predonation can be used to limit the need for allogeneic transfusion during and after operations of many types [229–231]. Factors that may limit the use of this technique in cardiac surgery patients include: (i) insufficient lead time, (ii) preoperative anaemia, and (iii) cardiac instability. In addition, autologous predonation is more expensive than allogeneic transfusion [232]. When 2 U of red blood cells are harvested over a 2–3-week period, the preoperative hemoglobin typically falls by approximately 2 g/dl. Even for patients who are anticipating cardiac surgery, however, this practice is generally safe and well tolerated [233,234]. Erythropoietin has been shown to be useful, alone or in combination with iron, to improve the hematocrit in anaemic patients before cardiac surgery and may improve the yield of autologous predonation in some patients [235–237].

Intraoperative techniques A variety of intraoperative techniques are available to help reduce the need for

Complications of cardiopulmonary bypass and cardioplegia 307 Table 16.1 Estimated risk of infectious agent transmission. Variable Probability of infection (per allogeneic unit) Hepatitis C virus Hepatitis B virus HIV HTLV-I and HTLV-II Probability of disease Hepatitis C virus Persistent hepatitis Active hepatitis Cirrhosis Fulminant hepatitis Hepatitis B virus Carrier status Persistent hepatitis Active hepatitis Cirrhosis or cancer HIV AIDS HTLV-I and HTLV-II ATL or HAM Quality adjustments for various health states Persistent hepatitis Active hepatitis Cirrhosis or cancer Fulminant hepatitis HIV infection AIDS ATL or HAM

Estimate

0.0003 0.000005 0.0000067 0.000017

0.28 0.12 0.10 0.01 0.04 0.02 0.01 0.01 1.0 0.04 0.99 0.90 0.90 0 0.75 0.50 0.90

HIV, Human immunodeficiency virus; HTLV, human Tlymphocyte virus; AIDS, acquired immunodeficiency syndrome; HAM, HTLV-associated myelopathy; ATL, adult T-cell lymphoma. From Etchason J, Petz L, Keeler E et al. The cost effectiveness of preoperative autologous blood donations. N Engl J Med 1995; 332: 19–724 Copyright. © 1995 Massachusetts Medical Society. All rights reserved.

allogeneic blood transfusion. The importance of rigorous surgical technique to limit bleeding during the operation should be emphasized. In contrast to the historical use of a whole blood prime, the CPB circuit today is typically primed with an acellular, or asanguinous, solution. Relative degrees of anaemia during CPB, particularly at hypothermic temperatures, are well tolerated. Cell saving or pump suction (cardiotomy suction) devices are used during the operation to scavenge any shed blood. Any residual blood in the CPB pump is returned to the patient using the cell saver, ultrafiltration, or simply as unprocessed blood. Each of these techniques has its relative advantages and disadvantages.

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Table 16.2 Techniques for reducing blood product transfusion in cardiac surgery patients. Preoperative Autologous predonation of whole blood, red blood cells, FFP, platelets, erythropoietin Intraoperative Institutional program of guidelines for blood product transfusion Rigorous surgical technique Pre-CPB isovolemic hemodilution Pre-CPB pheresis of platelets and FFP Pheresis of FFP and platelets Non-sanguinous prime Whole blood collection at CPB onset Retransfusion of pump blood Cell saver or ultrafiltration of pump blood Drug therapy Antifibrinolytic agents DDAVP Postoperative Institutional program of guidelines for allogeneic blood product administration. Shed mediastinal blood transfusion CPB, cardiopulmonary bypass; FFP, fresh frozen plasma. From Brody SC, Morse DS. Coagulation, transfusion, and cardiac surgery. In: Spiess BD, Countis RB, Gould SA, eds. Perioperative Transfusion Medicine. Baltimore: Lippincott Williams & Wilkins, 1998; 443, with permission.

Preoperative harvesting of platelet-rich plasma (PRP) can be used to limit the exposure of platelets to CPB and is usually performed in the operating room before the initiation of CPB. Whole blood is collected, spun in a centrifuge to separate the PRP from the cells, and the blood is re-administered to the patient. This process is repeated until a sufficient volume of PRP has been obtained. Using this technique, approximately 9–30% of the circulating platelets can be harvested and stored safely for 2–3 h. The inability to harvest an adequate volume of platelets may currently limit the utility of this technique, but improvements in equipment and techniques may increase the yield of the harvest. Studies of intraoperative transfusion of PRP to reduce the need for postoperative allogeneic transfusion have produced mixed results [238–241]. Acute normovolemic hemodilution refers to the withdrawal of whole blood from the patient and replacement with crystalloid or colloid, usually before the initiation of CPB. Like harvesting of PRP, this technique protects blood elements from the deleterious effects of CPB. The withdrawal of blood can be accomplished either through a central venous catheter before heparinization (using citrate storage bags) or through the venous line of the CPB pump after heparinization. The volume of blood that can be withdrawn safely depends on the patient’s body size and preoperative hemoglobin level, but in a typical patient approximately 1000 ml of blood can be withdrawn. This technique appears to be safe and well tolerated in many patients and its efficacy in terms of reduction in allogeneic transfusion has been documented in several

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studies [242,243]. Proponents point to a higher platelet count after CPB as the mechanism for reduced bleeding and transfusion requirement [244,245].

Postoperative techniques Institutional guidelines or ‘triggers’ for blood product transfusion may limit unnecessary transfusion postoperatively. As an example, a ‘trigger’ point hematocrit of 24% in the early postoperative period might prompt automatic transfusion of 2 U of red blood cells. This practice carries the advantage that transfusion happens automatically at predetermined ‘trigger’ points. Unfortunately, though, automatic transfusion may not always be indicated for an individual patient. Autotransfusion of shed mediastinal blood in the early postoperative period has been advocated as another technique to reduce the need for postoperative transfusion. Most [246–248] but not all studies [249–251] have shown this technique to be effective, but despite years of clinical use there is still controversy regarding the safety of this technique. Potential complications with autotransfusion of shed mediastinal blood include altered coagulation [252], systemic fibrinolysis [253], and bacterial contamination [254].

Pathophysiological consequences of cardiopulmonary bypass The use of CPB produces pathophysiological effects in nearly all of the body’s organ systems. Although these effects might not be considered complications in the classic sense, they are a necessary byproduct of CPB and lead to much of the morbidity associated with its use. A complete discussion of these pathophysiological effects is beyond the scope of this chapter; the reader is referred to other sources for additional information [255,256]. For the purpose of this chapter, we confine our discussion to: the effects of CPB generated at the blood–surface interface; the consequences of hypothermia, which is often used in conjunction with CPB; the metabolic consequences of CPB; the effects of CPB on the lungs; the effects of CPB on the kidneys; and the neurological effects of CPB.

Consequences of the blood–surface interface Ordinarily, the blood and plasma come into contact only with endothelial lined vessels. During cardiac surgical procedures with the use of CPB, however, the blood and plasma are exposed to a variety of foreign surfaces, including not only the components of the perfusion circuit but also the exposed tissues in the open surgical wound. As a result of this contact at the blood–surface interface, a host of specific reactions are initiated that result in a systemic response to CPB [257]. Almost immediately after contact with a non-endothelial surface, plasma proteins are adsorbed onto that surface, producing a monolayer of many different proteins [258,259]. Fibrinogen is among the most important of the plasma proteins that is adsorbed [260,261]. The type and relative mix of proteins will be determined by the particular non-endothelial surface involved.

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Figure 16.3 Complement pathways. (From Colman RW, Marder VJ, Salzman EW et al. Overview of hemostasis. In: Colman RW, Hirsch J, Marder VJ et al. eds. Hemostasis and Thrombosis: Basic Principles and Clinical Practice, 3rd edn. Philadelphia: Lippincott, Williams & Wilkins, 1994; 9, with permission.)

For purposes of this discussion, we will discuss the resulting activation of the contact, intrinsic, and extrinsic coagulation pathways, fibrinolysis, and complement. We will also discuss the important effects on the platelets, endothelial cells, neutrophils, monocytes, and lymphocytes.

Contact activation system The adsorption of factor (F)XII (Hageman factor) onto a non-endothelial surface begins a cascade in the contact system pathway (Figure 16.3). In the presence of prekallikrein and high-molecular-weight kininogen (HMWK), the active proteases FXIIa and FXIIf are produced [262,263]. In the presence of kallikrein and HMWK, FXIIa activates factor (F)XI to FXIa, which initiates the intrinsic coagulation pathway, leading eventually to the formation of thrombin. Kallikrein and FXIIa are both direct agonists for neutrophils.

Intrinsic coagulation pathway The extrinsic coagulation pathway may be more important in the systemic response to CPB, but there is evidence that activation of the intrinsic coagulation pathway also plays a role [264]. The complex of factor VIIIa, factor (F)IXa, and phospholipids (PL) binds to factor (F)X and leads to the production of FXa, the entry into the common coagulation pathway.

Complications of cardiopulmonary bypass and cardioplegia 311

Extrinsic coagulation pathway Under ordinary circumstances, tissue factor is a membrane-bound protein that is not exposed to the blood. Activated monocytes and endothelial cells also express tissue factor [265,266]. During CPB, tissue factor acts with activated factor VIIa and phospholipid (PL) to promote activation of both FIX to FIXa and FX to FXa, the entry into the common coagulation pathway. As such, FXa is produced by both the intrinsic and extrinsic coagulation pathways. The intrinsic coagulation pathway is activated primarily in the perfusion circuit and the extrinsic coagulation pathway is activated primarily in the surgical wound. The result of both coagulation pathways is the production of the circulating protease, thrombin.

Fibrinolysis One of the effects of circulating thrombin is the activation of endothelial cells, leading to the release of tissue plasminogen activator (t-PA), which then binds to fibrin. The combination of t-PA, fibrin, and plasminogen cleaves plasminogen to plasmin. Plasmin then cleaves fibrin.

Complement Both the classic and alternative complement pathways are activated during CPB (Figure 16.3). In the perfusion circuit, the blood–surface contact leads to activation of the classic pathway via C1, C2, and C4 to form C3 convertase which cleaves C3 into C3a and C3b. The alternate pathway, through factors B and D, also leads to production of C3b and may be the more important pathway during CPB [193]. The classic pathway is also activated at the termination of CPB when protamine is administered and heparin–protamine complexes are formed [267]. C3b then cleaves C5 into C5a and C5b. C5b leads to production of the terminal complement complex (TCC) by binding with C6, C7, C8, and C9. TCC interacts with cell membranes, leading to lysis of cells. In addition, TCC also leads to increased thrombin formation [268]. The released factors C3a, C4a, and C5a are vasoactive. C5a is a major neutrophil agonist [269,270].

Platelets The circulating platelets are subject to a variety of adverse influences during CPB. Perhaps the first noticeable effect on the platelets is a reduction in their circulating numbers because of dilution with the pump prime volume. Heparin inhibits platelet binding to von Willebrand factor and increases the bleeding time [271,272]. Heparin leads to increased sensitivity of the platelet to circulating agonists, including thrombin [273], C5b [268], plasmin [274,275], cathepsin G, serotonin, and epinephrine, among others. All of these influences contribute to platelet loss and dysfunction. The numbers of circulating platelets are also reduced by platelet–platelet adhesion and aggregation. Activated platelets express a variety of cell-surface glycoproteins and receptors that promote aggregation [276–278]. In addition

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to platelet–platelet aggregation, activated platelets also form aggregates with monocytes and neutrophils [276,279]. A subset of the activated platelets will produce and release a variety of substances, including thromboxane A2 [280], platelet factor 4, α-thromboglobulin [281], P-selectin [276], serotonin, adenosine diphosphate (ADP), adenosine triphosphate (ATP), calcium, mitogens, acid hydrolases [282], and neutral proteases. Although the effect will depend on many factors, both with respect to the patient and the surgical procedure, the circulating platelet count typically falls by 30–50% during CPB [283,284]. In addition to intact platelets, there are often platelet fragments in the circulation after the termination of CPB [285]. The overall platelet function is reduced and there is typically a prolongation of the measured bleeding time after CPB [283].

Endothelial cells During CPB, endothelial cells are activated by thrombin, C5a, and a variety of cytokines [e.g. interleukin-1 (IL-1), tumor necrosis factor (TNF)] [286–288].

Neutrophils The neutrophils are responsible for much of the systemic inflammatory response after CPB. These cells are strongly activated during CPB by kallikrein and C5a, but other agonists such as FXIIa, heparin, leukotriene B4, IL-1α, IL-8, and TNF also activate neutrophils [263,270,289,290]. Activated neutrophils release a variety of detrimental substances, including elastase, cathepsin G, lysozyme, myeloperoxidase, defensins, acid hydrolases, bacterial permeability agent, lactoferrin, collagenase, hydrogen peroxide, hydroxyl radicals, hypobromous acid, and hypochlorous acid [291].

Monocytes Monocytes are activated by monocyte chemotactic protein-1 (MCP-1), C5a, immune complexes, endotoxin, and IL-1 [292,293]. Activated monocytes express tissue factor, both in the perfusion circuit and in the surgical wound [294]. In addition, these monocytes produce a variety of cytokines (e.g. IL-1, IL-6, and TNF-α) that peak in concentration several hours after CPB [295,296]. The number of circulating monocytes is not changed during CPB, but this number increases for several hours after CPB [297,298].

Lymphocytes The numbers and function of both B and T cells are decreased in the first few days after CPB [299–301].

Consequences of hypothermia Mild to moderate hypothermia (25–34 °C) is used in conjunction with CPB to provide some degree of organ protection from ischemic injury during the operation. This safety margin with respect to organ ischemia is provided by

Complications of cardiopulmonary bypass and cardioplegia 313

a temperature-related reduction in the organs’ oxygen demand and consumption [302]. In neural tissues, there is also a direct beneficial effect of hypothermia in terms of preservation of high-energy stores and a reduction in excitatory neurotransmitter release [303–306]. Because of a reduction in the body’s oxygen consumption during hypothermia, CPB can be maintained with lower flow rates. The use of lower flow rates produces several important benefits for the patient and surgeon, including less blood trauma and better visualization in the operative field [307,308]. Hypothermia produces a variety of effects in the body’s organs [309]. In nearly all tissues, hypothermia decreases the organ blood flow, but this effect is pronounced for the skeletal muscle, kidneys, splanchnic bed, heart, and brain. In the heart, hypothermia is associated with heart block and both atrial and ventricular arrhythmias. It is important that the patient’s temperature not be allowed to fall precipitously during opening and cannulation because any resulting arrhythmias may be difficult to control before the initiation of CPB. In the lung, hypothermia leads to decreased ventilation. In the kidneys, hypothermia leads to increased renal vascular resistance. There is a decrease in tubular reabsorption, the urine output may increase, and there is often spilling of glucose into the urine. The adjunctive technique of hemodilution during CPB may improve renal blood flow during CPB and limit renal injury. Hypothermia leads to decreased metabolic and excretory function in the liver, but clinically significant liver injury during hypothermic CPB is rare. Hypothermic CPB often leads to hyperglycemia. Gluconeogenesis and glycogenolysis are increased and endogenous insulin production is decreased. Moreover, hypothermia results in a relative insensitivity to exogenous insulin administration. The surgical team should monitor the serum glucose level closely and administer exogenous insulin, as needed. There is ample evidence that avoiding even modest degrees of hyperglycemia may reduce the incidence of postoperative wound infection [310]. Water and electrolyte changes also accompany hypothermia. Hypothermia leads to a decrease in the free water clearance and serum potassium concentration and to increases in serum osmolality. Hypothermia produces both systemic and pulmonary vasoconstriction at temperatures < 26 °C [193]. Arteriovenous shunts may appear at low temperatures and have a deleterious effect on tissue oxygen delivery. There is an increase in blood viscosity and red blood cell aggregation and rouleaux formation may further reduce tissue oxygen delivery. Attention to proper anesthesia, hemodilution, and administration of vasodilators may help to limit these unwanted effects.

Profound hypothermia and circulatory arrest For certain cardiovascular operations (e.g. aortic surgery), a period of circulatory arrest is helpful or necessary [302]. During periods of circulatory arrest, the use of profound hypothermia (16–20 °C) may help to limit ischemic central nervous system (CNS) neurological injury. Data regarding a ‘safe’ period of

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circulatory arrest have been conflicting, but periods as long as 30–45 min are relatively well tolerated at deep hypothermia. Neurological injury after profound hypothermia and circulatory arrest may manifest as choreoathetosis, seizures, transient metabolic encephalopathy, stroke, and neurocognitive disorders. Every effort should be made to make these techniques as safe as possible for the patient. Circulatory arrest should not be initiated until there has been sufficiency time for uniform cerebral cooling. Topical cooling of the head (i.e. packed in ice) may be a useful adjunct. The use of barbiturates and corticosteroids is advocated by many authorities as useful adjuncts as well.

Metabolic consequences of CPB The use of CPB produces a variety of changes in the endocrine, humoral, and metabolic functions of the body.

Pituitary hormones The serum concentration of vasopressin [antidiuretic hormone (ADH)] is increased significantly with the use of CPB and persists for several hours postoperatively [311–313]. This exaggerated ADH response may be due to a variety of causes, including: transient hypotension at the initiation of CPB, a decrease in the circulating blood volume with the initiation of CPB, and a decrease in left atrial pressure with the initiation of CPB. ADH produces an increase in the peripheral vascular resistance, a decrease in cardiac contractility, a decrease in coronary blood flow, an increase in renal vascular resistance, and an increase in the release of von Willebrand factor [314,315]. The use of pulsatile perfusion or adjunctive regional anesthetic techniques (e.g. thoracic epidural anesthesia) may blunt, but not eliminate the exaggerated ADH response during CPB [313,316–318].

Adrenal hormones During hypothermic CPB, the plasma epinephrine concentration is typically increased 10-fold and the plasma norepinephrine level is typically increased fourfold [319–322]. The increased concentrations of these catecholamines leads to increased peripheral vasoconstriction and changes in intraorgan blood flow [320–324]. The use of deeper anesthesia, regardless of the type of anesthesia, may reduce the catecholamine response to CPB [325–328]. The effect of pulsatile perfusion on the catecholamine response is not clear [320,329]. Cortisol is released in response to the stress of any major operation, usually with a quick rise in concentration and then a slow fall to baseline within 24 h [330]. With CPB, cortisol rises to a high concentration during CPB and remains markedly elevated for > 48 h postoperatively [331–333]. Some studies have shown a blunted cortisol response with greater degrees of hypothermia [334] and with the adjunctive use of thoracic epidural anesthesia [327,328]. There is also an increase in adrenocorticotropic hormone (ACTH) in response to CPB [335].

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Atrial natriuretic factor Although there is some conflicting evidence, most studies have shown reduced levels of atrial natriuretic factor during CPB, especially in those patients with high preoperative levels (e.g. those with valvular heart disease) [336–338]. For most patients, there is a relative increase in atrial natriuretic factor that starts during rewarming and persists for up to several days after CPB [336,338–340]. Outside the setting of CPB, atrial natriuretic factor is released in response to atrial distension and acts to increase glomerular filtration, inhibit renin release, reduce the serum aldosterone concentration, and reduce the arterial blood pressure. In patients undergoing CPB, the normal regulatory mechanisms are lost during CPB and are diminished for the first 24 h postoperatively [341,342].

Renin–angiotensin–aldosterone axis The role of the renin–angiotensin–aldosterone axis during CPB is unclear [343]. For patients undergoing non-pulsatile hypothermic CPB, renin, angiotensin II, and aldosterone concentrations are elevated during and shortly after CPB [344–346]. Angiotensin-converting enzyme concentrations, corrected for the degree of hemodilution, are probably not affected by CPB but are typically lower than normal during rewarming and for some period postoperatively [322,347]. Most evidence suggests that postoperative hypertension is not related to abnormal concentrations of renin, angiotensin II, or aldosterone [348,349].

Thyroid hormones Several studies have documented the presence of sick euthyroid syndrome in patients during and after CPB [350]. This syndrome is characterized by decreased T3 concentrations, normal or reduced T4 concentrations, decreased free thyroxine, and normal thyrotropin concentrations. Administration of heparin before CPB causes a slight increase in the free serum T3 and T4 concentrations because heparin displaces these hormones from various binding proteins [351,352]. Adjusted for the level of hemodilution, however, T3 concentrations are not altered by CPB [322]. During normothermic CPB, thyrotropin concentrations are normal, but during hypothermic CPB, thyrotropin levels fall with the initiation of CPB and then rise steadily during the period of CPB [351,353]. Based on the fact that T3 regulates the heart rate, contractility, and oxygen consumption, some authorities have advocated the administration of T3 perioperatively to improve cardiac function. In experimental models, T3 administration has been shown to improve myocardial contractility after CPB [354,355]. In human studies, however, the evidence has been conflicting [356,357].

Other serum changes With the initiation of CPB, there is a fall in the serum total and ionized calcium levels [358–362]. With crystalloid priming solutions, the fall in the calcium

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concentration is due to hemodilution. Historically, many surgeons and anesthesiologists have favored the administration of calcium empirically at the conclusion of CPB to help with weaning from CPB. The effectiveness of this approach is not certain, however. Excessive calcium administration (i.e. without a decrease in the ionized calcium concentration) may contribute to perioperative pancreatitis and reduce the effectiveness of α-adrenergic receptor agonists [362,363]. Similar to calcium, the serum concentrations of total and ultrafiltratable magnesium also fall with the initiation of CPB [362,364]. After CPB, serum magnesium levels return to normal only very slowly [361]. In the postoperative period, hypomagnesemia may predispose the patient to the development of both atrial and ventricular arrhythmias, so many authorities recommend empiric replacement or supplementation with magnesium during and early after CPB [364–366]. The serum potassium level can vary considerably during CPB. In the absence of cardioplegia, the serum potassium concentration typically falls during hypothermic CPB. In most patients, however, the use of hyperkalemic cardioplegia solutions will promote a tendency for a rise in the serum potassium concentration during CPB [367]. The serum potassium concentration should be monitored closely during CPB, but a normal concentration is not needed until after CPB and a normal electrical rhythm is needed [368]. After the termination of CPB, there is typically an exaggerated loss of potassium in the urine and the clinician should be alert to this possibility [369].

Effects of CPB on the lung The lungs are affected by CPB in several ways [370–375]. First, collapse of the lungs during CPB produces atelectasis that may persist postoperatively. Second, the lung is a target organ for the systemic inflammatory response to CPB. And lastly, pulmonary metabolic activity is affected by CPB.

Atelectasis Atelectasis is the most common pulmonary complication after cardiac surgery [371]. Many patients undergoing cardiac surgical procedures will be predisposed to the development of atelectasis on the basis of a smoking history, chronic bronchitis, obesity, or the presence of pulmonary edema. Even before the initiation of CPB, passive ventilation with a paralyzed diaphragm and a monotonous ventilatory pattern will predispose the patient to the development of atelectasis. During a typical cardiac surgical procedure, many technical aspects of the operation itself may contribute to atelectasis. If the left internal mammary artery (IMA) is used for revascularization, the left pleural space is typically entered. Once the left pleural cavity is exposed, blood and irrigation fluid may collect in the pleural space and cause compression of the lung. Because of this problem, some surgeons advocate an extrapleural dissection of the IMA. Once CPB is initiated, the heart rests on the left lower lobe and this may be one

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explanation for the high frequency of left lower lobe atelectasis after CPB. Endotracheal suctioning during the procedure may produce mucosal injury and lead to atelectasis. Surfactant may be inhibited during CPB and this, combined with increased lung water due to complement activation, may also predispose the patient to atelectasis. The degree of atelectasis will vary from patient to patient, but the functional residual capacity (FRC) will decrease by approximately 20% [372]. Because of atelectasis, the arterial-alveolar (A–a) oxygen gradient is elevated after CPB and remains elevated for at least 7 days postoperatively. Intrapulmonary shunting is also increased during CPB. Other mechanical changes that have been observed during or after CPB include a decrease in lung compliance and an increase in airway resistance, but it is difficult to determine the relative contribution of CPB (rather than other aspects of the operation) to these changes. Nonetheless, these changes lead to a situation in which there is increased work of breathing postoperatively. Efforts to prevent atelectasis during CPB have produced only mixed results. There is some evidence to suggest that avoiding entry into the pleural space(s) may lead to better lung compliance postoperatively. A variety of ventilator management strategies during CPB, including intermittent or low-pressure static inflation of the lungs, have produced conflicting results with regard to postoperative lung function [373]. At the conclusion of CPB, it may be helpful to administer a series of sighs, with airway pressures of approximately 30 cm H2O to help reverse any atelectasis that has developed during CPB. After operation, the most effective treatment for atelectasis is positive-pressure ventilation which is provided for most patients as routine care. The clinician should be aware that levels of positive end-expiratory pressure (PEEP) > 6 cm H2O may impair the cardiac output. As an alternative, relatively large tidal volumes (i.e. 12–15 ml/kg) may be helpful. A high A–a gradient postoperatively may also be due to underlying chronic lung disease or to the presence of pulmonary edema.

Acute lung injury Soon after the introduction of CPB in the 1950s, a syndrome of acute respiratory failure termed ‘pump lung’ was noted to carry a high mortality rate. This acute lung injury was originally thought to be due to microemboli, but the use of appropriate filters in the perfusion circuit did not eliminate this complication. Today, most acute lung injury is thought to be mediated by complement activation [374]. There is a significant relationship between the duration of CPB, the degree of elevation of the circulating levels of C3a, and the degree of lung dysfunction after CPB. In animal studies, complement produces pulmonary leukocyte sequestration and intrapulmonary release of thromboxane A2 that produces pulmonary vasoconstriction and hypertension. There is also an accompanying increase in pulmonary vascular permeability that leads to an increase in lung water.

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The incorporation of filters in the perfusion circuit is used to limit microembolization and its contribution to acute lung injury. Leukocyte filters have been used for leukocyte depletion during CPB, with varying effectiveness in preventing postoperative lung dysfunction [375]. Leukocyte depletion of the residual volume of blood in the pump at the conclusion of CPB can also be used to help improve postoperative lung function. Hemodilution and avoidance of pulmonary vascular distension (i.e. with appropriate left heart venting) may also help to improve postoperative lung function.

Renal effects of cardiopulmonary bypass Several factors associated with cardiac surgery, including not only CPB but also hypothermia and hemodilution, may produce an adverse effect on renal function postoperatively. The relative contributions of each of these factors remain uncertain. Although the frequency of postoperative renal failure has decreased in recent years, this complication still carries a poor prognosis [376–379]. Not only is there a high associated short- (approximately 50%) and long-term mortality rate, but this complication typically is associated with other early postoperative complications, prolongs the hospital stay, and is associated with a substantial increase in the cost of medical care [380]. The incidence of postoperative renal failure after cardiac surgery that necessitates dialysis is approximately 1% [377,381]. Postoperative renal failure has been associated with a variety of preoperative patient-related factors, including: impaired renal function, impaired preoperative cardiac function, diabetes, peripheral vascular disease, history of acute rheumatic fever, older patient age, more complex operations (i.e. valvular surgery rather than firsttime CABG), previous myocardial infarction, and the presence of congestive heart failure [378,380,382–386]. The contribution of CPB per se to postoperative renal dysfunction is not entirely clear. Hemodilution is thought to increase tissue microcirculatory blood flow and oxygen delivery because of a reduction in the blood viscosity, but this effect has not been demonstrated in the human kidney [387]. Most studies that have examined the effect of varying levels of hypothermia on postoperative renal function have failed to show a relationship [388]. Both animal and clinical studies of pulsatile vs. non-pulsatile perfusion have failed to show a relationship between perfusion technique and postoperative renal function [389–393]. With the use of membrane oxygenators and arterial line filters, there is a reduction in embolism during CPB and this, theoretically, should help to prevent embolic damage to the kidneys during CPB. The most important perioperative factors related to postoperative renal dysfunction are thought to be renal hypoperfusion due to either low perfusion pressures during CPB or to the use of vasoconstrictor agents. Dopamine administered intravenously at low dose (1–3 μg/kg per min) has been shown to increase renal blood flow. Although the practice of administering dopamine at low dose in the perioperative period is common, there is

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no conclusive evidence that dopamine can ameliorate postoperative renal dysfunction, whether the agent is administered before or after the renal dysfunction becomes apparent [394,395]. Recent studies of the selective dopamine-2 receptor agonist, fenoldopam, have shown that this agent, when administered prophylactically to patients undergoing intravenous dye tests, confers a degree of protection from postprocedure renal dysfunction [396]. This benefit has not yet been confirmed in cardiac surgical patients, however. Other agents such as clonidine [397], calcium channel blockers [398,399], and atrial natriuretic peptide analogs [400,401] have not shown a convincing benefit in preventing or treating postoperative renal failure.

Neurological effects of CPB Neurological complications after cardiac surgery can be categorized into three general types: encephalopathy, stroke, and neurocognitive disorders [402–405]. The incidence of major neurological complications after cardiac surgery is reported to be approximately 1–6%, but this figure does not include those with neurocognitive disorders [406–409]. In an alternative, and increasingly popular, classification, these complications have been categorized as type I [cerebral death, non-fatal stroke, new transient ischemic attack (TIA)] or type II (new intellectual deterioration or new seizures) [406]. The development of a major neurological complication is associated with a substantial higher perioperative mortality rate, a prolonged hospital stay, and markedly increased in- and out-of-hospital medical costs [406,407,410]. Identified risk factors for the development of a type I neurological complication include: proximal aortic atherosclerosis, a history of previous neurological event (e.g. TIA, stroke), use of an intraaortic balloon pump (IABP) during the surgical procedure, diabetes mellitus, hypertension, pulmonary disease, unstable angina, increasing patient age, perioperative hypotension, and the use of LV venting during the operation [406]. Increasing patient age may be the most important risk factor, with an approximately 2% risk of a type I neurological complication at age 40–49 years but an approximately 8% risk at age 70–79 years [406]. Although there is some overlap, the risk factors for the development of a type II neurological complication are somewhat different: increasing patient age, pulmonary disease, hypertension, history of excessive alcohol consumption, history of previous CABG, arrhythmias, history of peripheral vascular disease (PVD), and congestive heart failure (CHF) on the day of operation. In recent years, it has become apparent that neurocognitive (type II) complications are probably much more common than type I complications. At the time of discharge from the hospital, the prevalence of neurocognitive decline may be as high as 60%, depending on the testing methods used to document this complication [411–413]. In the early postoperative period, the results of testing may be influenced by poor patient cooperation due to pain, sleep deprivation, and the effects of medications. Deficits have been documented in psychomotor speed, attention and concentration, new learning ability, and

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short-term memory. These neurocognitive changes may persist for months after operation and have an immeasurable effect on the individual patient’s quality of life. Considerable efforts have been made to understand the relative contributions of many perioperative factors on the development of neurological complications after CPB. Nonetheless, it has been difficult to dissect out the individual contributions of potentially detrimental factors such as embolization, hypoperfusion, hypoxia, hypotension, arrhythmias, disorders in coagulation, dehydration, and inflammation. All patients undergoing CPB probably experience some degree of embolization, despite the presence of filters in the perfusion circuit [410,414–416]. Transcranial Doppler has been used to document the significant relationship between the rate of cerebral embolization during CPB and the risk of a subsequent neurological complication [414]. There is no convincing evidence that the mean perfusion pressure during CPB is related to the risk of neurological complications [417,418], but there can be no doubt that hypoperfusion regionally or in the microvasculature can contribute to neurological injury. Recently, there has been increased attention to the systemic inflammatory response and its effect on the brain [419]. Several potential neuroprotective agents, including thiopental, propofol, and nimodipine, have been suggested, but there is little evidence for their effectiveness [419]. In early trials, aprotinin has shown promise as a neuroprotective agent during CPB [419]. It may be the case that inflammatory mechanisms may be as important as embolism in the etiology of neurological complications after CPB. Several aspects of the conduct of CPB have a bearing on neurological function and the development of neurological complications after CPB. In the nonCPB setting, the brain is able to autoregulate cerebral blood flow with a mean arterial pressure of as low as 50–55 mmHg. Given the lack of reliable evidence linking mean perfusion pressure and neurological outcomes, it is prudent to target the arterial perfusion pressure to be at least in this autoregulatory range. It is probably prudent to maintain the mean perfusion pressure higher for patients at increased risk of cerebral hypoperfusion (e.g. known cerebral vascular disease, previous stroke). Although there have been some conflicting data, most reports suggest that the systemic temperature during CPB probably has little independent effect on the frequency of postoperative neurological complications, at least for degrees of moderate hypothermia (28 °C) through normothermia (37 °C) [413,420–422]. Systemic rewarming at the end of CPB should be conducted to avoid even small degrees (i.e. 39 °C) of systemic hyperthermia. Although higher glucose concentrations in experimental models have been associated with worse neurological outcome, studies have failed to document this association in the clinical setting of CPB [413,423,424]. It is prudent to maintain the glucose concentration in the physiological range of 150–250 mg/dl. There are conflicting reports on the effect of pH management during CPB in adult patients and the risk of neurological complications

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[425–428]. For adult patients at high risk of embolic events undergoing CPB at moderate hypothermia, alpha-stat pH management may be beneficial in reducing the embolic risk. Despite the considerable morbidity that accompanies neurological injuries after CPB, it is not a common practice to monitor for the development of these complications during CPB. Although the technical details are beyond the scope of this chapter, the methods that are available for this purpose include: measurement of jugular bulb oxyhemoglobin saturation [429]; near-infrared spectroscopy (NIRS) [430]; transcranial Doppler [431]; and electrophysiological monitors such as EEG and evoked potentials [432].

Complications of cardioplegia Pathophysiological aspects of myocardial ischemic injury In the beating heart, the myocardial oxygen consumption (MvO2) is a function of the heart rate, the stroke work, and the inotropic state [433,434]. During a typical cardiac surgical procedure, the MvO2 varies significantly. The MvO2 is lowest when the heart is arrested and is greatest just after release of the aortic cross clamp, when an oxygen debt must be repaid. The MvO2 is also influenced by temperature, with markedly decreased MvO2 at lower temperatures. Myocardial ischemia occurs when there is an imbalance between myocardial oxygen delivery and myocardial oxygen consumption. Anaerobic metabolism results in acidosis, mitochondrial dysfunction, and, eventually, myocardial necrosis. ATP stores are reduced almost immediately, there is impaired contractility after a few minutes, and there is irreversible myocardial injury after 30–40 min of warm (37 °C) ischemia. In its severe forms, this myocardial injury can be apparent visually in the operating room, with discoloration of an affected region of the heart. TEE may document regional wall motion abnormalities that are due to regional myocardial ischemia. Postoperatively, this injury can be documented by a rise in the serum creatinine kinase (CPK), its myocardial (MB) isoform, lactate dehydrogenase (LDH), and troponin [435]. The peak of the CPK curve is usually at 24 h after injury, but the LDH peak may occur 4–5 days after injury. The incidence of perioperative myocardial infarction, documented by elevation of the cardiac enzymes, is approximately 1–2%. There is a spectrum of myocardial dysfunction after cardiac surgery, and some myocardial injury may be reversible. Myocardial ‘stunning’ refers to the situation in which initially dysfunctional ischemic myocardium regains normal function after some period of time. For some patients, this situation may be a manifestation of poor myocardial protection during the operation. For patients with substantial amounts of stunned myocardium, it may take hours or days for this recovery to occur. This condition can be manifested by a low cardiac output syndrome that may require inotropic or intraaortic balloon (IABP) support until the myocardium has recovered.

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Myocardial protection The earliest cardiac operations were performed on the beating heart. It was the introduction, however, of CPB and controlled arrest of the heart that enabled complex coronary and intracardiac operations to be performed routinely. The use of a hyperkalemic ‘cardioplegia’ solution was first described in 1955. At that time, very high concentrations of potassium resulted in severe cardiac injury and these solutions were abandoned [436]. For operations that required a ‘still’ heart, fibrillatory arrest induced by hypothermia was widely used. It was not until the 1970s that cardioplegia solutions with lower potassium concentration were shown to avoid direct cardiac injury during use [437,438]. These solutions have enjoyed widespread use because asystolic arrest significantly reduces the myocardial oxygen consumption. Despite years of study, there are still clinical challenges in the area of myocardial protection [439]. In most applications, intermittent doses of cardioplegia are delivered to satisfy the low-level oxygen and substrate demands of the myocardium during cardioplegic arrest. Historically, hyperkalemic crystalloid solutions were used to achieve and maintain cardioplegic arrest of the heart. More recently, blood cardioplegic solutions in which oxygenated blood is mixed (1 : 1–8 : 1) with a hyperkalemic crystalloid solution have become the standard. In animal studies, blood cardioplegia has been shown to reduce irreversible myocardial injury, reduce anaerobic metabolism, preserve high-energy phosphate stores, and result in better postischemic ventricular function compared with crystalloid cardioplegia solutions [440,441]. Moreover, clinical studies of blood vs. crystalloid cardioplegia have shown better outcomes (e.g. reduced perioperative myocardial infarction, less postoperative low cardiac output syndrome, and improved operative mortality rates) for blood cardioplegia [442]. Historically, cold cardioplegia solutions were used most commonly because of the added benefit of reduced oxygen consumption in the colder myocardium. Often, cardioplegia solutions were supplemented with topical cold saline or slush to help ensure cooling of the myocardium. If cold saline or slush is used, however, the surgeon must be aware of the small risk of phrenic nerve injury due to cold injury [443–445]. If phrenic nerve paralysis occurs, the patient may require prolonged mechanical ventilation and other respiratory complications are more likely. More recently, it has been recognized that lowering the temperature of the myocardium provides only a small additive benefit in terms of oxygen consumption on top of cardioplegic arrest at normothermia [446]. This feature, combined with the finding that myocardial cooling results in slower recovery of postischemic ventricular function, has prompted many surgeons to move toward the use of normothermic (37 °C) or tepid (approximately 34 °C) cardioplegia solutions.

Antegrade cardioplegia Antegrade cardioplegia is administered directly into the aortic root. A pursestring suture is typically placed in the ascending aorta and a cardioplegia

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cannula or needle is introduced to deliver the cardioplegia. Cardioplegia is typically administered in an initial dose (to cause arrest of the heart) followed by maintenance doses every 15–30 min afterwards. In practice, the maintenance doses are usually given between anastomoses for CABG operations and at convenient points during valve or other procedures. The perfusion pressure is monitored by the perfusionist and should be maintained at approximately 70 mmHg. An inability to maintain an adequate perfusion pressure during administration of the cardioplegia solution during the initial dose may indicate aortic insufficiency. The perfusionist should be alert to this possibility and the surgeon should be vigilant for dilatation of the left ventricle that results in this situation. If this occurs, intermittent dosing (with periods of aortic root venting), manual closure of the aortic valve (by pinching), or the use of retrograde cardioplegia may be necessary. Before each maintenance dose of antegrade cardioplegia, the aortic root should be de-aired to prevent air entry into the coronary arteries. Cardioplegia achieves its desirable effects (e.g. cardiac arrest, cardiac cooling) by distribution throughout the myocardium. The distribution of the cardioplegia solution in the myocardium will be most complete in territories of unobstructed coronary arteries. To help ensure better distribution of the cardioplegia solution, the use of retrograde cardioplegia should be considered in patients with high-grade coronary stenoses or occluded coronary arteries. Complications related to aortic root delivery of antegrade cardioplegia are relatively uncommon, but include tearing of the aorta, local hematoma formation, dissection of the aorta, and dislodgement of intraluminal plaque with subsequent embolization. During cannulation, a site free of atherosclerotic disease should be selected; manual palpation, TEE, or epiaortic ultrasound should be used to help guide the surgeon. At the conclusion of the procedure, the cardioplegia cannula should be removed and the site should be secured with a suture. Late aortic dissection or pseudoaneurysm formation at this site are possible. For most CABG operations performed with the use of CPB, administration of continuous antegrade cardioplegia is not practical. During CABG procedures, continuous antegrade cardioplegia will flow through any unoccluded coronary arteries and will obscure the operative field at the coronary arteriotomy. As with beating heart surgery, a misted blower can be used to ‘spray away’ cardioplegia solution from the operative site if antegrade cardioplegia is administered at a low rate during creation of the anastomoses. During elevation of the heart for construction of bypass anastomoses on the lateral wall of the heart, kinking of the proximal coronary arteries may limit the ability to administer antegrade cardioplegia. During operations for aortic valve replacement (AVR), an initial dose of cardioplegia can be administered by cannula in the aortic root as described above. Once the aorta is opened to expose the aortic valve, however, another cardioplegic technique must be selected for subsequent administrations of the cardioplegia solution. Retrograde cardioplegia is used commonly

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in this situation [447], but ostial perfusion cannulas can be inserted into the coronary ostia to deliver antegrade cardioplegia either continuously or intermittently. If continuous cardioplegia delivery is desired, small, flexible, soft-tipped cannulas can be placed in each of the coronary ostia and sutured in place with fine silk or Prolene suture. These cannulas can be held out of the way with additional sutures. If intermittent cardioplegia delivery is satisfactory, the left and right coronary ostia can be cannulated successively with hand-held ostial perfusion cannulas. Whenever ostial perfusion cannulas are used, the perfusionist must be vigilant to the pressure of delivery and the surgeon must be vigilant for dislodgement of the cannulas. With either continuous or intermittent delivery, direct injury to the coronary ostia may occur and lead to early or late coronary occlusion. During operations for mitral valve repair (MVR) or replacement, either hand-held or self-retaining retractors used for left atrial exposure have the additional effect of rendering the aortic valve incompetent. As a result, maintenance doses of antegrade cardioplegia can be administered only if the retraction is released and the aortic root is vented of any air. This obviously disrupts the flow of the operative procedure. Most surgeons choose to use retrograde cardioplegia in this situation.

Retrograde cardioplegia The use of retrograde cardioplegia has come into widespread use, largely because of the problems with distribution of antegrade cardioplegia in situations with occlusion or high-grade stenoses of the coronary arteries [448,449]. Typically, the retrograde cardioplegia cannula is inserted through a pursestring suture in the right atrium and correct placement of the cannula in the coronary sinus is confirmed by palpation and/or TEE. If a balloon-tipped cannula and pressure monitoring line are used, inflation of the balloon should result in ‘ventricularization’ of the pressure waveform. The cannula should be placed in the most proximal position in the coronary sinus that allows proper fixation. Unlike antegrade cardioplegia, one particular advantage of retrograde cardioplegia is that repeated de-airing of the aortic root is not necessary. Because of the position of the posterior interventricular vein in the proximal portion of the coronary sinus, this vein will not receive cardioplegia solution if the tip (and balloon) of the retrograde cardioplegia cannula is passed beyond this vein. This may be the most important drawback of retrograde cardioplegia. If the cannula is advanced too far into the coronary sinus, the right side of the heart will not be perfused adequately [450–453]. Some authorities have suggested carefully ‘backing out’ the retrograde cardioplegia cannula while cardioplegia solution is administered at a low rate until the posterior interventricular vein is seen to fill. Alternatively, a suture snare can be placed around the coronary sinus, just proximal to the posterior interventricular vein, to prevent migration of the cannula into the right atrium.

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During administration of retrograde cardioplegia, the pressure in the coronary sinus should be measured continuously. Effective distribution of the cardioplegia solution requires coronary sinus pressures in the 25–40 mmHg range. Excessive pressure in the coronary sinus may cause localized disruption of this vessel and lead to hemorrhage [454]. When elevating or retracting the heart with a retrograde cardioplegia cannula in place, care should be taken to avoid direct injury of the coronary sinus with the cannula tip. Visible injuries to the coronary sinus should be repaired with fine suture. Occasionally, coronary sinus injuries remain occult until excessive blood is noticed in the pericardial sac at the conclusion of the operative procedure. Another unusual complication of retrograde cardioplegia that has been reported is inadvertent puncture of the inner wall of the right atrium [455].

Neurological protection Profound hypothermia and circulatory arrest are helpful for a variety of cardiovascular operations (see Chapter 17, Complications of Aortic Surgery). A variety of adjuncts are available to help prevent neurological injury during these operations and will be discussed elsewhere. Two adjuncts that relate to cardiopulmonary bypass are profound hypothermia and the use of retrograde cerebral perfusion.

Profound hypothermia During many routine cardiac surgical procedures (e.g. CABG, valve replacement/repair), the systemic temperature can be maintained at normothermia (37 °C) or at mild hypothermia (32–36 °C) to avoid the unwanted effects of systemic hypothermia. For operations on the aortic arch or thoracoabdominal aorta, however, an ‘open’ approach is often necessary and profound degrees of hypothermia (16–20 °C) with circulatory arrest can be used to reduce the cerebral or spinal cord oxygen requirements and help to limit neurological injury during the operation. The ‘safe’ period of circulatory arrest at profound degrees of hypothermia is probably 30–45 min [456–459]. Longer periods of circulatory arrest have been associated with increased risk of neurological injury. Some operations are only possible with the use of profound hypothermia and circulatory arrest. Nonetheless, profound hypothermia has a detrimental effect on platelet function and myocardial recovery postoperatively.

Retrograde cerebral perfusion Another adjunct that may be useful during periods of profound hypothermia and circulatory arrest is retrograde cerebral perfusion [460–466]. There is considerable debate about the practical details, however. In its typical application, a venous cannula or a cardioplegia-type cannula is inserted into the superior vena cava. A tape or snare is secured around the cannula and retrograde perfusion can be established. The perfusion should be measured and maintained in the range of 25–30 mmHg [467].

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References 1 Westaby S, Bosher C. Landmarks in Cardiac Surgery. Oxford: ISIS Medical Media, 1997; 49–89. 2 Gibbon JH. Application of mechanical heart and lung apparatus to cardiac surgery. Minn Med 1954; March: 171–185. 3 Melrose DG, Dreyer B, Bentall HH et al. Elective cardiac arrest. Lancet 1955; July 2: 21–22. 4 Lillihei CW, DeWall RA, Gott VL et al. The direct vision correction of calcified aortic stenosis by means of pump-oxygenator and retrograde coronary sinus perfusion. Dis Chest 1956; 30: 123–132. 5 Edmunds LH Jr, ed. Cardiac Surgery in the Adult. New York: McGraw-Hill, 1997. 6 Gravlee GP, Davis RF, Kurusz Utley JR, eds. Cardiopulmonary Bypass. Principles and Practice, 2nd edn. Philadelphia: Lippincott, Williams & Wilkins, 2000. 7 Taylor KM, ed. Cardiopulmonary Bypass. Principles and Management. Baltimore: Williams & Wilkins, 1986. 8 Casthely PA, Bregman D. Cardiopulmonary bypass. Physiology, related complications, and pharmacology. Mount Kisco, NY: Futura, 1991. 9 Estafanous FG, Barash PG, Reves JG, eds. Cardiac Anesthesia. Principles and Clinical Practice, 2nd edn. Philadelphia: Lippincott, Williams & Wilkins, 2001. 10 DiNardo JA, ed. Anesthesia for Cardiac Surgery, 2nd edn. Stanford, CT: Appleton & Lange, 1998. 11 Hessell EA II, Hill AG. Circuitry and cannulation techniques. In: Gravlee GP, Davis RF, Kurusz M, Utley JR, eds. Cardiopulmonary Bypass: Principles and Practice, 2nd edn. Philadelphia: Lippincott, Williams & Wilkins, 2000; 69–97. 12 Ambesh SP, Singh SK, Dubey DK et al. Inadvertent closure of the superior vena cava after decannulation: a potentially catastrophic complication after termination of bypass. J Cardiothorac Vasc Anesth 1998; 12: 723 [Letter]. 13 Ratnaraj J, Manohar G. Pulmonary artery catheter displacement during cannulation for CPB. J Cardiothorac Vasc Anesth 1991; 5: 648 [Letter]. 14 Troianos CA. Transesophageal echocardiographic diagnosis of pulmonary artery catheter entrapment and coiling. Anesthesiology 1993; 79: 602–604. 15 Horrow JC, Laucks SO. Coronary air embolism during venous cannulation. Anesthesiology 1982; 56: 212–214. 16 McGiffin DC, Kirklin JK. Cardiopulmonary bypass for cardiac surgery. In: Sabiston DC Jr, Spencer FC, eds. Surgery of the Chest, 6th edn. Philadelphia: W.B. Saunders, 1995; 1256–1271. 17 Toomasian JM, McCarthy JP. Total extrathoracic cardiopulmonary support with kinetic assisted venous drainage: experience in 50 patients. Perfusion 1998; 13: 137–143. 18 Davila RM, Rawles T, Mack MJ. Venoarterial air embolus: a complication of vacuumassisted venous drainage. Ann Thorac Surg 2001; 71: 1369–1371. 19 Bernstein EF, Gleason LR. Factors influencing hemolysis with roller pumps. Surgery 1967; 61: 432–442. 20 Indeglia RA, Shea MA, Forstrom R et al. Influence of mechanical factors on erythrocyte sublethal damage. Trans Am Soc Artif Intern Organs 1968; 14: 264–271. 21 Galletti PM, Brecher GA. Heart-Lung Bypass, Principle and Techniques of Extracorporeal Circulation. New York: Grune & Stratton, 1962; 184–188. 22 Harringer W. Capture of particulate emboli during cardiac procedures in which aortic cross-clamp is used. Ann Thorac Surg 2000; 70: 1119–1123. 23 Borger MA, Ivanov J, Weisel RD et al. Stroke during coronary bypass surgery: principal role of cerebral macroemboli. Eur J Cardiothorac Surg 2001; 19: 627–632.

Complications of cardiopulmonary bypass and cardioplegia 327 24 Barbut D, Grassineau D, Lis E et al. Posterior distribution of infarcts in strokes related to cardiac operations. Ann Thorac Surg 1998; 65: 1656–1659. 25 Béïque FA, Joffe D, Tousignant G et al. Echocardiographic-based assessment and management of atherosclerotic disease of the thoracic aorta. J Cardiothoracic Vasc Anesth 1998; 12: 206–220. 26 Wong BI, McLean RF, Naylor CD et al. Central-nervous-system dysfunction after warm or hypothermic cardiopulmonary bypass. Lancet 1992; 339: 1383–1384. 27 Hammeke TA, Hastings JE. Neuropsychologic alterations after cardiac operation. J Thorac Cardiovasc Surg 1998; 96: 326–331. 28 Shaw PJ, Bates D, Cartlidge NEF et al. Early neurological complications of coronary artery bypass surgery. Br Med J 1985; 291: 1384–1387. 29 Newman MF, Kirchner JL, Phillips-Bute B et al. Longitudinal assessment of neurocognitive function after coronary-artery bypass surgery. N Engl J Med 2001; 344: 395–402. 30 Henriksen L. Evidence suggestive of diffuse brain damage following cardiac operations. Lancet 1984; 331: 816–820. 31 Åberg T, Ronquist G, Tydén H et al. Adverse effects on the brain in cardiac operations as assessed by biochemical, psychometric, and radiologic methods. J Thorac Cardiovasc Surg 1984; 87: 99–105. 32 Weinstein GS. Left hemispheric strokes in coronary surgery: implications for end-hole aortic cannulas. Ann Thorac Surg 2001; 71: 128–132. 33 Bar-El Y, Goor DA. Clamping of the atherosclerotic ascending aorta during coronary artery bypass operations: its cost in strokes. J Thorac Cardiovasc Surg 1992; 104: 469–474. 34 Ohteki H, Itoh T, Natsuaki M et al. Intraoperative ultrasonic imaging of the ascending aorta in ischemic heart disease. Ann Thorac Surg 1990; 50: 539–542. 35 Wareing TH, Davilla-Roman VG, Barzilai B et al. Management of the severely atherosclerotic ascending aorta during cardiac operations: a strategy for detection and treatment. J Thoracic Cardiovasc Surg 1992; 103: 453–462. 36 Sylivris S, Calafiore P, Matalanis G et al. The intraoperative assessment of ascending aortic atheroma: epiaortic imaging is superior to both transesophageal echocardiography and direct palpation. J Cardiothorac Vasc Anesth 1997; 11: 704 –707. 37 Dávilla-Román VG, Phillips KJ, Daily BB et al. Intraoperative transesophageal echocardiography and epiaortic ultrasound for assessment of atherosclerosis of the thoracic aorta. J Am Coll Cardiol 1996; 28: 942–947. 38 Still RJ, Hilgenberg AD, Atkins CW et al. Intraoperative aortic dissection. Ann Thorac Surg 1992; 53: 374 –380. 39 Gott JP, Cohen CL, Jones EL. Management of ascending aortic dissections and aneurysms early and late following cardiac operations. J Card Surg 1990; 5: 2–13. 40 Aoyagi S, Tayama E, Nishimi M et al. Aortic dissections complicating open cardiac surgery: report of three cases. Surg Today 2000; 30: 1022–1025. 41 Ishino K, Murakami T, Teramoto S. Cannulation-induced coronary artery dissection: successful management with circulatory assist devices and coronary bypass grafting. Surg Today 1998; 28: 563–566. 42 Salama FD, Blesovsky A. Complications of cannulation of the ascending aorta for open heart surgery. Thorax 1970; 25: 604 –607. 43 Benedict JS, Buhl TL, Henney RP. Acute aortic dissection during cardiopulmonary bypass. Arch Surg 1974; 108: 810–813. 44 Carey JS, Skow JR, Scott C. Retrograde aortic dissection during cardiopulmonary bypass: “nonoperative” management. Ann Thorac Surg 1977; 24: 44 –48. 45 Gates JD, Bichell DP, Rizzo RJ et al. Thigh ischemia complicating femoral vessel cannulation for cardiopulmonary bypass. Ann Thorac Surg 1996; 61: 730–733.

328

Chapter 16

46 Sabik JF, Lytle BW, McCarthy PM et al. Axillary artery: an alternative site of arterial cannulation for patients with extensive aortic and peripheral vascular disease. J Thorac Cardiovasc Surg 1995; 109: 885–891. 47 Baribeau YR, Westbrook BM, Charlesworth DC et al. Arterial inflow via an axillary artery graft for the severely atherosclerotic aorta. Ann Thorac Surg 1998; 66: 33–37. 48 High KM, Bashein G, Kurusz M. Principles of oxygenator function. Gas exchange, heat transfer, and operation. In: Gravlee GP, Davis RF, Kurusz M, Utley JR, eds. Cardiopulmonary Bypass: Principles and Practice, 2nd edn. Philadelphia: Lippincott Williams & Wilkins, 2000; 49–68. 49 Nilsson L, Bagge L, Nyström S-O. Blood cell trauma and postoperative bleeding: comparison of bubble and membrane oxygenators and observations on coronary suction. Scand J Thorac Cardiovasc Surg 1990; 24: 65–69. 50 Tabak C, Eugene J, Stemmer EA. Erythrocyte survival following extracorporeal circulation: a question of membrane versus bubble oxygenator. J Thorac Cardiovasc Surg 1981; 81: 30–33. 51 Pearson DT. Gas exchange: bubble and membrane oxygenators. Semin Thorac Cardiovasc Surg 1990; 2: 313–319. 52 Peterson KA, Dewanjee MK, Kaye MP. Fate of indium 111-labeled platelets during cardiopulmonary bypass performed with membrane and bubble oxygenators. J Thorac Cardiovasc Surg 1982; 84: 39–43. 53 Edmunds LH Jr, Ellison N, Colman RW et al. Platelet function during cardiac operation: comparison of membrane and buddle oxygenators. J Thorac Cardiovasc Surg 1982; 83: 805–812. 54 Padayachee TS, Parsons S, Theobold R et al. The detection of microemboli in the middle cerebral artery during cardiopulmonary bypass: a transcranial Doppler ultrasound investigation using membrane and bubble oxygenators. Ann Thorac Surg 1987; 44: 298–302. 55 Pedersen TH, Karlsen HM, Semb G et al. Comparison of bubble release from various types of oxygenators: an in vivo investigation. Scand J Thorac Cardiovasc Surg 1987; 21: 73–80. 56 Hatori N, Yoshizu H, Haga Y et al. Biocompatibility of heparin-coated membrane oxygenator during cardiopulmonary bypass. Artif Organs 1994; 18: 904 –910. 57 Shigemitsu O, Hadama T, Takasaki H et al. Biocompatibility of heparin-bonded membrane oxygenator (Carmeda MAXIMA) during the first 90 minutes of cardiopulmonary bypass: clinical comparison with the conventional system. Artif Organs 1994; 18: 936–941. 58 Tayama E, Raskin SA, Nose Y. Blood pumps. In: Gravlee GP, Davis RF, Kurusz M, Utley JR, eds. Cardiopulmonary Bypass: Principles and Practice, 2nd edn. Philadelphia: Lippincott, Williams & Wilkins, 2000; 37–48. 59 Tempe DK, Khanna SK. Accidental hyperperfusion during cardiopulmonary bypass: suggested safety features. Ann Thorac Surg 1998; 65: 306 [Letter]. 60 Briceño JC, Runge TM. Tubing spallation in extracorporeal circuits. An in vitro study using an electronic particle counter. Int J Artif Organs 1992; 15: 222–228. 61 Noon GP, Harrell JE Jr, Feldman L et al. Development and evaluation of pulsatile roller pump and tubing for cardiac assistance. Artif Organs 1983; 7: 49–54. 62 Peek GJ, Thompson A, Killer HM et al. Spallation performance of extracorporeal oxygenation tubing. Perfusion 2000; 15: 457–466. 63 Kolff J, McClurken JB, Alpern JB. Beware centrifugal pumps: not a one-way street, but a potentially dangerous “siphon”. Ann Thorac Surg 1990; 50: 512 [Letter]. 64 Jenkins OF, Morris R, Simpson JM. Australasian perfusion incident survey. Perfusion 1997; 12: 279–288.

Complications of cardiopulmonary bypass and cardioplegia 329 65 Hessel EAII, Hill AG. Cardiotomy suction and venting. In: Gravlee GP, Davis RF, Kurusz M, Utley JR, eds. Cardiopulmonary Bypass: Principles and Practice, 2nd edn. Philadelphia: Lippincott, Williams & Wilkins, 2000; 98–104. 66 Edmunds LH Jr, Saxena NC, Hillyer P et al. Relationship between platelet count and cardiotomy suction return. Ann Thorac Surg 1978; 25: 306–310. 67 Pearson DT. Microemboli: gaseous and particulate. In: Taylor KM, ed. Cardiopulmonary Bypass: Principles and Management. Baltimore: Williams & Wilkins, 1986; 313–354. 68 Wright G, Sanderson JM. Cellular aggregation and trauma in cardiotomy suction systems. Thorax 1979; 34: 621–628. 69 Solis RT, Noon GP, Beall AC Jr et al. Particulate microembolism during cardiac operation. Ann Thorac Surg 1974; 17: 332–344. 70 Liu JT-F, Su Z-K, Ding W-X. Quantitation of particulate microemboli during cardiopulmonary bypass: experimental and clinical studies. Ann Thorac Surg 1992; 54: 1196–1202. 71 Brooker RF, Brown WR, Moody DM et al. Cardiotomy suction: a major source of brain lipid emboli during cardiopulmonary bypass. Ann Thorac Surg 1998; 65: 1651–1655. 72 Tabuchi N, de Haan J, Boonstra PW et al. Activation of fibrinolysis in the pericardial cavity during cardiopulmonary bypass. J Thorac Cardiovasc Surg 1993; 106: 828–833. 73 Siderys H. Pericardial fluid and hemolysis. Ann Thorac Surg 1993; 56: 595 [Letter]. 74 Orenstein JM, Sato N, Aaron B et al. Microemboli observed in deaths following cardiopulmonary bypass surgery: silicone antifoam agents and polyvinyl chloride tubing as sources of emboli. Hum Pathol 1982; 13: 1082–1090. 75 de Jong JCF, ten Duis HJ, Sibinga CTS. Hematologic aspects of cardiotomy suction in cardiac operations. J Thorac Cardiovasc Surg 1980; 79: 227–236. 76 Boonstra PW, van Imhoff GW, Eysman L et al. Reduced platelet activation and improved hemostasis after controlled cardiotomy suction during clinical membrane oxygenator perfusions. J Thorac Cardiovasc Surg 1985; 89: 900–906. 77 Wielogorske JW, Cross DE, Nwadike EVO. The effects of subatmospheric pressure on the hemolysis of blood. J Biomechan 1975; 8: 321–325. 78 Hirose T, Burman SO, O’Connor RA. Reduction of perfusion hemolysis by use of atraumatic low-pressure suction. J Thorac Cardiovasc Surg 1964; 47: 242–247. 79 Arom KV, Vinas JF, Fewel JE et al. Is a left ventricular vent necessary during cardiopulmonary bypass? Ann Thorac Surg 1977; 24: 566–573. 80 Burton NA, Graeber GM, Zajtchuk R. An alternate method of ventricular ventingathe pulmonary artery sump. Chest 1984; 85: 814–815. 81 Breyer RH, Meredity JW, Mills SA et al. Is a left ventricular vent necessary for coronary artery bypass operations performed with cardioplegic arrest? J Thorac Cardiovasc Surg 1983; 86: 338–349. 82 Olinger GN, Bonchek LI. Ventricular venting during coronary revascularization: assessment of benefit by intraoperative ventricular function curves. Ann Thorac Surg 1978; 26: 525–534. 83 Najafi H, Javid H, Goldin MD et al. Aortic valve replacement without left heart decompression. Ann Thorac Surg 1976; 21: 131–133. 84 Salerno TA, Charrette EJP. Elimination of venting in coronary artery surgery. Ann Thorac Surg 1979; 27: 340–343. 85 Utley JR, Stephens DB. Venting during cardiopulmonary bypass. In: Utley JR, ed. Pathophysiology and Techniques of Cardiopulmonary Bypass, Vol. II. Baltimore: Williams & Wilkins, 1983; 115–127. 86 Robicsek F, Duncan GD. Retrograde air embolization in coronary operations. J Thorac Cardiovasc Surg 1987; 94: 110–114.

330

Chapter 16

87 Tingleff J, Joyce FS, Pettersson G. Intraoperative echocardiographic study of air embolism during cardiac operations. Ann Thorac Surg 1995; 60: 673–677. 88 O’Connor BR, Kussman BD, Park KW. Severe hypercarbia during cardiopulmonary bypass: a complication of CO2 flooding of the surgical field. Anesth Analg 1998; 86: 264–266. 89 Kurusz M, Mills NL. Management of unusual problems encountered in initiating and maintaining cardiopulmonary bypass. In: Gravlee GP, Davis RF, Kurusz M, Utley JR, eds. Cardiopulmonary Bypass: Principles and Practice, 2nd edn. Philadelphia: Lippincott Williams and Wilkins, 2000; 578–612. 90 Stoney WS, Alford WC, Burrus GR et al. Air embolism and other accidents using pump oxygenators. Ann Thorac Surg 1980; 29: 336–340. 91 Kurusz M, Butler B, Katz J et al. Air embolism during cardiopulmonary bypass. Perfusion 1995; 10: 361–391. 92 Mitchell S, Gorman D. The pathophysiology of cerebral arterial gas embolism. J Extra Corpor Technol 2002; 34: 18–23. 93 Kurusz M, Wheeldon DR. Risk containment during cardiopulmonary bypass. Semin Thorac Cardiovasc Surg 1990; 2: 400–409. 94 Dennis C. Perspective in press: one group’s struggle with development of a pumpoxygenator. Trans Am Soc Artif Intern Organ 1985; 31: 1–11. 95 Chaudhuri N, Hickey MS. A simple method of treating coronary air embolism after cardiopulmonary bypass. Ann Thorac Surg 1999; 68: 1867–1868. 96 Sandhu AA, Spotnitz HM, Dickstein ML et al. Retrograde cardioplegia preserves myocardial function after induced coronary air embolism. J Thorac Cardiovasc Surg 1997; 113: 917–922. 97 Butler BD, Laine GA, Leiman BC et al. Effect of the Trendelenberg position on the distribution of arterial air emboli in dogs. Ann Thorac Surg 1988; 45: 198–202. 98 Mehlhorn U, Burke EJ, Butler BD et al. Body position does not affect the hemodynamic response to venous air embolism in dogs. Anesth Analg 1994; 79: 734–739. 99 Watanabe T, Shimasaki T, Kuraoka S et al. Retrograde cerebral perfusion against massive air embolism during cardiopulmonary bypass. J Thorac Cardiovasc Surg 1992; 104: 532–533 [Letter]. 100 Rozanski J, Szufladowicz M. Successful treatment of massive air embolism. J Card Surg 1994; 9: 430–432. 101 Stark J, Hough J. Air in the aorta: treatment by reversed perfusion. Ann Thorac Surg 1986; 41: 337–338. 102 Hendricks FFA, Bogers AJJC, de la Riviere AB et al. The effectiveness of venoarterial perfusion in treatment of arterial air embolism during cardiopulmonary bypass. Ann Thorac Surg 1983; 36: 433–436. 103 Kern JA, Arnold S. Massive cerebral embolization: successful treatment with retrograde perfusion. Ann Thorac Surg 2000; 69: 1266–1268. 104 Lar LW, Lai LC, Ren LW. Massive arterial air embolism during cardiac operation: successful treatment in a hyperbaric chamber under 3 ATA. J Thorac Cardiovasc Surg 1990; 100: 928–930 [Letter]. 105 Armon C, Deschamps C, Adkinison C et al. Hyperbaric treatment of cerebral air embolism sustained during an open-heart surgical procedure. Mayo Clin Proc 1991; 66: 565–571. 106 Bitterman H, Melamed Y. Delayed hyperbaric treatment of cerebral air embolism. Israel J Med Sci 1993; 29: 22–26.

Complications of cardiopulmonary bypass and cardioplegia 331 107 Franklin C. The technique of radial artery cannulation. Tips for maximizing results while minimizing the risk of complications. J Crit Ill 1995; 10: 424–432. 108 Slogoff S, Keats AS, Arlund C. On the safety of radial artery cannulation. Anesthesiology 1983; 59: 42–47. 109 Wilkins RG, Lane N. Radial artery cannulation and ischaemic damage: a review. Anesthesia 1985; 40: 896–899. 110 Rose SH. Ischemic complications of radial artery cannulation: an association with a calcinosis, Raynaud’s phenomenon, esophageal dysmotility, sclerodactyly, and telangiectasia variant of scleroderma. Anesthesiology 1993; 78: 587–589. 111 Gronbeck C, Miller EL. Nonphysician placement of arterial catheters: experience with 500 insertions. Chest 1993; 104: 1716–1717. 112 Mangar D, Laborde RS, Vu DN. Delayed ischaemia of the hand necessitating amputation after radial artery cannulation. Can J Anesth 1993; 40: 247–250. 113 Grier D, Hartnell G. Percutaneous femoral artery puncture. Prac Anat Br J Radiol 1990; 63: 602–604. 114 Resar JR, Brinker JA. Peripheral arterial access. The large and small of it. Cathet Cardiovasc Diagn 1994; 33: 212–213. 115 Smith SMV, Galland RB. Late presentation of femoral artery complications following percutaneous cannulation for cardiac angiography or angioplasty. J Cardiovasc Surg 1992; 33: 437–439. 116 Polderman KH, Girbes ARJ. Central venous catheter use. Part 2: Infectious complications. Intens Care Med 2002; 28: 18–28. 117 Polderman KH, Girbes ARJ. Central venous catheter use. Part 1: Mechanical complications. Intens Care Med 2002; 28: 1–17. 118 Bambauer R, Inniger R, Pirrung KJ et al. Complications and side-effects associated with large-bore catheters in the subclavian and internal jugular veins. Artif Org 1994; 18: 318–321. 119 Herbst CA Jr. Indications, management, and complications of percutaneous subclavian catheters. Arch Surg 1978; 113: 1421–1425. 120 Conces DJ, Holden RW. Aberrant locations and complications in initial placement of subclavian vein catheters. Arch Surg 1984; 119: 293–295. 121 Smith BE, Model JH, Gaub ML et al. Complications of subclavian vein catheterization. Arch Surg 1965; 90: 228–229. 122 Robinson JF, Robinson WA, Cohn A et al. Perforation of the great vessels during central venous line placement. Arch Intern Med 1995; 155: 1225–1228. 123 Gray P, Sullivan G, Ostryzniuk P et al. Value of postprocedural chest radiographs in the adult intensive care unit. Crit Care Med 1992; 20: 1513–1518. 124 Duntley P, Siever J, Korwes ML. Vascular erosion by central venous catheters. Chest 1992; 101: 1633–1638. 125 Whitman ED. Complications associated with the use of central venous access devices. Curr Probl Surg 1996; 33: 309–378. 126 Snyder RH, Archer FJ, Endy T et al. Catheter infection: a comparison of two catheter maintenance techniques. Ann Surg 1988; 208: 651–653. 127 Flanagan JP, Gradisar IA, Gross RJ et al. Air embolus: a lethal complication of subclavian venipuncture. New Engl J Med 1969; 281: 488–489. 128 Reeves ST, Roy RC, Dorman BH. The incidence of complications after the double-catheter technique for cannulation of the right internal jugular vein in a university teaching hospital. Anesth Analg 1995; 81: 1073–1076.

332

Chapter 16

129 Shah KB, Rao TLK, Laughlin S et al. A review of pulmonary artery catheterization in 6,245 patients. Anesthesiology 1984; 61: 271–275. 130 Salmenpera M, Peltola K, Rosenberg P. Does prophylactic lidocaine control cardiac arrhythmias associated with pulmonary artery catheterization? Anesthesiology 1982; 56: 210–212. 131 Boscoe MJ, de Lange S. Damage to the tricuspid valve with a Swan-Ganz catheter. Br Med J 1981; 283: 346–347. 132 O’Toole JD, Wurtzbacher JJ, Wearner NE et al. Pulmonary-valve injury and insufficiency during pulmonary-artery catheterization. N Engl J Med 1979; 301: 1167–1168. 133 Bottiger BW, Schmidt H, Bohrer H. Nonsurgical removal of a knotted pulmonary artery catheter. J Cardiothorac Vasc Anesth 1991; 5: 647 [Letter]. 134 Feng WC, Singh AK, Drew T. Swan-Ganz catheter-induced massive hemoptysis and pulmonary artery false aneurysm. Ann Thorac Surg 1990; 50: 644 –646. 135 Cervenko FW, Shelley SE, Spence DG et al. Massive endobronchial hemorrhage during cardiopulmonary bypass: treatable complication of balloon-tipped catheter damage to the pulmonary artery. Ann Thorac Surg 1983; 35: 326–328. 136 Kron IL, Piepgrass W, Carabello B et al. False aneurysm of the pulmonary artery: a complication of pulmonary artery catheterization. Ann Thorac Surg 1982; 33: 629–630. 137 Urschel JD, Myerowitz PD. Catheter-induced pulmonary artery rupture in the setting of cardiopulmonary bypass. Ann Thorac Surg 1993; 56: 585–589. 138 Stone JG, Faltas AN, Khambatta HJ et al. Temporary unilateral pulmonary artery occlusion: a method for controlling Swan-Ganz catheter-induced hemoptysis. Ann Thorac Surg 1984; 37: 508–510. 139 McDaniel DD, Stone JG, Faltas AN et al. Catheter-induced pulmonary artery hemorrhage: diagnosis and management in cardiac operations. J Thorac Cardiovasc Surg 1981; 82: 1–4. 140 Pellegrini RV, Marcelli G, Di Marco RF et al. Swan-Ganz catheter induced pulmonary hemorrhage. J Cardiovasc Surg 1987; 28: 646–649. 141 Lemen R, Jones JG, Cowan G. A mechanism of pulmonary-artery perforation by SwanGanz catheters. N Engl J Med 1975; 292: 211–212. 142 Johnston WE, Royster R, Vinten-Johansen J et al. Influence of balloon inflation and deflation on location of pulmonary artery catheter tip. Anesthesiology 1987; 67: 110–115. 143 Daniel WG, Erbel R, Kasper W et al. Safety of transesophageal echocardiography: a multicenter survey of 10,419 examinations. Circulation 1991; 83: 817–821. 144 Seward JB, Khandheria BK, Oh JK. Critical appraisal of transesophageal echocardiography: limitations, pitfalls, and complications. J Am Soc Echocardiogr 1992; 5: 288–305. 145 Kallmeyer IJ, Collard CD, Fox JA et al. The safety of intraoperative transesophageal echocardiography: a case series of 7200 cardiac surgical patients. Anesth Analg 2001; 92: 1126–1130. 146 Hogue CW, Lappas GD, Creswell LL et al. Swallowing dysfunction after cardiac operations: associated adverse outcomes and risk factors including intraoperative transesophageal echocardiography. J Thorac Cardiovasc Surg 1995; 110: 517–522. 147 Savino JS, Hanson CW III, Bigelow DC. Oropharyngeal injury after transesophageal echocardiography. J Cardiothorac Vasc Anesth 1994; 8: 76–78. 148 Spahn DR, Schmid S, Carrel T et al. Hypopharynx perforation by a transesophageal echocardiography probe. Anesthesiology 1995; 82: 581–583. 149 Brinkman WT, Schanewise JS, Clements SD et al. Transesophageal echocardiography: not an innocuous procedure. Ann Thorac Surg 2001; 72: 1725–1726.

Complications of cardiopulmonary bypass and cardioplegia 333 150 Dewhirst WE, Stragand JJ, Fleming BM. Mallory-Weiss tear complicating intraoperative transesophageal echocardiography in a patient undergoing aortic valve replacement. Anesthesiology 1990; 73: 777–778. 151 Despotis GJ, Gravlee G, Filos K et al. Anticoagulation monitoring during cardiac surgery: a review of current and emerging techniques. Anesthesiology 1999; 91: 1122–1151. 152 Conrad J, LeCompte T, Horellou M et al. Antithrombin III in patients treated with subcutaneous or intravenous heparin. Thromb Res 1981; 22: 507–511. 153 Miciniak E, Gockerman J. Heparin induced decrease in circulating AT III. Lancet 1980; 2: 581–584. 154 Jordan RE, Oosta GM, Gardner WT et al. The kinetics of the hemostatic enzyme– antithrombin interactions in the presence of low molecular weight heparin. J Biol Chem 1980; 255: 10081–10090. 155 Sabbagh AH, Chung GKT, Shuttleworth P et al. Fresh frozen plasma: a solution to heparin resistance during cardiopulmonary bypass. Ann Thorac Surg 1984; 37: 466–468. 156 Anderson EF. Heparin resistance prior to cardiopulmonary bypass. Anesthesiology 1986; 64: 504–507. 157 Blakeman B. Management of heparin-induced thrombocytopenia: a cardiovascular surgeon’s perspective. Semin Hematol 1999; 36 (Suppl. 1): 37–41. 158 Cohen M. Heparin-induced thrombocytopenia and the clinical use of low molecular weight heparins in acute coronary syndromes. Semin Hematol 1999; 36 (Suppl. 1): 33–36. 159 Walenga JM, Jeske WP, Wood JJ et al. Laboratory tests for heparin-induced thrombocytopenia: a multicenter study. Semin Hematol 1999; 36 (Suppl. 1): 22–28. 160 Kelton JG. The clinical management of heparin-induced thrombocytopenia. Semin Hematol 1999; 36 (Suppl. 1): 17–21. 161 Body SC, Morse DS. Coagulation, transfusion, and cardiac surgery. In: Spiess BD, Counts RB, Gould SA, eds. Perioperative Transfusion Medicine. Baltimore: Williams & Wilkins, 1998; 419–460. 162 Vender J, Matthew E, Silverman I et al. Heparin-associated thrombocytopenia: alternative managements. Anesth Analg 1986; 65: 520–522. 163 Fareed J, Callas D, Hoppensteadt DA et al. Antithrombin agents as anticoagulants and antithrombotics: implications in drug development. Semin Hematol 1999; 36 (Suppl. 1): 42–56. 164 Sodian R, Loebe M, Gorman KF et al. Heparin induced thrombocytopenia: experiences in 12 heart surgery patients. ASAIO J 1997; 43: M430–M433. 165 Smith RE, Townsend GE, Berry BR. Enoxaparin for unstable angina and ancrod for cardiac surgery following heparin allergy. Ann Pharmacother 1996; 30: 476–480. 166 Arén C. Heparin and protamine therapy. Semin Thorac Cardiovasc Surg 1990; 2: 364–372. 167 Bull BS, Korpman RA, Huse WM et al. Heparin therapy during extracorporeal circulation. I. Problems inherent in existing heparin protocols. J Thorac Cardiovasc Surg 1975; 69: 674–684. 168 Bull BS, Huse WM, Brauer FS et al. Heparin therapy during extracorporeal circulation. II. The use of a dose–response curve to individualize heparin and protamine dosage. J Thorac Cardiovasc Surg 1975; 69: 685–689. 169 Akl B, Vargas G, Neal J, Robillard J, Kellp P. Clinical experience with the activated clotting time for the control of heparin and protamine therapy during cardiopulmonary bypass. Thorac Cardiovasc Surg 1980; 79: 98–102. 170 Culliford A, Gitel SN, Starr N et al. Lack of correlation between activated clotting time and plasma heparin during cardiopulmonary bypass. Ann Surg 1981; 193: 105–111.

334

Chapter 16

171 O’Neill AI, McAllister C, Corke CF et al. A comparison of five devices for the bedside monitoring of heparin therapy. Anesth Intens Care 1991; 19: 592–601. 172 Esposito RA, Culliford AT, Colvin SB et al. The role of the activated clotting time in heparin administration and neutralization for cardiopulmonary bypass. J Thorac Cardiovasc Surg 1983; 85: 174–185. 173 Hurt R, Perkins HA, Osborn JJ et al. The neutralization of heparin by protamine in extracorporeal circulation. J Thorac Surg 1956; 32: 612–619. 174 Bull MH, Huse WM, Bull BS. Evaluation of tests used to monitor heparin therapy during extracorporeal circulation. Anesthesiology 1975; 43: 346–353. 175 Anido G, Freeman DJ. Heparin assay and protamine titration. Am J Clin Pathol 1981; 76: 410–415. 176 Jaques L. A study of the toxicity of the protamine, salmine. Br J Pharmacol 1949; 4: 135. 177 Lowenstein E, Johnston WE, Lappas DG et al. Catastrophic pulmonary vasoconstriction associated with protamine reversal of heparin. Anesthesiology 1983; 59: 470–473. 178 Horrow JC. Protamine allergy. J Cardiothorac Anesth 1988; 2: 225–242. 179 Frater RWM, Oka Y, Hong Y et al. Protamine-induced circulatory changes. J Thorac Cardiovasc Surg 1984; 87: 687–692. 180 Levy JH, Schwieger IM, Zaidan JR et al. Evaluation of patients at risk for protamine reactions. J Thorac Cardiovasc Surg 1989; 98: 200–204. 181 Morel DR, Mo Costabella PM, Pittet J-F. Adverse cardiopulmonary effects and increased plasma thromboxane concentrations following the neutralization of heparin with protamine in awake sheep are infusion rate-dependent. Anesthesiology 1990; 73: 415–424. 182 Horrow J. Management of coagulation and bleeding disorders. In: Kaplan JA, ed. Cardiac Anesthesia. Philadelphia: W.B. Saunders, 1983; 951–994. 183 Keller R. Interrelations between different types of cells. II. Histamine-release from the mast cells of various species by cationic polypeptides of polymorphonuclear leukocyte lysosomes and other cationic compounds. Int Arch Allergy Appl Immunol 1968; 34: 139–144. 184 Stoelting RK, Henry DP, Verburg KM et al. Haemodynamic changes and circulating histamine concentrations following protamine administration to patients and dogs. Can Anesth Soc J 1984; 31: 534 –540. 185 Parsons RS, Mohandas K. The effect of histamine-receptor blockade on the hemodynamic responses to protamine. J Cardiothorac Anesth 1989; 3: 37–43. 186 Sethna D, Gray R, Bussell J et al. Further studies on the myocardial metabolic effect of protamine sulfate following cardiopulmonary bypass. Anesth Analg 1982; 61: 476–477. 187 Michaels IAL, Barash PG. Hemodynamic changes during protamine administration. Anesth Analg 1983; 62: 831–835. 188 Iwatsuki N, Matsukawa S, Iwatsuki K. A weak negative inotropic effect of protamine sulfate upon the isolated canine heart muscle. Anesth Analg 1980; 59: 100–102. 189 Hird RB, Wakefield TW, Mukherjee R et al. Direct effects of protamine sulfate on myocyte contractile processes: cellular and molecular mechanisms. Circulation 1995; 92 (Suppl. II): II-443–II-446. 190 Doolan L, McKenzie I, Krafchek J et al. Protamine sulfate hypersensitivity. Anesth Intens Care 1981; 9: 147–149. 191 Levy JH, Zaidan JR, Faraj B. Prospective evaluation of risk protamine reactions in patients with NPH insulin-dependent diabetes. Anesth Analg 1986; 65: 739–742. 192 Samuel T, Kolk AHJ, Rümke P et al. Autoimmunity to sperm antigens in vasectomized men. Clin Exp Immunol 1975; 21: 65–74.

Complications of cardiopulmonary bypass and cardioplegia 335 193 Kirklin JK, Chenoweth DE, Naftel DC et al. Effects of protamine administration after cardiopulmonary bypass on complement, blood elements, and the hemodynamic state. Ann Thorac Surg 1986; 41: 193–199. 194 Lakin JD, Blocker TJ, Strong DM et al. Anaphylaxis to protamine sulfate mediated by a complement-dependent IgG antibody. J Allergy Clin Immunol 1978; 61: 102–107. 195 Lowenstein E, Zapol WM. Protamine reactions, explosive mediator release, and pulmonary vasoconstriction. Anesthesiology 1990; 73: 373–374 [Editorial]. 196 Hobbhahn J, Conzen PF, Zenker B et al. Beneficial effect of cyclooxygenase inhibition on adverse hemodynamic responses after protamine. Anesth Analg 1988; 67: 253–260. 197 Morel DR, Lowenstein E, Nguyenduy T et al. Acute pulmonary vasoconstriction and thromboxane release during protamine reversal of heparin anticoagulation in awake sheep: evidence for the role of reactive oxygen metabolites following nonimmunological complement activation. Circ Res 1988; 62: 905–915. 198 Nuttall GA, Murray MJ, Bowie EJW. Protamine-heparin-induced pulmonary hypertension in pigs: effects of treatment with a thromboxane receptor antagonist on hemodynamics and coagulation. Anesthesiology 1991; 74: 138–145. 199 Schumacher W, Heran C, Ogletree M. Effect of thromboxane receptor antagonism on pulmonary hypertension caused by protamine–heparin interaction in pigs. Circulation 1988; 78: 207. 200 Colman RW. Humoral mediators of catastrophic reactions associated with protamine neutralization. Anesthesiology 1987; 66: 595–596 [Editorial]. 201 Godal H. A comparison of two heparin-neutralizing agents: protamine and polybrene. Scand J Clin Lab Invest 1960; 12: 446–457. 202 Weiss W, Gilman J, Catenacci A, Osterberg A. Heparin neutralization with polybrene administered intravenously. JAMA 1958; 166: 630–637. 203 Toyofuku T, Koyama S, Kobayashi T et al. Effects of polycations on pulmonary vascular permeability in conscious sheep. J Clin Invest 1989; 83: 2063–2069. 204 Egerton W, Robinson C. The antiheparin, anticoagulant and hypotensive properties of hexadimethrine and protamine. Lab Invest 1987; 56: 170–179. 205 Ransdell HT Jr, Haller JA Jr, Stowens D et al. Renal toxicity of polybrene (hexadimethrine bromide). J Surg Res 1965; 5: 195–199. 206 Yang VC, Port FK, Kim J-S et al. The use of immobilized protamine in removing heparin and preventing protamine-induced complications during extracorporeal blood circulation. Anesthesiology 1991; 75: 288–297. 207 Teng C-LC, Kim J-S, Port FK et al. A protamine filter for extracorporeal blood heparin removal. ASAIO Trans 1988; 34: 743–746. 208 Kim J-S, Vincent C, Teng C-LC et al. A novel approach to anticoagulation control. ASAIO Trans 1989; 35: 644 –646. 209 Despotis GJ, Summerfield AL, Joist JH et al. In vitro reversal of heparin effect with heparinase: evaluation with whole blood prothrombin time and activated partial thromboplastin time in cardiac surgical patients. Anesth Analg 1994; 79: 670–674. 210 Langer R, Linhardt RJ, Hoffberg S et al. An enzymatic system for removing heparin in extracorporeal therapy. Science 1982; 217: 261–263. 211 Cook JJ, Niewiarowski S, Yan Z et al. Platelet factor 4 efficiently reverses heparin anticoagulation in the rat without adverse effects of heparin–protamine complexes. Circulation 1992; 85: 1102–1109. 212 Levy JH, Cormack JG, Morales A. Heparin neutralization by recombinant platelet factor 4 and protamine. Anesth Analg 1995; 81: 35–37.

336

Chapter 16

213 Bernabei A, Gikakis N, Maione TE et al. Reversal of heparin anticoagulation by recombinant platelet factor 4 and protamine sulfate in baboons during cardiopulmonary bypass. J Thorac Cardiovasc Surg 1995; 109: 765–771. 214 Williams RD, D’Ambra MN, Maione TE et al. Recombinant platelet factor 4 reversal of heparin in human cardiopulmonary bypass blood. J Thorac Cardiovasc Surg 1994; 108: 975–983. 215 Dehmer GJ, Fisher M, Tate DA et al. Reversal of heparin anticoagulation by recombinant platelet factor 4 in humans. Circulation 1995; 91: 2188–2194. 216 Despotis GJ, Filos KS, Zoys TN et al. Factors associated with excessive postoperative blood loss and hemostatic transfusion requirements: a multivariate analysis in cardiac surgical patients. Anesth Analg 1996; 82: 13–21. 217 Moulton MJ, Creswell LL, Mackey ME et al. Reexploration for bleeding is a risk factor for adverse outcomes after cardiac operations. J Thorac Cardiovasc Surg 1996; 111: 1037–1046. 218 Dacey LJ, Munoz JJ, Baribeau YR et al. Reexploration for hemorrhage following coronary bypass grafting: incidence and risk factors. Northern New England Cardiovascular Disease Study Group. Arch Surg 1998; 133: 442–447. 219 Despotis GJ, Skubas NJ, Goodnough LT. Optimal management of bleeding and transfusion in patients undergoing cardiac surgery. Semin Thorac Cardiovasc Surg 1999; 11: 84–104. 220 Slaughter TF, Greenberg CS. Antifibrinolytic drugs and perioperative hemostasis. Am J Hematol 1997; 56: 32–36. 221 Peters DC, Noble S. Aprotinin: an update of its pharmacology and therapeutic use in open heart surgery and coronary artery bypass surgery. Drugs 1999; 57: 233–260. 222 Sundt TM III, Kouchoukos MD, Saffitz JE et al. Renal dysfunction and intravascular coagulation with aprotinin and hypothermic circulatory arrest. Ann Thorac Surg 1993; 55: 1418–1424. 223 Cosgrove DM III, Heric B, Lytle BW et al. Aprotinin therapy for reoperative myocardial revascularization: a placebo-controlled study. Ann Thorac Surg 1992; 54: 1031–1036. 224 Schulze K, Graeter T, Schaps D et al. Severe anaphylactic shock due to repeated application of aprotinin in patients following intrathoracic aortic replacement. Eur J Cardiothorac Surg 1993; 7: 495–496. 225 Etchason J, Petz L, Keeler E et al. The cost effectiveness of preoperative autologous blood donations. N Engl J Med 1995; 332: 719–724. 226 Tartter PI, Quintero S, Barron DM. Perioperative blood transfusion associated with infectious complications after colorectal cancer operations. Am J Surg 1986; 152: 479–482. 227 Dawes LG, Aprahamian C, Condon RE et al. The risk of infection after colon injury. Surgery 1986; 100: 796–803. 228 Murphy P, Heal JM, Blumberg N. Infection or suspected infection after hip replacement surgery with autologous or homologous blood transfusions. Transfusion 1991; 31: 212–217. 229 Love TR, Hendren WG, O’Keefe DD et al. Transfusion of predonated autologous blood in elective cardiac surgery. Ann Thorac Surg 1987; 43: 508–512. 230 Gluck D, Kubanek B, Ahnefeld F. Autologous transfusion. Objectives and benefits, limits and risks shown in a practical clinical concept. Anesthesia 1988; 37: 565–571. 231 Anderson BV, Tomasulo PA. Current autologous transfusion practices. Implications for the future. Transfusion 1988; 28: 394 –396. 232 Forbes J, Anderson M, Anderson G, Bleecher G, Rossi E, Moss G. Blood transfusion costs: a multicenter study. Transfusion 1991; 31: 318–323. 233 Britton L, Eastlund T, Dziuban S et al. Predonated autologous blood use in elective cardiac surgery. Ann Thorac Surg 1989; 47: 529–532.

Complications of cardiopulmonary bypass and cardioplegia 337 234 Owings DV, Kruskall MS, Thurer RL et al. Autologous blood donations prior to elective cardiac surgery. JAMA 1989; 262: 1963–1968. 235 Konishi T, Ohbayashi T, Kaneko T et al. Preoperative use of erythropoietin for cardiovascular operations in anemia. Ann Thorac Surg 1993; 56: 101–103. 236 Schmoekel M, Nollert G, Mempel M et al. Effects of recombinant human erythropoietin on autologous blood donation before open heart surgery. Thorac Cardiovasc Surg 1993; 41: 364–368. 237 Kyo S, Omoto R, Hirashima K, Eguchi S, Fujita T. Effect of human recombinant erythropoietin on reduction of homologous blood transfusion in open-heart surgery. A Japanese multicenter study. Circulation 1992; 86: 413–418. 238 Wong CA, Franklin ML, Wade LD. Coagulation tests, blood loss, and transfusion requirements in platelet rich plasmapheresed versus nonpheresed cardiac surgery patients. Anesth Analg 1994; 78: 29–36. 239 Jones JW, McCoy TA, Rawitscher RE et al. Effects of intraoperative plasmapheresis on blood loss in cardiac surgery. Ann Thorac Surg 1990; 49: 585–590. 240 Giordano GF, Rivers SL, Chung GKT et al. Autologous platelet-rich plasma in cardiac surgery: effect on intraoperative and postoperative transfusion requirements. Ann Thorac Surg 1988; 46: 416–419. 241 Del Rossi AJ, Cernaianu AC, Vertrees RA et al. Platelet-rich plasma reduces postoperative blood loss after cardiopulmonary bypass. J Thorac Cardiovasc Surg 1990; 100: 281–286. 242 Petry AF, Jost J, Sievers H. Reduction of homologous blood requirements by bloodpooling at the onset of cardiopulmonary bypass. J Thorac Cardiovasc Surg 1994; 107: 1210–1214. 243 Schönberger JPAM, Bredée JJ, Tjian D et al. Intraoperative predonation contributes to blood saving. Ann Thorac Surg 1993; 56: 893–898. 244 Lawson L, Ochsner J, Mills N, Leonard G. The use of hemodilution and fresh autologous blood in open heart surgery. Anesth Analg 1974; 53: 672–683. 245 Robblee JA. Pro: blood should be harvested immediately before cardiopulmonary bypass and infused after protamine reversal to decrease blood loss following cardiopulmonary bypass. J Cardiothorac Anesth 1990; 4: 519–521. 246 Schaff HV, Hauer J, Gardner TJ et al. Routine use of autotransfusion following cardiac surgery: experience in 700 patients. Ann Thorac Surg 1979; 27: 493–499. 247 Breyer RH, Engelman RM, Rousou JA et al. Blood conservation for myocardial revascularization: is it cost effective? J Thorac Cardiovasc Surg 1987; 93: 512–522. 248 Eng J, Kay PH, Murday AJ et al. Postoperative autologous transfusion in cardiac surgery. A prospective, randomised study. Eur J Cardiothorac Surg 1990; 4: 595–600. 249 Adan A, de la Rivière AB, Haas F et al. Autotransfusion of drained mediastinal blood after cardiac surgery: a reappraisal. Thorac Cardiovasc Surg 1988; 36: 10–14. 250 Axford TC, Dearani JA, Ragno G et al. Safety and therapeutic effectiveness of reinfused shed blood after open heart surgery. Ann Thorac Surg 1994; 57: 615–622. 251 Bouboulis N, Kardara M, Kesteven PJ et al. Autotransfusion after coronary artery bypass surgery: is there any benefit? J Card Surg 1994; 9: 314 –321. 252 de Haan J, Schönberger J, Haan J et al. Tissue-type plasminogen activator and fibrin monomers synergistically cause platelet dysfunction during retransfusion of shed blood after cardiopulmonary bypass. J Thorac Cardiovasc Surg 1993; 106: 1017–1023. 253 Griffith LD, Billman GF, Daily PO et al. Apparent coagulopathy caused by infusion of shed mediastinal blood and its prevention by washing of the infusate. Ann Thorac Surg 1989; 47: 400–406.

338

Chapter 16

254 Bland LA, Villarino ME, Ardunino MJ et al. Bacteriologic and endotoxin analysis of salvaged blood used in autologous transfusions during cardiac operations. J Thorac Cardiovasc Surg 1992; 103: 582–588. 255 Gravlee GP, Davis RE, Kurusz M, Utley JR, eds. Cardiopulmonary Bypass. Principles and Practice, 2nd edn. Philadelphia: Lippincott, Williams & Wilkins, 2000. 256 Edmunds LH Jr. Extracorporeal perfusion. In: Edmunds LH Jr, ed. Cardiac Surgery in the Adult. New York: McGraw-Hill, 1997; 255–294. 257 Blackstone EH, Kirklin JW, Stewart RW et al. The damaging effects of cardiopulmonary bypass. In: Wu KK, Roxy EC, eds. Prostaglandins in Clinical Medicine: Cardiovascular and Thrombotic Disorders. Chicago: Year Book, 1982; 355. 258 Uniyal S, Brash JL. Patterns of adsorption of proteins from human plasma onto foreign surfaces. Thromb Haemost 1993; 70: 253. 259 Ziats NP, Pankowsky DA, Tierney BP et al. Adsorption of Hageman factor (factor XII) and other human plasma proteins to biomedical polymers. J Lab Clin Med 1990; 116: 687–696. 260 Horbett TA. Principles underlying the role of adsorbed plasma proteins in blood interactions with foreign materials. Cardiovasc Pathol 1993; 2: 137S–148S. 261 Horbett TA. Proteins: structure, properties, and adsorption to surfaces. In: Ratner BD, Hoffman AS, Schoen FJ et al., eds. Biomaterials Science. An Introduction to Materials in Medicine. San Diego: Academic Press, 1996; 133–141. 262 Volanakis JE, Frank MM, eds. The Human Complement System in Health and Disease. New York: Marcel Dekker, 1998. 263 Colman RW. Surface-mediated defense reactions: the plasma contact activation system. J Clin Invest 1984; 73: 1249–1253. 264 Gikakis N, Khan MMH, Hiramatsu Y et al. Effect of factor Xa inhibitors on thrombin formation and complement and neutrophil activation during in vitro extracorporeal circulation. Circulation 1996; 94 (Suppl. II): II-341–II-346. 265 Drake TA, Ruf W, Morrissey JH et al. Functional tissue factor is entirely cell surface expressed on lipopolysaccharide-stimulated human blood monocytes and a constitutively tissue factor-producing neoplastic cell line. J Cell Biol 1989; 109: 389–395. 266 Grabowski EF, Rodriguez M, Nemerson Y et al. Flow limits factor Xa production by monolayers of fibroblasts and endothelial cells. Blood 1990; 76 (Suppl. I): 422 [Abstract]. 267 Wachtfogel YT, Harpel PC, Edmunds LH Jr. et al. Formation of Cîs-C1–inhibitor, kallikrien-Cî-inhibitor and plasmin-α2-plasmin-inhibitor complexes during cardiopulmonary bypass. Blood 1989; 73: 468– 471. 268 Wiedmer T, Esmon CT, Sims PJ. Complement proteins C5b-9 stimulate procoagulant activity through platelet prothrombinase. Blood 1986; 68: 875–880. 269 Berger M. Complement-mediated phagocytosis. In: Volanakis JE, Frank MM, eds. The Human Complement System in Health and Disease. New York: Marcel Dekker, 1998; 9–32. 270 Chenowith DE, Hugli TE. Demonstration of specific C5a receptor on intact human polymorphonuclear leukocytes. Proc Natl Acad Sci USA 1978; 75: 3943. 271 Ellison N, Edmunds LH Jr, Colman RW. Platelet aggregation following heparin and protamine administration. Anesthesiology 1978; 48: 65–68. 272 Sobel M, McNeill PM, Carlson PL et al. Heparin inhibition of von Willebrand factordependent platelet function in vitro and in vivo. J Clin Invest 1991; 87: 1787–1793. 273 Coughlin SR, Vu T-KH, Hung DT et al. Characterization of a functional thrombin receptor: issues and opportunities. J Clin Invest 1992; 89: 351–355. 274 Niewiarowski S, Senyi AF, Gillies P. Plasmin-induced platelet aggregation and platelet release reaction. J Clin Invest 1973; 52: 1647–1659.

Complications of cardiopulmonary bypass and cardioplegia 339 275 Lu H, Soria C, Cramer EM et al. Temperature dependence of plasmin-induced activation or inhibition of human platelets. Blood 1991; 77: 894. 276 Rinder CS, Bonner J, Rinder HM et al. Platelet activation and aggregation during cardiopulmonary bypass. Anesthesiology 1991; 74: 388–393. 277 Abrams CS, Ellison N, Budzynski AZ et al. Direct detection of activated platelets and platelet-derived microparticles in humans. Blood 1990; 75: 128–138. 278 Lefkovits J, Plow EF, Topol EJ. Platelet glycoprotein IIb/IIIa receptors in cardiovascular medicine. N Engl J Med 1995; 332: 1553–1559. 279 Rinder HM, Bonan JL, Rinder CS et al. Activated and unactivated platelet adhesion to monocytes and neutrophils. Blood 1991; 78: 1760–1769. 280 Addonizio VP Jr, Smith JB, Strauss JF III et al. Thromboxane synthesis and platelet secretion during cardiopulmonary bypass with bubble oxygenator. J Thorac Cardiovasc Surg 1980; 79: 91–96. 281 Hennessy VL Jr, Hicks RE, Niewiarowski S et al. Function of human platelets during extracorporeal circulation. Am J Physiol 1977; 232: H622–H628. 282 Addonizio VP Jr, Strauss JF III, Chang L-F et al. Release of lysosomal hydrolases during extracorporeal circulation. J Thorac Cardiovasc Surg 1982; 84: 28–34. 283 Edmunds LH Jr, Ellison N, Colman RW et al. Platelet function during cardiac operation: comparison of membrane and bubble oxygenators. J Thorac Cardiovasc Surg 1982; 83: 805–812. 284 Zilla P, Fasol R, Groscurth P et al. Blood platelets in cardiopulmonary bypass operations: recovery occurs after initial stimulation, rather than continual activation. J Thorac Cardiovasc Surg 1989; 97: 379–388. 285 Wenger RK, Lukasiewicz H, Mikuta BS et al. Loss of platelet fibrinogen receptors during clinical cardiopulmonary bypass. J Thorac Cardiovasc Surg 1989; 97: 235–239. 286 Saadi S, Plait JL. Endothelial cell responses to complement activation. In: Volanakis JE, Frank MM, eds. The Human Complement System in Health and Disease. New York: Marcel Dekker, 1998; 335–353. 287 Francis CW, Marder VJ. Physiologic regulation and pathologic disorders of fibrinolysis. In: Colman RW, Hirsch J, Marder VJ et al. Hemostasis and Thrombosis: Basic Principles and Clinical Practice, 3rd edn. Philadelphia: JB Lippincott, 1994; 1076–1103. 288 Asimakopoulos G, Taylor KM. Effects of cardiopulmonary bypass on leukocyte and endothelial adhesion molecules. Ann Thorac Surg 1998; 66: 2135–2144. 289 Ember JA, Jagels MA, Hugli TE. Characterization of complement anaphylatoxins and their biological responses. In: Volanakis JE, Frank MM, eds. The Human Complement System in Health and Disease. New York: Marcel Dekker, 1998; 241–244. 290 Insel PA. Analgesic-antipyretic and anti-inflammatory agents and drugs employed in the treatment of gout. In: Hardman IG, Limbird LE, eds. Goodman and Gillman’s Pharmacological Basis of Therapeutics. New York: McGraw-Hill, 1996; 618–619. 291 Wachtfogel YT, Kucich U, Greenplate J et al. Human neutrophil degranulation during extracorporeal circulation. Blood 1987; 69: 324 –330. 292 Enofsson M, Thelin S, Siegbahn A. Monocyte tissue factor expression, cell activation, and thrombin formation during cardiopulmonary bypass: a clinical study. J Thorac Cardiovasc Surg 1997; 113: 576–584. 293 Ernofsson M, Siegbahn A. Platelet-derived growth factor-BB and monocyte chemotactic protein-1 induce human peripheral blood monocytes to express tissue factor. Thromb Res 1996; 83: 307–320. 294 Chung JH, Gikakis N, Rao AK et al. Pericardial blood activates the extrinsic coagulation pathway during clinical cardiopulmonary bypass. Circulation 1996; 93: 2014 –2018.

340

Chapter 16

295 Frering B, Philip I, Dehoux M et al. Circulating cytokines in patients undergoing normothermic cardiopulmonary bypass. J Thorac Cardiovasc Surg 1994; 108: 636–641. 296 Kawahito K, Kawakami M, Fujiwara T et al. Interleukin-8 and monocyte chemotactic activating factor responses to cardiopulmonary bypass. J Thorac Cardiovasc Surg 1995; 110: 99–102. 297 Fingerle-Rowson G, Auers J, Kreuzer E et al. Down-regulation of surface monocyte lipopolysaccharide-receptor CD14 in patients on cardiopulmonary bypass undergoing aorta-coronary bypass operation. J Thorac Cardiovasc Surg 1998; 115: 1172–1178. 298 Haeffner-Cavaillon N, Roussellier N, Ponzio O et al. Induction of interleukin-1 production in patients undergoing cardiopulmonary bypass. J Thorac Cardiovasc Surg 1989; 98: 1100–1106. 299 Roth JA, Golub SH, Cukingnan RA et al. Cell-mediated immunity is depressed following cardiopulmonary bypass. Ann Thorac Surg 1981; 31: 350–356. 300 Ide H, Kakiuchi T, Furuta N et al. The effect of cardiopulmonary bypass on T cells and their subpopulations. Ann Thorac Surg 1987; 44: 277–282. 301 Nguyen DM, Mulder DS, Shennib H. Effect of cardiopulmonary bypass on circulating lymphocyte function. Ann Thorac Surg 1992; 53: 611–616. 302 Kirklin JW, Barratt-Boyes BG. Hypothermia, circulatory arrest, and cardiopulmonary bypass. In: Cardiac Surgery, 2nd edn. New York: Churchill Livingstone, 1993; 61–127. 303 Swain JA, McDonald TJ Jr, Griffith PK et al. Low-flow hypothermic cardiopulmonary bypass protects the brain. J Thorac Cardiovasc Surg 1991; 102: 76–84. 304 Michenfelder JD. The hypothermic brain. In: Michenfelder JD, ed. Anesthesia and the Brain. New York: Churchill Livingstone, 1998; 23–34. 305 Rothman SM, Olney JW. Glutamate and the pathophysiology of hypoxic-ischemic brain damage. Ann Neurol 1986; 19: 105–111. 306 Busto R, Globus MY-T, Dietrich WD et al. Effect of mild hypothermia on ischemia-induced release of neurotransmitters and free fatty acids in rat brain. Stroke 1989; 20: 904 –910. 307 Hickey RF, Hoar PF. Whole-body oxygen consumption during low-flow hypothermic cardiopulmonary bypass. J Thorac Cardiovasc Surg 1983; 86: 903–906. 308 Nussmeier NA, Arlund C, Slogoff S. Neuropsychiatric complications after cardiopulmonary bypass: cerebral protection by a barbiturate. Anesthesiology 1986; 64: 165–170. 309 Davies LK. Hypothermia: physiology and clinical use. In: Gravlee GP, Davis RF, Kurusz M, Utley JR, eds. Cardiopulmonary Bypass: Principles and Practice, 2nd edn. Philadelphia: Lippincott, Williams & Wilkins, 2000; 197–213. 310 Furnary AP, Zerr KJ, Grunkemeier GL et al. Continuous intravenous insulin infusion reduces the incidence of deep sternal wound infection in diabetic patients after cardiac surgical procedures. Ann Thorac Surg 1999; 67: 352–360. 311 Knight A, Forsling M, Treasure T et al. Changes in plasma vasopressin concentration in association with coronary artery surgery or thymectomy. Br J Anesth 1986; 58: 1273–1277. 312 Wu W-h, Zbuzek VK, Bellevue C. Vasopressin release during cardiac operation. J Thorac Cardiovasc Surg 1980; 79: 83–90. 313 Kaul TK, Swaminathan R, Chatrath RR et al. Vasoactive pressure hormones during and after cardiopulmonary bypass. Int J Artif Organs 1990; 13: 293–299. 314 Baylis PH. Vasopressin, diabetes insipidus, and syndrome of inappropriate antidiuresis. In: DeGroot LJ, Jameson JL, eds. Endocrinology, 4th edn, Vol. 1. Philadelphia: W.B. Saunders, 2001; 363–376. 315 Heyndrickx GR, Boettcher DH, Vatner SF. Effects of angiotensin, vasopressin, and methoxamine on cardiac function and blood flow distribution in conscious dogs. Am J Physiol 1976; 231: 1579–1587.

Complications of cardiopulmonary bypass and cardioplegia 341 316 Philbin DM, Levine FH, Emerson CW et al. Plasma vasopressin levels and urinary flow during cardiopulmonary bypass in patients with valvular heart disease: effect of pulsatile flow. J Thorac Cardiovasc Surg 1979; 78: 779–783. 317 Kuitunen A, Hynynen M, Salmenperä M et al. Anesthesia affects plasma concentrations of vasopressin, von Willebrand factor and coagulation factor VIII in cardiac surgical patients. Br J Anesth 1993; 70: 173–180. 318 Kehlet H. Surgical stress. The role of pain and analgesia. Br J Anesth 1989; 63: 189–195. 319 Anand KJS, Hickey PR. Halothane-morphine compared with high-dose sufentanil for anesthesia and postoperative analgesia in neonatal cardiac surgery. N Engl J Med 1992; 326: 1–9. 320 Landymore RW, Murphy DA, Kinley CE et al. Does pulsatile flow influence the incidence of postoperative hypertension? Ann Thorac Surg 1979; 28: 261–268. 321 Hirvonen J, Huttunen P, Nuutinen L et al. Catecholamines and free fatty acids in plasma of patients undergoing cardiac operations with hypothermia and bypass. J Clin Pathol 1978; 31: 949–955. 322 Reed HL, Chernow B, Lake CR et al. Alterations in sympathetic nervous system activity with intraoperative hypothermia during coronary artery bypass surgery. Chest 1989; 95: 616–622. 323 Balasaraswathi K, Glisson SN, El-Etr AA et al. Effect of priming volume on serum catecholamines during cardiopulmonary bypass. Can Anesth Soc J 1980; 27: 135–139. 324 Reves JG, Karp RB, Buttner EE et al. Neuronal and adrenomedullary catecholamine release in response to cardiopulmonary bypass in man. Circulation 1982; 66: 49–55. 325 Samuelson PN, Reves JG, Kirklin JK et al. Comparison of sufentanil and enfluranenitrous oxide anesthesia for myocardial revascularization. Anesth Analg 1986; 65: 217–226. 326 Ng A, Tan SSW, Lee HS et al. Effect of propofol infusion on the endocrine response to cardiac surgery. Anesth Intens Care 1995; 23: 543–547. 327 Stenseth R, Bjella L, Berg EM et al. Thoracic epidural anesthesia in aortocoronary bypass surgery II. Effects on the endocrine metabolic response. Acta Anesthesiol Scand 1994; 38: 834–839. 328 Moore CM, Cross MH, Desborough JP et al. Hormonal effects of thoracic extradural analgesia for cardiac surgery. Br J Anesth 1995; 75: 387–393. 329 Minami K, Körner MM, Vyska K et al. Effects of pulsatile perfusion on plasma catecholamine levels and hemodynamics during and after cardiac operations with cardiopulmonary bypass. J Thorac Cardiovasc Surg 1990; 99: 82–91. 330 Hume DM, Bell CC, Bartter F. Direct measurement of adrenal secretion during operative trauma and convalescence. Surgery 1962; 52: 174 –186. 331 Flezzani P, Croughwell ND, McIntyre RW et al. Isoflurane decreases the cortisol response to cardiopulmonary bypass. Anesth Analg 1986; 65: 1117–1122. 332 Lacoumenta S, Yeo TH, Paterson JL et al. Hormonal and metabolic responses to cardiac surgery with sufentanil-oxygen anesthesia. Acta Anesthesiol Scand 1987; 31: 258–263. 333 Uozumi T, Manabe H, Kawashima Y et al. Plasma cortisol, corticosterone, and nonproteinbound cortisol in extra-corporeal circulation. Acta Endocrinol 1972; 69: 517–525. 334 Taggart DP, Fraser WD, Borland WW et al. Hypothermia and the stress response to cardiopulmonary bypass. Eur J Cardiothorac Surg 1989; 3: 359–364. 335 Taylor KM, Walker MS, Rao LGS et al. Plasma levels of cortisol, free cortisol and corticotrophin during cardio-pulmonary by-pass. J Endocrinol 1975; 67: 29P–30P. 336 Terán N, Rodríguez-Iturbe B, Parra G et al. Atrial natriuretic peptide levels in brain venous outflow during cardiopulmonary bypass in humans: evidence for extracardiac hormonal production. J Cardiothorac Vasc Anesth 1991; 5: 343–347.

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337 Kharasch ED, Yeo K-T, Kenny MA et al. Influence of hypothermic cardiopulmonary bypass on atrial natriuretic factor levels. Can J Anesth 1989; 36: 545–553. 338 Curello S, Ceconi C, De Giuli F et al. Time course of human atrial natriuretic factor release during cardiopulmonary bypass in mitral valve and coronary artery diseased patients. Eur J Cardiothorac Surg 1991; 5: 205–210. 339 Northridge DB, Jamieson MP, Jardine AG et al. Pulmonary extraction and left atrial secretion of atrial natriuretic factor during cardiopulmonary bypass surgery. Am Heart J 1992; 123: 698–703. 340 Pasaoglu I, Erbas B, Varoglu E et al. Changes in the circulating endothelin and atrial natriuretic peptide levels during coronary artery bypass surgery. Jpn Heart J 1993; 34: 693–706. 341 Amano J, Suzuki A, Sunamori M et al. Attenuation of atrial natriuretic peptide response to sodium loading after cardiac operation. J Thorac Cardiovasc Surg 1995; 110: 75–80. 342 Hynynen M, Palojoki R, Heinonen J et al. Renal and vascular effects of atrial natriuretic factor during cardiopulmonary bypass. Chest 1991; 100: 1203–1209. 343 Feddersen K, Aurell M, Delin K et al. Effects of cardiopulmonary bypass and prostacyclin on plasma catecholamines, angiotensin II and arginine-vasopressin. Acta Anesthesiol Scand 1985; 29: 224 –230. 344 Hedner J, Towle A, Saltzman L et al. Changes in plasma atrial natriuretic peptideimmunoreactivity in patients undergoing coronary artery bypass graft placements. Regulatory Peptides 1987; 17: 151–157. 345 Diedericks BJS, Roelofse JA, Shipton EA et al. The renin–angiotensin–aldosterone system during and after cardiopulmonary bypass. S Afr Med J 1983; 64: 946–949. 346 Canivet JL, Larbuisson R, Damas P et al. Plasma renin activity and during α2-microglobulin during and after cardiopulmonary bypass: pulsatile vs nonpulsatile perfusion. Eur Heart J 1990; 11: 1079–1082. 347 Smallridge RC, Chernow B, Snyder R et al. Angiotensin-converting enzyme activity: a potential marker of tissue hypothyroidism in critical illness. Arch Intern Med 1985; 145: 1829–1832. 348 Weinstein GS, Zabetakis PM, Clavel A et al. The renin–angiotensin system is not responsible for hypertension following coronary artery bypass grafting. Ann Thorac Surg 1987; 43: 74–77. 349 Taylor KM, Morton IJ, Brown JJ et al. Hypertension and the renin–angiotensin system following open-heart surgery. J Thorac Cardiovasc Surg 1977; 74: 840–845. 350 Thrush DN, Austin D, Burdash N. Cardiopulmonary bypass temperature does not affect postoperative euthyroid sick syndrome? Chest 1995; 108: 1541–1545. 351 Bremner WF, Taylor KM, Baird S et al. Hypothalamo–pituitary–thyroid axis function during cardiopulmonary bypass. J Thorac Cardiovasc Surg 1978; 75: 392–399. 352 Schwartz HL, Schadlow AR, Faierman D et al. Heparin administration appears to decrease cellular binding of thyroxine. J Clin Endocrinol Metab 1973; 36: 598–600. 353 Holland FWII, Brown PS Jr, Weintraub BD et al. Cardiopulmonary bypass and thyroid function: a “euthyroid sick syndrome”. Ann Thorac Surg 1991; 52: 46–50. 354 Novitzky D, Human PA, Cooper DKC. Inotropic effect of triiodothyronine following myocardial ischemia and cardiopulmonary bypass: an experimental study in pigs. Ann Thorac Surg 1988; 45: 50–55. 355 Novitzky D, Human PA, Cooper DKC. Effects of triiodothyronine (T3) on myocardial high energy phosphates and lactate after ischemia and cardiopulmonary bypass: an experimental study in baboons. J Thorac Cardiovasc Surg 1988; 96: 600–607.

Complications of cardiopulmonary bypass and cardioplegia 343 356 Novitzky D, Cooper DKC, Barton CI et al. Triiodothyronine as an inotropic agent after open heart surgery. J Thorac Cardiovasc Surg 1989; 98: 972–978. 357 Klemperer JD, Klein I, Gomez M et al. Thyroid hormone treatment after coronary-artery bypass surgery. N Engl J Med 1995; 333: 1522–1527. 358 Das JB, Eraklis AJ, Adams JG Jr et al. Changes in serum ionic calcium during cardiopulmonary bypass with hemodilution. J Thorac Cardiovasc Surg 1971; 62: 449–453. 359 Yoshioka K, Tsuchioka H, Abe T et al. Changes in ionized and total calcium concentrations in serum and urine during open heart surgery. Biochem Med 1978; 20: 135–143. 360 Gray R, Braunstein G, Krutzik S et al. Calcium homeostasis during coronary bypass surgery. Circulation 1980; 62 (Suppl. I): I-57–I61. 361 Robertie PG, Butterworth JFIV, Prielipp RC et al. Parathyroid hormone responses to marked hypocalcemia in infants and young children undergoing repair of congenital heart disease. J Am Coll Cardiol 1992; 20: 672–677. 362 Robertie PG, Butterworth JFIV, Royster RL et al. Normal parathyroid hormone responses to hyocalcemia during cardiopulmonary bypass. Anesthesiology 1991; 75: 43–48. 363 Butterworth JFIV, Royster RL, Prielipp RC et al. Should calcium be administered prior to separation from cardiopulmonary bypass? Anesthesiology 1991; 75: 1121–1122. 364 Aglio LS, Stanford GG, Maddi R et al. Hypomagnesemia is common following cardiac surgery. J Cardiothorac Vasc Anesth 1991; 5: 201–208. 365 Harris MNE, Crowther A, Jupp RA et al. Magnesium and coronary revascularization. Br J Anesth 1988; 60: 779–783. 366 Abraham AS, Rosenmann D, Kramer M et al. Magnesium in the prevention of lethal arrhythmias in acute myocardial infarction. Arch Intern Med 1987; 147: 753–755. 367 Munday KA, Blane GF, Chin EF et al. Plasma electrolyte changes in hypothermia. Thorax 1958; 13: 334–342. 368 Manning SH, Angaran DM, Arom KV et al. Intermittent intravenous potassium therapy in cardiopulmonary bypass patients. Clin Pharmacol 1982; 1: 234–238. 369 Cohn LH, Angell WW, Shumway NE. Body fluid shifts after cardiopulmonary bypass. I. Effects of congestive heart failure and hemodilution. J Thorac Cardiovasc Surg 1971; 62: 423–430. 370 Oster JB, Sladen RN, Berkowitz DE. Cardiopulmonary bypass and the lung. In: Gravlee GP, Davis RF, Kurusz M, Utley JR, eds. Cardiopulmonary Bypass: Principles and Practice, 2nd edn. Philadelphia: Lippincott, Williams & Wilkins, 2000; 367–390. 371 Sladen R, Jenkins L. Intermittent mandatory ventilation and controlled mechanical ventilation without positive end-expiratory pressure following cardiopulmonary bypass. Can Anesth Soc J 1978; 25: 166–172. 372 Dobbinson T, Miller J. Respiratory and cardiovascular responses to PEEP in artificially ventilated patients after cardiopulmonary bypass surgery. Anesth Intens Care 1981; 9: 307–313. 373 Berry CB, Butler PJ, Myles PS. Lung management during cardiopulmonary bypass: is continuous positive airways pressure beneficial? Br J Anesth 1993; 71: 864–868. 374 Chenowith DE, Cooper SW, Hugli TE et al. Complement activation during cardiopulmonary bypass: evidence for generation of C3a and C5a anaphylotoxins. N Engl J Med 1981; 304: 497–502. 375 Morioka K, Muraoka R, Chiba Y et al. Leukocyte and platelet depletion with a blood cell separator: effects on lung injury after cardiac surgery with cardiopulmonary bypass. J Thorac Cardiovasc Surg 1996; 111: 45–54. 376 Werner HA, Wensley DF, Lirenman DS et al. Peritoneal dialysis in children after cardiopulmonary bypass. J Thorac Cardiovasc Surg 1997; 113: 64 –70.

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377 Fleming F, Bohn D, Edwards H et al. Renal replacement therapy after repair of congenital heart disease in children. J Thorac Cardiovasc Surg 1995; 109: 322–331. 378 Mangos GJ, Brown MA, Chan WYL et al. Acute renal failure following cardiac surgery: incidence, outcomes and risk factors. Aust NZ J Med 1995; 25: 284 –289. 379 McCullough PA, Wolyn R, Rocher LL et al. Acute renal failure after coronary intervention: incidence, risk factors and relationship to mortality. Am J Med 1997; 103: 368–375. 380 Mangano CM, Diamondstone LS, Ramsay JG et al. Renal dysfunction after myocardial revascularization: risk factors, adverse outcomes, and hospital resource utilization. The multicenter study of perioperative ischemia research group. Ann Intern Med 1998; 128: 194–203. 381 Zanardo G, Michielon P, Paccagnella A et al. Acute renal failure in the patient undergoing cardiac operation: prevalence, mortality rate, and main risk factors. J Thorac Cardiovasc Surg 1994; 107: 1489–1495. 382 Butterworth JF, Legault C, Royster RL et al. Factors that predict the use of positive inotropic drug support after cardiac valve surgery. Anesth Analg 1998; 86: 461– 467. 383 Cohen Y, Raz I, Merin G et al. Comparison of factors associated with 30-day mortality after coronary artery bypass grafting in patients with versus without diabetes mellitus. Am J Cardiol 1998; 81: 7–11. 384 Lema G, Meneses G, Urzua J et al. Effects of extracorporeal circulation on renal function in coronary surgical patients. Anesth Analg 1995; 81: 446–451. 385 Chertow GM, Lazarus JM, Christiansen CL et al. Preoperative renal risk stratification. Circulation 1997; 95: 878–884. 386 Picca S, Principato F, Mazzera E et al. Risks of acute renal failure after cardiopulmonary bypass surgery in children: a retrospective 10-year case–control study. Nephrol Dial Transplant 1995; 10: 630–636. 387 Crystal GJ, Salem MR. Myocardial and systemic hemodynamics during isovolemic hemodilution alone and combined with nitroprusside-induced controlled hypotension. Anesth Analg 1991; 72: 227–237. 388 Regragui IA, Izzat MB, Birdi I et al. Cardiopulmonary bypass perfusion temperature does not influence perioperative renal function. Ann Thorac Surg 1995; 60: 160–164. 389 Taylor KM, Bain WH, Maxted KJ et al. Comparative studies of pulsatile and nonpulsatile flow during cardiopulmonary bypass. I. Pulsatile system employed and its hematologic effects. J Thorac Cardiovasc Surg 1978; 75: 569–573. 390 Dapper F, Neppl H, Wozniak G et al. Effects of pulsatile and nonpulsatile perfusion mode during extracorporeal circulationaa comparative clinical study. Thorac Cardiovasc Surg 1992; 40: 345–351. 391 Gaer JAR, Shaw ADS, Wild R et al. Effect of cardiopulmonary bypass on gastrointestinal perfusion and function. Ann Thorac Surg 1994; 57: 371–375. 392 Taylor KM. Pulsatile cardiopulmonary bypass: a review. J Cardiovasc Surg 1981; 22: 561–568. 393 Hickey PR, Buckley MJ, Philbin DM. Pulsatile and nonpulsatile cardiopulmonary bypass: review of a counterproductive controversy. Ann Thorac Surg 1983; 36: 720–737. 394 Myles PS, Buckland MR, Schenk NJ et al. Effect of “renal-dose” dopamine on renal function following cardiac surgery. Anesth Intens Care 1993; 21: 56–61. 395 Perdue PW, Balser JR, Lipsett PA et al. “Renal dose” dopamine in surgical patients: dogma or science? Ann Surg 1998; 227: 470– 473. 396 Tumlin JA, Wang A, Murray PT et al. Fenoldopam mesylate blocks reductions in renal plasma flow after radiocontrast dye infusion: a pilot trial in the prevention of contrast nephropathy. Am Heart J 2002; 143: 894 –903.

Complications of cardiopulmonary bypass and cardioplegia 345 397 Kulka PJ, Tryba M, Zenz M. Preoperative α 2-adrenergic receptor agonists prevent the deterioration of renal function after cardiac surgery: results of a randomized, controlled trial. Crit Care Med 1996; 24: 947–952. 398 Bertolissi M, Antonucci F, De Monte A et al. Effects on renal function of a continuous infusion of nifedipine during cardiopulmonary bypass. J Cardiothorac Vasc Anesth 1996; 10: 238–242. 399 Amano J, Suzuki A, Sunamori M et al. Effect of calcium antagonist diltiazem on renal function in open heart surgery. Chest 1995; 107: 1260–1265. 400 Allgren RL, Marbury TC, Rahman SN et al. Anaritide in acute tubular necrosis. N Engl J Med 1997; 336: 828–834. 401 Rahman SN, Kim GE, Mathew AS et al. Effects of atrial natriuretic peptide in clinical acute renal failure. Kidney Int 1994; 45: 1731–1738. 402 Hogue CW Jr, Sundt TM III, Goldberg M et al. Neurological complications of cardiac surgery: the need for new paradigms in prevention and treatment. Semin Thorac Cardiovasc Surg 1999; 11: 105–115. 403 Puskas JD, Winston AD, Wright CE et al. Stroke after coronary artery operation: incidence, correlates, outcome and cost. Ann Thorac Surg 2000; 69: 1053–1056. 404 Salazar JD, Wityk RJ, Grega MA et al. Stroke after cardiac surgery: short- and long-term outcomes. Ann Thorac Surg 2001; 72: 1195–1202. 405 Ahlgren E, Arén C. Cerebral complications after coronary artery bypass and heart valve surgery. Risk factors and onset of symptoms. J Cardiothorac Vasc Anesth 1998; 12: 270–273. 406 Roach GW, Kanchuger M, Mangano CM et al. Adverse cerebral outcomes after coronary bypass surgery. N Engl J Med 1996; 335: 1857–1863. 407 Wolman RL, Nussmeier NA, Aggarwal A et al. Cerebral injury after cardiac surgery: identification of a group at extraordinary risk. The multicenter study of perioperative ischemia (McSPI) research group and the ischemia research and education foundation (IREF) investigators. Stroke 1999; 30: 514 –522. 408 van Dijk D, Keizer AMA, Diephuis JC et al. Neurocognitive dysfunction after coronary artery bypass surgery: a systematic review. J Thorac Cardiovasc Surg 2000; 120: 632–639. 409 Borger MA, Peniston CM, Weisel RD et al. Neuropsychologic impairment after coronary bypass surgery: effect of gaseous microemboli during perfusionist interventions. J Thorac Cardiovasc Surg 2001; 121: 743–749. 410 Barbut D, Lo Y-W, Gold JP et al. Impact of embolization during coronary artery bypass grafting on outcome and length of stay. Ann Thorac Surg 1997; 63: 998–1002. 411 McKhann GM, Goldsborough MA, Borowicz LM Jr et al. Cognitive outcome after coronary artery bypass: a one-year prospective study. Ann Thorac Surg 1997; 63: 510–515. 412 Vingerhoets G, Van Nooten G, Vermassen F et al. Short-term and long-term neuropsychological consequences of cardiac surgery with extracorporeal circulation. Eur J Cardiothorac Surg 1997; 11: 424 –431. 413 Mora CT, Henson MB, Weintraub WS et al. The effect of temperature management during cardiopulmonary bypass on neurologic and neuropsychologic outcomes in patients undergoing coronary revascularization. J Thorac Cardiovasc Surg 1996; 112: 514 –522. 414 Pugsley W, Klinger L, Paschalis C et al. The impact of microemboli during cardiopulmonary bypass on neuropsychological functioning. Stroke 1994; 25: 1393–1399. 415 Barbut D, Yao F-SF, Lo Y-W et al. Determination of size of aortic emboli and embolic load during coronary artery bypass grafting. Ann Thorac Surg 1997; 63: 1262–1267. 416 Stump DA, Rogers AT, Hammon JW et al. Cerebral emboli and cognitive outcome after cardiac surgery. J Cardiothorac Vasc Anesth 1996; 10: 113–119.

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417 Savageau JA, Stanton B-A, Jenkins CD et al. Neuropsychological dysfunction following elective cardiac operation. I. Early assessment. J Thorac Cardiovasc Surg 1982; 84: 585–594. 418 Kolkka R, Hilberman M. Neurologic dysfunction following cardiac operation with lowflow, low-pressure cardiopulmonary bypass. J Thorac Cardiovasc Surg 1980; 79: 432–437. 419 Murkin JM. Attenuation of neurologic injury during cardiac surgery. Ann Thorac Surg 2001; 72: S1838–S1844. 420 Martin TD, Craver JM, Gott JP et al. The Warm Heart Investigators. Randomized trial of normothermic versus hypothermic coronary bypass. Prospective, randomized trial of retrograde warm blood cardioplegia: myocardial benefit and neurologic threat. Ann Thorac Surg 1994; 57: 298–304. 421 Martin TD, Craver JM, Gott JP et al. Prospective, randomized trial of retrograde warm blood cardioplegia: myocardial benefit and neurologic threat. Ann Thorac Surg 1994; 57: 298–304. 422 Plourde G, Leduc AS, Morin JE et al. Temperature during cardiopulmonary bypass for coronary artery operations does not influence postoperative cognitive function: a prospective, randomized trial. J Thorac Cardiovasc Surg 1997; 114: 123–128. 423 Dietrich WD, Alonso O, Busto R. Moderate hyperglycemia worsens acute blood–brain barrier injury after forebrain ischemia in rats. Stroke 1993; 24: 111–116. 424 Metz S, Keats AS. Benefits of a glucose-containing priming solution for cardiopulmonary bypass. Anesth Analg 1991; 72: 428–434. 425 Murkin JM, Martzke JS, Buchan AM et al. A randomized study of the influence of perfusion technique and pH management strategy in 316 patients undergoing coronary artery bypass surgery. II. Neurologic and cognitive outcomes. J Thorac Cardiovasc Surg 1995; 110: 349–362. 426 Patel RL, Turtle MR, Chambers DJ et al. Alpha-stat acid-base regulation during cardiopulmonary bypass improves neuropsychologic outcome in patients undergoing coronary artery bypass grafting. J Thorac Cardiovasc Surg 1996; 111: 1267–1279. 427 Stephan H, Weyland A, Kazmaier S et al. Acid-base management during hypothermic cardiopulmonary bypass does not affect cerebral metabolism but does affect blood flow and neurological outcome. Br J Anesth 1992; 69: 51–7. 428 Bashien G, Townes BD, Nessly ML et al. A randomized study of carbon dioxide management during hypothermic cardiopulmonary bypass. Anesthesiology 1990; 72: 7–15. 429 Clauss RH, Hass WK, Ransohoff J. Simplified method for monitoring adequacy of brain oxygenation during carotid artery surgery. N Engl J Med 1965; 273: 1127–1131. 430 Brown R, Wright G, Royston D. A comparison of two systems for assessing cerebral venous oxyhaemoglobin saturation during cardiopulmonary bypass in humans. Anesthesia 1993; 48: 697–700. 431 Spencer MP, Thomas GI, Moehring MA. Relation between middle cerebral artery blood flow velocity and stump pressure during carotid endarterectomy. Stroke 1992; 23: 1439–1445. 432 Edmunds HL Jr, Griffiths LK, van der Laken J et al. Quantitative electroencephalographic monitoring during myocardial revascularization predicts postoperative disorientation and improves outcome. J Thorac Cardiovasc Surg 1992; 103: 555–563. 433 Silverman NA. Myocardial oxygen consumption after reversible ischemia. J Cardiac Surg 1994; 9 (Suppl.): 465–468. 434 Krukenkamp IB, Silverman NA, Sorlie D et al. Characterization of postischemic myocardial oxygen utilization. Circulation 1986; 74 (Suppl. III): III-125–III-129. 435 Etievent J-P, Chocron S, Toubin G et al. Use of cardiac troponin I as a marker of perioperative myocardial ischemia. Ann Thorac Surg 1995; 59: 1192–1194.

Complications of cardiopulmonary bypass and cardioplegia 347 436 Melrose DG, Dreyer B, Bentall HH et al. Elective cardiac arrest. Lancet 1955; 2: 21–22. 437 Weisel RD, Lipton IH, Lyall RN et al. Cardiac metabolism and performance following cold potassium cardioplegia. Circulation 1978; 58 (Suppl. I): I-217–I-226. 438 Gay WA. Potassium-induced cardioplegia. Ann Thorac Surg 1975; 20: 95–100. 439 Cohen G, Borger MA, Weisel RD et al. Intraoperative myocardial protection: current trends and future perspectives. Ann Thorac Surg 1999; 68: 1995–2001. 440 Feindel CM, Tait GA, Wilson GJ et al. Multidose blood versus crystalloid cardioplegia. J Thorac Cardiovasc Surg 1984; 87: 585–595. 441 Fremes SE, Christakis GT, Weisel RD et al. A clinical trial of blood and crystalloid cardioplegia. J Thorac Cardiovasc Surg 1984; 88: 726–741. 442 Christakis GT, Fremes SE, Weisel RD et al. Reducing the risk of urgent revascularization for unstable angina: a randomized clinical trial. J Vasc Surg 1986; 3: 764 –772. 443 Allen BS, Buckberg GD, Rosenkranz ER et al. Topical cardiac hypothermia in patients with coronary disease: an unnecessary adjunct to cardioplegic protection and cause of pulmonary morbidity. J Thorac Cardiovasc Surg 1992; 104: 626– 631. 444 Efthimiou J, Butler J, Woodham C et al. Diaphragm paralysis following cardiac surgery: role of phrenic nerve cold injury. Ann Thorac Surg 1991; 52: 1005–1008. 445 Tripp HF, Bolton JWR. Phrenic nerve injury following cardiac surgery: a review. J Card Surg 1998; 13: 218–223. 446 Buckberg GD, Brazier JR, Nelson RL et al. Studies of the effects of hypothermia on regional myocardial flow and metabolism during cardiopulmonary bypass. I. The adequately perfused beating, fibrillating, and arrested heart. J Thorac Cardiovasc Surg 1977; 73: 87–94. 447 Menasché P, Kural S, Fauchet M et al. Retrograde coronary sinus perfusion: a safe alternative for ensuring cardioplegic delivery in aortic valve surgery. Ann Thorac Surg 1982; 34: 647–658. 448 Gott VL, Gonzalez JL, Zuhdi MN et al. Retrograde perfusion of the coronary sinus for direct vision aortic surgery. Surg Gynecol Obstet 1957; 104: 319–328. 449 Salerno TA, Houck JP, Barrozo CAM et al. Retrograde continuous warm blood cardioplegia: a new concept in myocardial protection. Ann Thorac Surg 1991; 51: 245–247. 450 Partington MT, Acar C, Buckberg GD et al. Studies of retrograde cardioplegia. I. Capillary blood flow distribution to myocardium supplied by open and occluded arteries. J Thorac Cardiovasc Surg 1989; 97: 605–612. 451 Menasché P, Subayi J-B, Veyssié L et al. Efficacy of coronary sinus cardioplegia in patients with complete coronary artery occlusions. Ann Thorac Surg 1991; 51: 418–423. 452 Crooke GA, Harris LJ, Grossi EA et al. Biventricular distribution of cold blood cardioplegic solution administered by different retrograde techniques. J Thorac Cardiovasc Surg 1991; 102: 631–638. 453 Stirling MC, McClanahan TB, Schott RJ et al. Distribution of cardioplegic solution infused antegradely and retrogradely in normal canine hearts. J Thorac Cardiovasc Surg 1989; 98: 1066–1076. 454 Panos AL, Ali IS, Birnbaum PL et al. Coronary sinus injuries during retrograde continuous, normothermic blood cardioplegia. Ann Thorac Surg 1992; 54: 1137–1138. 455 He G-W. Rare complication of retrograde cardioplegia: inner wall perforation of the right atrium. Ann Thorac Surg 1997; 63: 539–541. 456 Griepp RB, Stinson EB, Hollingsworth JF et al. Prosthetic replacement of the aortic arch. J Thorac Cardiovasc Surg 1975; 70: 1051–1063. 457 Svennson LG, Crawford ES, Hess KR et al. Deep hypothermia with circulatory arrest: determinants of stroke and early mortality in 656 patients. J Thorac Cardiovasc Surg 1993; 106: 19–31.

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458 Kimura T, Muraoka R, Chiba Y et al. Effect of intermittent deep hypothermic circulatory arrest on brain metabolism. J Thorac Cardiovasc Surg 1994; 108: 658–663. 459 Newburger JW, Jonas RA, Wernovsky G et al. A comparison of the perioperative neurologic effects of hypothermic circulatory arrest versus low-flow cardiopulmonary bypass in infant heart surgery. N Engl J Med 1993; 329: 1057–1064. 460 Mills NL, Ochsner JL. Massive air embolism during cardiopulmonary bypass. J Thorac Cardiovasc Surg 1980; 80: 708–717. 461 Lytle BW, McCarthy PM, Meaney KM et al. Systemic hypothermia and circulatory arrest combined with arterial perfusion of the superior vena cava: effective intraoperative cerebral protection. J Thorac Cardiovasc Surg 1995; 109: 738–743. 462 Safi HJ, Brien HW, Winter JN et al. Brain protection via cerebral retrograde perfusion during aortic arch aneurysm repair. Ann Thorac Surg 1993; 56: 270–276. 463 Deeb GM, Jenkins E, Bolling SF et al. Retrograde cerebral perfusion during hypothermic circulatory arrest reduces neurologic morbidity. J Thorac Cardiovasc Surg 1995; 109: 259–268. 464 Yamashita C, Nakamura H, Nishikawa Y et al. Retrograde cerebral perfusion with circulatory arrest in aortic arch aneurysms. Ann Thorac Surg 1992; 54: 566–568. 465 Miyamoto K, Kawashima Y, Matsuda H et al. Optimal perfusion flow rate for the brain during deep hypothermic cardiopulmonary bypass at 20°C. J Thorac Cardiovasc Surg 1986; 92: 1065–1070. 466 Reich DL, Uysal S, Ergin A et al. Retrograde cerebral perfusion as a method of neuroprotection during thoracic aortic surgery. Ann Thorac Surg 2001; 72: 1774 –1782. 467 Usui A, Oohara K, Liu T-L et al. Determination of optimum retrograde cerebral perfusion conditions. J Thorac Cardiovasc Surg 1994; 107: 300–308.

CHAPTER 17

Complications of aortic surgery Thoralf M Sundt III, Whitney M Burrows

Background Cardiovascular surgeons may be called on to treat aneurysmal disease involving the ascending aorta and aortic root, the aortic arch, or the descending thoracic and thoracoabdominal aorta. Surgery may be indicated for the management of degenerative disease, dissection, or the prevention of complications of connective tissue disorders. Although these procedures represent a relatively small proportion of the practice of most surgeons, they may be indicated emergently, behooving all surgeons to become familiar with their conduct. Operations on the aorta are often complex, and patients requiring them often have significant comorbidities. Complications are therefore not uncommon. Despite a wide spectrum of underlying conditions and pathological anatomical characteristics, most aortic surgical procedures present common challenges. These operations generally involve interrupting or redirecting the circulation to some or all of the organ beds for a period, with end-organ ischemia being an obvious concern. The procedures may be lengthy, most often requiring extracorporeal support, which predisposes patients to hemorrhagic complications. Furthermore, many patients who have a surgical procedure for complex aortic problems have underlying pulmonary disease or renal dysfunction. Therefore, we have organized our comments by organ system rather than by type of procedure, with a focus on the recognition, treatment, and, most importantly, prevention of the common complications. Although we subscribe to the concept of evidence-based practice, complex aortic procedures remain relatively uncommon and sufficiently heterogeneous so that few centers perform enough aortic procedures to permit rigorous analysis of risk factors and prevention. Therefore, many of our recommendations are based on anecdotal experience.

Vascular complications Patients undergoing aortic procedures often have a systemic vasculopathy, so that the site of cannulation for perfusion assistance is an abnormal vessel, as are the vessels at the limits of any repair. Vascular complications are the most immediate and prominent technical challenges in aortic surgery. 349

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Vascular access Most aortic reconstructions in the adult require temporary circulatory support as either full cardiopulmonary bypass or partial left heart bypass. Traditionally, arterial inflow has usually been achieved through femoral arterial cannulation; however, these vessels are often diseased with either local atherosclerosis or dissection. Therefore, attention must be paid to the potential for significant local vessel trauma with the disruption of atherosclerotic debris that may embolize proximally during perfusion or move anterograde through the limb after decannulation. Local thrombosis may also occur as a consequence of endothelial damage or elevation of local plaque. Malperfusion due to cannulation of the false lumen in dissections that have propagated beyond the common femoral artery, or as a result of an iatrogenic retrograde dissection, may also occur. In addition, pathological features of the abdominal aorta pose potential problems whenever retrograde perfusion is instituted with dislodgement of thrombotic or atheroembolic material that may be propelled cephalad to the kidneys or brain. Early recognition of the local complications of thrombosis or iatrogenic stenosis of the femoral artery permits the most expeditious management, which is in the operating room at the termination of the procedure. A satisfactory femoral pulse should always be verified manually or by Doppler analysis. Similarly, pedal pulses, which must be accurately documented preoperatively, must be identified. Reexploration of the arteriotomy can then be readily performed with local endarterectomy or patch arterioplasty as indicated. When there is significant concern that plaque has been disrupted, we approach local endarterectomy and reconstruction aggressively, with a small patch of synthetic material. Evidence of distal embolization should also be investigated before the drapes are removed entirely. Intact popliteal pulses with loss of a pedal pulse or mottling of the distal lower extremity may be addressed by passing an embolectomy catheter distally from the femoral arteriotomy. Occasionally, popliteal exploration is requiredain either case, prompt recognition of the problem minimizes limb ischemia and the risk of tissue loss. As disheartening as such problems may be in the operating theater after a long procedure, the news comes much harder several hours later, after the patient is in the intensive care unit, with the prospect of remobilizing the operating room staff. Malperfusion syndromes may be more difficult to recognize. Unfortunately, their consequences, which are obvious, may be more grave. One must consider the possibility of malperfusion whenever peripheral perfusion is initiated. It may be evidenced by a decrease in urine output when the renal vessels are involved or by acidosis when the viscera are ischemic. These are non-specific signs, and they may not become apparent until later during the procedure. Some surgeons advocate the use of bilateral radial artery lines, particularly with acute dissection, when the risk of malperfusion is probably the greatest. The onset of a significant gradient between radial artery pressures may then be taken as evidence of malperfusion. If this occurs at the initiation of perfusion,

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its discontinuance and an attempt at alternative cannulation are indicated. If malperfusion becomes evident when an aortic cross clamp is placed for acute dissection, removal of the cross clamp and cooling to hypothermic circulatory arrest are indicated. Perhaps most vexing is retrograde embolization of local debris from the cannulation site or from thoracoabdominal disease. The consequences are usually appreciated only postoperatively when stroke or visceral infarction becomes apparent. Preoperatively and intraoperatively, the surgeon must be attentive to the potential for retrograde embolization and should consider all possible perfusion strategies. The risk of retrograde embolization may be minimized by a preference for central cannulation, an approach that has gained popularity recently and with which we agree. Ascending aortic aneurysms are rarely lined with thrombus as are abdominal aneurysms. Preoperative computed tomography (CT) can help to exclude thrombus. Furthermore, although atherosclerotic disease may be present, most often it consists of medial calcification. Intraoperative transesophageal echocardiography or intraoperative aortic surface echocardiography can help to rule out shaggy intraluminal disease that is more likely to embolize. When forced to cannulate in the groin, either because of central disease or when using left heart bypass, we have preferred the time-honored approach of sewing a ‘chimney’ of 8–10 mm of Dacron (DuPont, Wilmington, DE, USA) to the common femoral artery before heparinization [1]. A 22-Fr or 24-Fr arterial cannula easily fits into such a chimney, essentially eliminating all concerns of the perfusionist about arterial line pressure. It also permits a careful, atraumatic entry into the arterial system, minimizing the risk of retrograde dissection or elevating a proximal plaque with the tip of our inflow cannula. Local vessel trauma is also minimized, and perfusion of the extremity throughout the procedure is permitted. At the termination of bypass, the chimney can be oversewn, leaving a small Dacron patch arterioplasty. Often the chimney can be sewn to the femoral artery simultaneously with intubation and placement of the pulmonary artery catheter. When the patient must be repositioned (e.g., for thoracoabdominal aneurysm repair), the chimney graft may be tucked inside the groin wound and the skin closed with staples to be reopened after the patient is rolled into a right lateral decubitus position. An alternative site of arterial cannulation is the subclavian artery [2]. This approach avoids retrograde perfusion of a diseased thoracoabdominal aorta and facilitates early antegrade reperfusion of the brachiocephalic vessels during arch reconstruction. It is accomplished most easily with a chimney graft and is gaining popularity rapidly. Femoral venous cannulation for partial femorofemoral bypass or full cardiopulmonary bypass may be complicated by disruption of the vessel proximally during placement of the cannula. This complication is most often recognized by acute and sometimes nearly catastrophic volume loss. When this occurs, rapid extension of the femoral incision and retroperitoneal

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exploration can be lifesaving. To avoid this complication we prefer to use an over-the-wire system, of which several are available. The most common late complication of femoral venous access is deep vein thrombosis. To minimize local trauma, we have abandoned circumferential dissection and control of the vessel in favor of exposure of the ventral surface only and placement of a narrow, longitudinally orientated purse-string suture on the top of the vessel. The vein can then be accessed and the purse-string suture secured, disrupting only a limited portion of the vessel and permitting venous return from the distal extremity around the cannula. This avoids plethora of the limb. On decannulation, the purse-string suture can be secured without narrowing the vessel.

Anastomotic complications Anastomotic complications may occur early or late after major aortic reconstruction. Early problems include dislodgement of atheroembolic disease and tissue failure with anastomotic disruption and hemorrhage. Late postoperative pseudoaneurysms are most likely an underdiagnosed complication. The site of distal anastomosis is often diseased, particularly in arch and thoracoabdominal aneurysms. If the material is calcific, local endarterectomy may be necessary to make distal anastomosis possible. The prophylactic value of local endarterectomy on distal embolization is unclear, however, because there is usually no discrete border to the lesion and a shaggy ledge often remains. More frequently, the material is soft, like silt on the bottom of a slow-moving stream. Therefore, we usually try to minimize disruption of the material rather than attempt to remove it. Occasionally, we have created a ‘sandwich’ of Teflon felt (DuPont), first basting two strips of the material at the site of anastomosis with 4–0 suture in a continuous horizontal mattress pattern and then sewing the graft to the sandwich itself. Late pseudoaneurysms may be diagnosed when their sequelae of rupture or mass effect occur. Preferably, they should be identified by routine noninvasive imaging studies, such as CT or magnetic resonance imaging. Although there are no evidence-based guidelines for the appropriate frequency of postoperative imaging studies, it is clear from articles about abdominal aortic grafts that the frequency of diagnosis of postoperative pseudoaneurysms is much greater in series including routine surveillance studies [3]. Therefore, our view is that long-term surveillance, perhaps on an annual or biannual basis, should be undertaken of all patients who have undergone major aortic reconstructions. This practice also provides surveillance for the formation of subsequent aneurysms in other locations, because multiple aneurysms may occur. The risk of late pseudoaneurysm formation may be minimized by meticulous surgical technique. Kouchoukos et al. [4] have demonstrated that, for composite aortic root replacement, fewer late pseudoaneurysms result from an ‘open’ technique that consists of creation of separate coronary artery buttons for reimplantation, complete transection of the distal aorta to ensure

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full-thickness sutures, and avoidance of wrapping the remaining aneurysmal aorta around the repair. This approach permits repair of any imperfections in the anastomoses during the initial operative procedure and prevents inadvertent covering of potential problems. Of course, this technique is only possible because low-porosity grafts and excellent suture material are available. Another potential contributor to late pseudoaneurysm formation is infection. Placement of a graft in an infected field is uncommon, but it must be recognized. Therefore, when the suspected cause of an aneurysm is mycotic, either grossly or on CT, or when a patient with a known aneurysm exhibits bacteremia, the use of antibiotic impregnated grafts and lifelong antibiotic therapy should be considered. The value of aortic homografts in this setting is not yet widely accepted [5]. Finally, the surgeon should recognize the existence of collagen vascular disease, such as the Marfan syndrome, that may predispose to late aneurysm formation. It is now well recognized, for example, that complete root replacement rather than separate valve and graft repair is necessary to address adequately pathological lesions of the aortic root or dissection in Marfan syndrome, because sinus tissue left behind will dilatate with time. Therefore, one is well advised to consider the existence of connective tissue disease when operating for aneurysmal disease, particularly in young patients, because this finding may influence a surgeon’s intraoperative decisions.

Myocardial complications Complications related to myocardial ischemia and infarction are among the most common causes of death after aortic surgery. The cornerstone of dealing with these complications is prevention, and the most important step is adequate preoperative evaluation. Our practice is to perform coronary arteriography on all patients who are undergoing work on the ascending aorta or aortic arch for which the surgical approach will be a median sternotomy and for which cardioplegic arrest will be required. Occasionally concerns are raised about the risk of embolization of material from the aneurysm by the angiography catheter; however, from a practical standpoint this is quite rare and the information gathered is of sufficient value to warrant the risk. The notable exception to this policy is acute aortic dissection. Although some surgeons have defended the value of preoperative angiography in this setting, the majority now think that the yield of useful information obtained from angiography is not worth the required time and the accompanying risk imposed by the delay in surgery. We do, however, prepare the legs of all patients who have aortic dissection and manually perform intraoperative inspection of the coronary arteries. We are liberal with the placement of saphenous vein grafts to vessels with palpable disease and for patients with preoperative evidence of myocardial ischemia or significant involvement of the coronary ostia by the dissection flap.

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For operations on the thoracic or thoracoabdominal aorta, we prefer cardiac catheterization whenever circulatory arrest is planned. In our experience, the use of thallium or dobutamine echocardiographic non-invasive studies may result in underestimating the extent of disease in a substantial number of cases, and we are concerned about the stress imposed on the myocardium during ventricular fibrillation as the patient cools. We prefer coronary angiography in instances of circulatory arrest because we think the magnitude of myocardial insult is greater in these situations. We have seen the extent of disease dramaticallyaand fatallyaunderestimated by the reliance on non-invasive studies. When left heart partial bypass is planned, we are more willing to accept the results of non-invasive imaging. The principles of intraoperative management to minimize ischemia are familiar to cardiothoracic surgeons. The debate over cardioplegia composition and routes of its delivery need not be repeated here. However, with the use of ventricular fibrillation, either when an ascending aorta cannot be clamped or when the thoracic or thoracoabdominal aorta is approached through the left side of the chest, the mean perfusion pressure must be maintained > 75 mmHg to maintain adequate myocardial perfusion. In order to prevent left ventricular distension, we are liberal with placement of a left ventricular vent through the cardiac apex when we operate in the left side of the chest. Ventricular fibrillation is contraindicated for patients with severe left ventricular hypertrophy or with significant aortic regurgitation. The existence of these conditions should be evaluated by preoperative echocardiography.

Pulmonary complications Respiratory failure is a common complication of aortic surgery, probably because of the high incidence of concomitant emphysema in these patients. Tobacco use is rampant among those with degenerative aneurysmal disease and may lead to destructive airway disease and aneurysmal disease by the common pathophysiological mechanism. Recognition of respiratory failure is not difficult, and its management is supportive, but its impact on survival is profound (Figure 17.1) [6]. Prevention of pulmonary complications begins with the patient. Tobacco use should be discontinued before aneurysm repair, but that is often impractical. Intraoperatively the surgeon should minimize lung manipulation through a collaborative approach with the anesthesiologists. During deflation of the left lung, the right lung must not be hyperinflated. Full cardiopulmonary bypass averts problems with intraoperative oxygenation but probably exacerbates postoperative lung dysfunction. When operating on patients who have extensive pulmonary disease preoperatively, we use heparin-bonded circuits in the hope that we will minimize cytokine activation. In addition, we use aprotinin as a pulmonary protective agent. However, we avoid performing full bypass whenever possible in patients with the worst lung disease, and we have occasionally used an oxygenator spliced into the left heart circuit to

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Figure 17.1 Kaplan–Meier survival curves for patients with and without respiratory failure. The effect of pulmonary failure on survival after repair of thoracoabdominal aortic aneurysm is highly significant and supports efforts to minimize the risk of this common complication. (From Svensson et al. [6]. By permission of The Society for Vascular Surgery and North American chapter, International Society for Cardiovascular Surgery.)

permit partial bypass. When repairing thoracoabdominal aneurysms, we avoid complete division of the diaphragm so as to maintain its function postoperatively [7].

Renal complications Renal dysfunction ranks second in frequency, behind respiratory failure, as a complication of thoracoabdominal aneurysm repair. Renal dysfunction is less common after repair of proximal aortic disease, even when circulatory arrest is required. In our experience, only a mild elevation in serum creatinine occurs after proximal aortic repair, provided that the circulatory arrest time is < 1 h and the temperature is ≤ 18 °C. Significant renal dysfunction is uncommon when the thoracic aortic aneurysmal disease is confined to the chest and left heart bypass is used. Again, preexisting renal dysfunction is probably important, and it is aggravated by intraoperative ischemia. Like the effect of pulmonary failure, the effect of renal failure on survival is profound (Figure 17.2) [8]. To prevent renal dysfunction, we aggressively replace fluids and administer furosemide intraoperatively. Postoperatively we adequately hydrate patients

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Figure 17.2 Kaplan–Meier curve of cumulative survival for patients with (Yes) and without (No) renal failure. Renal failure after repair of thoracoabdominal aortic aneurysm has a profound effect on survival, probably acting as a marker for perioperative difficulties and predisposing the patient to subsequent complications. (From Svensson et al. [8]. By permission of Elsevier.)

and maintain urine output at > 100 ml/h. For thoracoabdominal aneurysm repair with left heart bypass, we have adopted a routine of visceral perfusion with blood through a sidearm of the pump and an ‘octopus’ with cannulas in each of the vessels when the visceral segment of the aorta is open [9]. This practice reduces the incidence of renal dysfunction significantly in our patients and permits a careful, unhurried repair.

Neurological complications Neurological complications of aortic surgery can profoundly affect the patient’s quality of life. They are certainly the most common bases for litigation, and their effect on survival is significant (Figure 17.3) [8]. Cerebral ischemia may be due to inadequate flow during the bypass run or to atheroembolic phenomena. Either is a significant risk with surgery on the ascending aorta or aortic arch or when circulatory arrest is used to repair the thoracoabdominal aorta. Preoperative carotid evaluation may be useful, although its effect on perioperative stroke has not been clearly proven. Central or subclavian cannulation minimizes the risk of dislodged debris in the thoracic aorta being propelled cephalad, as previously noted. When circulatory arrest is used, adequate cerebral cooling is critical. Patience during this phase of the operation is rewarding. We cool for at least 30 min, maintaining a gradient

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Figure 17.3 Kaplan–Meier curve of cumulative survival for patients with (Yes) and without (No) paraplegia or paraparesis. Patients who experience paraplegia after repair of thoracoabdominal aortic aneurysm have significantly worse early and late survival rates. (From Svensson et al. [8]. By permission of Elsevier.)

of no more than 10 °C between arterial inflow and core temperature to ensure uniform cooling. Some authors find the intraoperative use of electroencephalography helpful [10–12], and we have recently adopted this protocol as well. When using circulatory arrest, we work to minimize the cerebral ischemic time. Retrograde cerebral perfusion has been advocated by many, and it may be helpful in aortic arch surgery, particularly for flushing air and debris from the head vessels. We do not think that it should be relied on, however, to extend the ‘safe’ period of circulatory arrest. We have been unable to demonstrate any objective improvement in outcomes when retrograde perfusion was used in our series at Washington University (St Louis, MO, USA), and we currently use it selectively for cases in which aortic arch surgery is planned or in which we anticipate a prolonged episode of arrest for technical reasons. With careful control of central venous pressure at < 20 mmHg, we have seen few adverse consequences (such as cerebral edema). Cerebral ischemic time can be limited best by early antegrade perfusion, which may be accomplished by immediate cannulation of the brachiocephalic vessels. For this purpose, we use retrograde cardioplegia cannulas with manually inflating balloons. In this case, retrograde cerebral perfusion can be initiated after placement to remove air from the system before initiating antegrade perfusion. This may be particularly useful during aortic arch reconstructions. If the head vessels can be reimplanted as a single patch, early antegrade perfusion can be provided by anastomosing to the head vessels a 20-mm graft

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Figure 17.4 Multiple logistic regression analysis of the risk of paraplegia or paraparesis by the extent of the aortic repair according to clamp time. The risk of paraplegia after repair of thoracoabdominal aortic aneurysm is clearly related to the extent of resection. (Crawford extent: I, proximal descending to upper abdominal aorta; II, entire descending thoracic and abdominal aorta to below the renal arteries; III, distal descending thoracic and abdominal aorta; IV, entire abdominal aorta, including the visceral segment.) (From Svensson et al. [8]. By permission of Elsevier.)

with a 10-mm sidearm for arterial inflow before performing the anastomosis to the distal thoracic aorta, as described by Griepp and colleagues [13], without the risk of disrupting debris from the brachiocephalic vessels during direct cannulation [14]. In most instances, this anastomosis can be completed in < 30 min. Although spinal cord ischemia has been the subject of many book chapters and articles, paraplegia remains a vexing problem in thoracoabdominal aneurysm repair. Clearly, the risk of paraplegia relates to the extent of the aneurysm (Figure 17.4), a point that should be remembered when interpreting study results. Proposed solutions have relied on decreasing the metabolic demands of the spinal cord by cooling during reconstructionawhen it is presumably most vulnerable to injuryaand on maintaining distal perfusion to augment collateral flow during repair. Most protocols involve a combination of both strategies. Although pharmacological interventions to diminish injury have been proposed and studied in the laboratory, they have not been implemented clinically.

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Routine use of femorofemoral bypass to achieve profound hypothermia for circulatory arrest during repair has been advocated by Kouchoukos and Rokkas [15] and has gained a loyal following. Good results with low rates of paraplegia have been reported with this technique. Other authors, however, have expressed concern that the physiological insult imposed by this strategy is too great, essentially trading death for paraplegia. An alternative means of cooling the spinal cord, proposed by Cambria and Davison [16], entails cold epidural perfusion to accomplish topical cooling. This process is typically performed without distal perfusion. Distal perfusion during thoracic aortic occlusion may be accomplished by various means, including partial femorofemoral bypass, which demands complete heparinization, and left-atrial-to-femoral partial bypass, which can be accomplished with minimal anticoagulation. Additional measures to improve spinal cord perfusion during the vulnerable period include drainage of cerebrospinal fluid and vigorous support of blood pressure to maintain mean pressures > 75–80 mmHg above and below the clamp. The value of reimplantation of intercostal vessels is questioned by some authors, but the trend is certainly in favor of this approach [17]. Some authors use intraoperative motor evoked potentials as well to help guide this process. We think that a thoughtful, integrated approach to the prevention of spinal cord ischemia is appropriate. We prefer to use partial left heart bypass whenever possible with strict adherence to segmental occlusion techniques. This practice permits an unhurried operation. Drainage of cerebrospinal fluid is routine [18]. We take advantage of the benefits of mild hypothermia and permit the systemic temperature to decrease to 34 °C during aortic reconstruction. The temperature is returned to normal with an in-line heat exchanger before discontinuing bypass. We routinely reimplant sizable intercostal vessels between T8 and the visceral segment and have recently begun using motor evoked potentials. We are compulsive about maintaining adequate blood pressure postoperatively, and we emphasize to the house staff and nursing staff that hypotension is far more dangerous than hypertension in these patients. When left heart bypass is not possible because atherosclerotic disease at the left subclavian artery prevents placement of a cross clamp, we use circulatory arrest. In this instance, we do not use a spinal drain because we are concerned about a subdural hematoma developing and compressing the cord. We reserve circulatory arrest for special instances because we are concerned about the pulmonary insult and hematological abnormalities imposed by this approach.

Hematological complications Although less often fatal, hematological derangements are common with aortic surgeryamuch to the consternation of surgeons and anesthesiologists. Coagulopathy is often a problem after extensive aortic procedures involving

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circulatory arrest. A lengthy pump run and hypothermia lead to platelet dysfunction, and extensive suture lines as well as large surface areas of Dacron consume platelets and clotting factors. This is particularly true for the elephant trunk procedure, possibly because of sequestration of clotting factors outside the distal trunk. Prompt and aggressive replacement of clotting factors is usually satisfactory, but it is critical that all clotting factors arrive in the operating room simultaneously. When using left heart bypass, ongoing follow-up of the replacement of clotting factors during the period of partial bypass is critical. A strategy of waiting to give clotting factors until after partial bypass is completed can be disastrous. Therapy with adjunctive medication such as aprotinin or other antifibrinolytics may be helpful. Our early experience with aprotinin raised concerns about its safety during circulatory arrest, and we prefer to administer the drug only after the arrest episode is complete [19]. Also, adequate concentrations of heparin must be maintained. Although there is much enthusiasm for using various glues and sealants, we find meticulous attention to surgical technique, care in handling tissues, and smooth passage of suture needles to be of far greater importance.

Conclusion Complications after major aortic surgery are common, in part because the patients undergoing the procedures have underlying multisystem disease. The procedures themselves are often complex, with unique challenges. A coordinated team approach with meticulous attention to detail is critical to achieving the best possible results. With such an approach, excellent results can be achieved even when replacing extensive portions of the aorta. Therefore, it is likely that optimal results will be achieved by concentrating the experience among surgical teams with a special interest in this area.

References 1 Vander Salm TJ. Prevention of lower extremity ischemia during cardiopulmonary bypass via femoral cannulation. Ann Thorac Surg 1997; 63: 251–252. 2 Gillinov AM, Sabik JF, Lytle BW et al. Axillary artery cannulation. J Thorac Cardiovasc Surg 1999; 118: 1153. 3 Edwards JM, Teefey SA, Zierler RE et al. Intraabdominal paraanastomotic aneurysms after aortic bypass grafting. J Vasc Surg 1992; 15: 344 –350. 4 Kouchoukos NT, Wareing TH, Murphy SF et al. Sixteen-year experience with aortic root replacement. Results of 172 operations. Ann Surg 1991; 214: 308–318. 5 Vogt P, Pasic M, von Segesser L et al. Cryopreserved aortic homograft for mycotic aneurysm. J Thorac Cardiovasc Surg 1995; 109: 589–591. 6 Svensson LG, Hess KR, Coselli JS et al. A prospective study of respiratory failure after high-risk surgery on the thoracoabdominal aorta. J Vasc Surg 1991; 14: 271–282. 7 Engle J, Safi HJ, Miller CC III et al. The impact of diaphragm management on prolonged ventilator support after thoracoabdominal aortic repair. J Vasc Surg 1999; 29: 150–156.

Complications of aortic surgery 361 8 Svensson LG, Crawford ES, Hess KR et al. Experience with 1509 patients undergoing thoracoabdominal aortic operations. J Vasc Surg 1993; 17: 357–368. 9 Safi HJ, Miller CC III, Yawn DH et al. Impact of distal aortic and visceral perfusion on liver function during thoracoabdominal and descending thoracic aortic repair. J Vasc Surg 1998; 27: 145–152. 10 Stecker MM, Cheung AT, Pochettino A et al. Deep hypothermic circulatory arrest. I. Effects of cooling on electroencephalogram and evoked potentials. Ann Thorac Surg 2001; 71: 14–21. 11 Coselli JS, Crawford ES, Beall AC Jr et al. Determination of brain temperatures for safe circulatory arrest during cardiovascular operation. Ann Thorac Surg 1988; 45: 638–642. 12 Sebel PS. Central nervous system monitoring during open heart surgery: an update. J Cardiothorac Vasc Anesth 1998; 12 (Suppl. 1): 3–8. 13 Galla JD, McCullough JN, Griepp RB. Aortic arch replacement for dissection. Oper Tech Thorac Cardiovasc Surg 1999; 4: 58–76. 14 Hagl C, Ergin MA, Galla JD et al. Neurologic outcome after ascending aorta-aortic arch operations: effect of brain protection technique in high-risk patients. J Thorac Cardiovasc Surg 2001; 121: 1107–1121. 15 Kouchoukos NT, Rokkas CK. Hypothermic cardiopulmonary bypass for spinal cord protection: rationale and clinical results. Ann Thorac Surg 1999; 67: 1940–1942. 16 Cambria RP, Davison JK. Regional hypothermia with epidural cooling for spinal cord protection during thoracoabdominal aneurysm repair. Semin Vasc Surg 2000; 13: 315–324. 17 Safi HJ, Miller CC III, Carr C et al. Importance of intercostal artery reattachment during thoracoabdominal aortic aneurysm repair. J Vasc Surg 1998; 27: 58–66. 18 Coselli JS, LeMaire SA, Schmittling ZC et al. Cerebrospinal fluid drainage in thoracoabdominal aortic surgery. Semin Vasc Surg 2000; 13: 308–314. 19 Sundt TM III, Kouchoukos NT, Saffitz JE et al. Renal dysfunction and intravascular coagulation with aprotinin and hypothermic circulatory arrest. Ann Thorac Surg 1993; 55: 1418–1424.

CHAPTER 18

Complications of valvular surgery Jeffrey T Sugimoto, Anthony D Bruno, Karen A Gersch

Aortic valve surgery Anatomy The aortic valve is a tri-leaflet structure which separates the left ventricular outflow tract and the aorta or Sinuses of Valsalva. There are three leaflets or cusps, the left, the right and non-coronary, which are attached in a semicircular path to the base of the aorta at the fibrous annulus. For each leaflet the annular attachment does not lie in a single plane, being half moon in shape with the nadir at the mid-point of the leaflets and the peak at the commissural posts. There is a slight dilatation of the aorta above the valve associated with each of the leaflets, the Sinuses of Valsalva. This dilatation creates a vortex of blood flow important in valve closure. The sinuses end at the sino–tubular junction which is the narrowest portion of the ascending aorta. Below and in continuity with the left and non-coronary cusps is the anterior leaflet of the mitral valve. The ventricular septum lies below the right coronary cusp and within it a portion of the conduction system, most importantly the left bundle, and bundle of His. The left main coronary artery arises from the left Sinus of Valsalva. Its ostium lies directly posterior near the level of the sino–tubular junction. The left main coronary artery runs to the left under the pulmonary artery before dividing into the left anterior descending and circumflex arteries. Anatomic variants have been described and it is important to identify and avoid injury to the ostium as well as the artery as it courses behind the aorta near the annulus. The left main coronary artery can run perilously close to the commissure between the left and right coronary cusps. The right coronary ostium is an anterior structure located above the right coronary cusp. Its position tends to be more variable and is often displaced with aneurysmal changes in the aorta. Awareness of these anatomic relationships is critical to the safe conduct of aortic valve surgery (see Figure 18.1).

Incisions and cardiopulmonary bypass Recently ‘less invasive’ incisions or approaches to the aortic valve have been described; transverse sternotomy, partial sternotomy, right para-sternotomy, manubrial inverted ‘T’, reversed Z sternotomy, ‘J/j’ incision and upper right anterior thoracotomy have all been utilized successfully [1–4]. Each can be useful and generally do provide adequate exposure of the valve. However, if 362

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Figure 18.1 Surgeons view aortic valve. LMCA, Left main coronary artery; RCA, right coronary artery; LC annulus, left coronary annulus; ALMV, anterior leaflet mitral valve; NC annulus, non-coronary annulus; RC annulus, right coronary annulus. Demonstrates the attachment of the mitral valve at the aortic valve annulus and the proximity of the conduction system.

one is to utilize these approaches one must understand the potential benefits and risks and be prepared to deal with the specific limitations which may be imposed. To date, median sternotomy remains the most common incision for aortic valve surgery. With an aging population and often the need for a combined coronary revascularization procedure or partial aortic root replacement, this is often a compelling reason to consider the median sternotomy for most patients. This incision has been well tolerated for years and has few complications. It is necessary to place the patients on cardiopulmonary bypass to replace the aortic valve. Each institution has developed protocols and techniques that work well to achieve this. It is beyond the scope of this chapter to discuss the technique of cardiopulmonary bypass or its complications. However, it is important to emphasize the critical importance of myocardial protection particularly in the thick, hypertrophied ventricle. Our preference has been both systemic cooling, 28–30 °C, with a combination of cold anterograde and retrograde blood cardioplegia. Occasionally this is supplemented with direct coronary ostial administration of cardioplegia primarily for the right coronary artery. Topical cooling is performed with slush applied directly to the anterior surface of the right ventricle. A left ventricular vent placed through the right superior pulmonary vein is employed which aids in visualization and is important in the removal of air. Various protocols have been devised for removal of air prior to removal of the aortic cross clamp. We rely heavily on the use of the left ventricular vent and the ascending aortic cardioplegia needle for this.

Aortotomy To approach the aortic valve either a transverse or oblique incision can be utilized (see Figure 18.2). This is placed at least 1 cm above the right coronary

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Figure 18.2 Surgeons viewaaortotomy. Oblique incision in aorta carried down through the sino–tubular junction in the non-coronary sinus of valsalva.

ostium to avoid compromise on closure which can result in right ventricular or inferior infarction. With an aging population calcifications of the aortic root involving the Sinuses of Valsalva, sino–tubular junction and ascending aorta are common. Attempts to avoid these areas when feasible are recommended. Otherwise limited endarterectomy and debridement, or aortic reconstruction may be necessary to allow for successful closure. If the ascending aorta is heavily calcified, consideration of femoral artery cannulation, deep hypothermia and circulatory arrest without aortic cross clamping must be made to avoid embolization, stroke, as well as to allow for the successful completion of the operation. Epi-aortic and transesophageal echo may be a useful adjuncts [5]. In most cases it will be possible to place the aortic cannula, the aortic cross clamp and aortotomy in the ascending aorta, avoiding calcified areas. Post-stenotic dilatation or pure aneurysmal disease will cause thinning and enlargement of the aorta with the potential catastrophic complication of aortic dissection. Great care in controlling blood pressure and flow while on cardiopulmonary bypass, with particular attention to detail with the blood pressure at cannulation, cross clamp placement and removal as well as when weaning the patient from cardiopulmonary bypass, is critical to avoid this complication. Aggressive anesthetic management and communication with the anesthesiologist are particularly important to avoid wide fluctuations in blood pressure. The transverse aortotomy is made above the sino–tubular junction, avoiding the right coronary ostium with the oblique incision directed towards the mid portion of the non-coronary leaflet through the sino–tubular junction. Rarely is the aorta completely transected except with the implant of some stentless valves. A longitudinal T-shape aortotomy can also be used [6]. Uncontrolled tearing of the aortotomy must be avoided. More room for insertion of the prosthesis is achieved by utilizing the oblique incision which opens the narrow sino–tubular junction. Closure of the aorta often depends on the strength and thickness of the aorta. A secure closure in select cases can be achieved with a single running mono-filament suture line (4–0 Prolene RB-1®).

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In a thin or diseased aorta, a two-layer closure is recommended with an initial horizontal mattress everting suture line followed by a single running over an over suture line. This suture line can also be performed buttressing the initial horizontal mattress suture with strips of Teflon felt or strips of a Hemashield® Dacron graft or pericardium. At the completion of the closure there is rarely bleeding, though, with the force of left ventricular contraction as the patient is weaned from cardiopulmonary bypass, bleeding may occur. It is best to control all bleeding while on cardiopulmonary bypass, controlling flow and blood pressure. Early removal of cannulas should be avoided. Resumption of 364a brief period of cardiopulmonary bypass is preferable to tearing of the suture line which may then require major revision. Strict control of the blood pressure and anesthetic management is critical at this phase. With the availability of Bioglue®, it is often best to consider aortic repair of the friabledebrided areas prior to suturing. One can apply the Bioglue® protecting adequately the prosthesis prior to suturing of the aortotomy.

Aortic valve removal Removal of the aortic valve for insufficiency is usually straight forward. It is best to leave a thin rim of valve tissue and not to excise the annulus completely. Any excess valve tissue can be trimmed leaving a solid annulus. In calcific disease it is often possible to achieve the same result, though invariably the annulus, subannular region, mitral valve can be involved with calcifications. Careful debridement is required to avoid detaching the aorta from the left ventricle below. A pituitary rongeur can be used to crush the calcium into smaller particles and then remove the calcium, leaving the aorta, aortic annulus as well as left ventricle intact. Crushing horizontally along the axis of the annulus is safer than vertically. Tears in the aorta, annulus and mitral valve can occur with over-aggressive force trying to remove the calcium. If tears occur, repair is achieved with pledgeted horizontal mattress sutures brought from below. These can be later used to secure the valve. Extensive calcification below the right coronary annulus may require debridement with the potential hazard of heart block. Calcium often extends into the anterior leaflet of the mitral valve from the non-coronary annulus. Superficial debridement to allow for placement of sutures and valve seating can be performed without perforating the valve. One should avoid debriding calcium from the walls of the Sinuses of Valsalva unless it is protruding significantly or will not allow for proper seating of the prosthesis. If the calcifications of the annulus extend directly into and up the wall of the sinuses, very limited debridement may be applied avoiding the coronary ostia. This should avoid the need for extensive reconstruction or root replacement. Rarely should this be necessary even when extensive calcification is identified, and should be avoided when possible. All debris must be accounted for, with the potential for losing calcium into the left ventricle and coronary ostia, particularly the left. Sponges, tampons, and balloons have been utilized to prevent the loss of calcium into the left ventricular cavity [7]. Small pieces of gauze (nu-gauze®) or cotton-tip applicators

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can be utilized to obstruct the coronary ostium temporarily. Vigorous irrigation of the left ventricular cavity, the outflow tract, the annulus and aorta up to the aortic cross clamp should be performed prior to valve implant and after completion of debridement. Cold saline should be utilized which has the added benefit of myocardial preservation. We perform vigorous irrigation after debridement, after the sutures are placed and after seating of the valve.

Valve replacement For stented bio-prosthetic and mechanical valves we place the sutures from below the annulus, exiting slightly above it into the aorta (supra-annular). Pledgeted 2–0 Dacron (Ticron®) sutures are utilized with little to no space between the sequential horizontal mattress sutures. One must avoid taking too wide a bite which can cause bunching of the tissue and a resultant paravalvular leak. For a size 21 mm bioprosthesis this generally requires 12–13 sutures. Since the native annulus is not in a single plane, it is often more difficult to place a mechanical valve than a bioprosthetic. At the commissures it sometimes works well to resect more annular tissue and utilize a single suture which crosses the commissure as opposed to beginning and ending a suture at the commissure. One can then lower the plane of the ‘annular’ suture line in this manner (see Figure 18.3). This also avoids the problem of overlapping pledgets at the commissures, which is an inherent problem if placing the pledgets from below the annulus. Alternatively, at the commissures one can place simple horizontal mattress sutures without pledgets to avoid the problem of overlapping pledgets in this region. Though rarely a problem, the left main coronary artery should be avoided when suturing. It runs for a short distance along the posterior aspect of the aorta and comes very near the commissure between the left and right coronary cusps as it rises to be at the level of the left main coronary ostium. Deep sutures may damage the artery in this region requiring revascularization. Deep sutures in the muscle below the right coronary leaflet or at the nadir of the right coronary leaflet may damage the conduction system. If heart block occurs, a

Figure 18.3 Aortic valve replacement. Lowering the plane of the annulus at the commissures by crossing the annulus with a single horizontal mattress suture, can use pledgeted or non-pledgeted sutures.

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permanent transvenous pacemaker can be placed postoperatively. Removal and replacement of the sutures should not be attempted. Damage to the right coronary artery or ostium can also lead to stenosis or acute right ventricular failure intraoperatively [8]. After removal of the aortic valve below the noncoronary and left coronary leaflet, the anterior leaflet of the mitral valve is obvious. Small defects can be repaired with monofilament suture. Though discussions about what to do with the small aortic root will follow, it is often helpful in a small annulus to place the sutures along the non-coronary annulus from outside the aorta and bring it directly through or above the non-coronary annulus, leaving the pledgets outside the aorta. This often avoids the need for placing the valve obliquely above either the non-coronary annulus or the aortic root enlargement. If the aorta in the region appears thin, these sutures should exit the aorta directly through the annulus. The pledgets lay on the outside of the aorta. Seating the valve at the lowest point of each annular leaflet is critical. In general, it is best to tie one suture at the point lowest in each cusp before tying all others. This ensures proper seating of the valve and confidence that the valve will fit before having to remove multiple sutures for an oversized prosthesis or before deciding that an aortic root enlargement procedure may be necessary. The coronary ostia must always be identified and reconfirmed while seating the valve. At times this does require the use of a small dental mirror to re-identify the right coronary ostium. When tying the sutures one should avoid contact of the suture with the leaflets, particularly for a bioprosthetic valve. Though it is often difficult to tie the sutures along the axis of the valve ring, it is generally best to avoid tying the sutures across the valve in a perpendicular manner. The bioprosthetic valve should be moistened regularly to prevent drying. Once the valve is seated and tied into position, one should carefully inspect the suture line using a small suction tip (Frazier) for possible paravalvular leaks. Additionally, one can take a final look for any potential debris which might have been dislodged from the Sinuses of Valsalva in tying down the valve. Mechanical prostheses should be tested for unrestricted leaflet motion. It is generally good practice to irrigate the left ventricular outflow tract, suture line and aorta at this point prior to aortic closure.

The small aortic root, aortic valve replacement Critical to the success of operations for aortic stenosis is the placement of a prosthesis that does not leave the patient with significant residual aortic stenosis (patient–prosthetic mismatch). In general, for the stented bioprosthesis, this would mean the use of at least a size 21 mm valve and for a mechanical valve a size 19 mm. It is also important to consider the fragility and size of the patient when making the decision for aortic root enlargement. Each of the various prosthetic devices utilizes a different set of sizers and it is not recommended to interchange them. The sizer should fit comfortably into the annulus, particularly when the aortic root is stiff, thickened or calcified. Once the appropriate sized valve is chosen, it is generally good practice to check to

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Figure 18.4 Aortic valve replacement. ‘Tilting’ the aortic valve prosthesis by placing sutures slightly above the annulus in the non-coronary cusp. This often eliminates the need to enlarge the annulus.

be sure that the prosthesis will fit into the orifice before placing the sutures into the sewing ring. If there is concern about placement of the valve, one simple option that does not prolong the operation is to ‘tilt’ the valve placing the suture line in the noncoronary cusp above the true annulus in the wall of the aorta (see Figure 18.4). This will often increase the size of the prosthesis by one and avoid the need to enlarge the aortic root. This can be done with any of the stented bioprostheses. However, care must be taken when considering this for a mechanical valve, given the potential for leaflet impingement by the non-coronary annular tissue below. If a single-leaflet mechanical prosthesis is utilized, the major orifice should be directed towards the patient’s right side to allow for unrestricted maximal opening. If aortic root enlargement is still desired, multiple procedures have been described. The simplest is extension of the aortotomy to the mid point of the non-coronary annulus [9]. One does not necessarily need to transect the annulus. An elliptical piece of Dacron graft (Hemashield®) is then sutured which allows for aortic root enlargement just above the aortic annulus in the non-coronary cusp. One does not necessarily need to enter the roof of the left atrium or cut into the mitral valve to perform this procedure. The prosthesis can then be sutured in a tilted position again a few millimeters above the true annulus incorporating the patch as part of the valve suture line (see Figure 18.5). We perform this procedure with a small patch of a Hemashield® Dacron graft and utilize a running 4.0 Prolene® suture. The graft is sutured in place to a point a few millimeters above where we believe the valve will be sutured to the patch. After placement of the valve we complete this suture line. This suture line below the prosthesis must be placed carefully and securely. It is virtually inaccessible once the prosthesis is placed. Troublesome bleeding generally cannot be controlled with simple sutures. We have found this procedure to

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Figure 18.5 (a) Aortic root enlargement with incision carried down to and through the annulus in the non-coronary sinus. One does not necessarily need to extend this through the annulus on to the mitral valve. (b) Reconstruction with elliptical piece of Dacron graft.

be particularly useful in the elderly patient with the small annulus and calcification at the sino–tubular junction which can be resected and replaced with a slightly larger patch. Though the adult cardiac surgeon should be familiar with the more complex outflow tract reconstruction procedures, aorto-ventriculo-septolplasty (Konno–Rastan) [10], which require a right ventricular patch and a left ventricular outflow tract subannular patch, these procedures are generally reserved for children in whom one is attempting to place an adult-size prosthesis. Attempting to place a prosthesis that is too large creates multiple problems, including tearing of the aorta, distortion of the prosthesis with a flexible annulus or struts, impingement of the coronary arteries and the need to perform a complex reconstruction or ultimately replace the valve with a smaller than ideal prosthesis. Generally safe and effective aortic valve replacement can be achieved with good patient selection, proper preoperative evaluation and an efficient, safe operation which provides relief of either aortic obstruction or aortic insufficiency. Even in the elderly, it is sometimes best to perform a slightly more complex operation to avoid one of the more disastrous complications which can occur or which might ultimately require placement of a less than ideal prosthesis.

Mitral valve surgery Anatomy The mitral valve is a bi-leaflet structure separating the left atrium from the left ventricle, allowing for the unidirectional flow of blood into the left ventricle. The base of the leaflets is attached at the annulus, a fibrous connection in continuity with a number of important structures, with the free edge and undersurface of the leaflets giving rise to primary and secondary chordae

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Figure 18.6 Mitral valve anatomy. LCCA, Left circumflex coronary artery; ALMV, anterior leaflet mitral valve; PLMV, posterior leaflet mitral valve. Demonstrates the proximity of structures to the mitral valve annulus.

tendinae. These attach to the papillary muscles and the ventricular wall. The major papillary muscles give rise to chordae that support both the anterior and posterior leaflets. Given the proximity of the annulus to nearby structures, it is important to be knowledgeable about this. The annulus is an ovoid structure with the anterior or aortic leaflet attachment making up approximately onethird of the circumference. This leaflet at the annulus is in continuity with the annulus of the non-coronary and left coronary cusps of the aortic valve. The posterior leaflet annulus makes up the remaining two-thirds of the circumference of the valve. The two leaflets meet at the anterolateral and the postero-medial commissures. The circumflex coronary artery runs in the atrioventricular groove as it branches from the left main coronary artery near the anterolateral commissure and terminates after coursing along the posterior annulus for approximately two-thirds of its length. Similarly, the coronary sinus runs in the atrio-ventricular groove from the base of the atrial appendage to the region of the postero-medial commissure. In this region the atrioventricular (AV) nodal artery courses to the AV-node (see Figure 18.6).

Incisions and cardiopulmonary bypass Median sternotomy remains the most frequently utilized incision to approach the mitral valve. For years an anterolateral right thoracotomy has been utilized for an improved cosmetic result and recently a variety of ‘less invasive’ incisions have been introduced to theoretically reduce pain, blood loss, recovery time and improve cosmetic results. Our preference when utilizing a ‘less invasive’ approach has been the right parasternal incision through the 4th and 5th costo-chondral cartilages. Robotics have entered into the field of cardiac surgery and appear in certain hands to be a useful adjunct in limiting incisions [11]. Whatever the preference of the surgeon, the limitations of each incision

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must be carefully weighed in preparation for anticipated surgery. Often multivalve corrective procedures and concomitant coronary artery disease preclude the use of incisions other than a median sternotomy. Exposure of the mitral valve dictates the type of venous cannulation for cardiopulmonary bypass. With a large left atrium, venous cannulation through the right atrial appendage with a two-stage single venous cannula and direct incision at the interatrial groove into the left atrium achieved (vertical left atriotomy). This incision runs in front of the right pulmonary veins and can be extended safely under the inferior vena cava (IVC). It can also be extended under the superior vena cava (SVC), though it is more difficult to close this region safely. Incising the lateral pericardial attachments of the superior and inferior vena cavae, being careful to avoid the right phrenic nerve as it courses in a postero-lateral relation to the superior and inferior vena cavae, is generally performed to assist in elevation of the heart. Careful dissection to avoid thinning of the cavae is critical to avoid tears caused by retraction. Occasionally exposure remains inadequate without vigorous retraction. Uncontrolled tearing of the atria or cavae should be avoided. One can place a right angle cannula in the SVC with a caval tourniquet, replace the two-stage single venous cannula with an IVC cannula and caval tourniquet and then transect the SVC about 1 cm above the SVC and right atrial junction. When placing the SVC tourniquet one should dissect in the plane between the anterior surface of the right pulmonary artery and SVC to avoid damage to the azygous vein. This gives excellent exposure to the mitral valve. Alternatively, the valve can be approached through the dome of the left atrium utilizing a two-stage single venous cannula, though this does require more mobilization of the aorta as one enters the left atrium between the aorta and SVC and right atrium (superior approach). Calcification of the ascending aorta is a contraindication to this approach given the need for retraction of the aorta and aortic valve, and there is some increased risk of damage to the sinus node artery with atrial dysrhythmias. Bi-caval cannulation with caval tourniquets is employed for patients with normal or small atria. Cannulation of the SVC is direct to give more room within the right atrium to work with cannulation of the IVC low in the right atrium. Exposure of the valve is through the right atrium, the fossa ovalis and the atrial septum (trans-septal approach). The incision in the septum is vertical and extended to the lower edge of the fossa, avoiding the coronary sinus and superiorly into the septum. The roof of the left atrium under the aorta can be avoided. Most repairs and replacements can be performed without extending the incision outside of the confines of the septum (see Figure 18.7). Use of two small retractors works well to avoid tearing of the septal incision. Closure of the septum and right atrium as separate incisions with a running monofilament suture is straightforward. Cardioplegia can be administered directly into the coronary sinus. A vent is generally placed through the right superior pulmonary vein down into the left atrium. The right atrial closure can be achieved while rewarming after cross clamp removal and after removal of

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Figure 18.7 Trans-septal approach to mitral valve. Exposure of the atrial septum and fossa ovalis through the right atrium. Most valve repairs and replacements can be achieved without extending the incision beyond the confines of the septum. Dotted line denotes septal incision. TV, Tricuspid valve.

all left-sided air. If exposure through the septum is inadequate, this approach can be converted to the superior septal or extended vertical trans-septal approach extending the septal incision to meet the right atrial incision and into the roof of the left atrium [12,13]. Closure of this incision is more complex and often the sinus node artery is transected as the incision courses around the right atrial appendage, then onto the roof of the left atrium. Excellent exposure of the valve is created. A transverse trans-septal approach through the right atrium, septum and pulmonary veins has been described which also gives excellent exposure [14]. Care must be taken to limit the medial extent of the septal incision to the edge of the fossa ovalis, or the incision can tear into the mitral valve annulus. Administration of retrograde cardioplegia during maneuvers to remove air from the left side of the heart aids in the evacuation of air as well as being useful in filling the left ventricle and left atrium with no inflow coming from the right heart. Trans-esophageal echo is useful in air detection, but meticulous maneuvers to remove air from the left side of the heart are the mainstay for avoiding air embolus.

Mitral valve operations Operations of the mitral valve include open commissurotomy, mitral valve replacement and mitral valve repair or reconstruction. Each has its own inherent complications.

Mitral valve commissurotomy With the patient on cardiopulmonary bypass, the left atrium is opened and direct visualization of the mitral valve obtained. The stenotic orifice identified

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as well as the fused commissures. The fusion point is incised with a #15 scalpel protecting the underlying chordae and papillary muscles which may be fused and foreshortened below with a right angle clamp. One must avoid extending the commissurotomy through the annulus and serial testing of the valve must be performed to avoid creating severe insufficiency. To gain increased mobility of the valve leaflets one often has to split chordae which are fused. This at times also involves splitting partially the papillary muscle. If significant mitral insufficiency is created, early valve replacement should be considered, though if the leaflets are pliable, a mitral valve reparative procedure may be possible. Generally, if extensive debridement of calcium from the leaflets and annulus is required to achieve a commissurotomy, the patient is best served by replacement of the valve with chordal preservation.

Mitral valve replacement Removal of the mitral valve for replacement begins with downward traction on the mid portion of the anterior leaflet with either a stay suture or an Allis clamp. The valve is incised 2–3 mm from the true annulus. Utilizing the remaining leaflet as traction, the anterior annulus is exposed well and valve sutures can be placed serially as one removes the remainder of the leaflet. If the entire leaflet is removed prior to placement of valve sutures it is sometimes difficult to visualize well the anterior annulus without undue upward traction. Our practice has been to place the sutures from the ventricular side up through the annulus utilizing pledgeted horizontal mattress sutures of 2–0 Dacron (Ticron®) suture. These sutures are placed a few millimeters apart. Once the commissures are reached, a decision can be made whether or not to attempt chordal preservation. In most cases, the posterior leaflet tissue can be left in place, except in valves that are heavily calcified or severely scarred and foreshortened. One must remove or reposition most of the anterior leaflet tissue prior to suturing in the valve, otherwise it is likely that systolic anterior motion (SAM) of the anterior leaflet and left ventricular outflow tract obstruction can develop, particularly with the use of a bioprosthetic valve. Anterior chordal preservation must be performed precisely to avoid interference with proper valve function. This is particularly important when utilizing a mono-leaflet mechanical prosthesis. Care must be taken to avoid bunching of tissue at the annulus which may protrude below the annulus of the prosthetic valve. If one elects not to preserve the anterior chordae, they should be transected flush with the papillary muscle tip to avoid interference with proper valve function. Over-zealous traction on the valve leaflets still attached to papillary muscles can tear the posterior ventricular wall, creating a muscular defect which is often difficult to close but must be recognized immediately. This requires deep ventricular sutures of pledgeted 2–0 Dacron avoiding the nearby coronary arteries, particularly the posterior descending artery for a postero-medial papillary muscle tear. To achieve adequate valve seating it is often necessary to remove annular calcium. In general this calcification involves the posterior leaflet more heavily

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Figure 18.8 Mitral valve replacement. Atrio-ventricular discontinuity caused by removal of calcium from the posterior annulus of the mitral valve. This can be repaired with pledgeted sutures brought up through ventricular muscle, annular and left atrial tissue. Sutures can be used to anchor the prosthesis or annuloplasty ring.

than the anterior leaflet, and sometimes spreads into the posterior ventricular wall. Great care must be taken to avoid losing debris as one removes the calcifications into either the left atrium, pulmonary veins, or left ventricle. Again vigorous irrigation and immediately accounting for any debris are the mainstay of avoiding calcific emboli. Over-aggressive debridement of the annulus and calcifications may result in a significant defect separating the left ventricle from the left atrium (atrio-ventricular discontinuity), ventricular rupture or atrial dissection. Resultant atrio-ventricular groove hematoma, pseudoaneurysm and posterior rupture have been described [15–18]. This is repaired with pledgeted sutures brought from below beginning in the ventricular muscle up through the atrial wall at the level of the annulus. The sutures ultimately can be utilized to anchor the valve (see Figure 18.8). Preservation of both the valvular and subvalvular apparatus reduces the risk of ventricular rupture [19]. Both the circumflex coronary artery and coronary sinus are at some risk if a large defect has been created. Great care most be taken to avoid damaging these structures during reconstruction, which may require revascularization of the circumflex system. At times it is more prudent to leave calcium in place, utilizing large needles to go around the calcific deposits, or one can place the valve inside the calcified annulus taking smaller bites of primarily valvular tissue and using a smaller prosthesis. To circumvent the problem of an uneven surface on which the valve must sit, a strip of Teflon felt can be fashioned and sandwiched between the prosthetic valve ring and annular tissue. This allows one to seat the valve on a very irregular surface without the need for extensive debridement. When placing sutures in or around the annulus the anatomic structures in close proximity must always be kept in mind (see Anatomy). Creating aortic insufficiency because of anterior annular sutures placed too deeply or myocardial infarction secondary to circumflex artery damage should not occur. With bioprostheses, the valve should be orientated to avoid positioning a strut directly posterior. Leaving posterior leaflet tissue in place has reduced

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the rare complication of posterior ventricular rupture secondary to strut protrusion. It is still recommended to orientate the valve with one of the struts at the 4 : 00 position and the second at the 8 : 00 with the third strut directly anterior at the 12 : 00 position. This also avoids the complication of strut obstruction anteriorly of the left ventricular outflow tract. Bi-leaflet mechanical valves are orientated with the hinges at the 12 : 00 and 6 : 00 positions. Mono-leaflet valves are orientated with the major orifice opening anteriorly. Most mechanical valves can now be rotated within the sewing ring and unrestricted leaflet motion tested in virtually any position. Chordal preservation must be precise to avoid interference with mechanical valve function. Excess tissue sutured at the annulus may prevent proper leaflet excursion. Hemorrhage or hematoma in the atrio-ventricular groove on the posterior aspect of the heart represents posterior ventricular rupture and must be dealt with immediately by removal of the prosthesis, repair of the defect with sutures buttressed with Teflon, and then re-replacement of the valve. The incidence of ventricular rupture with mitral valve replacement is 0.5%. Izzat [20] described three influences together which are necessary to produce a ventricular rupture: a predisposition by an underlying weakened myocardium, i.e. inferior infarction, factors that may initiate this primary tear which include debridement of calcium, and dynamic forces which include immediate perioperative hypertension and left ventricular strain. Clearly all of these increase the risk of this complication, which in various series has carried a 75% mortality rate. Most survivors of this complication were recognized in the operating room at the time of the initial valve replacement. Prior to tying down the bioprosthetic valve but after seating of the valve, one should inspect the valve struts to be sure that none of the sutures has become entangled on the struts. If the struts cannot be well visualized, often a small dental mirror will expedite the process. A suture entangled in a strut will result in both central valve insufficiency and a paravalvular leak. If a vent is utilized and after tying the valve, the vent is moved from its position in the left atrium across the valve prosthesis. For a bi-leaflet mechanical prosthesis, it should be placed across the central orifice. For a mono-leaflet mechanical valve it should be placed across the minor orifice to avoid the complication of closure of the valve on the vent and forces that will not allow the vent to be removed. Internal closure of the left atrial appendage is recommended with either a purse-string suture or a double running over and over suture, being careful not to take a deep bite which could compromise the circumflex coronary artery. As the left atrium is being closed, meticulous maneuvers to remove air from the left side of the heart must be performed prior to aortic cross clamp removal. Simultaneously aspirating from the left ventricular vent and the ascending aorta, one should be able to evacuate all of the air. Once the cross clamp is removed, one should avoid over-distension of the left ventricle by controlling the vent volume until the heart begins to beat. For combined aortic and mitral valve surgery one should always repair or replace the mitral valve first to avoid retraction and damage to the aorta or

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the aortic valve prosthesis caused by retraction to expose the mitral valve. Similarly, if coronary bypasses are to be performed, particularly those to the circumflex system, these should be performed prior to either mitral valve repair or replacement or aortic valve replacement. One should avoid lifting the heart once the prosthesis is in place, which can cause posterior ventricular rupture.

Mitral valve reparative procedure Valve repair or valvuloplasty for mitral insufficiency vs. valve replacement under appropriate circumstances is the operation of choice, with a decrease in both long-term thromboembolic complications and mortality when properly reconstructed [21]. The experience of the surgeon dictates valve replacement vs. valve repair because of the potential for leaving significant mitral insufficiency or creating mitral stenosis when not performed adequately. Though reconstructive procedures can be done through any of the previously described approaches, adequate visualization is critical for successful reconstruction. It is also best to visualize the valve without excessive retraction, which may distort the valve. Preoperative and intraoperative assessment of the pathology with trans-esophageal echocardiography is often helpful in dictating the type of repair, and necessary after completion to assess for residual mitral insufficiency, mitral stenosis or systolic anterior motion of the mitral valve with left ventricular outflow tract obstruction, all of which conditions require correction prior to leaving the operating room. Numerous techniques have been described to reduce the length of the posterior annulus, which is almost always increased relative to the anterior leaflet when mitral insufficiency is encountered. Figure-of-eight sutures placed evenly on each side of the posterior annulus just below the commissures often suffice to eliminate mitral regurgitation. A ‘Kay-Reed’ measured annuloplasty plicating the posterior leaflets at the commissures has been used for years and is a simple, safe and effective technique when posterior annular dilatation is the pathology [22,23]. Though acutely quite effective since the entire posterior annulus is not supported by the repair, there is the potential for progressive posterior annular dilatation and recurrence of mitral insufficiency over time. Additionally, because of the height of the posterior leaflet tissue, there is the potential for causing systolic anterior motion of the anterior leaflet of the mitral valve and left ventricular outflow tract obstruction. If the height of the posterior leaflet with any of the reconstructive procedures is > 1 cm, one must consider plication of the posterior leaflet to prevent this complication. One of the commonest indications for mitral valve repair is mitral insufficiency secondary to a myxomatous valve plus or minus ruptured chordae to the posterior leaflet. The anatomy can be well delineated with echocardiography preoperatively, and although patients with severe mitral insufficiency may initially tolerate it well, their long-term prognosis is poor and a mitral valve reconstructive procedure is generally indicated [24].

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Figure 18.9 Mitral valve repair. Posterior leaflet quadrangular resection and sliding advancement annuloplasty allows for removal of significant portions of the posterior leaflet and reapproximation without tension. (a) Dotted line indicates resected area of posterior leaflet. (b) Final reconstructed appearance.

Reconstructive procedures address the flail segments of the valve, the redundant posterior leaflet tissue and the posterior annular dilatation. Quadrangular resection of the flail segment with primary repair of the posterior leaflet and a supporting annuloplasty ring, either flexible or rigid, often suffices. If primary repair of the posterior leaflet can be performed without tension, a sliding annuloplasty is generally not required. Utilizing monofilament suture, one must attempt to place the knots on the ventricular side of the leaflet tissue. There is otherwise the potential for perforation of the anterior leaflet as the leaflets coapt. 4–0 or 5–0 GoreTex® suture is a reasonable alternative and avoids this complication. The annuloplasty sutures are placed in or through the fibrous annulus and not into valvular tissue or left atrial tissue. The sutures at the commissures are placed deeply into the fibrous trigones. One must avoid placing sutures into the much weaker atrial tissue with the potential for tearing when tying. The annuloplasty ring size is based on the size of the anterior leaflet or the length of the anterior leaflet annulus as measured between the fibrous trigones. Avoiding distortion of the anterior annulus by choosing a ring size which is either too small or too large is critical. To reduce the posterior annular size, one travels in the posterior annular tissue further than in the annuloplasty ring. Placing the central posterior annular stitch into the annuloplasty ring first often facilitates correct spacing. Once the ring is lowered and tied, one should test for residual mitral insufficiency by filling the ventricle with saline or blood. Two problems may occur with quadrangular resection and primary repair of the posterior leaflet. Tension on the posterior leaflet tissue will cause the sutures to tear through, or the height of the posterior leaflet and redundant posterior leaflet tissue will cause systolic anterior motion of the mitral valve with left ventricular outflow tract obstruction. Both of these problems can be avoided by performing a simple sliding advancement annuloplasty (see Figure 18.9). This serves to both reduce the height of the posterior leaflet and eliminate tension on the primary repair. One can excise the redundant tissue or imbricate it. Occasionally, anterior leaflet chordae require shortening or

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even replacement. Excellent visualization is a prerequisite. Fine sutures placed through the chordae at about 1/2 of the distance required for shortening are placed. The papillary muscle is carefully split and the chordae imbricated. Small pledgets avoid cutting of suture into muscular tissue. Too deep a bite in the papillary muscle and tying the suture too tightly may cause necrosis of the muscle with resultant tip necrosis, detachment and severe mitral insufficiency. If there are multiple anterior leaflet chordae which are elongated, though repair may be possible, resection and primary repair of the anterior leaflet is generally not advocated. Since the anterior leaflet is responsible for most of the competency of the valve, one must be extremely careful when considering this. Replacement is generally indicated, though occasionally small segments of the anterior leaflet can be repaired utilizing posterior leaflet chordae (the flip-over technique) [25]. Mitral stenosis can be created in the repair of mitral insufficiency by choosing an annuloplasty ring which is too small or by failing to recognize that the leaflet tissue is thickened or stiff secondary to rheumatic heart disease. Intraoperative trans-esophageal echocardiography at the end of the reparative procedure is mandatory, and though often fixated on the small residual jet of mitral insufficiency, one must be alert for mitral stenosis and check appropriate velocities. If mitral stenosis is created, reinstituting cardiopulmonary bypass and correction are performed, which require removal of the annuloplasty ring, resizing and occasionally replacement of the valve. Systolic anterior motion of the mitral valve causing left ventricular outflow tract obstruction has been described with rigid and flexible annuloplasty rings, though more commonly with rigid rings [26]. Redundant anterior and posterior leaflet tissue as well as a large annulus, a bulging septum, a narrow mitralaortic angle, a non-dilatated hyperdynamic LV and anteriorly displaced mitral coaptation line are predispositions. One can often avoid this by replacing a rigid ring with a flexible ring, shortening the anterior leaflet chordae, reducing the height of the posterior leaflet, or by some combination of these. Our practice has been to eliminate posterior leaflet height as a cause by always performing a height-reducing sliding advancement annuloplasty when the height of the posterior leaflet is > 1 cm, as well as by always utilizing a flexible annuloplasty ring. With any of the mitral valve replacement or reparative procedures, low cardiac output can occur. A variety of factors may be causative, including long-standing disease with impaired left ventricular function, marginal myocardial protection, coronary insufficiency with previous infarction, as well as the importance of maintaining both left and right ventricular geometry by preservation of the chordal-papillary muscle continuity [19]. Clearly posterior leaflet preservation can be achieved in most cases. Numerous techniques to preserve anterior continuity have been described [27–29]. Understanding the complex physiology, anatomy, and techniques, and awareness of the preventable complications, will allow for the safe conduct of mitral valve surgery and improvement in both the quality and quantity of life for patients.

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Figure 18.10 Tricuspid valve surgeon’s view. SVC, Superior vena cava; FO, fossa ovalis; CS, coronary sinus; IVC, inferior vena cava; ALTV, anterior leaflet tricuspid valve; PLTV, posterior leaflet tricuspid valve; SLTV, septal leaflet tricuspid valve.

Tricuspid valve surgery Anatomy As the name implies, there are three leaflets: the septal, the posterior and the larger anterior leaflet. The leaflets are attached to the fibrous annulus which separates the atrium from the ventricle, and have chordae tendinae which connect to papillary muscles and the ventricular wall. Important anatomically is the conduction system, with the AV node within the Triangle of Koch in the region of the septal leaflet. The Triangle of Koch is bounded by the septal leaflet, the opening of the coronary sinus and the central fibrous body. The bundle of His runs through the central fibrous body to enter the ventricular septum. There are occasionally accessory leaflets between the major leaflets (see Figure 18.10).

Incisions and cardiopulmonary bypass Though multiple approaches have been described for isolated tricuspid valve surgery, commonly tricuspid valve insufficiency is secondary to mitral or aortic valvular disease, and these also require corrective procedures necessitating a median sternotomy approach. By whatever approach utilized, bi-caval cannulation with caval tourniquets is utilized. A longitudinal incision in the wall of the right atrium at least 1.5 cm away from the AV groove is made to avoid compromise of the right coronary artery on closure. Injury to the sinus node artery can occur if the incision is carried around the atrial appendage. Direct injury to the node can also occur if the incision is placed in proximity. Either anterograde or retrograde cardioplegia is utilized or a decision made to perform the surgery with the heart beating. Other valvular corrective procedures or coronary revascularization should be completed prior to tricuspid valve

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reconstruction. Often the surgeon elects to repair the tricuspid valve while rewarming and after the aortic cross clamp has been removed. The atrial incision is closed with a single layer of a 4–0 monofilament suture utilizing an inverting horizontal mattress suture technique which avoids troublesome bleeding from a thin atrial wall.

Tricuspid valve repair Generally tricuspid valve insufficiency results from secondary enlargement of the right ventricle and annulus, with correction primarily restoring the annular dimensions. A reparative procedure should be entertained whenever moderate insufficiency is documented or if there is significant right ventricular enlargement without severe right ventricular dysfunction or severe irreversible pulmonary hypertension given the likelihood of progressive insufficiency.

DeVega annuloplasty With the valve exposed a pledgeted double armed 2–0 monofilament suture is begun in the annulus at the posterior-septal leaflet commissure, with bites taken in the annulus every 5 mm to encircle the valve to the region of the anterior-septal commissure. Tension on the valve with a nerve hook often helps to identify the annular tissue. The other end of the suture is placed similarly, resulting in a double row of sutures encircling the annulus but avoiding the septal leaflet. The suture is then tied over pledgets plicating the annulus. A prosthetic valve sizer can be placed when tying to prevent over-tightening of the annuloplasty repair. It is important to incorporate the fibrous annulus into the suture line, otherwise the suture will tear out of the thin valve tissue and weak atrial tissue. This repair avoids placing sutures along the septal leaflet and the potential damage to the AV node and conduction system. There have been variable reports of both excellent and at times only moderate long-term success with this procedure [30].

Bicuspidization (Kay) Another technique is plication of the posterior leaflet with either figure-ofeight sutures or pledgeted mattress sutures placed at the posterior-septal leaflet commissure and the posterior-anterior leaflet commissure to essentially eliminate the posterior leaflet [31]. Results with this technique are variable. However, it has the advantage of avoiding the septal leaflet and the potential for conduction disturbances, and is a simple technique which can be added to a complex multivalve procedure without significantly increasing morbidity.

Carpentier–Edwards annuloplasty This repair is designed to plicate the posterior leaflet and commissures with a semirigid ring which is open along a portion of the septal leaflet to avoid placing sutures near the conduction system (see Figure 18.11). With the valve exposed the ring is sized by either measuring the septal annulus or by using

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Figure 18.11 Tricuspid valveaCarpentier– Edwards annuloplasty. Open area along septal leaflet avoids injury to the conduction system. SLTV, Septal leaflet tricuspid valve; ALTV, anterior leaflet tricuspid valve; PLTV, posterior leaflet tricuspid valve; CS, coronary sinus.

the size of the anterior leaflet. Horizontal mattress sutures of 2–0 Dacron (Ticron®) are placed in the annulus beginning about the mid point of the septal leaflet and moving towards the posterior leaflet, being careful to avoid the coronary sinus. Bites are longer in the annular tissue of the valve than in the annuloplasty ring along the posterior leaflet and commissures, thereby plicating this region. The sutures continue around the annulus and anterior leaflet to the antero-septal commissure. Again, it is critical to place the sutures in the stronger annular tissue. The Carpentier–Edwards annuloplasty repair has been used successfully with excellent long-term results [32]. Variations of the ring annuloplasty include the flexible Cosgrove annuloplasty ring and the Puig–Massana ring, which can both be tailored to perform the appropriate plication of the posterior leaflet region.

Tricuspid valve commissurotomy Tricuspid valve commissurotomy, though rare, is performed by identifying the fusion between the septal-posterior leaflet and between the posterioranterior leaflets. Once identified the fused commissures are split with a #15 scalpel towards but not to include the annulus. The anterior-septal commissure should not be incised with the likely production of valvular insufficiency or conduction disturbances. If insufficiency occurs and the leaflets are pliable, an annular repair can be performed.

Tricuspid valve replacement Endocarditis may damage or destroy multiple leaflets necessitating replacement, and though resection of the valve without replacement in the setting of active endocarditis has been described, the long-term prognosis of these patients is marginal [33,34]. Ultimately the right ventricle fails and replacement is indicated. In general, immediate reconstruction has become more accepted with a low incidence of early recurrent prosthetic valve endocarditis [35,36]. This has been achieved with both bioprosthetic and mechanical valves. When possible, the septal leaflet and its chordae should be retained to add additional strength for anchoring of the sutures. The anterior and posterior

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leaflets and chordae are then resected to the papillary muscles. Placement of a prosthesis generally requires annular plication which is performed primarily along the anterior and posterior leaflets. Sutures can be placed from either above or below the annulus. We have utilized pledgeted 2–0 Dacron sutures placing the pledgets below the annulus on the ventricular side. This is particularly useful when portions of the septal leaflet can be left in place to buttress the annulus and avoid placing sutures too deeply, potentially damaging the AV node and conduction system. Given the large size of the ventricle, it is unlikely that the struts of a bioprosthesis will impinge on the ventricular muscle or that mechanical valve leaflet excursion will be affected. Suturing at the anteroseptal commissure must be precise to avoid a paravalvular leak and damage to the conduction system. There have been numerous reports of mechanical valve thrombosis, particularly involving tilting disc valves [37–39]. For that reason, except in the very young patient, bioprosthetic valves have become the valve of choice, with a lower propensity to thrombosis and the theoretical advantage of increased longevity in a low-pressure system. Prognosis with tricuspid valve repair or replacement is often dictated by the left-sided lesion and the potential for pulmonary hypertension reversal. At times, however, with a corrected left-sided lesion, tricuspid valve insufficiency and right ventricular failure persist and progress despite a reduction in pulmonary hypertension. There are, unfortunately, no reliable tests to determine if right ventricular failure will improve with valve repair or replacement in patients with progressive symptoms of right heart failure and tricuspid insufficiency. Echocardiographic improvement of right ventricular function with intensive medical therapy as well as clinical improvement with intensive medical therapy may be our best guide. Obviously, it is critical for the cardiac surgeon to understand the anatomy, physiology and potential corrective procedures of the tricuspid valve so that he may employ them under appropriate circumstances in the management of complex heart surgery patients.

References 1 Gundry SR, Shattuck OH, Razzouk AJ et al. Facile minimally invasive cardiac surgery via ministernotomy. Ann Thorac Surg 1998; 65: 1100–1104. 2 Nair RU, Sharpe DA. Minimally invasive reversed Z sternotomy for aortic valve replacement. Ann Thorac Surg 1998; 65: 1165–1166. 3 Svensson LG, D’Agostino RS. Minimal-access aortic and valvular operations, including the ‘J/j’ incision. Ann Thorac Surg 1998; 66: 431–435. 4 Olin CL, Peterffy A. Minimal access aortic valve surgery. Eu J Cardiothorac Surg 1999; 15 (Suppl.): S32–S38. 5 Byrne JG, Aranki SF, Cohn LH. Aortic valve operations under deep hypothermic circulatory arrest for the porcelain aorta: ‘no-touch’ technique. Ann Thorac Surg 1998; 65: 1313–1315. 6 Angell WW, Pupello DF, Bessone LN. Universal method for insertion of unstented aortic autografts, homografts, and xenografts. J Thorac Cardiovasc Surg 1992; 103: 642–648.

Complications of valvular surgery 383 7 Khonsari S. Cardiac Surgery Safeguards and Pitfalls in Operative Technique. Rockville, MD: Aspen Publishers, Inc., 1988. 8 Tomasco B, Di Natale M, Minale C. Coronary ostial stenosis after aortic valve replacement. Ital Heart J 2002; 3: 133–136. 9 Nicks R, Cartmill T, Bernstein L. Hypoplasia of the aortic root: the problem of aortic valve replacement. Thorax 1970; 25: 339–346. 10 Roughneen PT, Deleon SY, Cetta F et al. Modified Konno-Rastan procedure for subaortic stenosis: indications, operative techniques, and results. Ann Thorac Surg 1998; 65: 1368–1375. 11 Jacobs S, Falk V. Pearls and pitfalls: lessons learned in endoscopic robotic surgeryathe da Vinci experience. Heart Surg Forum 2001; 4: 3007–3110. 12 Masiello P, Triumbari F, Leone R et al. Extended vertical transseptal approach vs. conventional left atriotomy for mitral valve surgery. J Heart Valve Dis 1999; 8: 440–444. 13 Guiraudon GM, Ofiesh JG, Kaushk R. Extended verticle transatrial septal approach to the mitral valve. Ann Thorac Surg 1991; 52: 1058–1060. 14 Brawley RK. Improved exposure of the mitral valve in patients with a small left atrium. Ann Thorac Surg 1980; 29: 179–181. 15 Cheng LC, Chiu CS, Lee JW. Left ventricular rupture after mitral valve replacement. J Cardiovasc Surg 1999; 40: 339–342. 16 El Asmar B, Acker M, Couetil JP et al. Mitral valve repair in the extensively calcified mitral valve annulus. Ann Thorac Surg 1991; 52: 66–69. 17 Craver JM, Jones EL, Guyton RA et al. Avoidance of transverse midventricular disruption following mitral valve replacement. Ann Thorac Surg 1985; 40: 163–171. 18 Giovanni R, Speziale G, Voci P et al. ‘Patch-Glue’ annular reconstruction for mitral valve replacement in severely calcified mitral annulus. Ann Thorac Surg 1997; 63: 570–571. 19 Le Tourneau T, Grandmougin D, Foucher C et al. Anterior chordal transection impairs not only regional left ventricular function but also impairs right ventricular function in mitral regurgitation. Circulation 2001; 104 (Suppl. I): 41–46. 20 Izzat MB, Smith GH. Rupture of the left ventricle after mitral valve repair: case report and new technique of repair. Br Heart J 1993; 69: 366–367. 21 Onnasch JF, Scheider F, Mierzwa M. Mitral valve repair vs. mitral valve replacement. Z Kardiol 2001; 90: 75–80. 22 Kay GL, Kay JH, Zubiate P et al. Mitral valve repair for mitral regurgitation secondary to coronary artery disease. Circulation 1996; 74: I–88. 23 Reed GE, Tice DA, Clauss RH. Asymmetric exaggerated mitral annuloplasty: repair of mitral insufficiency with hemodynamic predictability. J Thor Cardiovasc Surg 1965; 49: 752. 24 Reul RM, Cohn LH. Mitral valve reconstruction for mitral insufficiency. Prog Cardiovasc Dis 1997; 39: 567–599. 25 El-Khoury G, Noirhomme P, Verhelst R et al. Surgical repair of the prolapsing anterior leaflet in degenerative mitral valve disease. J Heart Valve Dis 2000; 9: 75–80. 26 Shah PM, Raney AA. Echocardiographic correlates of ventricular outflow obstruction and systolic anterior motion following mitral valve repair. J Heart Valve Dis 2001; 10: 302–306. 27 Smedira NG, Selman R, Cosgrove DM et al. Repair of anterior leaflet prolapse: chordal transfer is superior to chordal shortening. J Thorac Carciovasc Surg 1996; 112: 287–292. 28 Timek TA, Nielsen SL, Green GR et al. Influence of anterior mitral leaflet second order chordae on leaflet dynamics and valve competence. Ann Thorac Surg 2001; 72: 535–541. 29 Moon MR, DeAnda A, Daughters GT et al. Experimental evaluation of different chordal preservation methods during mitral valve replacement. Ann Thorac Surg 1994; 58: 931–944.

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30 Chidamgaram M, Abdulai SA, Baliga BG. Long-term results of DeVega tricuspid annuloplasty. Ann Thorac Surg 1987; 43: 185–188. 31 Kay JH, Mendez AM, Zubiate P. A further look at tricuspid annuloplasty. Ann Thor Surg 1976; 22: 498. 32 Cohn LH. Tricuspid regurgitation secondary to mitral valve disease: when and how to repair. J Card Surg 1994; 9 (Suppl. 2): 37–41. 33 Nihoyannopoulos P. Tricuspid valvectomy following tricuspid valve endocarditis in an intravenous drug addict. Heart 2001; 86: 144. 34 Couie EK, Lin SS, Reynetson SI et al. Pressure and volume loading of the right ventricle have opposite effects on left ventricular ejection fraction. Circulation 1995; 92: 819–824. 35 Katsumata T, Westaby S. Mitral homograft replacement of the tricuspid valve for endocarditis. Ann Thorac Surg 1997; 63: 1480–1482. 36 Tanaka M, Abe T, Hosokawa S et al. Tricuspid valve candida endocarditis cured by valve sparing debridement. Ann Thorac Surg 1989; 48: 857–858. 37 Thorburn CW, Morgan JJ, Shanahan MX. Long-term results of tricuspid valve replacement and the problem of prosthetic valve thrombosis. Am J Cardiol 1983; 51: 1128–1132. 38 Boskovic D, Elezovic J, Boskovic D. Late thrombosis of the Bjork-Shiley tilting disc valve in the tricuspid position: thrombolytic treatment with streptokinase. J Thorac Cardiovasc Surg 1986; 91: 1–8. 39 Shapira Y, Nili M, Hirsch R et al. Mid term clinical and echocardiographic follow up of patients with CarboMedics valves in the tricuspid position. J Heart Valve Dis 2000; 9: 396–402.

CHAPTER 19

Postpericardiotomy syndrome William A. Gay Jr

Postpericardiotomy syndrome (PPS) is an illness, which occurs after an intrapericardial intervention, and is characterized by fever, malaise and pleuro-pericardial pain. The condition usually has its onset in the second or third week after surgery, and is often accompanied by a pericardial and/or pleural friction rub. The incidence of PPS has been reported between 10 and 60% following intrapericardial surgery [1–7], but the condition is uncommon in children less than 2 years of age [8]. An identical illness has been reported to occur in some patients following acute myocardial infarction [9]. Some authors now refer to the condition as post cardiac injury syndrome [5]. PPS was first described in association with closed mitral valvotomy, occurring in 30% of patients [10]. Initially, clinicians felt that the symptom complex represented a recurrence of acute rheumatic fever in the postoperative period [11]. These observers noted that the syndrome typically had its onset during the second week after surgery, and described the pain as pleuropericardial, in that it was aggravated by ‘swallowing and change of position’. They also noted that about 5% of the afflicted patients developed a small pleural effusion. Today, PPS is most commonly seen following cardiac surgery using cardiopulmonary bypass, but it has also been reported after epicardial pacemaker lead placement [12,13], percutaneous transluminal coronary angioplasty [14], RF ablation of accessory conduction pathways [15] and following insertion of transvenous pacemaker leads [16,17]. When PPS was described in patients without prior rheumatic fever [18], and when no evidence of rheumatic activity could be found in these patients [19–21] the theory of a rheumatic etiology was discarded. Similarly, although a relationship was seen between PPS and viral illness [8], there has been no evidence of an infectious etiology [22]. The thinking in this regard is that the viral illness may condition the immune system so that the trauma associated with cardiac surgery results in the development of antibodies against the myocardium. The presence of these heart-reactive antibodies correlates well with other manifestations of the syndrome [23,24]. These antibodies are directed against both the sarcolemma (IgG) and the myofibrils (IgM) [24]. This antigen–antibody activity, along with the circulating immune complexes, produces both local and systemic symptoms. The diagnosis of PPS requires a high index of suspicion by the clinician. Fever is common in cardiac surgery patients during the early postoperative 385

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period. The usual causes include complement activation by cardiopulmonary bypass, early stasis atelectasis and sensitivity reactions (drugs, transfusions, etc.). Fevers due to wound infection usually have onset after 1–2 weeks, and are obvious on close examination of the patient. Urinary tract infections most often present with specific symptoms and are easy to detect by urinalysis and blood counts. When postoperative fever persists, and/or is not due to one of the conditions mentioned above, the clinician should consider PPS as a possible cause. The fever is usually in the range of 38–39 °C, but may be higher, particularly in children. While fever is virtually always present, other symptoms often vary. These may include malaise, irritability (particularly in children), decreased appetite, arthralgias and pleuro-pericardial pain (i.e. sharp pain intensified by deep breaths, lying down, swallowing or other movements). A pericardial friction rub may or may not be present early to assist in making the diagnosis, but such a rub is almost always audible at some time during the course of the illness. A tachycardia, out of proportion to the fever, is often present. Pleural effusions, when present, are usually left-sided and small, and may be difficult to detect clinically. Although pericardial effusions are usually present to some extent, tamponade is rare, but can be a devastating complication when it occurs. The finding of a weak, thready pulse, narrow pulse pressure, distended neck veins, shortness of breath of hepatomegaly should alert the clinician to this possibility. If there is difficulty with cardiac filling other signs may be present, such as ankle edema or ascites. A leukocytosis in the range of 10 000–15 000/mm3 with neutrophilic preponderance is usually present, as is elevation of the sedimentation rate and C-reactive protein. ECG findings of elevation of the ST segments in the limb and lateral precordial leads are helpful when present, but may be obscured by post-surgical changes. The most specific blood test for PPS remains the finding of anti-heart antibodies in the serum using immunoflourescence, recently enhanced by employing monoclonal antibodies directed against human IgG [25]. Conventional X-ray of the chest usually reveals moderate cardiomegaly, and may show evidence of pericardial effusion, but these changes are not specific for PPS. Indeed, modest cardiac enlargement is a common finding on early postoperative films, and pericardial effusion may be difficult to appreciate in patients with open communication between the pericardial and pleural spaces. Large pericardial and/or pleural effusions are more easily detected and, in the presence of cardiac restriction, may be accompanied by radiographic evidence of pulmonary congestion. The presence of a pericardial effusion is not diagnostic of PPS, since many, if not most, patients undergoing cardiac surgery develop a small effusion postoperatively [26]. The extensive use of echocardiography in the postoperative cardiac surgery patient has made the finding of pericardinal effusions common. Small effusions are usually posterior, and may sometimes be recognizable only during ventricular systole, whereas larger effusions may extend all around the heart and be visible throughout the cardiac cycle. Collapse or indentation of the atria, and

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sometimes the right ventricle, during diastole indicate interference with cardiac filling suggestive of tamponade. Despite the fact that PPS and echocardiographic evidence of pericardial effusions are common following cardiac surgery, tamponade is rare [27,28]. Late cardiac tamponade has been reported to have an incidence of 0.1–6%, usually occurring in patients taking anticoagulants and probably unrelated to PPS [29,30]. Additionally, although constrictive pericarditis can occur late after cardiac surgery, there appears to be no relation to PPS [31]. Remembering that PPS is largely a diagnosis of exclusion, other causes of fever, malaise and chest pain should be considered and ruled out before starting treatment for PPS. This treatment consists of various anti-inflammatory agents, starting with the most benign and proceeding from there. Salicylates in anti-inflammatory doses (30–75 mg/kg per day) are usually effective in alleviating the symptoms in adults. Children may require lower doses. From personal experience, indomethacin has proved quite effective, although some patients experience GI upset with this drug. Ibuprofen has also been useful. More severe cases, and those with large pericardial effusions, may require the administration of steroids. Indeed, patients given steroids will respond more rapidly than those treated with salicylates [32]. However, the prophylactic use of steroids pre-operatively has not been effective in preventing the subsequent development of PPS [33]. Those patients who develop large effusions resulting in tamponade will require more invasive treatment. An initial pericardiocentesis to relieve the tamponade can be life-saving and definitive. However, in the most severe cases the effusion may return, necessitating surgical drainage (pericardial window) or, more rarely, pericardiectomy [34]. PPS is usually a benign, self-limited condition which responds to rest and anti-inflammatory agents. The necessity for more aggressive therapy is rare. The long-term prognosis is good.

References 1 Clapp SK. Postoperative inflammatory syndromes. In: Garson A, Bricker JT, Fisher DJ, Neish SR, eds. The Science and Practice of Pediatric Cardiology, 2nd edn. Baltimore: Williams and Wilkins, 1998; 1817–1821. 2 Livelli FD Jr, Johnson RA, McEnany MT et al. Unexplained in-hospital fever following cardiac surgery. Natural history, relation to postpericardiotomy syndrome, and a prospective study of therapy with indomethacin versus placebo. Circulation 1978; 57: 968–975. 3 McCabe JC, Ebert PA, Engle MA et al. Circulating heart-reactive antibodies in the postpericardiotomy syndrome. J Surg Res 1973; 14: 158–163. 4 McClendon CE, Leff RD, Clark EB. Postpericardiotomy syndrome. Drug Intell Clin Pharmacol 1986; 20: 20–23. 5 Kahn AH. The postcardiac injury syndromes. Clin Cardiol 1992; 15: 67–74. 6 Engelman RM, Spencer FC, Reed GE et al. Cardiac tamponade following cardiac surgery. Circulation 1970; 41(Suppl): 1165–1171. 7 Kirsh MM, McIntosh K, Kahn DR et al. Postpericardiotomy syndromes. Ann Thor Surg 1970; 9: 158–179.

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8 Engle MA, Zabriskie JB, Senterfit LB et al. Viral illness and the postpericardiotomy syndrome. A prospective study in children. Circulation 1980; 62: 1151–1158. 9 Dressler W. A post-myocardial infarction syndrome: preliminary report of complication resembling idiopathic, recurrent, benign pericarditis. JAMA 1956; 160: 1379–1384. 10 Janton OH, Glover RP, O’Neill JE et al. Results of the surgical treatment of mitral stenosis. Circulation 1952; 6: 321–333. 11 Soloff LA, Zatuchui J, Janton DH et al. Reactivation of rheumatic fever following mitral commissurotomy. Circulation 1953; 8: 481–493. 12 Gillette PC, Shannon C. Cardiac pacing in children. In: Dreifus LS, ed. Pacemaker Therapy. Philadelphis: FA Davis, 1983; 209–221. 13 Wang RYC, Mok CK. Erosion of an epicardial pacemaker secondary to postpericardiotomy syndrome. Pace 1983; 6: 33–36. 14 Velander M, Grip L, Mogenson L et al. The postcardiac injury syndrome following percutaneous transluminal coronary angioplasty. Clin Cardiol 1993; 16: 353–354. 15 Rouang KS, Hee TT, Pogano TV et al. Dressler syndrome complicating radiofrequency ablation of an accessory atrioventricular pathway. Pacing Clin Electrophysiol 1993; 16: 251–253. 16 Hargreaves M, Bashir Y. Postcardiotomy syndrome following transvenous pacemaker insertion. Eur Heart J 1994; 15: 1005–1008. 17 Lau CP, Fong PC, Tai YT et al. Postpericardiotomy syndrome complicating transvenous dual chamber, rate-adaptive pacing: diagnosis aided by transesophageal echocardiography. Am Heart J 1992; 123: 1388–1393. 18 Ito T, Engle MA, Goldberg HP. Postpericardiotomy syndrome following surgery for nonrheumatic heart disease. Circulation 1958; 17: 549–555. 19 Elster SK, Wood HF, Seely RD. Clinical and laboratory manifestations of the postpericardiotomy syndrome. Am J Med 1954; 17: 826–831. 20 Epstein S. Is the postcommissurotomy syndrome of rheumatic origin? Arch Int Med 1957; 99: 253–257. 21 Larson DL. Relation of postcommissurotomy syndrome to the rheumatic state. Circulation 1957; 15: 203–208. 22 Harthorne JW, Williams C, Bland EF. Postpericardiotomy and related syndromes. In: Andrus EC, ed. The Heart and Circulation: second national conference on cardiovascular diseases. Washington, DC, 1964. Fed Am Soc Exper Biol 1965; 1: 513–521. 23 DeScheerder I, Wulfrank D, Van Renterghem L et al. Association of anti-heart antibodies and circulating immune complexes in the postpericardiotomy syndrome. Clin Exp Immunol 1984; 57: 423–428. 24 Maisch B, Berg PA, Kochesiek K. Clinical significance of immunopathological findings in patients with postpericardiotomy syndrome. 1. Relevance of antibody pattern. Clin Exp Immunol 1979; 38: 189–196. 25 Kocazeybek B, Erenturk S, Calyk MK et al. An immunological approach to postpericardiotomy syndrome occurrence and its relation with autoimmunity. Acta Chirurgica Belgica 1998; 98: 203–206. 26 Stevenson LW, Child JS, Laks H et al. Incidence and significance of early pericardial effusions after cardiac surgery. Am J Cardiol 1984; 54: 848–854. 27 Clapp SK, Garson A Jr, Gutgesell HP et al. Postoperative pericardial effusion and its relation to postpericardiotomy syndrome. Pediatrics 1980; 66: 585–588. 28 Weitzman LB, Tinker WP, Kronzon J et al. The incidence and natural history of pericardial effusion after cardiac surgery: an echocardiographic study. Circulation 1984; 69: 506–517. 29 Merrill W, Donahoo JS, Brawley RK et al. Late cardiac tamponade: a potentially lethal complication of open-heart surgery. J Thorac Cardiovasc Surg 1976; 72: 929–932.

Postpericardiotomy syndrome 389 30 Hochberg MS, Merrill WH, Gruber M et al. Delayed cardiac tamponade associated with prophylactic anticoagulation in patients undergoing bypass grafting: early diagnosis with two-dimensional echocardiography. J Thorac Cardiovasc Surg 1978; 75: 777–781. 31 Ng ASH, Dorosti K, Sheldon WC. Constrictive pericarditis following cardiac surgery-the Cleveland Clinic experience. Cleve Clin Quart 1984; 50: 39–44. 32 Engle MA, Zabriskie JB, Senterfit LB. Heart-reactive antibody, viral illness and the postpericardiotomy syndrome: correlates of a triple-blind, prospective study. In: Transactions of the American Clinical and Climatological Association, 87th annual meeting. Baltimore: Waverly, 1975; 147–160. 33 Mott AR, Fraser CD Jr, Kusnoor AV et al. The effect of short-term prophylactic methlyprednisolone on the incidence and severity of postpericardiotomy syndrome in children undergoing cardiac surgery with cardiopulmonary bypass. J Am Coll Cardial 2001; 37: 1700–1706. 34 McCabe JC, Engle MA, Ebert PA. Chronic pericardial effusion requiring pericardiectomy in the postpericardiotomy syndrome, J Thor Cardiovasc Surg 1974; 67: 814–820.

CHAPTER 20

Pulmonary and pleural complications after cardiac surgery Jeffrey E Everett

Pulmonary complications are one of the leading causes of morbidity and mortality after cardiac surgery. They are associated with prolonged intensive care unit stay, ventilatory times, and increased hospital costs. The reported incidence ranges from 25 to 90% [1,2]. Included are atelectasis, pneumonia, pulmonary embolus, pulmonary edema, diaphragmatic weakness or paralysis, and disorders of the pleura. The following will attempt to identify preoperative risk factors, techniques to prevent their occurrence, keys to early diagnosis, and treatment planning for each of these postoperative complications following cardiac surgery.

Respiratory failure Postoperative respiratory failure, as defined by prolonged mechanical ventilation or abnormal gas exchange that adversely limits one’s physical endurance, is a significant concern in any patient undergoing a cardiothoracic procedure. Indeed, mortality approaches 30% in postoperative cardiac surgery patients requiring mechanical ventilatory support for > 3 days. Patients become susceptible to nosocomial pneumonia, stress ulceration, airway injury, and debilitation. It is known that postoperative pulmonary dysfunction is associated with prolonged operative time, the surgical site, advanced age, obesity, intrinsic lung disease, preoperative level of function, and tobacco abuse. Of these, advanced age, obesity, and tobacco abuse are also known risk factors for coronary artery disease, making a large percentage of cardiac surgery patients at potential risk of postoperative respiratory failure. The process begins with the induction of a general anesthetic. The supine position reduces functional reserve capacity (FRC) by 0.5–1 l, probably secondary to upward pressure of the abdominal contents and laxity of the diaphragm from the anesthetic. This then corresponds to the development of postoperative lower lobe atelectasis. With regard to surgical site, proximity to the diaphragm affords the greatest risk. There is up to a 40% decrease in vital capacity, total lung capacity, FRC, and inspiratory reserve capacity following a sternotomy incision alone. These values slowly return to normal but remain significantly lower until 4–7 months postoperatively [3]. The impact is even greater with a thoracotomy. 390

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Postoperative pain with resultant splinting, hypoventilation, atelectasis and ventilation–perfusion (VQ) mismatch is primarily responsible. Identifying at-risk patients, however, is complicated by the fact that no single test predicts poor outcome and clinical reviews report conflicting results [4]. The goal is to identify the high-risk patient in order to optimize their preoperative status or perhaps even exclude the highest risk patient in which risk exceeds the benefit. Screening begins with careful history specifically addressing exercise tolerance, extent of dyspnea, sputum production, cough and smoking habits. Physical examination looks for signs of intrinsic lung disease, specifically chest contour, clubbing, cyanosis, rales, rhonchi, wheezing, quality of breath sounds, respiratory rate and pattern, and use of accessory muscles [5]. A young, non-smoking patient with no discernable symptoms warrants no additional testing. The more risk factors identified the more helpful laboratory testing including chest X-ray, arterial blood gas, pulmonary function test, and sputum culture will be. Unfortunately, there has been no reported study that defines a lower limit of preoperative spirometry volume or capacity [6]. There are, however, some findings consistently identified throughout reported series that assign risk. An elevated blood pCO2 > 45 mmHg is associated with a higher mortality [2,7]. A diffusing capacity of CO2 (DLCO), a forced expiratory volume in 1 s (FEV1) or a forced vital capacity (FVC) < 50% have been shown to predict a higher incidence of postoperative pulmonary failure. Though none is prohibitive, they do serve as indicator of risk and alert to the need for pulmonary optimization and appropriate discussion with the patient and family. Having identified at-risk patients, preoperative maneuvers may serve to lower the incidence of postoperative pulmonary complications. When the luxury of time permits, patients will benefit from 2–4 weeks of chest physiotherapy [1,2,5]. First and foremost is cessation of smoking. It may take several weeks for sputum production and bronchorrhea to decrease in heavy smokers. Postural drainage and percussion for 10 min four times daily will facilitate clearance of secretions. Purulent sputum should be cultured and antibiotic therapy initiated as indicated. Diaphragm exercises are performed by deeply inspiring and then exhaling with pursed lips. An incentive spirometer is issued to give objective feedback and to familiarize one with proper technique prior to its postoperative use. Specialized pulmonary rehabilitation centers utilize graded inspiratory resistance as another technique to condition respiratory muscles. Bronchodilators are prescribed to relieve bronchospasm [1]. Anemia should be corrected to restore oxygen-carrying capacity and the fluid balance returned to euvolemia. Though no study has demonstrated a reduction in postoperative pulmonary failure or pneumonia, preoperative conditioning has been shown to reduce atelectasis significantly, lead to earlier extubation times, improve gas exchange, and reduce impairment of respiratory muscle function compared with controls [1,2]. Once ventilator dependence occurs, a multidisciplinary approach is necessary to achieve recovery. Proper nutritional support is initiated, preferably using the enteral route. Respiratory quotient analysis is performed to prevent overfeeding that

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produces excess CO2 and may impair the ability to wean. Physical and respiratory therapists are utilized to institute aggressive chest physiotherapy. Prophylaxis for both stress gastritis and deep venous thrombosis (DVT) is routinely administered. Ventilatory support must be tailored to the individual patient. Those with chronic obstructive pulmonary disease (COPD) have a significantly higher work of breathing. Auto-positive end pressure (PEEP) is responsible, as patients must overcome intrinsic elastic recoil. Adding external PEEP without causing hyperinflation reduces the work of breathing and may facilitate weaning. Bronchodilators and corticosteroids are used to decrease airway resistance. A short course of corticosteroids administered after postoperative day 2 does not adversely effect wound healing. In those patients with acute lung injury, intrapulmonary shunting occurs from increased lung water and loss of effective alveolar units. PEEP is optimized with a pulmonary artery catheter to monitor changes in cardiac output. This is a means to recruit alveoli and improve tissue oxygenation. Inverting the inspiratory to expiratory ratio improves oxygenation by increasing lung volume, recruiting alveoli, and enhancing collateral ventilation. Inhaled nitric oxide (NO) decreases right-toleft shunting and improves oxygenation. Allowing the CO2 to rise, permissive hypercapnea, allows lower tidal volumes which reduces barotraumas. Beneficial results, however, have been conflicting when compared with standard ventilation. Once stabilized, slow pressure support weaning is attempted. This gradually increases the work of breathing to allow for conditioning. High-volume, low-pressure endotracheal tube cuffs have proven safe, but after 2 weeks tracheostomy should be considered to facilitate weaning and pulmonary hygiene.

Atelectasis Atelectasis may be present in up to 90% of patients following cardiac surgery. The etiology is multifactorial, including decreased FRC, splinting from postoperative pain, phrenic nerve dysfunction, impaired cough, mucous plugging, and surfactant deficiency [8]. Atelectasis may be classified as major, that involving a segment, lobe, or lung, or minor when it affects a smaller distribution. The pathophysiology of atelectasis includes several mechanisms (Figure 20.1). Absorption atelectasis occurs distal to an obstruction where there is no aeration. Compressive atelectasis occurs secondary to such disorders as hemothorax, pleural effusion, and abdominal distension. Passive atelectasis arises from pneumothorax, hypoventilation or diaphragmatic dysfunction. Preoperative intrinsic lung disease and smoking are predisposing factors, but are more probably markers for patients with limited pulmonary reserves who will be compromised by loss of functioning alveolar units. Known swallowing disorders such as those occurring with neurological disease or previous head and neck surgery are also predisposing factors. Atalectatic changes are present even at 8 weeks’ follow-up.

Pulmonary and pleural complications after cardiac surgery 393

Figure 20.1 Mechanisms contributing to the development of postoperative atelectasis. COPD, chronic obstructive pulmonary disease.

Preconditioning with pulmonary rehabilitation may lessen the impact. Intraoperative maneuvers to reduce the incidence include evacuation of any pleural effusions, full lung expansion with positive pressure ventilation, and use of continuous positive airway pressure (CPAP) during cardiopulmonary bypass (CPB). Postoperatively pulmonary physiotherapy includes appropriate suctioning, use of incentive spirometry, intermittent positive pressure ventilation (IPPB), and CPAP following extubation. For sputum producers, percussion and postural drainage are used to clear secretions. When atelectasis involves an anatomic segment or larger, bronchoscopy should be performed to clear retained secretions. Bronchodilators aerosolized in normal saline help to mobilize viscous secretions. Patients with recurrent atelectasis secondary to retained secretions should be considered for tracheostomy. Pleural

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Figure 20.2 (A) Hypoxic vasoconstriction minimizes flow through underventilated areas minimizing shunt. (B) Vasodilators including milrinone, nitroglycerin, and nitroprusside abolish hypoxic vasoconstriction thereby promoting deoxygenated blood admixture. PA, pulmonary artery. Arrow represents flow of blood towards the left atrium.

effusions should be drained and pneumothorax treated. Early ambulation serves to increase FRC and reduce atelectasis. Judicious use of analgesics to alleviate pain without over-sedation facilitates co-operation with breathing exercises. Hypoxia following any surgical procedure is most commonly due to VQ mismatch. Shunting may also play a role and is associated with certain pharmacological agents used during cardiac surgery. Nitroglycerin is commonly prescribed for its beneficial effect on myocardial perfusion, reduction of pulmonary vascular resistance, prevention of arterial graft spasm and lowering of systemic pressure. The lowering of pulmonary vascular resistance abolishes the hypoxic vasoconstriction response and thus promotes pulmonary blood flow into underventilated areas (Figure 20.2). Shunting is the consequence, leading to hypoxia. Nitroprusside and milrinone are pulmonary vasodilators that likewise can lead to shunting. Application of PEEP to recruit underventilated areas will limit this effect [9].

Pneumonia Lower respiratory tract infection is one of the most frequent complications in intensive care unit patients and those requiring prolonged mechanical ventilatory support. Even with fast-track recovery of patients following cardiac surgery, postoperative pneumonia remains one the most common causes of morbidity, mortality and increased cost [10–12]. Pneumonia in this setting probably originates from microaspiration of upper respiratory tract flora [13]. A prospective study of 100 patients undergoing cardiac surgery had tracheal aspirates obtained at the time of intubation in the operating room. The

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incidence of lower respiratory tract infection was 31% (8/26) with positive bacteriology compared with 1.4% (1/72) in those with negative aspirates [11]. Patients with a prolonged preoperative in-hospital stay are likely to have oropharyngeal colonization by more virulent and resistant organisms that predispose to postoperative pneumonia. Tobacco use is also a known risk factor for pneumonia. In addition, host defenses are weakened following general anesthesia and cardiopulmonary bypass. Decreased levels of complement, gamma globulin, and fibronectin are noted postoperatively. There is also reduced mucociliary clearance and impaired cough reflex. Prolonged operative times and multiple blood transfusions have also been established risk factors. Postoperative risk factors include impaired cough reflex, impaired mucociliary clearance, and microaspiration. Prolonged endotracheal intubation increases the risk of developing pneumonia by 1–3% per day [14]. Postoperative pneumonia is defined as new radiographic infiltrate with three of the following: purulent sputum [> 25 white blood cells (WBC)], positive culture, leukocytosis (> 10 000 WBC), and fever > 38 °C. Sputum samples in the acute setting may be misleading, for they are more a reflection of upper airway and oropharyngeal colonization than the true distal airway infection. Pneumonia is therefore often over-diagnosed, but acceptably so in light of the potential mortality if not aggressively treated. If diagnosis is in doubt, fiberoptic bronchoscopy with lavage can have a negative predictive value (< 50% polymorphonuclear cells) approaching 100% [15]. Protected brush catheter samples from the distal airway also have improved yield with sensitivity and specificity of 95% [16]. The offending organisms vary amongst institutions, with Klebsiella pneumoniae, Pseudomonas aeruginosa, Staphylococcus aureus, Haemophilus influenzae, Streptococcus pneumoniae, and Gram-negative aerobes and anaerobes being most common. Sterilization of the upper respiratory tract would appear to be a preemptive strike. Colonization, however, does not always correlate with infection. This is perhaps more likely an indicator of underlying lung disease, specifically COPD. Inappropriate preoperative antimicrobials may lead to resistant strains, and secondary bacterial and fungal overgrowth. A more prudent approach would be cessation of smoking, optimized clearance of secretion with chest physiotherapy, and treatment of subclinical infection. Preoperative instruction on the use of an incentive spirometer and bronchodilators has been advocated as a way to lower postoperative pulmonary complications. Perioperative antimicrobials, usually administered for wound infection prophylaxis, may be of benefit if appropriate antibiotics for nosocomial pneumonia are selected [17]. Previous concern on pneumonia secondary to Gram-negative overgrowth with stomach acid neutralization has not been consistently reproduced in the prospective setting [18]. Intraoperative maneuvers include shorter bypass run and time under general anesthesia. Postoperative early extubation, ambulation, chest physiotherapy and perhaps intermittent positive pressure breaths will help to reduce the incidence. Early recognition and empiric antibiotics based on clinical setting and Gram stain are the first step in treatment. Hospital antibiograms help

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to tailor therapy. Antimicrobials together with aggressive chest physiotherapy should minimize the morbidity and mortality of postoperative pneumonia.

Adult respiratory distress syndrome Adult respiratory distress syndrome (ARDS) is a clinical entity characterized by radiographic infiltrates, impaired gas exchange and decreased lung compliance. It is associated with aspiration, sepsis, shock and trauma. It is in essence the lung injury resulting from the systemic inflammatory response. Reported mortality rates range from 40 to 70% when the lungs are the sole system affected [19]. This condition has also been linked to cardiac surgery and the use of cardiopulmonary bypass. The pathophysiology probably originates with complement activation with the onset of bypass and subsequent elaboration of C3a and C5a [20]. Neutrophils become activated and are sequestered in the lung where they release elastase and myeloperoxidase leading to tissue injury. A second insult may be induced by visceral hypoperfusion during CPB, especially with frequent use of neosynephrine to maintain mean arterial pressure. Endotoxins are released as bacterial translocation occurs [21]. Another predisposing factor in this patient population is complement activation by protamine via the classic pathway. The net result is pulmonary dysfunction secondary to injury at the capillary–alveolar interface. At onset this is an exudative process, yet in some it will progress to fibrosis and irreversible damage [19]. Increased capillary permeability results in alveolar flooding with proteinaceous fluid. Lung compliance is reduced and hypoxic respiratory failure ensues. Inflammatory cellular infiltrate follows with thickening of alveolar walls and further reduction in compliance. The late phase is characterized by a reduction in cellular infiltrate and progression of collagen deposition in the interstitium. Though rare, with an incidence of only 0.4–3% of cardiac cases, the mortality remains high. Cardiopulmonary bypass elicits the inflammatory cascade in all patients. Most, however, have only subtle alterations in pulmonary function. There have been retrospective reviews that attempt to identify the predisposing factors for ARDS. Age > 60 years, reoperative surgery, duration of CPB, smoking history, shock, emergent surgery, low cardiac output, preoperative amiodarone, and multiple transfusions have been identified. Attempts have been made to limit the inflammatory response with the use of pre-CPB corticosteroids, but conflicting results have been obtained [19]. Most would agree that there is little benefit. Leukocyte filters likewise have shown variable results. Though laboratory models suggest benefit, this has not proven useful in the clinical setting. This limits therapy to early detection and supportive measures. The diagnosis is established by the presence of tachypnea, bilateral pulmonary infiltrates, hypoxia, requirement of PEEP > 5, and absence of left heart failure with pulmonary capillary wedge (PCW) < 18. Management begins with eliminating any further mediators such as hypoperfusion, bacterial translocation, or tissue ischemia. Ventilator management includes avoidance of barotraumas, optimal PEEP levels, use of prone position to improve VQ

Pulmonary and pleural complications after cardiac surgery 397

mismatch, limit FiO2 < 0.6, paralysis or sedation to reduce oxygen consumption and facilitate mechanical ventilation, permissive hypercapnea, and inverse I/E raito [22,23]. Fluid management should be guided by pulmonary artery catheter monitoring. The goal is to reduce lung water without compromising end-organ perfusion. Low-dose NO may reduce shunting and improve oxygenation. The mortality from ARDS is usually secondary to multisystem organ failure. These supportive measures and preventing further complications remain the mainstay of therapy.

Pulmonary edema Postoperative pulmonary edema results from several conditions. First, there is capillary leak secondary to the inflammatory response elicited during CPB. This occurs even with normal left atrial pressure. The majority of patients will not have a significant clinical manifestation other than decreased pulmonary compliance and increased alveolar–arterial gradient [24]. This lung edema will resolve over the first few postoperative days and may be hastened by the use of diuretics. The next form of pulmonary edema develops after 3–5 days. It is associated with the mobilization of extravascular fluid retained during bypass. The left atrial pressures if measured may be elevated. Though usually selflimited, diuretics may speed recovery. Congestive heart failure is the last form of pulmonary edema. It is the most serious and difficult to manage. The etiology is systolic or diastolic dysfunction of the left ventricle. Left atrial pressures rise with resultant pulmonary congestion. In the immediate postoperative period, preload and afterload are optimized first with inotropic agents added as needed. Should the desired response not be obtained, intra-aortic balloon counterpulsation or a left ventricular assist device may be considered. In the later postoperative period, management includes afterload reducing agents, typically ACE inhibitors, diuretics (loop or spironolactone), and perhaps digitalis. For patients with marginal pulmonary status preoperatively, consideration should be given for off-pump strategies to avoid at least the inflammatory cascade. For those requiring the use of CPB, ultrafiltration during the run will reduce free water load and perhaps lower cytokine levels. Modified ultrafiltration popularized in pediatric cases has been shown to improve postoperative oxygenation compared with controls [25].

Pulmonary embolus Pulmonary embolus (PE) is an infrequent complication following cardiac surgery, with reported incidence ranging from 0.5 to 3.5% [26]. Even though resultant mortality may approach 40%, the net perioperative risk adjusts to only 0.3–1.7%, which is significantly lower than other surgical services which typically report PE mortality of 1–6% [27]. This difference is probably secondary to high-dose heparin intraoperatively, antiplatelet therapy postoperatively, platelet dysfunction resulting from CPB, and hemodilution.

Figure 20.3 Algorithm for management of patient with suspected postoperative pulmonary embolus. ABG, Arterial blood gas; CXR, chest radiograph; EKG, electrocardiogram; CT, computed tomography.

Pulmonary and pleural complications after cardiac surgery 399

The vast majority of PE arise from deep vein thrombosis (DVT) from the lower extremities or pelvic veins. Screening duplex imaging of postoperative cardiac patients yields a DVT incidence of 20–40%. Interestingly, the side distribution of DVT is equal, and therefore does not appear influenced by saphenous vein harvesting. Most are limited to the calf veins and have low rate of propagation and resultant PE. Indeed, routine duplex scanning has been shown not to be cost effective in prospective testing [27]. A high index of suspicion must be maintained and diagnostic testing obtained judiciously. Though symptoms of leg tenderness and swelling commonly occur in this patient population from surgical trauma and fluid overload, the onset of unilateral symptoms should be further investigated. Sound clinical judgement together with appropriate testing should allow for accurate and effective diagnosis (Figure 20.3). The diagnosis of PE is equally challenging. As mentioned, DVT, the precursor of PE, is accurately diagnosed by clinical criteria in < 5% of cases [27]. The clinical signs and symptoms of PE are often marked by postsurgical changes. Chest pain, tachycardia, tachypnea are attributed to the surgical trauma including the recent sternotomy, presence of pleural drainage tubes, and internal thoracic artery (ITA) harvesting. Routine narcotic administration further masks the clinical picture. Hypoxia, distended neck veins, and wheezing are just as likely from atelectasis, pleural effusion, fluid overload, or cardiac dysfunction which occur with higher frequency. Preventative measures begin by identifying high-risk groups. The classic triad of stasis, hypercoagulable state, and endothelial injury is relevant to most surgical patients. Specific patient groups are at even higher risk. Several series have shown that preoperative or postoperative bed rest for > 3 days significantly increases the incidence of PE. Congestive heart likewise is a risk factor consistently identified in separate reports. A variety of other factors have been reported and should be considered, but have not proven statistically significant in multivariate analysis. These include hyperlipidemia, obesity, history of DVT or PE, heparin-induced thrombocytopenia, and recent myocardial infarction. Other variables such as gender, race, age, tobacco use, varicose veins, diabetes mellitus and use of an intra-aortic balloon pump have not been associated with an increased risk of PE after cardiac surgery. In addition, patients undergoing valve operation have a significantly lower incidence of PE than other cardiac procedures such as coronary bypass. This difference is believed secondary to the use of anticoagulants in this patient group [26]. Prophylactic maneuvers begin with the avoidance of indwelling catheters in the lower extremities, and early ambulation, preferably on postoperative day 1. Antiplatelet therapy, which is standard practice, should be instituted and may decrease the incidence of DVT. The role of graded compression stockings (GCS) and sequential compression devices (SCD) is controversial. Studies from other surgical services have shown a significant reduction in DVT with the use of SCD. A prospective study of cardiac surgery patients, however, has shown no such benefit. The use of subcutaneous heparin has not undergone safety or efficacy study in this patient population. Concern over bleeding

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complication, the development of thrombocytopenia, and overall low incidence of PE in cardiac surgery patients explain the avoidance. It must be kept in mind, however, that reported series are taken from the general population of cardiac surgery patients, most of which ambulate early and may not have significant risk factors. A more aggressive approach should be applied to patients targeted at high risk. The use of SCD and even subcutaneous heparin should be considered for patients with delayed recovery, congestive heart failure or combination of previously mentioned risk factors. Diagnostic workup begins with clinical examination, chest X-ray, and arterial blood gas analysis. Ventilation–perfusion scanning has been the traditional screening examination. Although a high-probability scan may be used to confirm the diagnosis accurately, an intermediate or low-probability test cannot be used as confirmation of diagnostic exclusion. In fact, up to 54% of post-cardiac surgery patients with a low–intermediate VQ scan have been shown to have PE by pulmonary angiography or autopsy [28]. To improve diagnostic accuracy, Duplex evaluation of the lower extremities may be obtained. If both Duplex examination for DVT and VQ scanning together are negative, the incidence of PE falls to < 9%. Spiral computed tomography is now emerging as a rapid non-invasive screening tool to diagnose PE. In experienced centers diagnostic yield approaches angiography with sensitivity of 94% and specificity of 94% [29]. No large series have reported its use in cardiac surgery patients. The postoperative patient with unexplained dyspnea and hypoxia should have an aggressive workup. If VQ scanning is other than high probability, pulmonary angiogram should be obtained. Early detection will lead to therapy which decrease the likelihood of recurrent emboli as well as prevent propagation. Pulmonary embolism, once diagnosed, is classified based upon the patient’s hemodynamic status, oxygenation and percent pulmonary artery occlusion (Table 20.1). Classification schemes have been derived to guide therapy and prognosis. Patients with class I or II embolism are managed with anticoagulation alone. Heparin is administered to achieve a partial thromboplastin

Table 20.1 Classification of pulmonary embolism. Class

Symptoms

PaO2

% PA occlusion

Hemodynamics

I II III IV

None Anxiety, hyperventilation Dyspnea Shock, dyspnea

Normal < 80 < 65 < 50

< 20 20–30 30–50 > 50

V

Syncope

< 50

> 50

Normal Tachycardia CVP elevated, PA > 20 mmHg CVP elevated, PA > 25 mmHg, BP < 100 CVP elevated, PA > 40 mmHg, shock

PA, Pulmonary artery; CVP, central venous pressure; BP, blood pressure. (Adapted from Greenfield L. Complications in Surgery and Trauma. Philadelphia: JB Lippincott Co., 1984.)

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level two times control. Oral therapy with coumadin is initiated and the two overlapped until the INR reaches the therapeutic range. Patients with complications of anticoagulation therapy, recurrence despite therapeutic anticoagulation, hemodynamically compromising PE, or inability to comply with medical therapy are evaluated for placement of a caval filter. Class IV–V PE are managed with emergent emobolectomy via suction catheter or open technique.

Pleural disease Pleural effusions are evident in 50% of post-cardiac surgery cases. The majority are left sided and will resolve with no specific therapy. The onset may be immediately postoperative or delayed anywhere from days to weeks later. In the largest reported series of post-cardiac surgery patients, < 1% developed a large effusion, one which occupies > 25% of the hemithorax [30]. Congestive heart failure, pericardial inflammation, and pulmonary embolus are the most commonly identified causes. The majority, at least two-thirds, are idiopathic. Pleural effusions are characterized as bloody or serous. Bloody effusions occur sooner postoperatively, contain high lactate dehydrogenase, and typically resolve with 1–2 thoracenteses. They originate from postsurgical bleeding into the thoracic cavity. These effusions reach their maximal size on average 12 days postoperatively. Hemorrhage into the pleural space elaborates interleukin-5 by CD4 cells and may explain the presence of eosinophilia in fluid samples. Untreated bloody effusions may incite pleural fibrosis and lung entrapment [31]. Early drainage and lung expansion prevents this unusual but serious complication. Pleurectomy and decortication are necessary once entrapment has occurred. Non-bloody effusions are less likely to have an identifiable source, contain low LDH, reach their maximal size on average 1 month postoperatively and are lymphocytic. These effusions may be a form of hypersensitivity reaction. There is a direct correlation with pericardial effusions when screened using echocardiography, suggesting a potential relationship to the postcardiotomy syndrome. Indeed, mammals are known to have small fenestrations that provide direct communication between the pleural and pericardial spaces. In addition, harvesting of the internal thoracic artery (ITA) interrupts pleural lymphatics, impeding resorption of pleural fluid. There is also a higher incidence in cases in which topical hypothermia is used. Serous effusions are more likely to recur and require repeated interventions. Consideration may be given to the administration of non-steroidal anti-inflammatory agents or prednisone for recurrent cases. Treatment failures may be managed with mechanical or chemical pleurodesis.

Pneumothorax Pneumothorax is an uncommon complication following cardiac surgery, occurring in 0–1.4% of cases. The etiology is direct lung injury, usually ITA

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harvesting, spontaneous rupture of bullae or blebs from barotraumas, or from air drawn into the thoracic cavity from thoracostomy tube sites. Identifiable risk factors include intrinsic pulmonary disease such as emphysema and bronchitis, mainstem intubation with barotraumas, iatrogenic injury during placement of central venous catheters, and tobacco abuse. Presentation ranges from asymptomatic incidental chest X-ray finding to cardiopulmonary arrest. In the sedated and intubated patient an index of suspicion must be maintained. Restlessness, hypoxia, dysrrhythmia or increased airway pressure are suggestive in the intubated patient. Spontaneously breathing patient complaints may be vague, including chest pain, dyspnea or anxiety. Early diagnosis begins with physical examination. Obvious findings include unilateral absence of breath sounds and hyperresonace to percussion. Most, however, will not have such clear findings and if the clinical condition permits the diagnosis should be confirmed with chest X-ray. Observation may be all that is necessary for the small incidental pneumothorax. Others will require aspiration or thoracostomy tube drainage. Persistent air leak over 72 h may be managed by thoracoscopic stapling, pleural abrasion or pleurectomy, or chemical pleurodesis.

Phrenic nerve injury Diaphragmatic elevation or paralysis occurs in 7–11% of patients after cardiac surgery. Topical hypothermia has been shown both clinically and experimentally to cause phrenic nerve dysfunction with resultant hemidiaphragm elevation and lobar atelectasis. Phrenic nerve conduction velocity measuring also identifies prolonged cardiopulmonary bypass as a statistically significant risk factor. Slow resolution is the typical clinical course. By 6 months 44% normalize and by 1 year 90%. Diagnosis is suspected in patients with diminished breath sounds and poor diaphragmatic excursion during percussion and an elevated hemidiaphragm on chest X-ray. The diagnosis can be confirmed with videofluoroscopy or ultrasound of the diaphragm. Phrenic nerve conduction velocities are available in some centers. Observation is the mainstay of therapy, as most will resolve. Diaphragmatic plication is unusually applied to adult patients.

References 1 Castillo R, Haas A. Chest physical therapy: comparative efficacy of preoperative and postoperative in the elderly. Arch Phys Med Rehabil 1985; 66: 376–379. 2 Weiner P, Zeidan F, Zamir D et al. Prophylactic inspiratory muscle training in patients undergoing coronary artery bypass graft. World J Surg 1998; 22: 427– 431. 3 Ingwersen UM, Larsen KR, Bertelsen MT et al. Three different mask physiotherapy regimens for prevention of postoperative pulmonary complications after heart and pulmonary surgery. Intens Care Med 1993; 19: 294 –298. 4 Ingersoll GL, Grippi MA. Preoperative pulmonary status and postoperative extubation outcome of patients undergoing elective cardiac surgery. Heart Lung 1991; 20: 137–143.

Pulmonary and pleural complications after cardiac surgery 403 5 Nealon TF Jr, McNeil AG. Management of operations in the pulmonary cripple. Surg Clin North Am 1967; 47: 1223–1234. 6 Gass GD, Olsen GN. Preoperative pulmonary function testing to predict postoperative morbidity and mortality. Chest 1986; 89: 127–135. 7 Celli BR. What is the value of preoperative pulmonary function testing? Med Clin North Am 1993; 77: 309–325. 8 Johnson D, Thomson D, Mycyk T et al. Respiratory outcomes with early extubation after coronary artery bypass surgery. J Cardiothorac Vasc Anesth 1997; 11: 474 – 480. 9 Berthelsen P, St Haxholdt O, Husum B et al. PEEP reverses nitroglycerin-induced hypoxemia following coronary artery bypass surgery. Acta Anesthesiologica Scand 1986; 30: 243–246. 10 Carrel TP, Eisinger E, Vogt M et al. Pneumonia after cardiac surgery is predictable by tracheal aspirates but cannot be prevented by prolonged antibiotic prophylaxis. Ann Thoracic Surg 2001; 72: 143–148. 11 Carrel T, Schmid ER, von Segesser L et al. Preoperative assessment of the likelihood of infection of the lower respiratory tract after cardiac surgery. Thorac Cardiovasc Surg 1991; 39: 85–88. 12 Gould FK, Freeman R, Brown MA. Respiratory complications following cardiac surgery. The role of microbiology in its evaluation. Anesthesia 1985; 40: 1061–1064. 13 Harrington OB, Duckworth JK, Starnes CL et al. Silent aspiration after coronary artery bypass grafting. Ann Thoracic Surg 1998; 65: 1599–1603. 14 Fagon J, Chastre J, Domart Y et al. Nosocomial pneumonia in patients receiving continuous mechanical ventilation. Am Rev Resp Dis 1989; 139: 877. 15 Kirtland S, Corley D, Winterbauer R et al. The diagnosis of ventilator-associated pneumonia: a comparison of histologic, microbiologic, and clinical criteria. Chest 1997; 112: 445. 16 Wimberly N, Bass J, Boyd B et al. Use of a bronchoscopic protected catheter brush for the diagnosis of pulmonary infections. Chest 1982; 81: 556. 17 Bernard A, Pillet M, Goudet P et al. Antibiotic prophylaxis in pulmonary surgery. J Thorc Cardiovasc Surg 1994; 107: 896. 18 Poullis M. Chronic H2 receptor antagonist treatment and pulmonary complications post cardiac surgery. Ann Roy Coll Surg Engl 1999; 81: 239–241. 19 Milot J, Perron J, Lacasse Y et al. Incidence and predictors of ARDS after cardiac surgery. Chest 2001; 119: 884 –888. 20 Kutsal A, Ersoy U, Ersoy F et al. Complement activation during cardiopulmonary bypass. J Cardiovasc Surg 1989; 30: 359–363. 21 Berger D, Bolke E, Huegel H et al. New aspects concerning the regulation of the postoperative acute phase reaction during cardiac surgery. Clinica Chimica Acta 1995; 239: 121–130. 22 Brussel T, Hachenberg T, Roos N et al. Mechanical ventilation in the prone position for acute respiratory failure after cardiac surgery. J Cardiothorac Vasc Anesth 1993; 7: 541–546. 23 Matthay MA, Wiener-Kronish JP. Respiratory management after cardiac surgery. Chest 1989; 95: 424–434. 24 Thorsen MK, Goodman LR. Extracardiac complications of cardiac surgery. Semin Roentgenol 1988; 23: 32–48 [Review]. 25 Kiziltepe U, Uysalel A, Corapcioglu T et al. Effects of combined conventional and modified ultrafiltration in adult patients. Ann Thorac Surg 2001; 71: 684 –693. 26 Josa M, Siouffi SY, Silverman AB et al. Pulmonary embolism after cardiac surgery. J Am Coll Cardiol 1993; 21: 990–996. 27 Shammas N. Pulmonary embolus after coronary artery bypass surgery: a review of the literature. Clin Cardiol 2000; 23: 637–644.

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28 Ramos R, Salem BI, Haikal M et al. Critical role of pulmonary angiography in the diagnosis of pulmonary emboli following cardiac surgery. Catheter Cardiovasc Diagn 1995; 36: 112–117. 29 Ost D, Rozenshtein A, Saffran L et al. The negative predictive value of spiral computed tomography for the diagnosis of pulmonary embolism in patients with nondiagnostic ventilation-perfusion scans. Am J Med 2001; 110: 16–21. 30 Light RW, Rogers JT, Cheng D et al. Large pleural effusions occurring after coronary artery bypass grafting. Cardiovascular Surgery Associates, PC. Ann Intern Med 1999; 130: 891–896. 31 Lee YC, Vaz MA, Ely KA et al. Symptomatic persistent postcoronary artery bypass graft pleural effusions requiring operative treatment: clinical and histologic features. Chest 2001; 119: 795–800.

CHAPTER 21

Neurological complications in cardiac surgery George J Koullias, John A Elefteriades

Introduction The close correlation between the heartathat gives lifeaand the brainathat provides quality of lifeais such that on many occasions, neurological complications following cardiac surgical procedures severely minimize the beneficial effects of the operation. In the 1960s, severe neurological complications during cardiac surgery were appearing in 20% of patients [1,2]. In the 1970s and 1980s, with improvements in surgical technique, anesthesia and monitoring, the incidence fell to the range of 5% [3,4]. Recently, with the increased average age of the cardiac surgical patient, studies have shown that stroke rate is once again in the range of 5%. Prolonged encephalopathy occurs in about 10% of patients [5]. From a pathophysiological standpoint, three major mechanisms cause neurological injury during cardiac surgery: macroembolism, microembolism and reduced cerebral blood flow.

Systemic inflammatory response syndrome (SIRS) in cardiac surgery Cardiac surgery with cardiopulmonary bypass (CPB) is known to induce systemic inflammatory response syndrome (SIRS). SIRS is associated with increased morbidity and mortality, mainly due to organ and resultant hemodynamic failure. SIRS is diagnosed based on specific clinical criteria, but as a syndrome incorporates a conglomeration of pathophysiological alterations such as: 1 Reduction of circulating immunoglobulins (especially antibodies against endotoxin). 2 Leukocyte and complement system activation. 3 Immunological suppression. 4 Interleukin and inflammatory mediator release. 5 Diffuse endothelial damagealeaking. 6 Resultant hemodynamic failure and collapse. SIRS has long been described after cardiac surgery with the use of CPB. Intensive research efforts have focused on identifying patients at increased 405

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preoperative risk of SIRS, increased risk of SIRS during the first few postoperative hours, and finally on diminishing the morbid effects of SIRS or its resultant MODS (multiple organ dysfunction syndrome). The APACHE III immediate postoperative scoring system is a reliable predictor of postoperative SIRS. Cardiac surgical patients that have lower preoperative anti-endotoxin antibody levels release more anti- and proinflammatory cytokines during CPB. This increase in cytokines [IL-6, IL-8, IL-1β, C-reactive protein (CRP)] is higher in patients with longer CPB times [6,7]. Several aspects of the cell-mediated immune response are either severely depressed or greatly increased during CPB [8]. These actions are usually mediated by proinflammatory cytokines. Some of these proinflammatory molecules (specifically IL-8 and CRP) have been studied as impending SIRS markers in the immediate postoperative setting in cardiac surgical patients [9,10]. SIRS seems to be equal in conventional and minimally invasive cardiac surgery [11], but lower in ‘off-pump’ procedures [12]. Preoperative risk factors for SIRSabesides low anti-endotoxin antibody levelsainclude chronic use of ACE inhibitors, high preoperative CRP levels and preoperative respiratory infection [13,14]. One thing needs to be remembered: the single most important intraoperative risk factor for SIRS appears to be CPB duration [15]. The effects of SIRS on the brain have been studied in the contest of trauma and systemic infections, but not during the cardiac surgery postoperative state. In the event of SIRS, the central nervous system seems to react in a manner that mimics both protective adaptation and self-induced injury. The main SIRS-induced CNS adaptations are the following, and should always be considered in cases of neurological injury during cardiac surgery: 1 Cerebral vasodilatation followed by vasoconstriction. 2 Increase of the blood–brain barrier permeability. 3 Reduced neuronal metabolic rate. 4 Increased CSF pressure. 5 Neuronal membrane damage of various degrees. 6 Enhanced expression of leukocyte adhesion molecules. 7 Synthesis and release of nitric oxide, glutamate and aspartate, all of which act as neurotransmitters and later as potent neurotoxins.

Types of neurological injury in coronary and valve surgery Two main types of neurological injury during and after surgery have been described.

Type I neurological injuries Type I neurological injuries encompass all major and moderate focal neurological injuries, including shock and coma resulting from a major cerebral infarct. Major cerebral infarction incorporating a large portion of the cerebrum and/or the cerebellum occurs in 0.3–2% of all cardiac operations, depending

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on the study. Its incidence follows the general trend of decrease over the last 30 years, with an increase in the last decade. The overwhelming majority of these are of embolic origin. Detailed pathological studies have shown that the primary sites of damage reside in the posterior cortex, basal ganglia and cerebellum. Characteristically, the brain stem is pathologically spared in cases of major neurological injuries [6]. Aggregates of fibrin, fat particles, atheromatous particles and platelets are usually discovered in embolized small-caliber arteries and higher size atheromatous debris coated with platelets are discovered in occluded major arteries [16]. Focal cerebrovascular accidents incorporating smaller portions of the CNS appearing for a period of > 24 h are also classified as type I injuries and are usually seen after valve replacement procedures (10%), after coronary revascularization procedures (< 2%) and even after percutaneous transluminal coronary angioplasty (0.2%). Macroembolism (in contrast to microembolism showering) is identified as the major etiological factor in the appearance of cerebrovascular accidents during and after valve surgery. Clinically, in the majority of these cases, the patient has a left hemiparesis caused by embolism of a major branch of the right middle-cerebral artery. Although there is no solid explanation, the predilection for cardiogenic embolism of right cerebral vessels has been documented repeatedly in the literature. Decreased tolerance of the right cerebral hemisphere to micro- and macroembolism has also been hypothesized [7]. The remaining 20–30% of cerebrovascular accidents involve the sensory mechanisms and cerebellum, producing sensory deficits and postoperative balance disorders. Major epileptic seizures, another form of type I injury, are found in an average of 0.3–0.8% of cases. They are usually a consequence of cerebral infarction and have been described as early as immediately after the patient has been weaned from bypass. Usually seizures appear in the first postoperative week. Twenty percent to 30% of the cases are seen as late as 1 year after surgery. Unfavorable outcome correlates with seizures difficult to control initially and with seizures that appear as myoclonic crises [17,18]. Coma is an extreme form of decreased level of consciousness and its incidence is fortunately low. Approximately 50% of major cerebral functions manifest clinically as immediate postoperative coma. Bilateral preexistent carotid and cerebrovascular disease and postoperative acidosis are associated with poor outcome. Brain stem dysfunction, signs of decerebration or decortication and persistent absence of response to painful stimuli predict poor outcome. In comas of < 1 week duration, a 90–93% functional recovery has been observed. If the coma lasts 3.5–4 weeks, there is practically no chance of any functional recovery [19]. Spinal cord injury in non-aortic cardiac surgery is a rare complication and is evidenced by the appearance of postoperative hemiparesis or paraparesis. This complication is seen when an intra-aortic balloon pump is used and attributed to embolization and ischemia of the spinal cord vessels caused by atheromas dislodged locally from the aorta during balloon counterpulsation.

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Type II neurological injuries The collective category of type II injuries encompasses a wide variety of neurological injuries of either lesser magnitude or lesser duration. Ophthalmological complications, minor seizure disorders, focal deficits that last < 24 h, diffuse mild encephalopathy, disorders of attention, recent or remote memory, and affect, immediate or later psychiatric disorders, as well as dysfunction of components of the peripheral nervous system are included in this category. In general, the more immediate and more detailed the neurological assessment, the higher the discovered incidence of type II neurological injury. Ophthalmological disorders are encountered in 17–25% of cardiac surgical patients. Because of their short duration in the immediate postoperative setting of the cardiac surgical patient, ophthalmological disorders are frequently overlooked. They are caused by single, or more frequently, multiple fibrin and platelet microemboli to the retinal vessels [20]. Usually the patient complains of temporary partial loss of vision, hemianopic defects or intermittent ‘flashing lights’ vision. Relatively frequently, the patient also experiences cortical blindness (Anton syndrome) due to bilateral occipital lobe microembolism. The vast majority of the above ophthalmological disorders do not last more than 6 weeks [10] and permanent blindness after cardiac surgery is very rare.

Minor seizure disorders and diffuse mild encephalopathy Minor seizure disorders usually accompany clinically non-significant embolic ischemic lesions. Their overall incidence is 1–4% and they are easily controlled with short-term antiseizure medication regimens. Mild diffuse encephalopathy has been discovered in > 40% of patients after cardiac surgery [21,22]. This is associated with the appearance of abnormal (bilateral Babinski reflexes, corticomodullar reflexes) or primitive reflexes (grasping or sucking reflex). These reflexes are of minor clinical importance and are attributed to diffuse mild ischemic dysfunction of the frontal lobes during cardiopulmonary bypass [21,22].

Mental and cognitive dysfunction The incidence of diagnosed mental disorders after coronary and vascular surgery ranges from 30 to 80% [22–24]. This wide range is due to the use of different diagnostic criteria and cognitive tests in the literature. The sooner and more complete the neurocognitive testing, the higher the reported incidence of diagnosed dysfunction. These disorders usually manifest as disorders of recent and remote memory, judgement, affect and behavior. Initially in cardiac surgery, these disorders were attributed to stress after a major operation. Today all indications point to discrete diffuse hypoperfusion-related cerebral damage with or without additional microembolic phenomena. In comparative neurocognitive studies [25] of patients who underwent major surgery and patients who had cardiac surgery with cardiopulmonary bypass, it was proven that postoperative neurocognitive deficits were more pronounced in the cardiac surgery patient group.

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Nevertheless, two points need to be emphasized. First, in the vast majority of cardiac surgical patients, the observed neurocognitive deficits are not debilitating. Second, almost complete resolution of those deficits is observed clinically and during cognitive testing in 98–99% of these patients, 4–8 weeks after surgery [26,27].

Psychiatric complications Psychiatric complications after cardiac surgery are reported in 1–5% of the patients, and usually manifest as confusion, psychokinetic instability, paranoid ideation and irritability. They last between 1 and 3 weeks and their etiology (organic or psychiatric) is still debated. As in the case of postoperative cognitive dysfunction, the wide variation in the reported incidence is attributed to the variety of diagnostic criteria and timing [22,28–31]. Clinically, a differential diagnosis between the so-called ‘ICU psychosis’ and a psychiatric complication after cardiac surgery should be made. ICU psychosis usually starts after the third to fifth ICU stay day as opposed to psychiatric dysfunction after cardiac surgery that starts the first or second postoperative day. Peripheral nervous system complications are generally considered innocent and are not discovered unless the patient develops specific complaints. Their overall incidences ranges from 2.6 to 13%. Most such complications are related to brachial plexus injuries. Specifically the lower trunk of the plexus is injured more frequently, with resultant digit weakness or hypersthesia, especially in the ulnar distribution. The majority of these complaints significantly subside 4–8 weeks after surgery [31]. More infrequent complications are phrenic nerve damage, recurrent laryngeal nerve injury and peroneal nerve injury during saphenous vein harvesting [32].

Risk factors for neurological injury in coronary and valve surgery Several well-designed multicentre prospective randomized trials have identified risk factors for type I and type II neurological injuries in patients after cardiac surgery. Risk factors for type I injury after coronary artery bypass were proximal aortic atherosclerosis, prior neurological event, use of intra-aortic balloon pump (IABP), diabetes mellitus, hypertension, pulmonary disease, angina and age [33]. Risk factors for type II injury in coronary artery bypass grafting (CABG) were: history of pulmonary disease, age, the use of preoperative antihypertensives, systolic blood pressure > 180 mmHg on admission, excessive alcohol consumption, prior CABG, and dysrythmias on the day of surgery [5,33,34]. Several risk factors were also identified for the patient who underwent CABG plus an intracardiac procedure. Type I injury risk factors in these patients included the presence of atrial and ventricular thrombus, proximal

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Figure 21.1 Schematic correlation between the degree of proximal aortic atherosclerosis, the associated intraoperative emboli release and the resultant risk of neurological injury.

aortic atherosclerosis, intermittent aortic cross-clamping and a history of myocardial infarction [5,34,35]. Risk factors for type II injury in patients undergoing combined procedures included proximal aortic atherosclerosis, an admission systolic blood pressure > 180 mmHg, history of endocarditis, congestive heart failure immediately following surgery, alcohol abuse, and perioperative dysrythmia [5,34–36]. Proximal atherosclerosis was identified as the single most important risk factor for type I and type II injury in patients undergoing either CABG or CABG combined with an intracardiac (valvular) procedure. More than 75% of patients above the age of 75 have proximal aortic atheromas detected on transesophageal echocardiography or intraoperative epicardial echocardiography. In an excellent study by Barbut [36], 100% of patients undergoing coronary bypass surgery and/or valve surgery were found to have detectable emboli. They were detected in the aortic lumen during specific intraoperative phases: cannulation, aortic manipulation, clamping and unclamping. The average number of emboli in this study was 135 during coronary bypass surgery and 1030 during valve surgery. More importantly, the number of emboli correlated well with the stroke risk and the degree of proximal aortic atherosclerosis [36,37]. Another similar study failed to confirm such a correlation [38]. These observations and findings are depicted schematically in Figure 21.1. Other prospective studies [39] have identified additional risk factors for type I injury during coronary bypass surgery. Predictors for type I injury included cerebral vascular disease, peripheral vascular disease, diabetes, renal failure, perioperative myocardial infarction, hypertension and age > 70 years [40].

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Prevention of neurological injury in coronary artery and valve surgery Preoperative prevention—the role of carotid endarterectomy The presence of carotid disease is consistently identified as a predictor of neurological injury in cardiac surgery and is one factor that can be easily identified and treated preoperatively. Initial efforts to correlate carotid disease with the risk of type I neurological injury during cardiac surgery were focused on the preoperative detection of carotid bruits. Reed and coworkers reported that the risk of type I injury during cardiac surgery was 3.9 times higher when a carotid bruit was present preoperatively [41]. Two years later, Fagglioli showed that the incidence of type I neurological injury after cardiac surgery increased by 9.9-fold if carotid stenoses > 75% were not addressed pre- or intraoperatively [42]. The advantages of carotid endarterectomy in the general population are well documented. Two randomized trials defined the advantages of carotid endarterectomy compared with medical therapy for symptomatic carotid stenosis (> 70%). In the NASCET study [43], the risk of ipsilateral stroke in 2 years was 9% for the surgical arm as opposed to 26% for the non-surgical arm. In the European Carotid Surgery Trial [44], the stroke rate for the surgical arm was 10.3% compared with 16.8% for the non-surgical arm. Two additional randomized trials also defend the advantages of carotid endarterectomy for asymptomatic patients with ≥ 60% carotid stenosis. The 1993 VA Cooperative study [45] and the 1995 ACAS study showed significant stroke and survival advantages in asymptomatic patients (with carotid stenosis > 70%) who had elective carotid endarterectomy [46]. How does this demonstrated efficacy of carotid endarterectomy translate to the patient about to undergo cardiac surgery? In the only randomized study of combined coronary artery surgery and carotid endarterectomy in patients with unstable angina and high-grade asymptomatic carotid stenosis, Hetzer and coworkers [47] showed that the stroke rate in combined procedures was 2.8%, compared with a 14.4% for a staged approach (6.9% during initial CABG and 7.5% during the subsequent performed carotid endarterectomy). Combined cardiac and carotid procedures were also demonstrated by Akins [48] and Daily [49] to be cost effective, with very low associated morbidity and stroke rates. A factually based paradigm emerged from the presentation and discussion of Dr Akins’ paper at the adult postgraduate course of the 70th American Medical Association for Thoracic Surgery Meeting (New Orleans, April 16, 1999). Based on these comments and our own practice, we recommend [50]: 1 In making our decision on a patient with coronary artery and carotid disease, we should address operatively first the more compelling lesion, heart or carotid. Poorly compensated carotid lesions (in patients with transient ischemic attack (TIA), or with critically tight lesions) should be corrected before elective cardiac surgery. Critical cardiac disease should be corrected before non-compelling carotid disease.

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2 If the patient has a tight carotid lesion and unstable angina then he should undergo a combined operation. 3 If the patient has a tight carotid lesion and a contralateral but not tightly diseased carotid and unstable angina, he should undergo a combined correction, followed by an endarterectomy of the less diseased side in the near future. 4 In patients with unstable angina and asymptomatic high-grade carotid lesions, we proceed with CABG with systematic hypothermia (and IABP if the left main disease present) for cerebral protection.

Intraoperative prevention of neurological injury Aortic atheroma With the increasing use of transesophageal echocardiology (TEE), intraoperative epiaortic echocardiography (IEE) and transcranial doppler echocardiography (TCD), it has become feasible to estimate qualitatively and quantitatively the presence and degree of aortic atheroma as well as the amount of embolizing atherosclerotic debris. The presence and degree of aortic atheroma has emerged as the single most important risk factor for type I and type II neurological injury during cardiac injury [5,34]. Embolic neurological injury occurs mainly via embolization of atherosclerotic debris. To a lesser degree, air embolism, clot formation and embolization and cardiopulmonary bypass-related cerebral blood flow alterations can also cause neurological dysfunction. Using TEE, aortic atheromas have been graded as follows. Grade I (small to moderate wall thickening), grade II (severe aortic wall thickening), grade III (intraluminal protrusion < 5 mm), grade IV (intraluminal protrusion > 5 mm) and grade V (mobile intraluminal atheroma). Several investigators using TCD have identified emboli traveling through the mid-cerebral artery [37,38]. Important positive correlations have been made between the number of imaged embolizing atherosclerotic debris and incidence of type I and/or type II neurological injury in these patients. In one of these studies [36], it was prospectively determined that the presence of grade I aortic atheroma is associated with 0% neurological type I injury as opposed to a 30% incidence in patients with grade IV or V aortic atheromas. In most cardiac surgery centers, the introduction of the aortic cannula is preceded by manual aortic palpation and selection of the optimal cannulation site. Several well-designed studies [51–55] have proven that 30–70% of severe aortic atheromas cannot be localized effectively with manual palpation. In a series of 1200 patients to whom intraoperative epiaortic echocardiography was applied, 231 (19.25%) were found to have grade I–IV atheromas in areas that were by palpation characterized as ‘normal’ [56]. In 27 of these patients with grade IV atheromas, the ascending aorta was replaced with no incidence of type I injury. Yet, this aggressive approach has not been widely applied at other institutions. In another series of 168 patients with less significant aortic disease, application of epiaortic echocardiography resulted in technical modifications, such as

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femoral cannulation, avoidance of specific areas for aortic cross-clamping, modification in the placement of proximal graft anastomoses or institution of retrogradeainstead of antegradeacardioplegia [54]. All of these intraoperative modifications of the operative technique resulted in a significant decrease in the incidence of type I and type II injury [54]. In a series of 130 patients undergoing CABG, specific attention was paid to those patients with grade V aortic atheromas. Modifications of operative technique in a group of these patients again resulted in significantly lower stroke rate [53]. Additional studies have examined the role of intraoperative technique modifications, made based on epiaortic echo data, on the incidence of neuropsychological complications. The addition of transcranial Doppler data in these patients gave additional information regarding the number of aortic atherosclerotic debris flowing through the mid-cerebral artery. It was concluded [57] that the incidence of neuropsychological complications in patients who had smaller numbers of embolizing particles (< 100) was < 10%, as opposed to patients with a higher number of particles (> 1000) that had as a group a 40% incidence of neuropsychological morbidity. This provided direct evidence correlating the amount of embolic debris load and postoperative neurobehavioral outcome [58]. This work and other studies have demonstrated overwhelmingly the impact of aortic debris and embolization on neurological outcome and the dramatic importance of echocardiographic evaluation.

Prevention of air embolism Besides the traditional measures and air evacuation techniques, newer devices, extensive external filter application and technique modifications have been gradually introduced into daily practice, aiming at the decrease of incidence of type I and type II injury [59]. Examples include newer arterial cannulas with vents, insertion of venous cannulas during positive end expiratory pressure in patients with suspected atrial septal defect (ASD) or ventricular septal defect (VSD) or other intracardiac shunts and almost complete replacement of bubble oxygenations. More recently, extensive use of carbon dioxide flooding in our institution has dramatically decreased (among others) the incidence of type I injury. Furthermore, avoidance of gas exchange in venous return, use of bubble detectors and multiple arterial filters, use of closed compressible venous reservoir and nonobstructive arterial pumps have been utilized in our institution [60,61].

Prevention of thrombus formation Avoidance of thrombus formation during cardiac surgery focuses mainly on three factors: perioperative recognition of patients with a higher potential for coagulation, achievement, maintenance and monitoring of systemic heparinization during cardiopulmonary bypass, and research and development of less thrombogenic or thrombo-resistant synthetic materials, such as heparin-coated perfusion equipment [62–64].

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Figure 21.2 Application of an Edwards EMBOL-X® System intra-aortic filter. Courtesy of Edwards Lifesciences.

Intra-aortic filtration A new method of intra-aortic filtration has been developed and is undergoing testing in European centers. This intra-aortic filter (Edwards EMBOL-X®) System, Edwards Lifesciences Corp., Irvine, CA, USA) is introduced through a modified 24 Fr aortic cannula after the optimal cannulation site has been selected by palpation, TEE or intraoperative epiaortic echocardiography. Before aortic unclamping, this filter is introduced through a parallel port of the aortic cannula and expanded to cover the entire aortic lumen. The filter is removed with the removal of the aortic cannula [65] (Figure 21.2). The application of this intra-aortic filter device was presented for the first time in the USA by Dr J.A. Navia in a case demonstration of a low neurological injury risk patient that underwent coronary artery bypass grafting (Figure 21.3) [66]. The same was evident in a patient that underwent an aortic valve replacement [67]. At the same time, Reichenspurner and coworkers presented the first group of 77 patients, undergoing coronary artery bypass or valve procedures, in which the intra-aortic filter was used. The authors did not focus on the incidence of type I and type II injury. They concluded that virtually all of the

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Figure 21.3 Postoperative pictures of introduced intra-aortic filters. The presence of numerous particles can be seen, consisting of atheromatous debris, collagen and aortic wall particles.

77 intra-aortic filters had, on postoperative evaluation, significant amounts of captured atherosclerotic debris. Debris presence was assessed and evaluated quantitatively by visual inspection, pathological and microscopical examination and scanning electron microscopy. No evidence of hemolysis was detected and there was no evidence of aortic wall injury or dissection during and after the application of the device [65,68]. The International Council of Emboli Management (ICEM) is a continuing prospective project in 14 major European centers evaluating the efficacy of intra-aortic filter application and its possible contribution in the reduction of type I injury in cardiac surgery. Since 1997, several progressively larger series of patients have been reported [65,69–72] Last year, ICEM reported their final results on 445 patients who underwent coronary artery bypass and/or valvular procedures [73]. After the intra-aortic filter was used, it was preserved in formalin and sent to a core lab for histological analysis. In order to compare their data, ICEM reported their results in comparison with the prospective multicenter study by Roach [5] which assessed adverse cerebral outcomes during cardiac surgery in the USA. The preoperative data in the two studies were reported and are summarized in Table 21.1. The overall mortality was 4% and the incidence of type I injury was 1.8%, less than the 3.1% reported by Roach et al. [5]. The examined group in the ICEM study was overall at high risk of type I injury and experienced a lower incidence of type I neurological injury. Table 21.1 Comparisons of risk factors for type I and II neurological injury between patient groups at the ICEM and Roach studies. Risk factor

ICEM, %

Roach et al., %

Aortic atheroma Age > 70 years HTN IDDM

16.89 41.3 64.21 19.1

12.4 31.9 57.2 25.1

HTN, hypertension; IDDM, insulin dependent diabetes mellitus.

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Percent of filters

Pathology Fibrous atheroma Surgical debris Platelets and fibrin Thrombus Number of particles/filter Mean surface area of particles Percent of cases with discovered particles

65 7 52 21 8.3 7.1 mm2 99

Recognizing the established link between particulate emboli and type I neurological injury, the authors believe, and we concur, that this lower incidence is possibly related to the fact that a significant amount of embolizing debris was captured in almost 99% of the patients (Table 21.2).

Single vs. excluding clamp technique and stroke rate The single-clamp technique, proposed by Buckberg [74] and popularized by Salerno [75] and Aranki [76,77], was based on sound reasoning. By eliminating the second, partially occluding clamp, this method may potentially decrease the incidence of embolic stroke in CABG. However, clinical benefits of this method have not been demonstrated conclusively by either retrospective or prospective studies. Many surgeons realize that although avoiding the application of the conventional second clamp may decrease the number of aortic emboli [78], this technique necessarily results in longer cross clamp times and converts the otherwise closed bypass operation to an open procedure, with increased risk of cardiac and cerebral air embolization. The available studies in the literature comparing these two methods are either retrospective [76,79] or randomized prospective [80–83]. Only one of these studies has found a small cardiac preservation advantage and no type I injury advantage [81]. At our institution, we retrospectively examined 607 consecutive patients who underwent isolated coronary bypass operations over a 3-year period at Yale-New Haven Hospital. Three hundred and one (50%) were performed by one surgeon using exclusively the single-clamp technique and 306 (50%) were performed by a second surgeon using exclusively the two-clamp technique. Postoperative adverse effects were compared between these two groups. There were no differences in terms of postoperative stroke (1.7% single-clamp vs. 2.0% two-clamp; P = 0.78) or postoperative myocardial infarction (2.6% single-clamp vs. 0.7% two-clamp; P = 0.052). The two-clamp technique was not a significant predictor of stroke or any other type I injury by logistic regression analysis (P = 0.72). The sound rational expectation for decreased emboli with the single-clamp technique has not been confirmed clinically, probably because its benefit is overwhelmed by emboli due to the

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arterial cannula itself, the ‘jet-spray’ effect of arterial flow, and the (albeit single) cross clamp application. On the basis of the Yale study, we found no solid and compelling evidence for surgeons successfully utilizing either method of constructing their proximal anastomoses to change to the other technique [84].

Passive retrograde cerebral perfusion in routine cardiac surgery Of considerable interest is the study of Quigley et al. [85] from the Guthrie Clinic. This group has performed 3 min of passive retrograde cerebral perfusion in all valve operations. During this period of cerebral perfusion, central venous pressure is kept between 20 and 25 mmHg and simultaneous transcranial Doppler signals have demonstrated reversal of middle cerebral artery blood flow. The same methodology has been used by others but with no reported decrease in the incidence of type I injury [86]. The Guthrie group has reported 0% type I injury in 317 consecutive valve operations [85,87].

Neurological injury in off-pump cardiac surgery Many studies in the recent literature have compared the incidence of type I and II neurological injury in cardiac surgical patients operated with CPB (CAB) and off-pump coronary bypass (OPCAB). As regards the incidence of intraoperative and postoperative stroke, large prospective and retrospective studies have demonstrated no statistically significant stroke rate differences [88,89]. At the same time, other groups have reported lower stroke rates in the OPCAB group [90,91]. Although more multicenter randomized as well as meta-analyses are needed, advances in both CPB technology and beating heart techniques will continue to demonstrate gradually decreasing similar stroke rates in the average-risk cardiac patient. As regards type II injury and early and mid-term neuropsychological outcomes, OPCAB seems to be associated with lower incidences, although the precise reasons for this finding are yet to be determined [92]. The overall goal of improving neurological outcomes in cardiac and aortic surgery is related to research in CNS protection and technological evolution. This technology aims mainly to mimic normal biochemical and fluid mechanical conditions. Improvement in pump, occluding clamp and off-pump techniques as well as CNS protection strategies will ultimately provide the best protection for patients at risk of neurological injury.

Types of neurological injury in aortic surgery Cerebrovascular accident is a dreaded complication of surgery of the ascending aorta and aortic arch. Although not as intuitively obvious, type I neurological injury can occur as well from operations on the descending aorta. A stroke rate ranging from 5 to 15% has been found in 23 series on aortic surgery published the last decade [93–95].

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The same general classification of neurological injury pertinent to coronary and valvular surgery applies to aortic surgery.

Prevention of neurological injury in aortic surgery Type I neurological injuries in aortic surgery are mainly caused by one or more of the following pathophysiological entities [96]: 1 Systemic hypotension (especially with coexistent cerebrovascular disease). 2 Embolism (air, debris). 3 Reduced perfusion syndromes (in dissections). 4 Inadequate cerebral protection during deep hypothermic circulatory arrest (DHCA). 5 Reperfusion injury. The following will focus mainly on technical modifications for the prevention and intraoperative management of these entities.

Management of systemic hypotension The preoperative assessment of any cerebrovascular disease is as important in aortic surgery as in coronary or valvular surgery. Preoperative addressing of symptomatic or more hemodynamically significant (> 70%) asymptomatic carotid disease is recommended, if the patient is stable and can tolerate the waiting period between carotid endarterectomy and the aneurysm repair [96]. Preoperative arterial blood pressure patient readings constitute a useful indicator of the blood pressure that should be maintained intraoperatively and immediately postoperatively. Dramatically hypertensive patients may suffer at pressures of 80–120 mmHg. Since bleeding is the most frequent etiology of hypotension in aortic surgery, meticulous hemostasis emerges as the paramount factor for the maintenance of optimal intraoperative blood pressure. Additional hemostatic measures include (i) routine use of Teflon or pericardial strips for coronary (less accessible) button reinforcement, (ii) routine reinforcement of the posterior aortic anastomotic wall with interrupted pledgeted sutures in addition to the primary continuous suture line, (iii) wrapping of the anastomosis, particularly in cases of dissection, and (iv) utilization of the several available glue materials.

Prevention of air or particulate embolism Experience has shown that although primary lining by thrombus is rare in the ascending aorta, atheromatous debris are common in this area and in the aortic arch. This material is easily dislodged during aortic replacement manipulations. Patients with ascending aortic dissection usually have minimal atherosclerosis and atheromatous embolism is of lesser magnitude. Useful techniques to minimize atheromatic debris embolization include (i) meticulous cleaning and irrigation of the open aorta, (ii) head vessel exclusion, and (iii) retrograde cerebral perfusion.

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Embolization of atheromatous debris is somewhat counterintuitive in operations of the descending aorta because the descending aorta, being downstream from the head vessels, might not be expected to be a significant source of air or particulate matter in such operations [96]. In our experience, strokes do indeed occur with frequency in operations of the descending aorta. We believe that manipulation of the aortic arch for proximal control and femoral artery retrograde perfusion are two important causes of type I neurological injury in descending aortic operations. Technical modifications in aortic surgery to reduce type I neurological injury from particulate or air embolism include: 1 Avoidance of left atrial appendage cannulation in atrial fibrillation (Figure 21.4a). 2 Cannulation of the (L) superior or inferior pulmonary vein in these cases, or avoidance of cannulation entirely. 3 Subclavian (instead of femoral) artery cannulation in ascending aortic procedures in which descending or abdominal atheroma is detected. 4 In descending aortic procedures, application of proximal cross clamp before the initiation of (left atrial to femoral artery) CPB and removal of the clamp after discontinuation of CPB (Figure 21.4b). 5 Steep Trendelenburg positioning. 6 Carotid vessel occlusion during DHCA. 7 Carbon dioxide flooding of the operative field. 8 Meticulous and prolonged venting during rewarming. 9 Wide open de-airing through the suture line. 10 Trickle flow from below, to allow the atrial tree to fill slowly, like a well. 11 Repositioning of the arterial perfusion cannula from the femoral artery (used initially) to the graft itself (or to a side arm, small-caliber prefabricated graft) when perfusion is restarted in case of severe atherosclerotic debris (96).

Prevention of malperfusion syndromes Cerebral malperfusion syndromes can present before, during and after aortic operation. For dissections, Griepp has described intraoperative cerebral malperfusion as an ‘insidious problem with catastrophic consequences’. Fortunately, cerebral malperfusion is infrequent in aortic dissection at initial presentation. In the unfortunate event that a patient presents to the hospital with cerebral malperfusion, the treatment is immediate operation with ascending aortic replacement, as long as there is no evidence of completed stroke with cerebral necrosis. Malperfusion may present intraoperatively at two district phases: at the initiation of perfusion (usually via the femoral artery), and after the completion of the anastomoses of the ascending aortic graft when perfusion is resumed. In the first case of early intraoperative malperfusion, the femoral cannula may have been unintentionally misplaced in the false lumen. This can be recognized by a flaccid ascending aorta or head vessels after institution of perfusion. Corrective action should be taken immediately, before brain death results.

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(a)

(b) Figure 21.4 (a) Illustration of the correct order of aortic cross clamping, and (b) avoidance of left atrial appendage cannulation in patients with atrial fibrillation.

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Two alternative options exist. First one may cannulate the opposite femoral arteryaalthough there is sometimes no guarantee that this cannulation will recruit the true lumen. Alternatively, we recommend the selective cannulation of the carotid arteries to ensure cerebral perfusion, with simultaneous right radial artery blood pressure monitoring, which indicates the status of the innominate artery perfusion. In the case of cerebral malperfusion after completed replacement of the ascending aorta for type I dissection, early TEE and transcranial Doppler echocardiographic application can recognize and quantify cerebral malperfusion once the proximal and distal anastomoses are completed and circulation resumed for rewarming. If malperfusion is detected by the anesthesiologist after unclamping the new aorta, the cannula should immediately be replaced in the graft, thus restoring antegrade cerebral blood flow by decompressing the false channel and relieving the obstruction. If cerebral malperfusion is not recognized until the ICU after the entire operation is completed, immediate carotid fenestration or grafting are indicated, but almost invariably with poor results and a very high incidence of residual incapacitating neurological type I injury. In chronic type A dissections, inappropriate restoration of ‘single-barrel’ aorta can potentially cause a massive type I neurological injury. For acute type A dissections, we always reconstitute a single-barrel aorta by re-approximating the two dissected aortic wall layers. But in the case of chronic type A dissection, the chronic double-barrel aorta must be preserved. We fenestrate the distal flap and sew the graft to the adventitia only. By the chronic stage, important organs, including the brain and the kidneys, may be completely dependent on the false lumen for their perfusion [96].

Prevention of inadequate cerebral protection during DHCA Deep hypothermia and circulatory arrest is a term used when the circulation is deliberately suspended at pharyngeal temperatures < 20 °C. Hypothermia is achieved by cold perfusion in combination with ice packing around the head and a cooling blanket [97]. To prevent the numerous adverse reactions and their effects on cerebral homeostasis, numerous interventions must be undertaken. These practices include progressive vs. rapid systemic cooling [98], acid-base balance monitoring and correction [99], avoidance of hyperglycemia [100] and an arrest time of ≤ 45 min to ensure minimal cerebral side-effects. If periods of ≥ 60 min are anticipated (infrequent event), one has the following options: retrograde perfusion via the superior vena cava (SVC) or selective antegrade cerebral perfusion. If the right subclavian artery was cannulated already for CPB, simply resuming low flow in the arterial line and clamping across the base of the innominate artery will restore perfusion. The following additional cerebral protection guidelines in patients in whom DHCA was utilized have been proposed by Ergin and coworkers [101]: 1 Maintenance of cerebral perfusion pressure of 40–50 mmHg (by right radial artery trace) during selective cerebral perfusion.

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2 Application of brief retrograde cerebral perfusion before antegrade perfusion in case of patients with a high risk of type I neurological injury (extensive atheroma). 3 Occlusion of inferior vena cava when retrograde cerebral perfusion is used. 4 Avoidance of high pressures during continuous retrograde cerebral perfusion to avoid cerebral edema. 5 Avoidance of hyperglycemia and aggressive correction of acidosis.

Retrograde cerebral perfusion Retrograde cerebral perfusion, originally described by Mills [102] and popularized by Ueda [103] combined with hypothermia, is an alternative method for brain protection during DHCA. The SVC is perfused with cold blood at a pressure of 20–30 mmHg and a resultant flow of 250–800 ml/min. Numerous studies show that only a fraction of this flow actually perfuses the brain [104–106]. Nevertheless, several investigators have demonstrated brain oxygenation [107] and reduced type I neurological injury after aortic arch operations utilizing retrograde cerebral perfusion [104,105,108].

Direct antegrade cerebral perfusion Direct antegrade cerebral perfusion was first introduced by DeBakey [109] under normothermic conditions and was associated with high mortality and high incidence of type I neurological injury. In theory, direct antegrade cerebral perfusion should provide the best CNS protection, especially when combined with hypothermia. Bachet [110] renewed interest in the technique, demonstrating acceptable mortality and low incidence of type I injury (5%). Since then, multiple studies have shown benefits of direct antegrade cerebral perfusion [111–114] mainly by extending the ‘safe’ interval of DHCA for procedures on the aortic arch. Severe drawbacks of this method are its obligatory manipulation of the head vessels (with increased risk of embolization, wall trauma, or even dissection), the variability of perfusion protocols, and the cumbersome nature of the lines and cannulas. In any configuration the method relies on an intact circle of Willis for full brain perfusion. Despite favorable incidence of reported type I neurological injuries, direct antegrade cerebral perfusion is not universally practiced because of the enhanced potential of the dangers inherent in direct vessel manipulation and the cumbersome apparatus. Regarding the choice between deep hypothermic circulatory arrest, retrograde cerebral perfusion and direct antegrade cerebral perfusion, it is safe to say that knowledgeable experts prefer each technique. No advantage of one over another has been documented.

Prevention of stroke in aortic surgeryathe Yale experience We reviewed 317 thoracic aortic operations performed at Yale-New Haven Hospital with regard to incidence of stroke [115]. From these procedures, 206 (64.9%) were performed electively and 97 (35.1%) emergently. The overall incidence of stroke was 7.3%. When classified as emergent, the stroke incidence

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was 16.5% as opposed to 3.4% in elective procedures. When classified as ascending vs. descending aortic procedures, the stroke rate was 6.9% and 8.1%, respectively. Univariate analysis showed that only a preoperative history of diabetes was a significant preoperative risk factor for stroke. Of all the strokes encountered, 65.2% were embolic, 13% were ischemic and 13% were hemorrhagic. Patients with a stroke remained intubated an average of 8.9 days longer than those without a stroke (12.7 vs. 3.8 days) and stayed 17.1 days longer in the hospital after the operation, than those without (31.4 vs. 14.3 days). Long-term survival in stroke patients was dismal. Because intraoperative emboli were the overwhelming source of stroke in our study, we focused intensively on anti-embolic precautions and modifications to our operative technique. The following specific technical alterations were incorporated and are recommended: 1 Mobilizationaeven mobilization for operations on severely diseased descending aortas can liberate debris. The aortic arch should be gently manipulated for proximal control in descending aortic operations. 2 Debridementaon severely diseased aortic cuffs before anastomosis and restoration of circulation, meticulous debridement is essential. 3 Echocardiographyatransesophageal and epiaortic echocardiographic selection of the aortic cannulation site. In patients with severe, mobile atheroma of the descending aorta, avoidance of femoral cannulation and alternative perfusion through the subclavian or axillary artery are recommended. 4 Carbon dioxide flooding of the operative field, which displaces air and is quickly absorbed in case of air embolism, is strongly recommended. 5 Order of clamping in descending aortic surgery is paramount. We recommend the application of the proximal clamp before the initiation of femoral perfusion and similarly discontinuation of perfusion before the release of the proximal clamp. In this way, liberated debris is obligated away from the brain. 6 Avoidance of the left atrium (LA) in atrial fibrillation. In patients with atrial fibrillation, the appendage may contain clot. It is best to avoid cannulation of such an appendage for LA-femoral bypass. The clamp and sew technique of femoral artery-femoral vein bypass may be preferable. We observed a significant decrease in stroke rate for operations on the descending aorta in the time period after the embolic nature of stroke was documented and systemic anti-embolic measures instituted [115].

Mechanisms of spinal cord injury in aortic surgery Risk factors for spinal cord ischemia during aortic surgery Paraplegia and parparesis represent a devastating neurological complication in thoracic and thoraco-abdominal aortic surgery, and their incidence in the thoraco-abdominal literature varies from 4 to 38% [116]. Factors that affect these percentages are total aortic clamp time, extent of aorta replaced and the presence or absence of dissection [117]. From an operative standpoint, patients with few or no patent segmental arteries in the replaced aortic segment (especially in the T8–L2 region) have better neurological

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outcome, especially when atrio-femoral bypass is used [118]. Depending on the Crawford classification, the average incidence of spinal cord injury is 11–13% for type I, 28–30% for type II, 6–8% for type III, and 3–5% for type IV. Operation for extensive acute type B aortic dissection carries an exceptionally high risk of paraplegia or paraparesis. More recently, a biochemically medicated reperfusion spinal cord injury has been identified to play an important role in a subgroup of patients who develop deficits soon after surgery [119].

Pathophysiology of spinal cord injury The occurrence and the degree of spinal cord injury is dependent upon: 1 Duration of reduced blood flow. 2 Presence of collateral flow (with atrio-femoral bypass), or steal phenomena. 3 Neuronal metabolic rate. 4 Rate and amount of CSF pressure increase. 5 Rate and intensity of reperfusion injuries (neutrophil glutamate action). The exact pathophysiological cellular and subcellular mechanisms that are involved in spinal cord injury have not been completely elucidated. The amino acid glutamate has emerged as a basic mediator with an important role in acute spinal cord injury during ischemia and reperfusion [120]. The amino acids glutamate and aspartate are widely spread spinal cord neurotransmitters. Despite that, increased intraneuronal levels of these two amino acids have been shown to be highly neurotoxic to hypoxic or anoxic neurons. Under normal conditions, a well-perfused spinal cord has protective mechanisms to keep intraneuronal aspartate and glutamate levels to a minimum. In hypoxia, anoxia, or spinal cord trauma or severe inflammation, the energy (ATP)-dependent neuronal reabsorption systems fail and the intraneuronal glutamate level rises to a three to four-fold level even for 60–90 min after reperfusion. Glutamate exerts its action through three classes of receptors. The NMDA classes of receptors are membrane receptors connected to Ca2+/Na+ channels and glutamate action to these receptors leads to rapid influx of Ca2+, Na+ and Cl– into the neuronal cell with resulting intracellular edema and lysis. A delayed secondary form of spinal cord neuronal cell injury results from the rapid intracellular rise in Ca2+ concentration [121]. Ca2+ concentrations lead to phospholipid membrane disruption, arachidonic acid release and irreversible mitochondrial injury [122]. Specific pharmacological inhibitors of the above events are being developed and tested in animal models. These substances are either competitive or non-competitive inhibitors and blockers of the NMDA receptors. Competitive blockers have in general reduced in vivo potential because of their inability to effectively cross the blood–brain barrier. In contrast, non-competitive NMDA blockers are lipophilic and easily cross the blood–brain barrier with resultant high concentrations at the site of the injury [120]. Dextrophan has been shown to reverse glutamate-mediated neuronal injury in neuronal cell cultures and also in rabbit models. Similar results have been achieved with the administration of MK-801 in

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mice. In other studies, in patients under hypothermic circulatory arrest, besides glutamate, nitric oxide seems to be highly neurotoxic [121,122].

Spinal cord protection during aortic surgery The currently used clinical or evolving laboratory techniques for spinal cord protection include the following: 1 Pharmacological. 2 Mechanical. (a) CSF drainage (b) Peripheral perfusion (c) Hypothermia (i) Systemic (ii) Local (d) Sensory evoked potentials (SEP)/motor evoked potentials (MEP) guided intercostal artery ligation (e) Adamkiewicz artery imaging (f) Segmental artery reimplantation (T7–LI).

Pharmacological interventions Multiple pharmacological agents have been tested in animal and human studies. These include allopurinol, superoxide dismutase, naloxone, barbiturates, steroids, manitol, gangliosides, ACE inhibitors, NMDA inhibitors such as dextrophan, and MK-801 and adenosine [123]. Ongoing research suggests that a combination of different agents rather than a single agent may be the most effective for pharmacological protection and treatment of spinal cord injury in the future.

Mechanical Cerebrospinal fluid drainage It is known that the decrease in spinal cord perfusion is partially due to an increase in CSF pressure during the ischemic period. This is especially true when vasodilatation is used to decrease the proximal aortic pressure [124]. Sodium nitroprusside is frankly contraindicated (for this reason) in aortic surgery. In the 1960s, Blaisdell, Cooley [125] and Miyamoto [126] introduced CSF drainage during aortic cross clamping. Although these initial studies were optimistic, the efficacy of CSF drainage has not been tested alone. Favorable results have been reported regarding CSF drainage in combination with naloxone infusion [126] or the use of atriofemoral bypass [127] or intrathecal papaverin injection [118,128]. At our institution, CSF drainage is routinely employed for thoracic and thoracoabdominal aneurysms intraoperatively and for 48 h postoperatively. We try to maintain an intrathecal pressure of < 10 Torr.

Peripheral perfusion The high incidence of neurological injury during and after repairs for

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Crawford type I and type II thoracoabdominal aneurysms has resulted in the application of partial (atriofemoral) bypass during the repair of these aneurysms by the majority of reporting groups. Left atrial to femoral artery bypass is routinely used in our institution in these cases with mild heparinization and distal flow of 2.5–3.5 l. In the reported series, partial bypass is combined with CSF drainage [118,129] or concurrent aggressive reattachment of lower thoracic and upper lumbar arteries. This is our policy. We prefer a ‘cobrahead’ technique for safe, expedient intercostal reimplantation.

Hypothermia Hypothermia reduces metabolic demands at a cellular level. A 60% reduction in spinal cord metabolic rate has been observed in local hypothermia of 28–30°C. Hypothermia also increases spinal cord tolerance to ischemia by decelerating the membrane degeneration process, influx of Ca2+ ions, ATP storage depletion, and enzyme deactivation rate. There are four described hypothermia techniques aiming at reducing spinal cord injury. Total hypothermia with cardiopulmonary bypass Total hypothermia with cardiopulmonary bypass has been used with proven results in reducing postoperative paraplegia. The preferred method involves partial (atrio-femoral) bypass with mild hypothermia [31–33%] [130]. Arrhythmias are occasionally encountered. Risk of postoperative myocardial infarction is also increased. Local epidural cooling Local epidural cooling causing regional spinal cord hypothermia during aortic cross clamping has been effective in preventing spinal cord injury in animal models [131–133]. This technique has the main advantage of avoiding the undesirable side-effects of systemic hypothermia. The potential theoretical disadvantage of this method is that epidural administration of a cold solution could potentially cause a sharp rise in CSF pressure. Davidson and coworkers [133] have reported favorable results using this protection technique in eight patients with no adverse spinal cord results. Local aortic cold solution infusion Local aortic cold solution perfusion at an isolated aortic segment that gives vessels to the spinal cord has been utilized in animal models The main disadvantage of this method is that it incorporates a period of aortic perfusion during which the aorta is closed, with resultant prolongation of ischemia time and operation. There are no current clinical applications of this method today. Hypothermic circulatory arrest Hypothermic circulatory arrest was initially reported by Crawford and coworkers [134] in the late 1980s. Swensson and coworkers reported on 656 patients with a mean circulatory arrest time of 31 min. This study involved patients who had several types of aortic pathology, including ascending, aortic arch, and thoracoabdominal aneurysm

Neurological complications in cardiac surgery 427

patients. This study proved that the incidence of central and spinal cord injury significantly increases after 40 min of circulator arrest. Furthermore, the overall operative mortality increases markedly after 65 min of circulatory arrest. In a series of 96 patients with thoracoabdominal aneurysm repair, Kouchoukos and coworkers [135] reported a mortality of 7.3% and an incidence of paraplegia/paraparesis of 3.3%. Hypothermic circulatory arrest may be associated with a series of complications such as parenchymal pulmonary hemorrhage, acute respiratory distress syndrome and other pulmonary complications [134,136,137]. Several experts do not routinely use hypothermic circulatory arrest and prefer to use this method when (i) there is a need for aortic arch pathology repair, or (ii) there is difficulty in aortic cross clamping because of either rupture or extensive atherosclerosis [138]. For descending aortic operations we recommend deep hypothermic circulatory arrest when proximal control and repair involve the distal aortic arch.

Evoked potentials It has been shown in experiments since the 1960s that stimulation of the upper thoracic spinal cord and synchronous functional monitoring is a reliable indicator of ischemic injury based on the changes in the evoked potentials of the lower extremity skeletal muscles (MEPs). Also, sensory potentials (SEPs) have been monitored. Several technical modifications have been described. These in general involve modifications of neuromuscular blocking agent administration by the anesthesiologist and synchronous monitoring at the lower extremities. Hypothermia, anesthetics and intrathecal medications may affect evoked potentials and have to be accounted for when interpreting the evoked potential derived data [139.] When an intercostal vessel needs to be sacrificed prior to induction to CPB, one should proceed with temporary occlusion of the vessel, and then proceed with the division of this vessel [140]. SEP monitoring when employed is prudent to continue for the first 2–3 postoperative days. SEPs are not widely employed because of the technical complexity and because most surgeons see no impact on management: this surgical procedure must be performed as quickly and as safely as possible in all patients, not just those who manifest abnormal SEPs.

Adamkiewicz artery imaging and intercostal artery reimplantation In 90% of patients, the artery of Adamkiewicz starts between T7 and L1 and in 80% of cases this artery branches from the left segmental intercostal or the lumbar artery [141]. Although opinions vary [142], in the majority of cases intercostal artery reimplantation between T7 and L1 is performed. This reimplantation is not necessary when severe disease of the central portion of the descending aorta is present and has already obliterated the intercostal vessels. As regards the preoperative imaging of the Adamkiewicz artery, although technically feasible, it is time consuming and is associated with a small incidence of paraplegia or paraparesis. Because of that, it is not widely

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used [143]. As a technical means of re-implantation of the intercostal arteries, at our institution we use a ‘cobrahead’ technique [144].

Future directions The evolution in pump technology, pump materials, intraoperative techniques, neuroprotective agent development, and a more in-depth understanding of neuronal molecular mechanisms of injury, apoptosis and death seem to hold the key to the future decrease in the incidence in neurological injury in cardiac surgery. After death itself, neurological injury is the most devastating complication of cardiac surgery. With the advent of the 21st century, neurological injury remains essentially an unconquered frontier for the cardiac surgeon. The thoughtful, systematic, detailed investigation of perioperative stroke by our specialty has led to the observations and recommendations made in this chapter.

References 1 Gilman S. Cerebral disorders after open-heart operation. N Engl J Med 1965; 272: 489–498. 2 Javid H, Tufo HM, Najafi H et al. Neurologic abnormalities following open-heart surgery. J Thorac Cardiovasc Surg 1969; 58: 502–509. 3 Mills SA. Cerebral injury in cardiac operations. Ann Thorac Surg 1993; 56: 586–591. 4 Utley JR, Leyland SA, Johnson HD et al. Correlation of preoperative factors, severity of disease, type of oxygenation, and perfusion times with mortality and morbidity of coronary bypass. Perfusion 1991; 6: 15–22. 5 Roach GW, Kanchuger M, Mangano CM et al. for the multicenter Study of Perioperative Ischemia Group and Ischemia Research Foundation. Adverse cerebral outcomes after coronary bypass surgery. N Engl J Med 1996; 335: 1857–1863. 6 Rothenburger M, Soeparwata R, Deng MC et al. Prediction of clinical outcome after cardiac surgery: the role of cytokines, endotoxin, and antiendotoxin antibodies. Shock 2001; 16 (S1): 44–50. 7 Rothenburger M, Soeparwata R, Deng MC et al. The impact of antiendotoxin core antibodies and cytokine release and ventilation time after cardiac surgery. J Am Coll Cardiol 2001; 38: 124–130. 8 Markewitz A, Lante W, Franke A, Marohl K, Kuhlmann WD, Weihold C. Alterations of cell-mediated immunity following cardiac operations: clinical implications and open questions. Shock 2001; 16: 10–15. 9 Sablotzki A, Mann V, Simm A, Czeslick E. Changes in the cytokine network through escalating SIRS after heart surgery. Anas Intens Notfall Schmerz 2001; 36: 522–529. 10 Marie C, Muret J, Fitting C, Payen D, Cavaillon JM. Interleukin-1 receptor antagonist production during infectious and noninfectious SIRS. Crit Care Med 2000; 28: 2277–2282. 11 Hamano K, Kawamura T, Gohra H et al. Stress caused by minimally invasive cardiac surgery versus conventional cardiac surgery: incidence of SIRS. W J Surg 2001; 25: 117–121. 12 Vallely MP, Bannon PG, Kritharides L. The systemic inflammatory response syndrome and off pump surgery. Heart Surg For 2001; 4: 7–13. 13 Boeken U, Feindt P, Mohan E et al. Post-perfusion syndrome and disturbed microcirculation after cardiac surgery: the role of angiotensin-converting enzyme inhibitors. Thorac Cardiovasc Surg 1999; 47: 347–351.

Neurological complications in cardiac surgery 429 14 Boeken U, Feindt P, Zimmermann N et al. Increased preoperative CRP-values without signs of an infection and complicated course after cardiopulmonary bypass operations. Eur Jr Cardiothorac Surg 1998; 13: 541–545. 15 Furunaga A, Tsuboi H, Itoh H et al. Significance of SIRS at cardiopulmonary bypass. J Jap Ass Thorac Surg 1996; 44: 790–794. 16 Agnilar MJ, Gerbone F, Hill J. Neuropathologic complications of cardiac surgery. J Thorac Cardiovasc 1971; 61: 676–685. 17 Sotaniemi KA. Brain damage and neurological outcome after open-heart surgery. J Neurol Neurosurg Psychiatry 1980; 43: 127–135. 18 Shaw PJ, Bates D, Cartlidge NEF et al. An analysis of factors predisposing to neurological injury in patients undergoing coronary bypass operations. Q R Med 1989; 267: 633–646. 19 Levy DE, Bates D, Carponna JJ et al. Prognosis in non-traumatic coma. Ann Intern Med 1981; 94: 293–302. 20 Shaw PJ, Bates D, Cartlidge NEF et al. Neuro-ophthalmological complications of coronary artery bypass graft surgery. Acta Neurol Scand 1987; 76: 1–7. 21 Magee KR. Clinical analysis of reflexes. In: Vinken PJ, Bruyn GW, eds. Handbook of Clinical Neurology, Vol. 1. Amsterdam: North Holland, 1969; 237–256. 22 Shaw PJ, Bates D, Cartlidge NEF et al. Early neurological complications of coronary artery bypass surgery. Br Med J 1985; 291: 1384 –1387. 23 Newman S. The incidence and nature of neuropsychological morbidity following cardiac surgery. Perfusion 1989; 4: 93–100. 24 Stump DA, Rogers TA, Hammon WJ et al. Cerebral emboli and cognitive outcome after cardiac surgery. J Cardiothorac Vasc Anesthesia 1996; 10: 113–119. 25 Shaw PJ, Bates D, Cartlidge NEF et al. Neurologic and neuropsychological morbidity following major surgery. Comparison of coronary artery bypass and peripheral vascular surgery. Stroke 1987; 18: 700–707. 26 Stump D, Newman S, Coker L et al. Persistence of neuropsychol deficits following CABG. Anesthesiol 1990; 73: A113. 27 Stump DA, Hart S, Ruby BJ et al. New neuropsychol deficits one month following CABG. Anesth Anal 1994; 78: 5419. 28 Rabiner CJ, Willner AE, Fishman J. Psychiatric complications following coronary bypass surgery. J Nerv Ment Dis 1975; 160: 342–348. 29 Mills S, Prough D. Neuropsychiatric complications following cardiac surgery. Semin Cardiovasc Surg 1991; 3: 39– 46. 30 Aberg H, Torkel. Deviations of the normal postoperative course regarding cerebral function. American Association for Thoracic Surgery, Neurologic Injury during Cardiac Surgery III. New Orleans, April 16, 1999. 31 Morin JE, Lang R, Elleker MG et al. Upper extremity neuropathies following median sternotomy. Ann Thorac Surg 1982; 34: 181–185. 32 Lederman RJ, Breuer AC, Hanson MR et al. Peripheral nervous system complications of coronary artery bypass graft surgery. Ann Neurol 1982; 12: 297–302. 33 Newman MF, Wolman R, Kanchuger M et al. Multicenter preoperative stroke risk index for patients undergoing coronary artery bypass graft surgery. Multicenter Study of Perioperative Ischemia (McSPI) Research Group. Circulation 1996; 94 (Suppl. II): 74–80. 34 Roach GW. Neurologic injury in cardiac surgery: incidence, risk factors and cost impact. American Association for Thoracic Surgery, Neurologic Injury during Cardiac Surgery III. New Orleans April 16, 1999. 35 Wolman RL, Nussmeien N, Aggarwal A et al. For the Multicenter Study of Perioperative Ischemia Group and the Ischemia Research Foundation. Cerebral injury after cardiac surgery: identification of a group at extraordinary risk. Stroke 1999; 30: 514 –522.

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36 Barbut D. Aortic atheroma. Single largest predictor of stroke in cardiac surgery. American Association for Thoracic Surgery, Neurologic Injury during Cardiac Surgery III. New Orleans, April 16, 1999. 37 Llinas R, Barbut D, Caplan LR. Neurologic complications of cardiac surgery. Prog Cardiovasc Dis 2000; 43: 101–112. 38 Barbut D, Lo YW, Hartman GS et al. Aortic atheroma is related to outcome but not numbers of emboli during coronary bypass. Ann Thorac Surg 1997; 64: 454 –459. 39 Eugleman D, Cohn LH, Rizzo RJ. Incidence and predictors of transient ischemic attach and strokes following coronary artery bypass grafting. Report and collective review. American Association for Thoracic Surgery, Neurological Injury During Cardiac Surgery V, San Diego, May 5, 2001. 40 Eugleman D, Cohn LH, Rizzo RJ. Incidence and predictors of transient ischemic attach and strokes following coronary artery bypass grafting: report and collective review. Heart Surg Forum 1999; 2: 242–245. 41 Read GL, Scager GE, Picard EH et al. Stroke following coronary artery bypass surgery. N Engl J Med 1988; 319: 246–250. 42 Faggioli GL, Curl GR, Ricotta JJ. The role of carotid screening before coronary artery bypass. J Vasc Surg 1990; 12: 724 –731. 43 North American Symptomatic Carotid Endarterectomy Trial Collaborations. Beneficial effect of carotid endarterectomy in symptomatic patients with high-grade stenosis. N Engl J Med 1991; 325: 445–453. 44 European Carotid Surgery Trialists’ Collaborative Group. MRC European Carotid Surgery Trial: interim results for symptomatic patients with severe (70–90 percent) or with mid (0–29 percent) carotid stenosis. Laucet 1991; 337: 235–243. 45 Hobson RW, Weiss DG, Fields WS et al. Efficacy of carotid endarterectomy for asymptomatic carotid artery stenosis. N Engl J Med 1993; 328: 221–227. 46 Executive Committee for the Asymptomatic Carotid Endarterectomy Study. Endarterectomy for asymptomatic carotid artery stenosis. JAMA 1995; 273: 421–428. 47 Hetzer NR, Loop FD, Beven EG et al. Surgical staging for simultaneous coronary and carotid disease. A study including prospective randomization. Vasc Surg 1989; 9: 455–463. 48 Akins CW, Moncure AC, Daggett WM et al. Safety and efficacy of concomitant carotid and coronary artery operations. Ann Thorac Surg 1985; 60: 311–318. 49 Daily PO, Freeman RK, Dembitsky EWP et al. Cost reduction by combined carotid endarterectomy and coronary artery bypass grafting. J Thorac Cardiovasc Surg 1996; 111: 185–193. 50 Akins CW. The case for combined carotid and coronary artery surgery. Adult Cardiac Surgery Symposium. 79th Annual Meeting, American Association for Thoracic Surgery, New Orleans, April 18. 1999. 51 Davila-Roman VG, Barzilai B, Wareing TH, Murphy SF, Kouchoukos NT. Intraoperative ultrasonographic evaluation of the ascending aorta in 100 consecutive patients undergoing cardiac surgery. Circulation 1991; 84 (Suppl. III): 47–53. 52 Ribakove GH, Katz ES, Galloway AC et al. Surgical implications of transesophageal echocardiography to grade the atheromatous aortic arch. Ann Thorac Surg 1992; 53: 758–763. 53 Katz ES, Tunick PA, Rusinek H, Ribakove G, Spencer FC, Kronzon I. Protruding aortic atheromas predict stroke in elderly patients undergoing cardiopulmonary bypass: experience with intraoperative transesophageal echocardiography. J Am Coll Cardiol 1992; 20: 70–77.

Neurological complications in cardiac surgery 431 54 Wareing TH, Davila-Roman VG, Barzilai B, Murphy SF, Kouchoukos NT. Management of the severely atherosclerotic ascending aorta during cardiac operations. J Thorac Cardiovasc Surg 1992; 103: 453–462. 55 Nicolosi AC, Aggarwai A, Almassi GH, Olinger GN. Intraoperative epiaortic ultrasound during cardiac surgery. J Card Surg 1996; 11: 49–55. 56 Wareing TH, Davila-Roman VG, Daily BB et al. Strategy for the reduction of stroke incidence in cardiac surgical patients. Ann Thorac Surg 1993; 55: 1400–1407. 57 Pugsley W, Klinger L, Paschalis C, Treasure T, Harisson M, Newman S. The impact of microemboli during cardiopulmonary bypass on neuropsychological functioning. Stroke 1994; 25: 1393–1399. 58 Murkin JM. Methods of stratifying patients at risk for neurological injury: visualizing the aorta in cardiac surgery. In: Neurological Injury During Cardiac Surgery III. Mobilizing Multidisciplinary Resources. New Orleans, April 16, 1999; 35–39. 59 Tovar EAI, Campo C, Bosari A et al. Postoperative management of cerebral air embolism. Ann Thorac Surg 1995; 60: 1138–1142. 60 Mueller X, Tevaearai H, VanNess K et al. Air trapping ability of the Spiral GoldTM membrane oxygenator. Perfusion 1998; 13: 53–57. 61 Von Segesser LK, Ruchat P. Reduction of embolus production and prevention of neurologic injury. In: Neurologic Injury During Cardiac Surgery IV. Mobilizing Multidisciplinary Resources. Glascow, Scotland, September 4, 1999; 18–21. 62 Ruchat P, Bogousslawsky J, Hurni M et al. Systematic surgical closure of patent foramen ovale in selected patients with cerebrovascular events due to paradoxical embolism. Eur J Cardiothorac Surg 1997; 11: 824 –827. 63 Von Segesser LK, Weiss B, Pasic M et al. Risk and benefit of low systematic heparinization during open heart operations. Ann Thorac Surg 1994; 58: 391–398. 64 Von Segesser LK. Rationale for surface modification of arterial filter media. In: Neurologic Injury During Cardiac Surgery III. Mobilizing Multidisciplinary Resources. New Orleans, April 16, 1999; 44–45. 65 Reichenspruner H. Intraaortic filtration captures significant particulate debris during cardiac surgery. In: Neurologic Injury During Cardiac Surgery III. Mobilizing Multidisciplinary Resources. New Orleans, April 16, 1999; 46–49. 66 Navia JA. Intraaortic filtration. Case demonstration of effective capture of particulate emboli. In: Neurologic Injury During Cardiac Surgery III. New Orleans: American Association for Thoracic Surgery, April 16, 1999. 67 Navia JA. Video demonstration of a new surgical method of intraaortic filtration during cardiopulmonary bypass. In: Neurologic Injury During Cardiac Surgery III. A Call to Arms. Washington, DC: May 5, 1988. 68 Reichenspurner H, Navia JA, Berry G et al. Particulate emboli capture by an intraaortic filter device during cardiac surgery. J Thorac Cardiovasc Surg 2000; 119: 233–241. 69 Reichenspurner H. Arterial filtration during cardiac surgery. Report of the first series of patients. In: Neurologic Injury During Cardiac Surgery I. American Association for Thoracic Surgery Meeting, 1997. 70 Reichenspurner H. Validating emboli management during cardiac surgery: initial clinical experience with a new aortic filter device. A feasibility study. In: Neurologic Injury During Cardiac Surgery II. A Call to Arms. American Association for Thoracic Surgery Meeting, 1998. 71 Moritz A. International Council for Emboli Management (ICEM): a prospective observational studyathe Frankfurt experience. In: Neurologic Injury During Cardiac Surgery III. Mobilizing Multidisciplinary Resources. American Association for Thoracic Surgery Meeting, 1999.

432

Chapter 21

72 Wimmer-Greineker G, Gerber J, Dietrich M et al. Extraction of particulate emboli during cardiac surgery: International Council of Emboli Management Study Group Report. In: Neurologic Injury During Cardiac Surgery IV. Emerging Consensus. American Association for Thoracic Surgery Meeting, 2000. 73 Reichenspurner H. Risk factors and neurologic outcomes: International Council of Emboli Management Study Group results. In: Neurologic Injury During Cardiac Surgery. V. American Association for Thoracic Surgery Meeting, 2001. 74 Buckberg GD. A proposed solution to the cardioplegia controversy. J Thorac Cardiovasc Surg 1979; 77: 803–815. 75 Salerno TA. Single aortic cross-clamping for distal and proximal anastomeses in coronary surgery: an alternative to conventional techniques. Ann Thorac Surg 1982; 33: 518–520. 76 Aranki SF, Rizzo RJ, Adams DH et al. Single-clamp technique: an important adjunct to myocardial and cerebral protection in coronary operations. Ann Thorac Surg 1994; 58: 296–303. 77 Aranki SF, Sullivan TE, Cohn LH. The effect of the single aortic cross-clamp technique on cardiac and cerebral complications during coronary bypass surgery. J Card Surg 1995; 10: 498–502. 78 Barbut D, Hinton RB, Szatrowski TP et al. Cerebral emboli detected during bypass surgery are associated with clamp removal. Stroke 1994; 25: 2398–2402. 79 Yamaguchi A, Katamura N, Kawashima M et al. Clinical preeminence of single aortic cross-clamping for proximal anastomoses in coronary artery bypass surgery. Nippon Kyobu Geka Gakkai Zasshi (J Jpn Assoc Thorac Surg) 1993; 41: 1194 –1198. 80 Rajalin A, Kuttila K, Niinikoski J et al. Myocardial reperfusion after coronary artery bypass surgery. suture of only distal of all anastomoses with the aorta cross-clamped? Scand J Thorac Cardiovasc Surg 1995; 29: 175–180. 81 Bertolini P, Santini F, Montalbano G et al. Single aortic cross-clamp technique in coronary artery surgery: a prospective randomized study. Eur J Cardiovasc Surg 1997; 12: 413–419. 82 Hammon JW Jr, Stump DA, Kon ND et al. Risk factors and solutions for the development of neurobehavioral changes after coronary artery bypass grafting. Ann Thorac Surg 1993; 63: 1613–1618. 83 Musumeci F, Feccia M, MacCarthy PA et al. Prospective randomized trial of single-clamp technique versus intermittent ischemic arrest: myocardial and neurological outcome. Eur J Cardiothorac Surg 1998; 13: 702–709. 84 Kim RW, Mariconda DC, Tellides G et al. Single-clamp technique does not protect against cerebrovascular accident in coronary artery bypass grafting. Eur J Cardiothorac Surg 2001; 20: 127–132. 85 Quigley RL, Fuller BC, Sampson LN, Reitknecht FL. Passive retrograde cerebral perfusion during routine cardiac valve surgery reverses middle cerebral artery blood and reduces the risk of stroke. J Heart Valve Dis 1997; 6: 288–291. 86 Diesfeld T, Lajos TZ, Schimert G. Arterial venous bridge on cardiopulmonary bypass. J Card Surg 1994; 9: 128–130. 87 Quigley RL, Pym J, Highbloom YR et al. Passive retrograde cerebral perfusion following routine cardiac surgery may eliminate risk of perioperative embolic cerebral vascular accidents. In: Neurologic Injury During Cardiac Surgery V. American Association for Thoracic Surgery Meeting, San Diego, May 2001. 88 Iaco AL, Contini M, Theodori G et al. Off or on bypass? What is the safety threshold? Ann Thorac Surg 1999; 68: 1486–1489. 89 Kshettry VR, Flavin TH, Emery RW, Nicoloff DM. Does multivessel, off-pump coronary artery bypass (OPCAB) reduce postoperative morbidity? 36th Annual Meeting of the Society of Thoracic Surgeons, Fort Lauderdale, FL, Jan 31–Feb 2, 2000.

Neurological complications in cardiac surgery 433 90 BhaskerRao B, VanHimbergen D, Edmonds HL et al. Evidence of improved cerebral function after minimally invasive bypass surgery. J Card Surg 1998; 13: 27–31. 91 Bergsland J, Hasnain S, Lajos TZ, Salerno TA. Elimination of cardiopulmonary bypass: a prime goal in reoperative coronary artery bypass surgery. Eur J Cardiothorac Surg 1998; 14: 59–62. 92 Hernandez F, Cohn W, Baribeau YR et al. In-hospital outcomes of off-pump versus onpump coronary bypass procedures: a multicenter experience. Ann Thorac Surg 2001; 72:1528–1534. 93 Miller DC. Surgical management of aortic dissection: indications, perioperative management and long-term results. In: Doroghazi RM, Slater EE, eds. Aortic Dissection. New York: McGraw-Hill, 1983; 193–245. 94 Miller DC, Mitchell RS, Oyer PE et al. Independent determinants of operative mortality for patients with aortic dissections. Circulation 1984; 70: 1–153. 95 Griepp RB, Ergin MA, Lansman SL et al. The physiology of hypothermic circulatory arrest. Sem Thorac Cardiovasc Surg 1991; 3: 188. 96 Elefteriades JA. Postgraduate Lecture on ‘Cerebral Protection in Aortic Surgery’: 1999 American Association for Thoracic Surgery Meeting, New Orleans, April, 1999. 97 Griepp RB, Ergin MA, Lansman JL et al. The physiology of hypothermic arrest. Sem Thorac Cardiovasc Surg 1991; 3: 188–194. 98 Daries LK. Hypothermia: physiology and clinical use. In: Gravlee GP, Davis RF, Utley JR, eds. Cardiopulmonary Bypass. Baltimore: Williams & Wilkins, 1993; 140–150. 99 Swan H. The importance of acid-base management for cardiac and cerebral presentation during open heart operations. Surg Gynecol Obstet 1984; 158: 391–395. 100 Ekroth R, Thompson RJ, Lincoln C et al. Elective deep hypothermia with total circulatory arrest: changes in plasma creatine kinase BB, blood glucose and clinical variables. J Thorac Caridovasc Surg 1989; 97: 30–36. 101 Ergin MA, Galla JD, Lansman SL et al. Hypothermic circulatory arrest in operations on the thoracic aorta. Determinants of operative mortality and neurologic outcome. J Thorac Cardiovasc Surg 1994; 107: 788–789. 102 Mills NL, Ochsyer JL. Massive air embolism during cardiopulmonary bypass: causes, prevention and management. J Thorac Cardiovasc Surg 1980; 80: 708–714. 103 Ueda Y, Miki S, Kusuhara K et al. Surgical treatment of aneurysm of dissection involving the ascending aorta and aortic arch, utilizing circulatory arrest and retrograde cerebral perfusion. J Thorac Cardiovasc Surg 1982; 82: 249–257. 104 Lytle BW, McCarthy PM, Meaney KM et al. Cardiopulmonary bypass myocardial management and support techniques. J Thorac Cardiovasc Surg 1995; 109: 738–749. 105 Deep GM, Jenkins E, Bolling SF et al. Retrograde cerebral perfusion during hypothermic circulatory arrest reduces neurologic morbidity. J Thorac Cardiovasc Surg 1995; 109: 259–265. 106 de Brux JL, Subayi JB, Pegis JD, Pillet J. Retrograde cerebral perfusion. Anatomic study of the distribution of blood to the brain. Ann Thorac Surg 1995; 60: 1294 –1302. 107 Winsborrow BG, Koslowski P, Figueiras CL et al. 31P Spectroscopic imaging of pig brains during circulatory arrest. Can J Appl Spect 1994; 39: 135–140. 108 Ergin MA, Griepp RB, Lansman SL et al. Hypothermic circulatory arrest and other methods of cerebral protection during operations on the thoracic aorta. J Cardiac Surg 1994; 9: 525–532. 109 Debakey ME, Crawford ES, Cooley DA et al. Successful resection of fusiform aneurysm of aortic arch with replacement with homograft. Surg Gynecol Obstet 1957; 105: 657–701. 110 Bachet J, Guilment D, Boudot B et al. Cold cerebroplegia: a new technique for cerebral protection during operations on the transverse aortic arch. J Thorac Cardiovasc Surg 1991; 102: 85–92.

434

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111 Kazui T, Kimura N, Yamada O, Komatsu S. Surgical outcome of aortic arch aneurysms using selective cerebral perfusion. Ann Thorac Surg 1994; 57: 904 –911. 112 Alamanni F, Agrifoglio M, Pompilio G et al. Aortic arch surgery: pros and cons of selective cerebral perfusion: a multivariate analysis for cerebral injury during hypothermic circulatory arrest. J Cardiovasc Surg 1995; 36: 31–39. 113 Kazui T, Yamada O, Komatsu S. Emergency graft replacement of the aortic arch for acute type A dissection. J Cardiovasc Surg 1992; 33: 211–218. 114 Tabayashi K, Ohmi M, Togo T et al. Aortic arch aneurysm repair using selective cerebral perfusion. Ann Thorac Surg 1994; 57: 1305–1311. 115 Goldstein LJ, Davies RR, Rizzo JA et al. Stroke in surgery of the thoracic aorta: incidence, impact, etiology and prevention. J Thorac Cardiovasc Surg 2001; 122: 935–945. 116 Panneton JM, Hollier LH. Basic data underlying clinical decision making. Section d. Ann Vasc Surg 1995; 9: 503. 117 Coselli JS. Thoracoabdominal aortic aneurysms: experience with 372 patients. J Card Surg 1994; 9: 638–643. 118 Svensson LG, Crawford ES, Hess KR, Coselli JS, Safi HI. Experience with 1509 patients undergoing thoracoabdominal aortic operations. J Vasc Surg 1993; 17: 357–370. 119 Olney JW, Ho OL, Rhee V et al. Neurotoxic effects of glutamate. N Engl J Med 1973; 289: 374–375. 120 Kern JA. Mechanisms of spinal cord injury. In: Adult Cardiac Surgery Symposium. 79th Annual Meeting, American Association for Thoracic Surgery, New Orleans, April 18–21, 1999. 121 Brock MV, Blue ME, Lowenstein CJ et al. Induction of neuronal nitric oxide following hypothermic circulatory arrest. Ann Thorac Surg 1996; 62: 313–320. 122 Tseng EE, Brock MV, Lange MS et al. Neuronal nitric synthase inhibition reduces neuronal apoptosis after hypothermic circulatory arrest. Ann Thorac Surg 1997; 64: 639–647. 123 Swensson LG. New and future approaches for spinal cord protection. Semin Thorac Cardiovasc Surg 1997; 9: 18–33. 124 Gelman S, Reves JG, Fowler K et al. Regional blood flow during aortic crossclamping of the thoracic aorta and infusion of sodium nitroprusside. J Thorac Cardiovasc Surg 1983; 85: 287–293. 125 Blaisdell FW, Cooley DA. The mechanisms of paraplegia after temporary thoracic aortic occlusion and its relationship to spinal fluid pressure. Surgery 1962; 51: 351–355. 126 Miyamoto K. A new and simple method of preventing spinal cord damage following temporary occlusion of the thoracic aorta by draining the cerebrospinal fluid. J Cardiovasc Surg 1960; 16: 188–199. 127 Safi HI. Neurologic deficit in patients at high risk with thoracoabdominal aortic aneurysms: the role of cerebral spinal fluid drainage and distal aortic perfusion. J Vasc Surg 1994; 20: 343–443. 128 Mantrand-Workshop Group. Thoracoabdominal aortic aneurysms with special reference to technical problems and complications. Eur J Vasc Surg 1993; 7: 725–730. 129 Safi HI, Campbell MP, Miller CC et al. Cerebral spinal fluid drainage and distal aortic perfusion decrease the incidence of neurological deficit: the results of 343 descending and thoracoabdominal aortic aneurysm repairs. Eur J Vasc Endovasc Surg 1997; 14: 118–124. 130 Frank SM, Parker SD, Rock P et al. Moderate hypothermia, with partial bypass and segmental sequential repair for thoracoabdominal aortic aneurysm. J Vasc Surg 1994; 19: 687–683. 131 Berguer R, Porto J, Fedoronko B et al. Selective deep hypothermia of the spinal cord prevents paraplegia after aortic crossclamping in the dog model. J Vasc Surg 1992; 15: 62–68.

Neurological complications in cardiac surgery 435 132 Wisselink W, Becker MO, Nguyen JH et al. Protecting the ischemic spinal cord during aortic clamping: the influence of selective hypothermia and spinal cord perfusion pressure. J Vasc Surg 1994; 19: 788–794. 133 Marsala M, Vanicky I, Galik J et al. Panmyelic epidural cooling protects against ischemic spinal cord damage. J Vasc Surg 1994; 20: 304 –310. 134 Crawford ES, Coselli JS, Safi HJ. Partial cardiopulmonary bypass, hypothermic circulatory arrest and posteriolateral exposure for thoracic aortic aneurysm operation. J Thorac Cardiovasc Surg 1987; 94: 824 – 831. 135 Rokkas CK, Kouchoukos NT. Profound hypothermia with spinal cord protection in operations on the descending thoracic and thoracoabdominal aorta. Semin Thorac Cardiovasc Surg 1998; 10: 57–60. 136 Szempetery S, Crisler C, Grinnan GLB. Deep hypothermic arrest and left thoracotomy for repair of difficult thoracic aneurysms. Ann Thorac Surg 1993; 55: 830–833. 137 Safi HI, Miller CC III, Subramanian MH et al. Thoracic and thoracoabdominal aortic aneurysm repair using cardiopulmonary bypass, profound hypothermia, and circulatory arrest via left side of the chest incision. J Vasc Surg 1998; 28: 591–598. 138 Coselli JS. Left atrial to femoral bypass vs circulatory arrest. In: Adult Cardiac Surgery Symposium. 79th Annual Meeting, American Association for Thoracic Surgery, New Orleans, April 18–21, 1999. 139 Svensson LG. Commentary on the DeHaan and colleagues: efficacy of the transcranial motor evoked myogenic potentials to detect spinal cord ischemia during operations for thoracoabdominal aneurysms. J Thorac Cardiovasc Surg 1997; 113: 100 –101. 140 Galla JD, Ergin MA, Sadeghi AM et al. A new technique using somatosensory evoked potential guidance during descending and thoracoabdominal aortic repairs. J Card Surg 1994; 9: 662–667. 141 Svensson LG, Crawford ES. Cardiovascular and Vascular Disease of the Aorta. Philadelphia: W.B Saunders, 1997. 142 Griepp RB, Ergin MA, Galla JD et al. Looking for the artery of Adamkiewicz: a quest to minimize paraplegia after operations for aneurysms of the descending thoracic and thoracoabdominal aorta. J Thorac Cardiovasc Surg 1996; 112: 1202–1213. 143 Svensson LG. Intraoperative identification of spinal cord blood supply during descending and thoracoabdominal aortic repairs. J Thorac Cardiovasc Surg 1996; 112: 1455–1461. 144 Elefteriades JA, Coady MA, Nikas DJ, Kopf GS, Gusberg RJ. ‘Cobrahead’ graft for intercostal artery implantation during descending aortic replacement. Ann Thorac Surg 2000; 69: 1282–1284.

Index

Note: page numbers in italics refer to figures, those in bold refer to tables. abdominal herniation 150 abscess, subphrenic 191 achalasia 186 pneumatic dilatation 209 undiagnosed in antireflux surgery 186 activated clotting time (ACT) 302 Adamkiewicz artery imaging 427 adenosine 59 adrenal hormones 314 adrenocorticotrophic hormone (ACTH) 314 adult respiratory distress syndrome (ARDS) 396–7 amiodarone 57 air embolism lung transplantation 128–9 massive in cardiopulmonary bypass 293–5 postoperative treatment 295, 296 prevention 413, 418–19 venous 284 air leaks bronchoplasty 96 chest tube 77, 78, 117 hypocapnia 117 intraoperative management 112–13, 114, 115–17 lung volume reduction procedures 109, 112–13, 114, 115–18 massive 109 peri-extubation period 117 persistent 75 postoperative management 117–18 prolonged 77–8 tracheal resection 104 air swallowers 195 airway compression 233 late complications in lung transplantation 132–3 management 101–2 measurement 101 postoperative from tracheal resection/reconstruction 103–4 resistance reduction 392 stenosis 132 airway pressure release ventilation 40 aldosterone 315 Allen test 259, 295

alveolopleural fistula 77–8 aminopyrine breath test 162 amiodarone 57, 274 analgesia antireflux surgery 199 chest wall reconstruction 157 epidural 94, 119 lung volume reduction procedures 118–19, 121 postoperative optimization 38 thoracic surgery 252 ancrod 302 anemia correction 391 aneurysmal disease 349, 351, 355, 356, 358, 364 CSF drainage 425 infected 353 thoracic aorta 355, 425 thoracoabdominal aorta 349, 355, 356, 358 CSF drainage 425 hypothermic circulatory arrest 426–7 repair 425–6 angina, unstable 412 angiotensin converting enzyme (ACE) 315 annuloplasty 377 Carpentier–Edwards 380–1 Cosgrove 381 DeVega 380 Kay–Reed measured 376 Puig–Massana 381 ring size 378 antibiotics bronchopleural fistula 81, 82 pneumonia 395, 396 nosocomial 120 postoperative 39 thoracotomy wound infections 29–30 anticoagulation cardiopulmonary bypass 300–5 oral 164 reversal 303–5 antidiuretic hormone (ADH) 314 antifibrinolytic therapy 305–6 aortic surgery 360 antiplatelet therapy 399 antireflux surgery 183–200 analgesia 199 bleeding 197 437

438

Index

antireflux surgery (cont’d) bowel dysfunction 198–9 cardiopulmonary complications 194 complete obstruction 197 dysphagia 195–6, 196 endoscopy 185 esophageal injuries 191–2 external fistulization 198 failure 199 flatulence 195 gas bloat 194–5 gastric perforations 192 herniated wrap 195, 196, 197 internal fistulization 197, 198 intraoperative pitfalls 188–9 leaks 198 motility disorders 186 operation selection 187–8 outcome 183 paraesophageal herniation 192–3 perioperative complications 189–94 postoperative complications 194–9 post-thoracotomy neuralgia 199 preoperative evaluation 184–6 preoperative strictures 196 redo 197, 199 vascular injuries 190, 191 visceral perforation 192 antithrombin III (ATIII) 301 Anton syndrome 408 anxiety disorders, preoperative 126 aorta/aortic surgery 349–60 air embolism 418–19 anastomotic complications 352–3 antibiotic-impregnated grafts 353 ascending aneurysmal disease 349, 351 atheroembolization 258 calcification 364, 371 replacement 273 atheroma 412–13 embolization 418–19 atherosclerosis 410 bleeding 418 calcified 258 cannulation 263–4, 287–8 air introduction 293 complications 288 cardiac catheterization 354 cardioplegia 323 cardiopulmonary bypass 350 cerebral ischemia 356–8 circulatory arrest 359 clamping 423 coronary arteriography 353 debridement 423 descending 264, 423 aneurysmal disease 349 cross clamp 419 double-barrel 421

emboli 410, 412, 413, 418–19 intra-aortic filtration 414–16 embolization distal 350 retrograde 351 femorofemoral bypass 359 hematological complications 359–60 hemostasis 418 injury 236–7 intramural hematoma 288 local cold solution infusion 426 long-term surveillance 352 malperfusion syndromes 350–1 mobilization 423 myocardial complications 353–4 neurological complications 356–9 neurological injury 417–19, 420, 421–3 prevention 418–19, 420, 421–3 systemic hypotension management 418 partial left heart bypass 350 patch repairs 273 pericardial patch 273 plaque 272 post-stenotic dilatation 364 pseudoaneurysms 352–3 pulmonary complications 354–5 renal dysfunction 355–6 repair of friable-debrided areas 365 shaggy intraluminal disease 351 single-barrel 421 spinal cord cooling 359 spinal cord injury 423–7 mechanical interventions 425–7 pathophysiology 424–5 pharmacological interventions 425 prevention 425–7 risk factors 423–4 stroke prevention 422–3 tears 273–4 thoracic 354, 355 occlusion 359 thoracoabdominal 349, 355, 356, 358 hypothermic circulatory arrest 426–7 profound hypothermia for operations 325 surgery 354 thrombosis 350 tube graft 274 vascular access 350–2 vascular complications 349–53 see also aneurysmal disease aortic arch atheroembolization 258 atherosclerotic disease 237 profound hypothermia for operations 325 reconstruction 357 aortic regurgitation 354

Index 439 aortic root aneurysmal disease 349 calcification 364 de-airing 274 dissection 274 replacement 352–3, 363 small 367–9 venting 292 aortic valve/aortic valve surgery 362–9 anatomy 362 bioprosthetic 367–8 stented 367, 368 too large 369 calcification 365 combined mitral valve surgery 375–6 incisions 362–3 insufficiency 365 pledgets 366, 367 removal 365–6 replacement 323–4, 366–7 small aortic root 367–9 aortotomy 363–5 transverse 364–5 aorto–ventriculo–septoplasty 369 aprotinin 305–6, 320, 354 aortic surgery 360 argatroban 302 arrhythmias, post-operative 48–62 atrial 48–9, 51, 52–5, 250 characteristics 48–50 drug prophylaxis 56–9 hemodynamic stability 59 incidence 48–50 influence on outcome 51 mechanisms 51–6 post-esophagectomy 163 post-sympathectomy 250 postpericardiotomy syndrome 386 pulmonary artery catheter insertion 299 risk factors 50–1 supraventricular 48–9, 51, 52 treatment 59, 60, 61–2 ventricular 50, 55–8, 123, 274, 277 malignant 61 see also atrial fibrillation arterial cannulation 286–9 arterial catheters, continuous blood pressure monitoring 295, 297 arteriotomy, distal 271 Ashman’s phenomenon 56 Aspergillus 132 asthma, atelectasis 37, 38 atelectasis, postoperative 36–9, 390, 392–4 absorption 392 bronchoplasty 99 cardiopulmonary bypass 316–17 compressive 392 esophageal resection 167 etiology 69 fibrotic structures 97

lobar torsion differential diagnosis 87 management 37–9 mediastinal surgery 251 passive 392 predisposing factors 392 preoperative conditioning 391 prevention 69, 317 pulmonary resection 67, 68, 69, 70 recurrent 393 susceptibility 36–7 thoracoscopy 143 treatment 69 atherosclerotic disease aorta 410 aortic arch 237 atrial fibrillation 48, 51, 52–3, 54 electrical cardioversion 62 flecainide 58 left atrial cannulation avoidance 419, 420 left atrium avoidance 423 lung volume reduction 123, 124 mediastinal surgery 250–1 atrial flutter 53–4 atrial natriuretic factor 315 atrial premature contractions 52, 53 atrial tachycardia, multifocal 55 atrioventricular groove 370 hemorrhage/hematoma 375 atrioventricular node 52 block 53 conduction depression 61 refractory 52 atrium, right inner wall puncture 325 venous cannulas 284 axillary artery cannulation 289 azygos vein tears 236 Babinski reflex, bilateral 408 balloon dilating systems 202, 203, 222 achalasia 209 barotrauma 402 Barrett’s esophagus 185, 196 Belsey Mark IV repair 187, 189, 190, 191 internal fistulization 198 post-thoracotomy neuralgia 199 Belsey’s artery 191 Bioglue® 365 blindness, cortical 408 blood autologous predonation 306, 308 scavenging 291 ultrafiltration 307 blood pressure arterial 315 continuous monitoring 295, 297 blood product transfusion 305, 307 reduction 306–9 trigger points 309

440

Index

blood transfusion autotransfusion of shed mediastinal blood 309 avoidance of allogeneic 306–9 bone resorption 10 bougies, mercury-filled 202–3 brachial plexus damage 89, 409 sympathectomy 250 brachiocephalic vessels, cannulation 357 brain, systemic inflammatory response 320, 406 bronchial anastomosis complications in lung transplantation 130–1 tension avoidance 94–5 bronchial dehiscence 152 bronchial fistula closure 75, 79 bronchial granulation 97 bronchial laceration 238 bronchial stenosis 99 bronchoscopy 102 bronchial stents 97, 133 bronchial strictures 97, 99 bronchoscopy 102 bronchiolitis, lymphocytic 133 bronchiolitis obliterans/bronchiolitis obliterans syndrome 133 bronchitis, acute 111–12 bronchodilators 391, 392, 393 pneumonia prevention 395 bronchomalacia 132 bronchoplasty 92 anesthetic management 94 complication management 97–8 dehiscence of anastomosis 97–8 morbidity/mortality 99–100 patient evaluation 93 postintubation pneumonia 94 surgical technique 94–7 bronchopleural fistula 77, 78–82 drainage 81 infection control 81 management 98 prevention 145 treatment 80–2 bronchopulmonary secretions 38 bronchoscopy bronchoplasty patient evaluation 93 bronchopleural fistula 80 pleural effusion 137 tracheal pathology evaluation 101, 102 tracheal resection 104 tracheobronchial resection 97–8 tube placement 94 bronchoscopy, fiberoptic 38, 39 atelectasis 70 bronchial anastomotic complications 131 intrapleural spaces 75 bronchospasm 391 bronchovascular fistula 98

C-reactive protein 406 calcium ion concentrations 424 calcium levels 315–16 Candida 132 capillary leak 397 carbon dioxide intra-abdominal insufflation 194 operative field flooding 293, 413, 419, 423 respiratory failure 391, 392 carbon dioxide retention 109, 121 lung volume reduction procedure 120–1 cardiac catheterization 251 cardiac herniation 84–6 extrapleural pneumonectomy 150, 151–2 cardiac index 275 cardiac tamponade coronary artery bypass graft 277 extrapleural pneumonectomy 150 postpericardiotomy syndrome 387 cardiomegaly, postpericardiotomy syndrome 386 cardioplegia 280–1 antegrade 292, 322–4 aorta 323 aortic valve surgery 363 cold solutions 322 complications 321–5 delivery 264, 323–4 mitral valve surgery 371–2 myocardial protection 322–5 neurological protection 325, 413 retrograde 323–4, 324–5 retrograde cerebral perfusion 325 techniques 281 cardiopulmonary bypass 237, 280–1 acute lung injury 317–18 adrenal hormones 314 adult respiratory distress syndrome 396 anemia toleration 307 anticoagulation 300–5 monitoring 302–3 antifibrinolytic therapy 305–6 aortic surgery 350 aortic valve surgery 362–3 arterial cannulas/cannulation 286–9 aortic 286–8 axillary 289 femoral 288–9 arterial catheters 295, 297 atrial natriuretic factor 315 bleeding 305 blood conservation techniques 306–9 blood–surface interface 309–12 calcium levels 315–16 cardiotomy suction 291 catheters 284 cell saver 291 central venous catheters 297–8 central venous pressure 285 cerebral hypoperfusion 320

Index 441 circuit components 281, 282, 283–93 circulatory arrest 313–14 complement pathways 310–11 continuous positive airway pressure 393 electrical failure 293 endothelial cells 312 failure to separate from 275–6 heat exchanger 290 hemodilution 313, 318 hypothermia 312–14, 318 total 426 lung effects 316–18 lymphocytes 312 magnesium levels 316 massive air embolism 293–5 postoperative treatment 295, 296 mechanics 281, 282, 283–93 complications 293–5 metabolic consequences 314–16 mitral stenosis 378 mitral valve surgery 370–2 monitoring 295, 297–300 monocytes 312 neurocognitive complications 319–20 neurological complications 319–21 neuroprotective agents 320 neutrophils 312 organ ischemic injury protection 312–14 pathophysiological consequences 309–21 perfusion circuit filters 318 peripheral cannulation 284 pH management 320–1 pituitary hormones 314 platelets 312 potassium levels 316 pulmonary artery rupture 299 pulmonary edema 397 pump oxygenator 289–90, 294 renal effects 318–19 renin–angiotensin–aldosterone axis 315 rewarming 320 systemic heparinization 413 systemic inflammatory response 405–6 thyroid hormones 315 transesophageal echocardiography 299–300 tricuspid valve surgery 379–80 ultrafiltration of blood 307 venous cannulas/cannulation 283–4, 371 venous drainage 285 augmented 285–6 venous reservoir 285 venting of left heart 291–3 cardiopulmonary compromise 298 Cardiopulmonary Risk Index (CPRI) 50 cardiotomy suction 291, 307 cardioversion chemical 60, 61–2

DC synchronous electrical 60, 61 semielective electrical 62 carotid disease 411–12 carotid endarterectomy 258 neurological injury prevention 411–12 carotid fenestration 421 carotid stenosis 258 Carpentier–Edwards annuloplasty 380–1 cartilage resorption 10 Celestin tube 206–7, 213–14 cell saving 291, 307 central nervous system, systemic inflammatory response-induced changes 406 central venous catheters 297–8 central venous pressure (CVP) 276, 285 cerebral artery, middle 413 blood flow reversal 417 cerebral hypoperfusion 320 cerebral infarction 406–7 cerebral ischemia, aortic surgery 356–8 cerebral malperfusion see malperfusion syndromes cerebral perfusion antegrade 422 selective 421 retrograde 325, 357, 422 passive 417 cerebral vessel embolism 407 cerebrospinal fluid (CSF) drainage 425 cerebrovascular accident 417 focal 407 see also stroke Chamberlain procedure see mediastinotomy, anterior chemotherapy esophageal stents 222 germ cell tumors 244, 245–6 seminomas 244 teratoma 244 chest tube air leak 77, 78, 117 bronchopleural fistula 81 coronary artery bypass graft 278 drainage of esophagectomy leak 165 pneumothorax 131 chest wall defects 155 chest wall reconstruction 155–9 local cancer recurrence 158 with lung resection 158, 159 mortality 158 outcome 158–9 prosthetic materials 156, 157 seroma 157 soft tissue reconstruction 156–7 suction drains 156 chest wall resection 157 atelectasis susceptibility 36 children aorto–ventriculo–septoplasty 369

442

Index

children (cont’d) median sternotomy 11 mediastinal masses 233 mediastinal tumors 249 posterolateral thoracotomy 18 postpericardiotomy syndrome 387 chronic obstructive pulmonary disease (COPD) 395 atelectasis 37, 38 multifocal atrial tachycardia 55 ventilatory support 392 chylothorax 82–4 esophageal resection 168–9 leak identification 83 mediastinal mass resection 246–7 chylous effusions 84 chylous fistula 168–9 circulatory arrest 313–14, 359 hypothermic 426–7 cisterna chyli 82 clamshell incision 24–5 clotting factors 310–11 sequestration 360 coagulation pathway common 310, 311 extrinsic 311 intrinsic 310 coagulopathy, aortic surgery 359–60 cognitive dysfunction 408–9 collagen vascular disease 353 colon, esophageal reconstruction 174–5, 176, 179, 180, 181 coma 407 complement pathways 310–11 compression stockings graded 399 intermittent pneumatic 164 computed tomography (CT) bronchial anastomotic complications 131 bronchoplasty patient evaluation 93 esophageal perforation 205 pleural disease 135, 136 pleural effusion 137 congestive heart failure 397 lung volume reduction 123 pleural effusion 401 continuous positive airway pressure (CPAP) 393 coronary annulus, right 365 coronary arteriography 353 coronary artery circumflex 370 main left 362, 366 open endarterectomy 271 patch closure 271 stenosis 259 coronary artery bypass graft (CABG) 257–78 anastomosis distal 264–6

end-to-side 266, 271 side-to-side 267, 268, 269 anastomotic techniques 266–7, 268, 269 cobra-hood 272 proximal 272–3 aortic atheroma 413 aortic root dissection 274 aortic tear 273–4 arteriotomy 265 artery harvesting 259–61 bleeding anastomotic 272 postoperative 277 predisposition 257–8 cannulation 263–4 cardiac tamponade 277 cardioplegia delivery 264, 323 cell saver 291 chest tube 278 conduits axial orientation 275 failure 276 selection 259 coronary angiogram 258 emboli 410 embolic stroke rate 416–17 endarterectomy 269–73 harvesting techniques 259–62 heart reperfusion 274–5 intra-aortic filtration 414–16 mitral valve surgery 376 myocardial infarction 276 myocardial protection 264 neurological complications 258, 409–10 off-pump techniques 275 order of distals 266 parachute technique 269, 272 pericardial tamponade 276–7 postoperative complications 276–8 preoperative assessment 257–62 reoperative 273 sternotomy 262–3 supraventricular arrhythmias 277 T-grafting 263 target site selection 264 –6 vascular spasm 275 vein harvesting 261–2 ventricular tachycardia 277 wound complications 277–8 Y-grafting 263 Coronary Artery Calcification Index (CAC) 50 coronary artery disease lung volume reduction 123–4 neurological injury prevention 411–17 coronary endarterectomy coronary artery bypass graft 269–73 techniques 270–2 coronary ostia 365–6 aortic valve replacement 367

Index 443 coronary ostium, right 362, 363–4, 365–6 aortic valve replacement 367 coronary revascularization, combined 363 coronary sinus 370 pressure 325 corticomodular reflexes 408 corticosteroids see steroids cortisol 314 Cosgrove annuloplasty 381 cough reflex, impaired 395 coumadin 401 crystalloid solutions, hyperkalemic 322 cuff injuries 100–1 Cushing’s syndrome 231 cyanoacrylate glue 116 cyclosporine 131 cytokines 406 cytomegalovirus (CMV) 132 bronchiolitis obliterans syndrome 133 Dacron grafts 273, 274 aortic valve replacement 368, 369 Dacron patch arterioplasty 351 deep hypothalamic circulatory arrest (DHCA) 418, 419 prevention of inadequate cerebral protection 421–3 deep venous thrombosis antireflux surgery 194 esophageal resection 164 femoral vein 352 lung volume reduction procedures 125 prophylaxis 392 preoperative 164 pulmonary embolus 399 thoracoscopy 143 depression, post operative 126 DeVega annuloplasty 380 dextran, low-molecular weight 302 dextrorphan 424 diaphragm division 43 elevation 74, 89 exercises 391 extrapleural pneumonectomy 149 reconstruction 152 transplantation 72–3 diaphragm patch disruption 150, 151 digoxin 57–8, 59, 60 ventricular rate control 61 dilatation systems 202–4 polyvinyl wire 202, 203–4, 222 diltiazem 58, 59, 60 ventricular rate control 61 diuresis, edema management 104 dobutamine stress echocardiography 124 dopamine 318–19 dumbbell tumors 249 dumping syndrome 166, 180, 181, 199 dysphagia

antireflux surgery 195–6 esophageal reconstruction 179, 181 esophageal resection 165 peptic strictures 187 total fundoplication 188 echocardiography dobutamine stress 124 transesophageal 130 electrocautery 3 median sternotomy 4, 5 posterolateral thoracotomy 17 elephant trunk procedure 360 Eloesser flap, bronchopleural fistula 81 emphysema antireflux surgery 194 end-stage 108, 109, 125–6 lung transplantation 128 lung volume reduction 125–6 tracheal resection 104 empyema 111 cavity obliteration 81, 82 drainage 75, 76 extrapleural pneumonectomy 152 fibrinolytic therapy 142 mature and thoracotomy 144–5 pleural effusion 137 pulmonary resection 78–82 thoracoscopy 141, 142–3 encephalopathy, diffuse mild 408 endocarditis, tricuspid valve damage 381 endothelial cells 312 endothelin receptor antagonists 42 endotracheal tube, tracheal resection 102, 103 epidural cooling 426 epileptic seizures 407 epinephrine 104 plasma concentration 314 epsilon-aminocaproic acid (EACA) 305 Epstein–Barr virus (EBV) 132 erythromycin, gastric emptying 167, 181 erythropoietin 306 esophageal hiatus 184 esophageal instrumentation 202–25 achalasia 209 see also esophagus, perforation esophageal reconstruction 173–81 anastomosis location 177 anastomotic leak 173, 176, 177 treatment 178–9 anastomotic technique 177–8 anatomic complications 173 choice of organs 174–6 colon utilization 174–5, 176, 179, 180, 181 complications 180, 181 dysphagia 179, 181 functional complications 179–81 jejunum utilization 175–6, 179 route 176

444

Index

esophageal reconstruction (cont’d) stomach utilization 174, 175, 179, 180, 181 stricture formation 173, 179 esophageal resection 161–70 anastomotic dehiscence 164–5 anastomotic stricture 165–6 cardiac complications 163 chylothorax 168–9 delayed gastric emptying 166–7 dumping syndrome 166 dysphagia 165 esophageal perforation 207, 208 leaks 165 anastomotic 164–5 morbidity 162 mortality 161–2 patients preparation 30 selection 162–3 recurrent laryngeal nerve injury 169–70 respiratory complications 167 scoring system 163 thromboembolism 164 vocal cord paralysis 170 esophageal sphincter function 185 esophageal stents 207, 208, 211–23 airway obstruction 220, 222 benign disease 223 bleeding 222 coiled 219, 220 conventional 216–17 expandable 216–17 complications 219–20, 221, 222–3 insertion of additional 218, 219 migration 219–20, 221 misplacement 218, 219, 220 mortality 223 perforation 219, 223 pressure necrosis 222 tumor overgrowth 220 types 216, 217 esophageal varices 212–14, 215 tamponade of bleeding 214 esophagectomy recurrent laryngeal nerve injury 42 supraventricular arrhythmias 49 total for scleroderma 187 esophagitis diagnosis 185 intractable 187 reflux 166 esophagogastrectomy 166, 167 cervical 178 esophagogastric anastomosis 207, 208 esophagogastric fistula 197, 198 esophagostomy, cervical 207 esophagus dilatation 179, 202–4 perforation diagnosis/treatment 204–9 pneumatic 209, 210

distal dysfunction 196 distal obstruction 206–7 diversion procedures 207–9 endoscopy foreign body removal 224 perforation 205 exclusion procedures 207–9 foreign body removal 223–5 intraoperative injuries in antireflux surgery 191–2 laser therapy 210–12 manometry 185–6 perforation 202–4 contrast radiographic studies 204, 205 controlled fistula creation 213 CT 205 diagnosis/treatment 204–9 endoscopy 205 following pneumatic dilatation 210 foreign bodies 225 laser therapy complication 211–12 mediastinoscopy 238 non-operative therapy 205–6 sclerotherapy 212–14, 215 stenting 213–14, 217, 219, 223 surgical treatment 206–9 tissue debridement 206 recurrent carcinoma 166, 179 rupture 196 sclerotherapy 212–14, 215 intramural hematoma 214, 215 stapling 208 strictures 165–6, 173, 179 antireflux surgery 185 dilatation 202–4 malignant 210 tenting 150 tortuous 210 tumors 211 excluding-clamp technique 416–17 extracorporeal membrane oxygenation (ECMO) 42 lung transplantation 129 factor XII 310 feeding tubes, enteric 209 femoral artery 264 cannulation 288–9, 297, 419, 421 Dacron chimney 351 stenosis 350 thrombosis 350 femoral vein cannulation 351–2 femorofemoral bypass 359 fenoldopam 319 fever, benign localized mesothelioma 146 fibrin 311 fibrin glue 77, 82, 84 air leaks 116 fibrinogen 309 fibrinolysis 305, 311

Index 445 fibrinolytic therapy in empyema 142 fibrothorax thoracoscopy 143 thoracotomy 144–5 FK506 131 flecainide 58, 61 fluid excessive intake in pulmonary edema 42 management 40 foreign bodies, esophagogastric 223–5 fundoplication external fistula 198 paraesophageal herniation 192–3 partial 187, 188, 189, 190, 191 internal fistulization 198 post-thoracotomy neuralgia 199 total 187 dysphagia 188 see also Nissen fundoplication furosemide 355 ganciclovir 132 gas bloat 194–5 gastric arteries, short 190, 198 gastric emptying 180, 181 delayed 166–7 gastric mucosa, edema 167 gastric outlet obstruction 166–7 gastritis, stress 392 gastro–esophageal junction avulsion 192 Collis gastroplasty 188 complete obstruction 197 dilatation for achalasia 209 esophageal hiatus 184 resection 174, 175 stapling 208 gastroesophageal reflux disease (GERD) 183 misdiagnosis 186–7 pH monitoring 186 preoperative evaluation 184–6 recurrence 199 scleroderma 186–7 see also antireflux surgery gastrointestinal tract bleeding 125 lung volume reduction procedures 124–5 perforation 124–5 transesophageal echocardiography 300 gastrointestinal tract, upper endoscopy 202–4 foreign body removal 224–5 perforation diagnosis/treatment 204–9 foreign body removal 223–5 gastropexy, Hill posterior 189 gastroplasty Collis 187, 188, 189, 192 complications 196 Hill 191 gastrostomy 208

gluconeogenesis 313 glutamate/glutamate receptors 424 glycogenolysis 313 grasping reflex 408 Haemophilus influenzae 395 Hageman factor 310 heart complications in lung volume reduction 123– 4 congenital abnormalities 128 partial left bypass 350, 359 reperfusion 274–5 venous return obstruction 284 venting of left 291–3 see also cardioplegia heat exchanger 290 hemi-clamshell incision 25 hemithorax, air leakage inspection 116 hemodilution 313, 318 acute normovolemic 308–9 hemodynamic stability, atrial tachyarrhythmia 59 hemorrhage, lung volume reduction procedures 122–3 hemostasis pinpoint 3 median sternotomy 5 posterolateral thoracotomy 17 hemothorax 36 thoracocentesis 137 thoracoscopy 141, 143–4 heparin 280 allergy 302 cardiopulmonary bypass 300–1 complications 301 dosage monitoring 301 low-molecular weight 302 platelet effects 311 preoperative prophylaxis 164 pulmonary embolus 400–1 rebound 304 resistance 301 thrombocytopenia induction 301–2 thrombus formation prevention 413 thyroid hormone levels 315 heparin-binding proteins 304 heparin-induced thrombocytopenia (HIT) 301–2 heparin-induced thrombocytopenia and thrombosis (HITT) 302 heparin–protamine complexes 304, 305 heparinase 305 herpes 132 hexadimethrine 304 Hill gastroplasty 191 hirudin 302 histamine release 304 Horner’s syndrome 89, 231, 249 sympathectomy 250

446

Index

hypercalcemia 231 hypercapnia lung volume reduction procedure 120–1, 122 permissive 40, 392 hyperglycemia 313 hypertension 231 postoperative 315 hypocapnia, air leaks 117 hypoglycemia, benign localized mesothelioma 146 hypothermia 312–14, 318 circulatory arrest 426–7 phrenic nerve dysfunction 402 profound 313–14 circulatory arrest 325 spinal cord protection during aortic surgery 426–7 hypoventilation, lung volume reduction procedure 121 hypovolemia, thoracocentesis complication 137 hypoxia, postoperative 394 ibutilide 61 ICU psychosis 409 immunoglobulin E (IgE) 304 immunosuppression, lung transplantation 131 imuran 131 incisional hernia, median sternotomy 11 infection bronchopleural fistula 81 lung transplantation 131–2 pleural 137 pleural spaces 135 subphrenic abscess 191 thoracoscopy port site 141 thoracotomy incisions 29–30 see also respiratory tract infection; wound infections inferior vena cava cannulation for mitral valve surgery 371–2 entrapment 150 inflammation/inflammatory disease intrapleural space risk 71 trachea 101 inflammatory cascade 396 innominate artery injury 236–7 intercostal artery reimplantation 427 intermittent positive pressure ventilation (IPPV) 40, 393 atelectasis 38 International Council of Emboli Management (ICEM) 415–16 intra-aortic balloon pump 275 intra-aortic filtration 414–16 intra-operative epiaortic echocardiography (IEE) 412–13, 423

intra-operative epiaortic ultrasound 258 intraperitoneal hematoma 87 intrapleural spaces 71–5, 76 prevention 71–4 recurrent 78 reduction 75 see also pleural spaces inverse ratio ventilation 40 jejunostomy, feeding 209 jejunum, esophageal reconstruction 175– 6, 179 kallikrein 310 Karnofsky index 162 keloid 13 ketorolac 119 kidneys aortic surgery 355–6 cardiopulmonary bypass 318–19 Klebsiella pneumoniae 395 Langer’s lines 3, 13 laser ablation bronchial neoplasms 92 esophageal 210–12 leukocyte filters 318 leukocytosis, postpericardiotomy syndrome 386 Linton tube 214 lobectomy air leak closure 115 atelectasis 70 atrial arrhythmias 48–9 bronchopleural fistula 80 sleeve 92 tumor recurrence 98 low cardiac output syndrome 321 mitral valve replacement/repair 378 lung(s) acute injury 317–18 cardiopulmonary bypass effects 316–18 compliance loss 71 expansion 142 functional residual capacity 317 gangrene 87, 88 hernia with thoracotomy incisions 28 injury 401 lobar torsion 86–8 parenchymal hematoma 123 re-expansion 115–16, 143 resection with chest wall reconstruction 158, 159 torn tissue 115 see also lobectomy lung cancer bronchoplasty 99, 100 lymph node classification for staging 234, 235 recurrence with sleeve lobectomy 98

Index 447 resection apical 89 atrial arrhythmias 51 recurrent laryngeal nerve injury 89 lung clamps 115 lung transplantation 128–33 acute rejection 131, 133 atelectasis susceptibility 36 bronchiolitis obliterans/bronchiolitis obliterans syndrome 133 early complications 128–31 immunosuppression 131 infection 131–2 late complications 131–3 retransplantation 133 vascular anastomotic complications 130 lung volume reduction procedures 108–26 complications 112–13, 114, 115–26 extubation 121 morbidity 111 mortality 109, 110, 111 nutritional supplementation 111 preoperative preparation 111–12 reintubation for respiratory failure 120, 121 staple line buttress 113, 114, 115 lymph node classification for lung cancer staging 234, 235 lymphocytes 312 magnesium levels 316 magnetic resonance imaging (MRI), pleural disease 135 malperfusion syndromes 350–1 prevention 419, 421 mammary artery grafts 259, 316 Marfan syndrome 353 meat bolus obstruction 225 mediastinal cysts 230 mediastinal masses 230–4, 235, 236–8 cervical mediastinoscopy 233–4, 235 choriocarcinomas 245 clinical features 231 diagnosis 231–3 embryonal cell carcinoma 245 germ cell tumors 243–6 metastases 245 serum markers 244, 245–6 imaging 232 lesion biopsy 232–3 lymph nodes 234, 235 malignant neoplasms 231 needle biopsy 232 resection anterior 241–8 complications 246–8 posterior 248–9 seminomas 244, 245 serologic evaluation 232

teratomas 243–4, 245 thoracoscopic sympathectomy 249–50 see also thymoma mediastinal surgery 230–52 mediastinal tumors 230, 231 fibrosis 238 metastases 248 incisional 238 neurogenic 248–9 resection 43, 246, 247–8, 249 spinal column extensions 249 mediastinitis 7, 111 post-thymectomy 241 mediastinoscopy 25–7 bronchoplasty patient evaluation 93 cervical 233–4, 235 complications 236–8 contraindications 234 esophageal perforation 238 hemorrhage 236 incisional metastases 238 mediastinal masses 232–3 mediastinotomy 25–7, 232 anterior 43 parasternal 26–7 mediastinum 230 germ cell tumors 243–6 medical complications of surgery 250–2 post-cardiopulmonary bypass bleeding 305 meningitis, post-thoracotomy 29 mental dysfunction 408–9 mesothelioma, benign localized 146 mesothelioma, malignant 135, 139 diagnosis 145 extrapleural pneumonectomy 146, 148–52 pleural 146–7 pleurectomy/decortication 147–8 port site recurrence 141 recurrence 148 surgery 145–52 mesothelium 146 methotrexate 133 metoclopramide 181 metoprolol 59 ventricular rate control 61 microaspiration 395 milrinone 394 mitral stenosis 378 mitral valve 362 anatomy 369–70 calcification 373–4 insufficiency 376, 378 myxomatous 376 mitral valve surgery 369–78 annuloplasty 376 cardiopulmonary bypass 370–2 combined aortic surgery 375–6 commissurotomy 372–3

448

Index

mitral valve surgery (cont’d) incisions 370–2 operations 372–6 posterior annulus length reduction 376, 377 postpericardiotomy syndrome 385 reconstruction 376, 377 repair 376–8 cardioplegia 324 indications 376 posterior leaflet 376, 377 replacement 373–6 bioprostheses 374–5 prostheses 373, 375 venous cannulation 371–2 MK-801 425 mobilization, early 119 monocytes 312 motility disorders 186 mucociliary clearance, impaired 395 multiple organ dysfunction syndrome (MODS) 406 muscle flaps bronchoplasty 97 bronchopleural fistula 82 chest wall reconstruction 156–7 intrapleural spaces 75 median sternotomy 10, 11 muscle-sparing incisions 23 myasthenia gravis thymectomy 238–41 thymoma 241, 242 mycophenilate mofetil 131 myocardial infarction coronary artery bypass graft 276 esophageal resection 163 lung volume reduction 123, 124 mediastinal surgery 251 myocardial ischemia lung volume reduction 123, 124 pathophysiology 321 myocardial protection 264, 322–5 aortic valve surgery 363 myocardial stunning 321 myocardium cardioplegia solution distribution 323 oxygen consumption 321 myocutaneous flaps, median sternotomy 11 myoplasty, empyema cavity obliteration 81 naso-tracheal suctioning, lung volume reduction procedures 119–20 National Emphysema Treatment Trial (NETT) 108 nerve injury 89 neuralgia intercostal 28 upper limb 250

neurocognitive deficit 408–9 neurological complications 405 neurological injury, postoperative 406–10 air embolism prevention 413 aortic surgery 417–19, 420, 421–3 embolic 412 intra-aortic filtration 414–16 intra-operative prevention 412–17 off-pump cardiac surgery 417 passive retrograde cerebral perfusion 417 prevention 411–17 preoperative 411–12 risk factors 409–10 type I 406–7, 410 prevention 419, 420 type II 408–10 neuromuscular transfer 89 neuroprotective agents 320 neutrophils 312 nimodipine 320 Nissen fundoplication 185, 187–8, 189, 191 gas bloat 194–5 reherniation 193 slipped 196, 197 nitric oxide inhaled 42, 129, 392 neurotoxicity 425 nitroglycerin 394 nitroprusside 394 NMDA receptors 424 Nocardia 132 nutritional supplementation in lung volume reduction procedures 111 off-pump coronary artery bypass (OPCAB) 417 omentum bronchopleural fistula closure 81, 82 chest wall reconstruction 156–7 intrapleural space obliteration 75 ophthalmological disorders 408 orgaran 302 osteoarthropathy, pulmonary 146 osteochondritis 10 osteomyelitis, median sternotomy 7, 8, 10 osteoporosis of sternum 13 oxygen, myocardial consumption 321 Pancoast’s syndrome 249 panic attacks 126 papaverine 275 papillary muscles 370 paraesophageal hernia 192–3 paraplegia post-thoracotomy 29 thoracoabdominal aortic aneurysm repair 358 patient positioning intermittent prone 40 supine 390

Index 449 peptic strictures, dysphagia 187 perfusion scintigraphy, dipyridamole thallium-201 124 pericardectomy 86 pericardial defect closure 85–6 pericardial effusion 401 postpericardiotomy syndrome 386, 387 pericardial friction rub 386 pericardial inflammation, pleural effusion 401 pericardial patch 86 dehiscence 150, 151–2 replacement in empyema 152 pericardiocentesis 387 peripheral nervous system complications 409 peripheral perfusion, spinal cord protection during aortic surgery 426 peristalsis, intermittent mass 181 peroneal nerve injury 409 phenylephrine 119 phospholipids 310 photopheresis 133 phrenic nerve conduction velocity 402 crush 72 phrenic nerve injury 42–3, 89, 240–1, 409 mediastinal mass resection 246 paralysis 322 postoperative 402 physiotherapy pneumonia prevention 395, 396 postoperative 38, 39, 393 lung volume reduction procedures 119 preoperative 391 pituitary hormones 314 plasmapheresis 240 plasmin 311 platelet factor 4 305 platelet-rich plasma, preoperative harvesting 308 platelets 311–12 pleura 135 abrasion 117 excessive drainage 41 infection 137 malignant mesothelioma 146–7 sarcoma 148 solitary fibrous tumour 135 thickening 135, 136 pleural disease adhesive 113 bulky 137, 139 diagnosis 135, 136 malignant 137 postoperative 401 thoracoscopy 138–42 thoracotomy 144 pleural effusion 137 bronchoscopy 137

esophageal anastomotic leak 165 loculated 138 malignant 142 percutaneous drainage 139 postoperative 401 postpericardiotomy syndrome 386 ring enhancement 145 thoracoscopy 139 pleural envelope resection 148 pleural fluid collections 135, 136, 137 pleural spaces 135–52 drainage 299 infection 135 obliteration 113 surgical evaluation 137–42 see also intrapleural spaces pleural tent 72, 117 pleurectomy 117 parietal 144 pleurectomy/decortication, malignant pleural mesothelioma 146, 147–8 pleurodesis 84 talc use 141, 142, 146 pleuroperitoneal shunts 84 Pneumocystis carinii pneumonia (PCP) 132 pneumomediastinum, antireflux surgery 194 pneumonectomy 39 arrhythmias 51 atrial arrhythmias 49 bronchopleural fistula 79–80, 81 chylothorax 82 completion 97, 98 extrapleural complications 150–2 malignant pleural mesothelioma 146, 148–52 pain management 151 pulmonary artery injury 237 pulmonary edema 41–2 recurrent laryngeal nerve injury 42, 89 pneumonia bronchoplasty 99 diagnosis 395 esophageal resection 167 lung volume reduction procedures 118 nosocomial 120, 122 postintubation 94 postobstructive 97 postoperative 39, 394–6 risk factors 395 susceptibility 36 thoracoscopy 143 pneumonitis 132 radiation 148 pneumoperitoneum 72, 74 lung volume reduction 125 pneumothorax 36 antireflux surgery 194 central venous catheters 298 chest tube 131

450

Index

pneumothorax (cont’d) esophageal anastomotic leak 165 management 402 mediastinoscopy 238 pleural disease 135, 136 postoperative 401–2 tension 298 thoracocentesis complication 137, 138 positive end-expiratory pressure (PEEP) 392, 394 postcardiotomy syndrome 401 postpericardiotomy syndrome (PPS) 385–7 antibodies 385 potassium levels 316 premature ventricular complex 55–6 flecainide 58 procainamide 59, 61–2 propafanone 61 propofol 320 propranolol 58–9 prostacyclins 302 prostanoid drugs 42 protamine 303–4 protamine–heparin complexes 304, 305 Pseudomonas aeruginosa 395 Pseudomonas nosocomial pneumonia 120 psychiatric complications 409 lung volume reduction procedures 125–6 Puig–Massana annuloplasty 381 pulmonary artery air removal 298 anastomosis 129 flow 130 injury 237 pressure 276 resistance 41 rupture 299 thrombosis 130 pulmonary artery catheters 251, 298–9 pulmonary capillary leak syndrome 129 pulmonary disease, aortic surgery 354–5 pulmonary dysfunction, adult respiratory distress syndrome 396 pulmonary edema 397 post-pneumonectomy 41–2 pulmonary embolus 397, 398, 399– 401 antireflux surgery 194 classification 400–1 diagnosis 399, 400 esophageal resection 164 lung volume reduction procedures 125 mortality 397 pleural effusion 401 preoperative prophylaxis 164 prevention 399–400 pulmonary fibrosis 71, 74 lung transplantation 128 pulmonary function tests 93 lung transplantation 133 pulmonary hypertension, primary 128

pulmonary infarction 37 pulmonary ligament, inferior 113 division 114 pulmonary rehabilitation, atelectasis prevention 393 pulmonary resection 67–89 alveolopleural fistula 77–8 atelectasis 67, 68, 69, 70 atrial arrhythmias 51 bronchopleural fistula 78–82 cardiac herniation 84–6 chylothorax 82–4 incidence of complications 68 intrapleural spaces 71–5, 76 lobar torsion 86–8 nerve injury 89 risk factors for complications 67 pulmonary vascular disease 128 pulmonary vascular recruitment 42 pulmonary vein cannulation 419 pump lung 317 pump oxygenator 280–1, 289–90 bubble 289 bypass 289–90 centrifugal pump 290 heparin-coated 289 membrane 289 roller pump 290, 294 pump suction see cardiotomy suction pyloromyotomy 167, 180 pyloroplasty 167, 180, 181 bowel dysfunction 199 pylorospasm 180 pylorus, endoscopic balloon dilatation 181 QRS complex 53 premature ventricular complex 55, 56 ventricular tachycardia 57 quinidine 61, 62 radial artery catheter 295, 297 radial artery graft 259 harvesting 259–60 T-grafting 263 radiation therapy bronchial healing effects 97 bronchoplasty 97 esophageal stents 222 seminomas 244 teratoma 244 thymoma 243 re-sternotomy see sternotomy incisions, redo recurrent laryngeal nerve 102 palsy 237 recurrent laryngeal nerve injury 42–3, 89, 409 esophageal resection 169–70 mediastinal mass resection 246 mediastinoscopy 237 thymectomy 240–1

Index 451 red cells aplasia 241, 242 autologous predonation 306 renal failure, postoperative with cardiac surgery 318 renin–angiotensin–aldosterone axis 315 reperfusion response in lung transplantation 129–30 respiratory complications 36–43 esophageal resection 167 preoperative risk factors 40 respiratory failure acute 40–1 aortic surgery 354 cardiopulmonary bypass 317 lung volume reduction procedures 120–2 postoperative 390–2 risk 391 thymectomy for myasthenia gravis 240 respiratory insufficiency esophageal resection 167 extrapleural pneumonectomy 151 respiratory quotient analysis 391–2 respiratory tract infection management 120 nosocomial in lung volume reduction 109, 118–20 rib fractures, thoracoscopy 144 Robicsek weaving technique 9, 13 modification 10, 11 saphenous vein grafts 259 closure 271–2 saphenous vein harvesting 409 scapula, winging 20 scars, hypertrophied 13 scleroderma 186–7 sclerotherapy, esophageal varices 212–14, 215 seizure disorders 407, 408 Sengstaken–Blakemore tube 214 septic syndrome, thoracoscopy 143 sequential compression devices 399 seroma chest wall reconstruction 157 extrapleural pneumonectomy 152 muscle-sparing thoracotomy 19 shoulder complications in thoracotomy 18, 19, 20 shunting 394 single-clamp technique 416–17 sino–tubular junction 362 calcification 364 sinus rhythm 62 sinuses of Valsalva 362 calcification 364 sleeve pulmonary resection 36, 38 somatosensory evoked potentials (SSEPs) 427 d-sotalol 61

spinal column hematoma 249 spinal cord compression 249 cooling 359 hypothermia 426–7 injury 407 aortic surgery 423–7 peripheral perfusion 425–6 ischemia 358 neurotransmitters 424 protection during aortic surgery 425–7 spirometry, incentive 38, 119, 391, 393 esophageal resection 167 pneumonia prevention 395 spleen antireflux surgery 189–91 hematoma 197 Staphylococcus aureus 395 stapling devices 77 stellate ganglion, sympathectomy 250 stenting bronchial 97, 133 esophageal 207, 208, 211–23 sternal wires clamshell incision 24, 25 median sternotomy 6, 9, 10, 11, 12–13 partial sternotomy 14, 15 redo sternotomy 13 sternotomy bleeding 262 coronary artery bypass graft 262–3 median 109, 128, 233, 237 aortic valve surgery 363 mediastinal tumor resection 246 mitral valve surgery 370 sternal wires 6, 9, 10, 11, 12–13 partial 14, 15 redo 13 respiratory failure 390 thymectomy for myasthenia gravis 239 tracheoinnominate artery fistula 105 sternotomy incisions 3–16 bilateral submammary vertical 13–14 median 3–11, 13 advantages 4 antibiotic irrigation 9 muscle flap coverage 10 operative technique 4–7 patient preparation 4 suture technique 6–7 wound complications 7–11 median–bilateral subcostal 15–16 indications 15–16 partial 14–15 redo 12–13 sternum closure median sternotomy 6–11 median sternotomy–bilateral subcostal incision 16

452

Index

sternum (cont’d) partial sternotomy 14 redo sternotomy 13 debridement of infected 277–8 dehiscence 7, 8, 9 osteoporosis 13 removal 10 separation 10–11 steroids 392 bronchial healing effect 97 edema management 104 immunosuppression 131 weaning prior to lung volume reduction procedures 111 stomach esophageal reconstruction 174, 179, 180, 181 functional complications 180 intraoperative injuries in antireflux surgery 191–2 Streptococcus pneumoniae 395 stroke 407 clamp techniques 416–17 coronary artery bypass graft 258, 413, 416–17 mediastinoscopy 237 prevention in aortic surgery 422–3 risk 410, 411 subarachnoid–pleural fistula with pneumocephalus 29 subclavian artery cannulation 264, 351, 419 revascularization 248 subclavian vein division/revascularization 248 subcutaneous hematoma 137 subphrenic abscess 191 sucking reflex 408 superior vena cava cannulation 283 mitral valve surgery 371–2 obstruction 233 persistent left 284 retrograde perfusion 421, 422 superior vena caval syndrome 231, 233 suprahyoid laryngeal release 104 supraventricular arrhythmias 277 supraventricular tachycardia esophageal resection 163 lung volume reduction 123, 124 surgical site 390 suture technique aortic valve replacement 366, 367, 368 aortotomy 364–5 bronchoplasty 95–6 extrapleural pneumonectomy 152 median sternotomy 6–7 median sternotomy–bilateral subcostal incision 16 mitral valve

repair 376, 377 replacement 373, 374, 375 pledgets 366, 367 plication for air leaks 116 posterolateral thoracotomy 18–19 thoracoabdominal incision 23–4 tricuspid valve surgery 381, 382 wound infections 30 swallowing disorders 392 see also dysphagia Swan–Ganz catheter see pulmonary artery catheters systemic inflammatory response 320, 396, 397, 405–6 diagnosis 405 systemic sclerosis 186–7 talc 141, 142, 145 pleurodesis for malignant pleural mesothelioma 146 thiopental 320 thoracentesis 139 thoracic artery, internal flow capacity 273 graft anastomosis 266 harvesting 260–1, 401–2 pedicle 263 mobilization 261 skeletonization 261 spasm 275 T-grafting 263 thoracic duct 83 injury 83–4, 168 ligation 84, 168 surgical closure 247 trauma 247 thoracoabdominal incision 23–4 thoracocentesis 137–8 thoracoplasty 72, 73–4 empyema cavity obliteration 81 intrapleural spaces 75 thoracoscopy complications 141–2 drainage of esophagectomy leak 165 empyema 141, 142–3 fibrothorax 143 hemothorax 143–4 indications 139 malignant pleural effusion 142 mediastinal masses 232, 233, 249 multiport video 140–2, 143 pleural disease 138–42 port site infection 141 rib fractures 144 single-port 139, 140, 142, 143 mesothelioma diagnosis 145 sympathectomy 249–50 talc poudrage 141, 142, 145 thymectomy for myasthenia gravis 239– 40

Index 453 tumor seeding in tract 141 video-assisted thoracic surgery (VATS) 27, 81 pleural disease 138–42 thoracosternotomy, bilateral 24–5 thoracostomy bronchopleural fistula 81 pneumothorax 402 thoracostomy tube 299 thoracotomy air removal from pulmonary artery 298 chylothorax 168 epidural analgesia 94 fibrothorax 144–5 mature empyema 144–5 mediastinal masses 232, 233 neuralgia 199 pleural disease 144 reoperative for esophagectomy leak 165 respiratory failure 40–1, 390–1 supraventricular arrhythmias 49 suture closure 152 vascular anastomosis complications 130 thoracotomy incisions 16–30 anterolateral 18 infections 29–30 lung hernia 28 muscle-sparing 19–23 neurological sequelae 29 posterolateral 16–19, 22 patient preparation 16–17 technique 17–18 reoperative 18 vertical axillary 19–20 thorax closure 18–19, 152 incisions 3–30 sternotomy 3–16 thoracotomy 16–30 video-assisted 27 malignancy 25, 26 surgery analgesia 252 side of operation 51 thrombin 310, 311 thrombocytopenia, heparin-induced 301–2 thrombosis aorta 350 femoral artery 350 pulmonary artery 130 thrombus formation prevention 413 thymectomy 239–41 myasthenia gravis 238–41 thymoma myasthenia gravis 241, 242 radiation therapy 243

recurrence 243 resection 241–3, 247 surgical excision 242 surgical resection 243 thyroid hormones 315 thyroplasty technique 89 thyrotoxicosis 231 thyrotropin 315 thyroxine (T4) 315 tissue plasminogen activator (t-PA) 311 torsade de pointes 61 trachea 100–1 burned 100 cuff injuries 100–1 high-risk conditions 100 inflammation 101 laceration 238 pathology evaluation 101 stenosis 104, 105 tracheal resection/reconstruction 100–1 airway management 101–2 complications management 103–5, 106 edema 104 granulations 104 postoperative airway 103–4 stenosis 104 surgical technique 102–3 tracheo-esophageal groove 102 dissection in recurrent laryngeal nerve injury 42 vocal cord paralysis 170 tracheobronchial resection 92–106 complication management 97–8 management 92 stenosis 97 see also bronchoplasty tracheobronchial tree compression 249 tracheoinnominate artery fistula 105 tracheostomy, percutaneous 39 airway management 102 tracheal resection 103, 104 tracheoinnominate artery fistula 105 tranexamic acid 305 transbronchial biopsy 131, 132 transcranial Doppler echocardiography 412, 413, 417 cerebral malperfusion 421 transdiaphragmatic access 43 transesophageal echocardiography (TEE) aortic atheroma 412 aortic cannulation 287, 294, 423 cardiopulmonary bypass 299–300 cardiopulmonary bypass catheters 284 cerebral malperfusion 421 de-airing maneuvers 293 descending aorta 264 intraoperative 300 mitral valve repair 376, 378 odynophagia 300 transesophageal endocardiography 275

454

Index

transjugular intrahepatic portal systemic shunting (TIPS) 212 trap door incision 25 triangle of Koch 379 tricuspid valve anatomy 379 insufficiency 382 leaflets 379 tricuspid valve surgery 379–82 annuloplasty techniques 380–1 bicuspidization 380 bioprosthesis 382 commissurotomy 381 incisions 379–80 prognosis 382 repair 380–1 replacement 381–2 triiodothyronine (T3) 315 tube graft 274 tuberculous disease, advanced refractory 148 two-clamp technique 416–17 ultrasonography intraoperative epiaortic 258 pleural disease 135 vagotomy 180 vagus nerve injury 89, 196, 199 vasopressin see antidiuretic hormone (ADH) venous cannulation 283–6 venous thrombosis venous catheterization 298 see also deep venous thrombosis ventilation, mechanical 38, 40, 392 air leaks 117–18 liquid 42 lung volume reduction 116 tracheal resection 102, 103 ventilation–perfusion (VQ) mismatch 394 ventilation–perfusion (VQ) scan 400 ventilator dependence 391 ventricle, left aortic valve removal 365–6 hypertrophy 354

outflow tract obstruction 378 venting 292–3 ventricle, right, failure 382 ventricular complex, premature 55–6 flecainide 58 lung volume reduction 123 ventricular fibrillation 274 ventricular rate control 61 ventricular rupture, posterior 375 ventricular tachycardia 56, 57 coronary artery bypass graft 277 ventricular vent, left 363 verapamil 59, 60 ventricular rate control 61 video-assisted thoracic surgery (VATS) 27 bronchopleural fistula 81 lung volume reduction procedures 109, 112, 113 vital capacity, esophageal resection 162 vocal cord medialization 89, 105 vocal cord paralysis 89, 104–5 esophageal resection 170 mediastinoscopy 237 von Willebrand factor 311, 314 warfarin 302 wound complications coronary artery bypass graft 277–8 lung volume reduction procedures 125 median sternotomy 7–11 wound infections chest wall reconstruction 157 coronary artery bypass graft 277–8 drainage 30 healing 30 median sternotomy 7–8, 9 diagnosis 9 incisional hernia 11 rate 5 mediastinoscopy/mediastinotomy 26 sternal 125 thoracoabdominal incision 23 thoracotomy incisions 29–30 tracheal resection 104 video-assisted thoracic surgery 27