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Edited by:

Douglas J. Mathisen, MD

Division of Thoracic Surgery
Massachusetts General Hospital
Harvard Medical School
Boston, Massachusetts

Christopher R. Morse, MD
Assistant Professor
Department of Surgery
Division of Thoracic Surgery
Massachusetts General Hospital
Harvard Medical School
Boston, Massachusetts
Series Editor:

Josef E. Fischer, MD, FACS

William V. McDermott Professor of Surgery

Harvard Medical School
Department of Surgery
Beth Israel Deaconess Medical Center
Boston, Massachusetts

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I would like to dedicate this book to my family, whose love, support, and sacrifice have meant so
much to me. Art and Virginia Mathisen, parents (deceased); Julie Quinn Mathisen, wife; Amy, Jen,
Beth, Kate Mathisen, daughters.
Douglas J. Mathisen
To my parents Frank and Beverley Morse, without whose sacrifice and support this would not have
been possible, and to my wife Andrea for her devotion, understanding, and strength.
Christopher R. Morse

Shair Ahmed, MD
Department of Cardiothoracic Surgery
Emory University School of Medicine
Atlanta, Georgia
Clemens Aigner, MD, MBA, FETCS
Associate Professor
Department of Surgery
Division of Thoracic Surgery
Medical University of Vienna
Vienna, Austria
James S. Allan, MD
Assistant Professor of Surgery
Department of Surgery
Division of Thoracic Surgery
Massachusetts General Hospital
Harvard Medical School
Boston, Massachusetts
Rafael S. Andrade, MD
Associate Professor of Surgery
Interim Chief Section of Thoracic and Foregut Surgery
Division of Cardiothoracic Surgery
University of Minnesota
Minneapolis, Minnesota
Andrew T. Arndt, MD
Cardiothoracic Surgery Fellow
Yale University School of Medicine
New Haven, Connecticut
Hugh G. Auchincloss, MD, MPH
General and Cardiothoracic Surgery
Massachusetts General Hospital
Boston, Massachusetts
Joshua N. Baker, MD
Assistant in Surgery
Department of Surgery
Division of Cardiac Surgery
Massachusetts General Hospital
Instructor in Surgery

Harvard Medical School

Boston, Massachusetts
Scott K. Berman, MD
Division of Thoracic Surgery
White Plains Hospital
White Plains, New York
Jamil F. Borgi, MD
Cardiothoracic Surgery Fellow
University of Washington Medical Center
Seattle, Washington
Ivan Bravio, MD
Thoracic Surgeon
Department of Cardiothoracic Surgery
Santa Marta Hospital
Lisbon, Portugal
Stephen R. Broderick, MD
Attending Surgeon
Barnes-Jewish Hospital
Department of Surgery
Division of Cardiothoracic Surgery
Washington University School of Medicine
St Louis, Missouri
Cynthia S. Chin, MD
Director of Womens Cancer Program Services
Division of Thoracic Surgery
White Plains Hospital
White Plains, New York
Traves D. Crabtree, MD
Attending Surgeon
Barnes-Jewish Hospital
Assistant Professor
Department of Surgery
Division of Cardiothoracic Surgery
Washington University School of Medicine
St. Louis, Missouri
Philippe Dartevelle, MD
Centre Chirurgical Marie Lannelongue

Department of Thoracic and Vascular Surgery and Heart-lung Transplantation

Institute of Thoracic Oncology
Hpital Marie Lannelongue
Le Plessis Robinson, France
Professor of Cardiothoracic Surgery
Paris Sud University
Le Kremlin Bictre, France
Pierre de Delva, MD
Assistant Professor
Department of Surgery
Division of Cardiothoracic Surgery
University of Mississippi Medical Center
Jackson, Mississippi
Frank C. Detterbeck, MD
Professor and Chief
Section of Thoracic Surgery
Yale University School of Medicine
New Haven, Connecticut
Dean M. Donahue, MD
Assistant Professor of Surgery
Harvard Medical School
Division of Thoracic Surgery
Massachusetts General Hospital
Boston, Massachusetts
Daniel P. Doody, MD
Pediatric Surgeon
Department of Surgery
Division of Pediatric Surgery
Massachusetts General Hospital
Associate Professor of Surgery
Harvard Medical School
Department of Pediatric Surgery
Massachusetts General Hospital
Boston, Massachusetts
Dominique Fabre, MD
Department of Thoracic and Vascular Surgery and Heart-Lung Transplantation
Thoracic Oncology Institute
Marie-Lannelongue Hospital
Paris Sud University
Le Plessis Robinson, France

Elie Fadel, MD, PhD

Centre Chirurgical Marie Lannelongue
Department of Thoracic and Vascular Surgery and Heart-lung Transplantation
Institute of Thoracic Oncology
Hpital Marie Lannelongue
Le Plessis Robinson, France
Professor of Cardiothoracic Surgery
Paris Sud University
Le Kremlin Bictre, France
Eric N. Feins, MD
Division of Thoracic Surgery
Massachusetts General Hospital
Harvard Medical School
Boston, Massachusetts
Matthew P. Fox, MD
Division of Thoracic Surgery
Massachusetts General Hospital
Harvard Medical School
Boston, Massachusetts
Julie Freischlag, MD
The William Stewart Halsted Professor
Department of Surgery
Division of Vascular Surgery
The Johns Hopkins Hospital
Baltimore, Maryland
Henning A. Gaissert, MD
Associated Visiting Surgeon
Division of Thoracic Surgery
Massachusetts General Hospital
Associate Professor of Surgery
Department of Surgery
Harvard Medical School
Boston, Massachusetts
Sidhu Gangadharan, MD
Department of Surgery
Division of Thoracic Surgery and Interventional Pulmonology

Beth Israel Deaconess Medical Center

Assistant Professor of Surgery
Harvard Medical School
Boston, Massachusetts
Jose P. Garcia, MD
Cardiac Surgery
Department of Surgery
Massachusetts General Hospital
Boston, Massachusetts
Natalia Glebova, MD, PhD
Fellow in Vascular Surgery
Department of Surgery
Division of Vascular Surgery
The Johns Hopkins Hospital
Baltimore, Maryland
Mahmoud Ismail, MD
Department of General, Visceral, Vascular, and Thoracic Surgery
Universittsmedizin Berlin
Charit Campus Mitte
Berlin, Germany
Jordan Kazakov, MD
C.E.T.O.C, Division of Thoracic Surgery
Centre Hospitalier de lUniversit de Montral
Clinical and Research Fellow, CETOC
Department of Thoracic Surgery
University of Montreal
Montral, Quebec
Mohamed Khereba, MBBCh
Thoracic Surgery Research Fellow
CHUM Endoscopic Tracheobronchial and Oesophageal Center (CETOC)
Division of Thoracic Surgery
University of Montreal
Montreal, Quebec, Canada
Doosang Kim, MD, PhD
Department of Thoracic and Cardiovascular Surgery
Veterans Health Service Medical Center
Seoul, Korea
Tad Kim, MD

Department of Surgery
Division of Cardiothoracic Surgery
University of Mississippi Medical Center
Jackson, Mississippi
Walter Klepetko, MD
Professor of Thoracic Surgery
Department of Surgery
Division of Thoracic Surgery
Medical University of Vienna
Vienna, Austria
John C. Kucharczuk, MD
Division of Thoracic Surgery
University of Pennsylvania
Philadelphia, Pennsylvania
Michael H. Kwon, MD
Department of Surgery
Massachusetts General Hospital
Boston, Massachusetts
Michael Lanuti, MD
Assistant Professor of Surgery
Harvard Medical School
Director of Thoracic Oncology
Division of Thoracic Surgery
Massachusetts General Hospital
Boston, Massachusetts
Moishe Liberman, MD, PhD
Department of Surgery
Division of Thoracic Surgery
Centre Hospitalier de lUniversit de Montral
Associate Professor
CHUM Endoscopic Tracheobronchial and Oesophageal Center (CETOC)
Department of Surgery
Division of Thoracic Surgery
University of Montreal
Montral, Quebec, Canada
Maria Lucia L. Madariaga, MD
Clinical Fellow Surgery

Department of Surgery
Division of Thoracic Surgery
Massachusetts General Hospital
Harvard Medical School
Boston, Massachusetts
Douglas J. Mathisen, MD
Division of Thoracic Surgery
Massachusetts General Hospital
Harvard Medical School
Boston, Massachusetts
Robert E. Merritt, MD
Assistant Professor of Cardiothoracic Surgery
Department of Cardiothoracic Surgery
Division of Thoracic Surgery
Stanford Hospitals and Clinics
Stanford University School of Medicine
Assistant Professor of Cardiothoracic Surgery
Division of Thoracic Surgery
Falk Cardiovascular Research Center
Stanford, California
Philippe Monnier, MD
Professor Emeritus and Former Chairman
Otolaryngology, Head & Neck Surgery Department
Professor Emeritus
Lausanne University
School of Biology and Medicine
University of Lausanne
University Hospital CHUV
Lausanne, Switzerland
Christopher R. Morse, MD
Assistant Professor
Department of Surgery
Division of Thoracic Surgery
Massachusetts General Hospital
Harvard Medical School
Boston, Massachusetts
Michael S. Mulligan, MD
Cardiothoracic Surgery

University of Washington Medical Center

Seattle, Washington
Ashok Muniappan, MD
Assistant Surgeon
Division of Thoracic Surgery
Massachusetts General Hospital
Instructor in Surgery
Harvard Medical School
Boston, Massachusetts
Basil S. Nasir, MBBCh
Interventional Thoracic Endoscopy Fellow
CHUM Endoscopic Tracheobronchial and Oesophageal Center (CETOC)
Division of Thoracic Surgery
University of Montreal
Montreal, Quebec, Canada
Francis C. Nichols, MD
Associate Professor of Surgery
Division of General Thoracic Surgery
Mayo Clinic
Rochester, Minnesota
Konstantinos Papadakis, MD
Instructor in Surgery
General Surgery
Department of Surgery
Boston Childrens Hospital
Boston, Massachusetts
Allan Pickens, MD
Assistant Professor of Surgery
Director of Minimally Invasive Surgery and Thoracic Oncology
Section of Cardiothoracic Surgery
Emory University Hospital Midtown
Atlanta, Georgia
Eitan Podgaetz, MD, MPH
Assistant Professor of Surgery
Section of Thoracic and Foregut Surgery
Division of Cardiothoracic Surgery
University of Minnesota
Minneapolis, Minnesota

Francesco Puma, MD
Professor of Surgery
Thoracic Surgery Unit
University of Perugia Medical School
Perugia, Italy
Dirk Van Raemdonck, MD, PhD
Surgical Director Lung Transplant Program
Department of Thoracic Surgery
University Hospital Gasthuisberg
Professor of Surgery
Laboratory for Experimental Thoracic Surgery
Department of Clinical and Experimental Medicine
KU Leuven
Leuven, Belgium
Nathalie Roy, MD
Assistant in Surgery
Department of Surgery
Division of Cardiac Surgery
Massachusetts General Hospital
Instructor in Surgery
Harvard Medical School
Boston, Massachusetts
Jens C. Rckert, MD
Department of General, Visceral, Vascular, and Thoracic Surgery
Universittsmedizin Berlin
Charit Campus Mitte
Berlin, Germany
Kishore Sandu, MD
Clinical Instructor
Otolaryngology, Head & Neck Surgery Department
Assistant Professor
Lausanne University
University Hospital CHUV
Lausanne, Switzerland
Ravi Shah, MD
Department of Surgery
Massachusetts General Hospital
Boston, Massachusetts

Robert C. Shamberger, MD
Department of Surgery
Boston Childrens Hospital
Robert E. Gross Professor of Surgery
Harvard Medical School
Boston, Massachusetts
K. Robert Shen, MD
Associate Professor of Surgery
Department of Surgery
Division of General Thoracic Surgery
Mayo Clinic
Rochester, Minnesota
Hon Chi Suen, MBBS (HK), DABS, DABThS
Center for Cardiothoracic Surgery, Inc
St. Louis, Missouri
Marc Swierzy, MD
Department of General, Visceral, Vascular, and Thoracic Surgery
Universittsmedizin Berlin
Charit Campus Mitte
Berlin, Germany
Mathew Thomas, MD
Senior Associate Consultant
Division of Cardiothoracic Surgery
Mayo Clinic
Jacksonville, Florida
Robert W. Thompson, MD
Attending Surgeon and Director
Center for Thoracic Outlet Syndrome
Department of Surgery
Section of Vascular Surgery
Barnes-Jewish Hospital
Professor of Surgery (Vascular Surgery), Radiology, and Cell Biology and Physiology
Washington University School of Medicine
St. Louis, Missouri
Jacopo Vannucci, MD
Thoracic Surgery Unit

University of Perugia Medical School

Perugia, Italy
Thomas K. Varghese Jr, MD, MS
Director of Thoracic Surgery
Harborview Medical Center
Associate Program Director
UW Cardiothoracic Surgery Residency
Associate Professor
Department of Surgery
Division of Cardiothoracic Surgery
University of Washington
Seattle, Washington
Chandu Vemuri, MD
Attending Surgeon
Department of Surgery
Section of Vascular Surgery
Barnes-Jewish Hospital
Assistant Professor of Surgery (Vascular Surgery) and Radiology
Washington University School of Medicine
St. Louis, Missouri
Garrett L. Walsh, MD
Department of Thoracic and Cardiovascular Surgery
MD Anderson Cancer Center
The University of Texas
Houston, Texas
Cameron D. Wright, MD
Visiting Surgeon
Division of Thoracic Surgery
Massachusetts General Hospital
Professor of Surgery
Harvard Medical School
Boston, Massachusetts
Peirong Yu, MD
Department of Plastic Surgery
MD Anderson Cancer Center
The University of Texas
Houston, Texas

Series Preface
This series of miniatlases is an outgrowth of Mastery of Surgery. As the series editor, I have
been involved with Mastery of Surgery since the third edition, when I joined two greats of
American surgery, Lloyd Nyhus and Robert Baker, who were the editors at that time. Surgical
atlases were common in those days, and Mastery of Surgery was one of several quality atlases
which existed then; of particular quality were those by Dr. John Madden of New York, Dr.
Robert Zollinger of Ohio State, and two others, with which the reader may be less familiar.
The first was by Professor Pietro Valdoni, Professor of Surgery at the University of Rome, who
ran 10 operating rooms simultaneously, and as the Italians like to point out to me, a
physician to three popes. One famous surgeon said to me, what can you say about Professor
Valdoni? Professor Valdoni said to three popes, take a deep breath, and they each took a
deep breath. This superb atlas, which is not well known, was translated from the Italian by
my partner when I was on the staff at Mass General Hospital, Dr. George Nardi. The second
was a superb atlas by Dr. Robert Ritchie Linton, an early vascular surgeon whose atlas was of
very high quality.
Atlases, however, fell out of style, and in the fourth and fifth editions of Mastery of Surgery,
we added more chapters that were textbooky types of chapters to increase access to the
growing knowledge base of surgery. In discussing with Brian Brown and others at Lippincott
Williams & Wilkins, as well as with some of the surgeons who subsequently became editors of
books in this present series, it seemed that we could build on our experience with Mastery of
Surgery by creating smaller, high-quality atlases, each focusing on the key operations of a
sharply circumscribed anatomical area. This we have accomplished due to the incredible
work of the editors who were chosen for their demonstrated mastery in their fields.
Why the return of the atlas? Is it possible that the knowledge base is somewhat more
extensive with more variations on the various types of proceduresthat as we learn more
about the biochemistry, physiology, genetics, and pathophysiology in these different areas,
there have gotten to be variations on the types of procedures that we do on patients in these
areas? This increase in the knowledge base has occurred simultaneously at a time when the
amount of time available for training physiciansand especially surgeonshas been steadily
declining. While I understand the hypothesis that brought the 80-hour work week upon us,
which limits the time that we have for instruction (though I do believe that it is well
intentioned), I still ask the question: Is the patient better served by a somewhat fatigued
resident who has been at the operation, and knows what the surgeon is worried about, or a
comparatively fresh resident who has never seen the patient before?
I dont know, but I tend to come down on the side that familiarity with the patient is
perhaps more important. And what about the errors of hand-off, which seem to be more of an
intrinsic issue with the hand-off itself (which we are not able to really remedy entirely),
rather than poor intentions?
This series of miniatlases is an attempt to help fill the void created by inadequate time for
training. We are indebted to the individual editors who have taken on this responsibility and
to the authors who have volunteered to share their knowledge and experience in putting
together what we hope will be a superb series. We have chosen surgeons who are inspired by
their experience of teaching residents and medical students (a high calling indeed), a quality

matched only by their devotion and superb care they have given to thousands of patients.
It is an honor to serve as the series editor for this outstanding group of miniatlases, which
we hope will convey the experiences of an excellent group of editors and authors to the
benefit of students, residents, and their future patients in an era in which time for education
seems to be increasingly limited.
Putting a book togetherespecially a series of booksis not easy, and I wish to
acknowledge the staff at Lippincott Williams & Wilkins, including Brian Brown, Keith
Donnellan, Brendan Huffman, and many others. I would also like to thank my personal staff
in the office, in particular, Edie Burbank-Schmitt, Ingrid Johnson, Abigail Smith, and Jere
Cooper. None of this would have been possible without them.
Josef E. Fischer, MD, FACS
Boston, Massachusetts

Dr. Josef Fischer has created a series of atlases designed to complement the textbook Mastery
of Surgery. These atlases are meant for students of all ages, medical students, residents,
practicing surgeons, academic surgeons, general surgeons, thoracic surgeons, and anyone
with an interest in surgical techniques. The two volumes in the series deal with thoracic
surgery procedures exclusive of esophageal surgery. We have contributions from leading
experts in thoracic surgery throughout the world. This international flavor should increase
the broad appeal of this surgical atlas. The focus has been on the authors personal
approaches. One of the great attractions of thoracic surgery is the wide array of disorders and
the number of procedures required to manage these problems. This is certainly true of these
two volumes. The topics covered range from the simple to the complex.
The texts have been organized to deal with thoracic surgical procedures not covered in Dr.
James Luketichs excellent volume on esophageal surgery. The chapters are organized with a
minimum of background, focusing on indications and contraindications, surgical techniques,
avoidance of pitfalls, the management of complications, and surgical results. The emphasis is
mainly on surgical technique. The technique sections are liberally supported with detailed
drawings. This approach should give the reader all that they need to know in order to
manage the surgical problems covered in the text. We have purposely provided only selected
references, if the reader wishes to learn more.
We have tried to organize these two volumes according to several broad topics. The first
general topic has to do with endoscopy. These rather straightforward procedures may be
familiar to most readers, but chapters in this portion emphasize different approaches, specific
indications, and problems that may be encountered.
The most common procedures thoracic surgeons perform are related to pulmonary
resections. This is the largest topic covered. Thoracic surgery is in a transition from open
procedures to minimally invasive procedures and we have tried to present both sides of that
argument with chapters devoted to open pulmonary resections and minimally invasive
pulmonary resections for each procedure.
Tracheobronchoplasty has become a much more common procedure for practicing thoracic
surgeons. Sleeve resections have become more commonplace in practice. The more advanced
carinal resections and reconstructions are still (for the most part) limited to units that have a
specialized interest in these procedures. These complex operations are covered by
acknowledged experts in the field.
Fistulas following pulmonary resections are challenges for all thoracic surgeons. Different
approaches are required in specific circumstances. Knowledge of these different approaches
should be invaluable to the practicing surgeon. The uses of well-vascularized, pedicled,
buttressing muscle or omentum are invaluable in handling these complex problems and are
covered in detail in these chapters.
Pulmonary transplantation and related procedures are important in contemporary thoracic
surgery. Specific techniques related to surgery for pulmonary transplantation are covered in
detail by acknowledged experts.
Disorders of the chest wall and diaphragm are uncommon procedures. Few surgeons have
developed extensive experience or expertise in these areas. Yet these conditions do present to

the practicing surgeon. Knowledge of these procedures is valuable for those occasions that
surgeons are confronted with these problems. These conditions encompass thoracic outlet
syndrome, pectus excavatum and carinatum, the paralyzed diaphragm, and conditions of the
mediastinum. We have chosen individuals who have developed specific expertise in these
Disorders of the trachea are uncommon problems. There are centers, however, that have
developed specific expertise in these areas. Because of the unusual and infrequent
presentation of these problems, detailed knowledge and understanding of the management of
these conditions is invaluable. Specific knowledge of techniques, avoidance of complications,
and managing complications when they occur should be invaluable to the surgeon unfamiliar
with these conditions.
Finally, there are groups of disorders that fit into a broad category of extended thoracic
operations. These are operations that have been designed by a handful of experts for specific
unusual problems and are quite demanding in their understanding and technical detail. While
these types of operations may not be practiced by a general population of thoracic surgeons,
knowledge of these procedures and who performs them should awaken the awareness of these
problems and the solutions that are available.
We hope these two volumes will be viewed by surgeons as a welcome addition to the
thoracic surgical literature. We have selected procedures in such a way that the surgeon
should be able to find specific information on any operation involved in thoracic surgery.
Douglas J. Mathisen, MD
Christopher R. Morse, MD

Series Preface


1 Lung Harvest/Techniques
Dirk Van Raemdonck and Ivan Bravio
2 Single Lung Transplantation
Ashok Muniappan
3 Double Lung Transplant
Clemens Aigner, Doosang Kim, and Walter Klepetko
4 Heart and Lung En Bloc Transplantation
Jose P. Garcia and Ravi Shah
5 ECMO and Lung Transplantation
Nathalie Roy and Joshua N. Baker
6 Lung Volume Reduction: Transsternal
Thomas K. Varghese Jr.
7 Lung Volume Reduction: VATS
Thomas K. Varghese Jr.
8 Monaldi Procedure
Tad Kim and Pierre de Delva
9 Cavernostomy (Aspergilloma)
Francis C. Nichols


10 Chest Wall/Pleural Space/Diaphragm: Thoracic Outlet SyndromeSupraclavicular

Thoracic Outlet Decompression
Robert W. Thompson and Chandu Vemuri
11 Thoracic Outlet Syndrome Requiring Vascular Reconstruction: Vein, Artery
Dean M. Donahue
12 Thoracic Outlet Syndrome: Transaxillary Approach
Julie Freischlag and Natalia Glebova


13 Pectus Excavatum: The Nuss Repair

Daniel P. Doody
14 Pectus RepairRavitch
Konstantinos Papadakis and Robert C. Shamberger


15 Open Reduction and Internal Fixation of Chest Wall Fractures
Hon Chi Suen
16 Chest Wall Resection/Reconstruction for Tumors
Francesco Puma and Jacopo Vannucci
17 Sternal Resection/Reconstruction
Eric N. Feins and Christopher R. Morse


18 Plication/Thoracotomy/VATS
Michael H. Kwon and Christopher R. Morse
19 Laparoscopic Diaphragmatic Plication
Eitan Podgaetz and Rafael S. Andrade
20 Diaphragmatic Pacing
Scott K. Berman and Cynthia S. Chin


21 Decortication: Thoracotomy and VATS
Robert E. Merritt

22 Pleurodesis, Indwelling Pleural Catheters

Jordan Kazakov and Moishe Liberman
23 Eloesser Flap and Clagett Procedures
Shair Ahmed and Allan Pickens
24 Thoracic Duct Ligation
Stephen R. Broderick and Traves D. Crabtree
25 Thoracic Sympathectomy
James S. Allan and Maria Lucia L. Madariaga


26 Robotic Resection: Thymus

Mahmoud Ismail, Marc Swierzy, and Jens C. Rckert
27 Transcervical Thymectomy
Henning A. Gaissert

28 Transsternal Thymectomy for Invasive Thymoma and Thymic Carcinoma

John C. Kucharczuk


29 Posterior Neurogenic Tumors VATS/Open
Frank C. Detterbeck and Andrew T. Arndt
30 Dumbbell Neurogenic
Mathew Thomas and K. Robert Shen


31 Release Maneuvers: Suprahyoid Laryngeal Release

Basil S. Nasir and Moishe Liberman
32 Release Maneuvers: Pericardial Release
Mohamed Khereba, Basil S. Nasir, and Moishe Liberman
33 T-Tube
Ashok Muniappan
34 Tracheal Dilation
Ashok Muniappan
35 Tracheal Resection
Ashok Muniappan
36 Laryngotracheal Resection
Matthew P. Fox and Douglas J. Mathisen
37 Pediatric Laryngotracheal Resection and Reconstruction
Kishore Sandu and Philippe Monnier
38 Tracheoesophageal Fistula
Hugh G. Auchincloss and Douglas J. Mathisen
39 Slide Tracheoplasty
Cameron D. Wright
40 Tracheoplasty
Sidhu Gangadharan
41 Closure of Persistent Tracheal Stoma
K. Robert Shen
42 Autologous Tracheal Replacement
Dominique Fabre and Philippe Dartevelle
43 Microvascular Reconstruction of Tracheal Defects
Peirong Yu and Garrett L. Walsh


44 Superior Vena Cava Resection/Reconstruction

Michael Lanuti
45 Extended Thoracic Resections with Cardiopulmonary Bypass
Elie Fadel and Philippe Dartevelle
46 Pulmonary Endarterectomy
Jamil F. Borgi and Michael S. Mulligan

Part I
Lung Transplantation/Chronic Lung

1 Lung Harvest/Techniques

Dirk Van Raemdonck and Ivan Bravio

Every potential organ donor should be considered as a potential lung donor. The ideal lung
donor criteria as defined in the early years of lung transplantation are listed in Table 1.1. The
perfect lung donor matching all these criteria has become very rare in Western Europe
because of the constant change in donor profile with a rising proportion of older donors
becoming brain death from cerebrovascular disease. The scientific evidence to rely on these
strict donor criteria was extensively reviewed by a panel of the Pulmonary Council of the
International Society for Heart and Lung Transplantation and found to be very low.
Recommendations were made to relax the acceptance criteria. The lung yield from all
available donors, therefore, varies between countries and between lung transplant centers
within the same country from 10% to nearly 50%. This percentage depends on (1) the
expertise of the local donor team with active donor management; (2) the confidence by the
recipient team to relax the preset lung donor criteria accepting pulmonary grafts from
extended criteria donors and from donors after cardiocirculatory death; and (3) the
willingness of the lung retrieval team to travel to the donor hospital to verify whether the
initial information regarding lung oxygenation capacity, appearance on chest x-ray, and
bronchoscopy findings provided at the time of organ offer, truly reflects lung quality
witnessed at final evaluation in the donor after endotracheal suctioning and maximal alveolar
As stated above, many potential lung donors will present with one of the more parameters
that do not match the ideal criteria listed in Table 1.1. Many of these should be considered as
relative contraindications as good immediate outcome is often possible. Nevertheless donors
with older age, significant smoking history, inferior oxygenation, and radiographic infiltrates
are considered to carry potential risk factors for the onset of chronic allograft dysfunction
resulting in impaired long-term survival although strong evidence is missing in published
literature. Some donor factors, however, should be considered as absolute contraindications
for lung use such as pneumonia or sepsis, significant underlying parenchymal or vascular
lung disease, history of recent malignancy (except skin cancer and some brain tumors), ABO
incompatibility, and seropositivity for human immunodeficiency virus or hepatitis B or C
virus in case of seronegative recipients.

TABLE 1.1 Ideal Lung Donor Selection Criteria

We prefer to send an experienced lung surgeon to the donor hospital as the decision process
whether or not to accept the lung is as important as proper lung preservation and excision.
Before leaving, the surgeon in charge should check with the scrub nurse and donor
coordinator whether all surgical instruments and preservation solutions are available.
Upon arrival in the donor hospital, the recipient team is quickly informed on the estimated
timing of cross clamp in the donor as unexpected delays in transport or start of donor
operation may have occurred.
An advice that is greatly appreciated by younger colleagues when joining for their first lung
retrieval is to take off their socks before entering the operating room. Otherwise they risk
returning home with a soaked pair after organ flush and additional topical cooling!
It is important to introduce the lung team to all members of the local donor team including
scrub nurse and anesthesiologist and to retrieval surgeons from other transplant centers.
In case of simultaneous heart procurement, a plan is discussed and agreed in advance with
the heart surgeon on the surgical steps to be taken. Some may not be familiar with
combined heart and lung retrieval!
It is the surgeons responsibility to check all relevant donor medical history, to verify the
blood group, and to check whether the death certificate was completed according to state
In case the donor is not yet fully installed on the operating table, we prefer to have both
arms next to the body to get more working space for both abdominal and thoracic teams.
The shoulders are lifted up with towels and the head is extended backwards to have the
neck free for better exposure to the trachea.
A broad-spectrum antibiotic and 1 g methylprednisolone is administered IV to the donor if
not done already.
We routinely ask the anesthesiologist in charge of the donor to switch the gas mixture on
the ventilator to 100% oxygen and to increase positive end-expiratory pressure to 5 cm
H2O if needed. Ventilatory parameters are checked paying attention to the tidal volume
and peak airway pressure so to have an idea on pulmonary compliance. A new arterial
blood gas sample can be taken after 5 minutes although we prefer to wait for intrathoracic

pulmonary vein blood sampling.

First a tracheal aspirate for culture is taken through the endotracheal tube followed by a
quick flexible bronchoscopy whenever possible to verify the correct position of the
endotracheal tube and to appreciate the amount and color of airway secretions, presence of
blood or stomach content, and degree of mucosal inflammation. After cleaning the airways,
we routinely perform a bronchoalveolar lavage with 2 50 mL of saline solution. The
returned fluid is aspirated for culture and cellular and biomolecular analysis. Purulent
secretions persistently bubbling up into the central airways are a bad sign indicative for the
presence of pneumonia.

A standard median sternotomy is performed usually in combination with median
laparotomy in case abdominal organ retrieval is scheduled. In case sternotomy is left to be
done by our own team (often the chest cavity is already opened by the abdominal team),
we prefer to split the sternum in apnea in order not to damage lung parenchyma protruding
into the retrosternal plane in a fully ventilated donor.
Lung Inspection and Evaluation
If not done yet by others, we open the pleural cavity on both sides by incising the
mediastinal pleura. Care must be taken not to damage lung parenchyma on its medial
aspect when using cautery. At this moment, we do not yet open the pericardium in order
not to destabilize the heart too much when inspecting the lungs.
Transection of the diaphragmatic muscles is a tremendous help to gain access with easier
exposure of the lower lobes.
The first step is to take a blood sample with a heparinized syringe by puncturing the
extrapericardial part of the lower or middle lobe vein on both sides to assess oxygenation
capacity (partial oxygen pressure in pulmonary vein = PpvO2) of left and right lungs
The next step is to inspect the lungs for abnormalities that may preclude safe
transplantation. We, therefore, ask the anesthesiologist to disconnect the endotracheal tube
from the ventilator after initial preoxygenation as described above. First, it offers the
possibility to observe the elasticity of both lungs (collapse test). If the lungs do not
collapse instantly or symmetrically, this may be indicative of retained secretions or
presence of interstitial lung pathology (edema, hemorrhage, pneumonia, emphysema).
Deflated lungs are easier to be eviscerated from the pleural cavity without too much
cardiac compression. We then quickly palpate both lungs looking for abnormal findings
(nodules, blebs, adhesions) that may need further attention during and after retrieval.
Significant structural abnormalities may finally exclude the lungs for transplantation.
The anesthesiologist is then asked to manually reinflate both lungs with 50% oxygen to a
sustained 30 cm H2O pressure for recruitment of all atelectactic lung segments helped with
gentle massage by the surgeon (Fig. 1.1). This maneuvre is also very indicative of lung

Once the blood gas results have returned and PpvO2 values fit with macroscopic findings,
the recipient team is called to inform that lungs fulfill quality requirements and what the
estimated cross-clamp time will be. Depending on the transport time and estimated
operative time needed to explant the native lungs, it is now about the moment to call the
recipient to the operating room and to prepare him for induction of anesthesia.
In case of discrepancy between healthy looking lungs and low oxygenation capacity
(PpvO2/FiO2 <300 mm Hg), blood gas analysis should be repeated to verify.
If any doubt about lung performance and quality, lungs can always be explanted for further
testing during ex vivo perfusion in the donor hospital or in the recipient hospital after
being transported back on ice in case the expertise and equipment is available.

Figure 1.1 All atelectatic parenchymal zones are recruited by pressure ventilation and gentle massage.

Lung Dissection
If not previously done by others, the next step is to open the pericardium and to suspend
both edges to the skin with heavy stitches.
In case the heart is retrieved for separate cardiac transplantation, much of the dissection is
usually carried out by the heart surgeon. The ascending aorta is freed from the main
pulmonary artery and encircled with a tape. The superior vena cava is mobilized from its
pericardial attachments and encircled with a heavy ligature distal to both innominate
veins. We do not favor to dissect or ligate the azygos vein as this maneuvre may cause
bleeding or result in inadvertent ligation of the upper lobe branch of the right pulmonary
artery. We have witnessed lobar infarction when arterial transection was not recognized or
ignored at implantation. The intrapericardial inferior vena cava is mobilized from its
pericardial attachments to facilitate adequate clamping. Passing a ligature is not needed as
many abdominal teams like to vent the liver into the pericardium.
A horizontal mattress suture is then placed in the anterior midportion of the ascending
aorta to secure the cardioplegia cannula once it is inserted.
For lung procurement without the heart, we advise to restrict the intrapericardial dissection
to a minimum to speed up the retrieval and to avoid too much cardiac manipulation risking
arrhythmias and premature cardiac arrest in an unstable donor. If no heart surgeon is
around, the help of a thoracic assistant is greatly appreciated for suctioning during lung

The placement of a purse-string suture on the main pulmonary artery is the only important
act that is needed in a beating heart procedure. We prefer a 4-0 polypropylene suture
widely placed for the introduction of a large-sized (18 to 24 Fr) pulmoplegia cannula
allowing a high-volume flush at low pressure. If the heart is being used, care should be
taken to stay distal to the pulmonary valve (>1.5 cm) but away from the pulmonary artery
bifurcation to prevent inadvertent selective cannulation of the left main pulmonary artery.
In case the heart is not used and not retrieved for the homograft bank, cannulation close to
the pulmonary valve is recommended (Fig. 1.2A).
Lung Preservation
Once the dissection of all organs is completed, the donor is heparinized with 25,000 units
through central venous access or direct intracaval injection. We prefer the abdominal
surgeons to insert their cannulas first, one in the abdominal aorta for flushing and a sump
in the abdominal vena cava for venting. Next the cardioplegia needle or thin cannula is
introduced. We ask the heart surgeon to secure his cannula with a ligature, so there is less
risk for dislocation during manipulation of heart and lungs while verifying adequate flush
especially in atelectatic lower lobes.

Figure 1.2 A: A large pulmoplegia cannula is inserted in the main pulmonary artery through a purse string proximal to the
pulmonary valve for antegrade flush. B: The pulmoplegia cannula has a wider tip at the end preventing from inadvertent
decannulation during flush.

A pulmonary artery incision is then made in the middle of the purse string with a sharp
blade no. 15 and the arteriotomy is sufficiently dilated to allow easy entrance of the flush
cannula. We prefer a cannula with a broader tip at the end, so that it stays intraluminal
when pulled back to verify the correct position in the main pulmonary artery (Fig. 1.2B).
This maneuvre may sometimes lead to significant blood loss and should, therefore, be done
at the very end when all teams are ready to start flushing the organs.

The purse string is snugged and a ligature is tied around the cannula for fixation. With the
cannula in the upright position, the height of the blood column is an indicator of the
arterial pressure in the pulmonary circulation. A three-way stopcock is connected to the
side hole in the cannula. This greatly helps to de-air once connected to the purged
pulmoplegia line.
Before initiating the flush, it is wise to reconfirm full expansion of the lung and if needed,
to recruit the alveoli in atelectatic zones.
A bolus of a strong vasodilator prostaglandin E1 alprostadil (Prostin VR 0.5 mg/mL, Pfizer),
prostaglandin I2 epoprostenol (Flolan 0.5 mg, GlaxoSmithKline), or nitroglycerine (Nitro
Pohl, 1 mg/mL, Pohl-Boskamp BV) is injected with a 50-mL syringe directly into the
pulmonary artery via the three-way stopcock on the cannula. It is wise to inform other
members that this bolus injection may result in a significant drop in systemic arterial
After circulation of the vasodilator through the lungs, inflow to the right heart is stopped by
ligating or clamping both vena cava. The inferior vena cava is hemitransected proximal to
the clamp for venting of the right heart and the tip of the left atrial appendage is transected
to decompress the left atrium. Alternatively, the left atrium can be incised in the middle of
the atrioventricular groove and the left pulmonary vein after the apex of the heart is lifted
in the cephalad position. The latter procedure is, however, less effective in draining the
large volume of lung preservation solution.
The aortic clamp is then placed and both cardioplegia and pulmoplegia lines are opened
verifying that both left and right ventricles are adequately decompressed once the solutions
start filling both atria. Larger incisions may be needed for adequate venting. If the heart is
not used and the abdominal team has put a clamp on the infradiaphragmatic part of the
descending aorta, no clamp on the ascending aorta is needed. In this way, the pulmoplegia
solution is injected by the left ventricle into the aorta flushing the bronchial arteries, so the
airways may be better preserved. The heart will stop beating by cold perfusion running into
the coronary arteries and by the additional topical cooling. The vascular clamp on the
inferior vena cava is then released for better venting of the liver.
Attention should be paid to the position of the tip of the pulmoplegia cannula. Inadvertent
cannulation of the left pulmonary artery is possible leading to inadequate flush of the right
lung. Gentle traction on the cannula may help to keep the cannula in the midline position
with the tip directed toward the pulmonary valve.
We flush both lungs by gravity (60 cm H2O) with one large bag (2.8 L) and one small bag
(1 L) of cold Perfadex preservation fluid (XVIVO AB, Gothenburg, Sweden) running
simultaneously. This will result in a total flush volume of 40 to 70 mL/kg body weight
(45 to 95 kg donor). The free outflowing perfusate from the left atrium should gradually
clear and must be monitored during the flush assuring equal distribution of Perfadex to
both lungs.
The pericardial suspension stitches are released and cold saline solution is poured on the
heart and lungs for additional topical cooling.
During the flush, ventilation is continued with the same tidal volume, PEEP 5 cm H2O and
FiO2 0.5. If needed, recruitment of atelectatic zones will result in more equal blanching of
the lungs.

When retrieving lungs from donors after cardiocirculatory death (Maastricht category III or
IV), the steps for lung procurement are somewhat reversed. After quick sternotomy, both
pleural cavities are widely opened and cold saline solution is poured over deflated lungs.
The pericardium is opened; a large sump drain is inserted in the inferior vena cava through
an opening in the right atrial appendage for decompression of the right heart. The
pulmoplegia cannula is inserted in the main pulmonary artery through the pulmonary valve
after incising the right ventricular outflow tract. The cannula is then secured by tying a
heavy ligature passed around the main pulmonary artery distal to the valve. The cannula is
de-aired and connected to the flushed pulmoplegia line. The left atrial appendage is
transected and antegrade flush with Perfadex is started while ventilation of both lungs is
regained. In experienced hands the whole procedure will not take longer than 3 to 5
minutes after skin incision.
In addition to the antegrade flush, lung preservation should be completed by an additional
retrograde flush with 1 L Perfadex (250 mL via each of the four pulmonary veins) once the
heart is extracted. This can be done with the same cannula gently wedged in the orifice of
the four veins (Fig. 1.3). Small clots and debris may flow out from the pulmonary artery. It
is believed that adding a retrograde flush improves airway preservation via
bronchopulmonary collaterals. We prefer to do this while the lungs are still in the body
attached to the trachea, so that ventilation can continue during the flush allowing better
distribution of the preservation solution. If performed on the back table the Perfadex used
for retrograde perfusion can be collected and utilized for lung storage.

Figure 1.3 The same pulmoplegia cannula is wedged in the orifice of the right superior pulmonary vein for retrograde flush.

Lung Extraction
Once both lungs and heart are sufficiently flushed and cooled, the organs can be extracted.
Decannulation is performed, the ventilator is disconnected leaving the endotracheal tube in
place, and pleural and pericardial cavities are emptied with heavy suction devices.
In case of planned combined heartlung transplantation, the organs are not split but
dissected and extracted en bloc. If the heart is used for a separate heart recipient or for the
homograft bank, this organ will be extracted first.
The first step is to completely transect the inferior vena cava and to dissect its attachment
up to the level of the right inferior pulmonary vein. Thereafter, the heart can be lifted and

turned completely with the apex pointing in the cephalad direction. In this way the left
atrium is maximally distended. A horizontal cut with a sharp blade is made in the
midportion of the left atrium in between the atrioventricular groove and the left pulmonary
vein. The left atrial incision is further extended parallel to the atrioventricular groove
toward the base of the left atrial appendage on the left side and toward the inferior edge of
the inferior vena cava on the right. The surgeon standing on the left side of the donor has
the best view from inside the left atrium on the orifices of both right-sided pulmonary
veins. The left atrial incision on the right side is then continued along the interatrial groove
(Waterston). We do not dissect the groove from the outside. A sufficient rim of left atrium
(minimum 1 cm) should be left as cuff for both the heart and the lungs. It is important not
to overstretch the heart as this may result in insufficient atrial cuff on the lung side once it
retracts. The scissors should always be kept in a horizontal position when completing
circular cuff excision. Attention should be paid not to incise the pulmonary arteries at this
The heart is put back in its normal position and the superior vena cava and ascending aorta
are transected at sufficient length needed for the heart recipient. Both vessels are then freed
from its attachments with the right pulmonary artery. Finally, the main pulmonary artery is
usually transected at the cannulation site unless a longer cuff is needed for a heart recipient
with a congenital abnormality. In case the lung will be hooked up to a device for ex vivo
lung perfusion, a longer segment of main pulmonary artery will facilitate arterial
After heart extraction, dissection of the double-lung bloc is to be continued by the lung
surgeon. The inferior pericardium is transected in a U-shape taking care not to injure the
lung at its attachment with the pulmonary ligament. This structure is transected carefully
by cephalad traction on the double-lung bloc. We leave the esophagus attached to the
vertebral body, so sharp dissection is carried out between the esophagus and posterior
pericardium. With the right lung moved over into the left pleural cavity, the azygos vein is
now transected. The same maneuvre is done on the left side now dividing the descending
aorta distal to the arch. The dissection in the posterior mediastinum is continued separating
the esophagus from the trachea as high as possible. Thereafter the innominate veins are
transected as well as all supra-aortic vessels and pleural attachments. The trachea is then
freed and vagal and recurrent nerves are transected.
Once all attachments are loosened, the double-lung bloc remains connected to the trachea
only. The endotracheal cannula is pulled back by the anesthesiologist (who has often left
the room by that time) guided by the surgeon, so that a sufficient length of trachea can be
harvested, especially when the airway will be hooked up to a device for ex vivo perfusion
and ventilation. Before dividing the trachea between two parallel linear stapler lines (TA
45-4.8 disposable stapler, Covidien, Mansfield, MA), the endotracheal tube is suctioned and
both lungs are manually and gently reinflated with 50% oxygen until all atelectatic zones
have been recruited. The staple lines are whipped with betadine solution. The inflated
double-lung bloc is then extracted out of the body after maximal spreading of the sternal
incision and pulling down the diaphragm.
Lung Packing

The double-lung bloc is immersed in cold Perfadex solution and covered with soaked
towels. Arterial and venous cuffs are inspected for sufficient length and iatrogenic tears
that may need repair on the bench prior to implantation (Fig. 1.4). Parenchymal
abnormalities like apical blebs, scarring, or tears may be stapled (ILA 100 reusable stapler,
Covidien, Mansfield, MA).
This is about the moment to give a third call to the recipient surgeon informing him on the
exact cross-clamp time and on any surgical issues discovered in the donor lungs.
We prefer to split the double-lung bloc already in the donor hospital, so that both lungs can
be packed and stored on ice individually as long as needed for sequential implantation.
The posterior pericardium is transected first followed by the left atrial cuff on the midline
(Fig. 1.5A). The pulmonary artery is transected at its bifurcation (Fig. 1.5B). The subcarinal
nodes and peritracheal fatty tissue are dissected freeing the orifice of both left and right
main bronchi. (The peribronchial tissue of the left and right main bronchi should be
preserved to avoid bronchial damage and for future buttressing of the anastomosis.) Lung
splitting is finished by stapling the left main bronchus close to the trachea using two
additional cartridges of the same stapler (Fig. 1.5C). If desired, the trachea can be resected
for culture by adding another stapler line on the orifice of the right main bronchus.
The individual left and right lungs are then triple bagged (Fig. 1.6). The first bag is filled
with cold Perfadex and the second bag with cold saline and crushed ice. We take care to
completely de-air the first bag, so that the lung is entirely surrounded by preservation
solution. Finally, the double-bagged lung is then secured inside a third sterile plastic bag.
Both lungs are then submerged in the cool box filled with ice. A label is attached clearly
indicating the position of the left and right lungs in the box that is now securely closed
ready for transport.

Figure 1.4 The left atrial cuff is inspected. Sufficient muscular tissue surrounding the pulmonary veins is present to safely
perform the left atrial anastomosis.

Figure 1.5 A: The posterior pericardium is transected first followed by the left atrial cuff on the midline. B: The pulmonary
arteries are divided at their bifurcation. C: Lung splitting is finished by double-stapling of the left main bronchus with a
linear stapler close to the trachea.

Figure 1.6 The lungs are each packed in three sterile bags. The first bag is filled with Perfadex solution and maximally deaired, so that the lung is completely surrounded by cold preservation solution. The second bag contains cold saline solution
and crushed ice. The third bag is dry and will protect the organs when covered by ice during storage in the cool box.

Before leaving the donor operating room, it is important to check for all surgical
instruments used during lung procurement and to gather all personal belongings.
Donor blood samples, lymphoid tissue, and chest x-ray whenever possible are collected and
stored to accompany the lungs to the donor hospital for further analysis and tissue typing.
It is very important to thank the local team for their help and hospitality. This is a token of
appreciation and motivates the local team members to offer potential donors in future.
When leaving the donor hospital, a fourth call is given to the recipient team with the exact
time of departure and the estimated time of arrival in the recipient operating room.

From experimental and clinical experience, it is well known that the lungs tolerate warm
ischemia up to about 1 hour, much longer compared to other solid organs. This results from
the alveolar oxygen reserve in ventilated or inflated lungs enabling cellular aerobic
metabolism to continue. Therefore, there is no reason whatsoever to panic during lung
retrieval in case an unexpected event happens to the donor (premature cardiac arrest,
major bleeding, or malposition of flush cannula). Even if the cardiac or abdominal team
decides to abort the procurement, lungs can still be harvested safely. We refer to the
procedure previously described for retrieving lungs from donors after cardiocirculatory
death. Lungs can always be cooled topically with cold saline and a flush cannula can be
quickly inserted via the right ventricular outflow tract through the pulmonary valve into
the pulmonary artery for antegrade flush. Lungs can also be flushed on the back table after
extraction. Deflated lungs can also be ventilated or inflated on the back table using a sterile
endotracheal tube connected to the ventilator or to a portable Ambu bag.
Structures at risk to be damaged during lung procurement are vascular cuffs and

parenchyma. The most frequent complication encountered is a short venous cuff especially
on the right side around the inferior pulmonary vein. Surgical techniques have been
described how to enlarge the venous cuff with surrounding donor pericardium and how to
reconstruct individual pulmonary veins inadvertently transected. A small tear in the
pulmonary artery may happen occasionally during dissection as the wall of the vessel is
often thin and fragile in a young donor. This can easily be repaired with a 6-0
polypropylene stitch. Tears in lung parenchyma resulting from pleural adhesions or
inadvertent cuts can usually be sealed with a linear stapler.

The success rate of lung donor procurement largely depends on the willingness of the surgical
team to travel to the donor hospital and on the acceptance rate of the retrieving surgeon
when donor lungs do not fit the ideal criteria. Once the decision is taken to accept the organs,
the technical success rate of lung procurement is very high in case all sequential steps and
principles of lung preservation are well respected. It is unusual that a donor lung is rejected
after retrieval. This may be the case if a tear is technically unrepairable or if significant
structural damage is observed once the lungs are inspected on the back table (edema,
contusion, pneumonia, or emphysema). If a suspicious nodule is found that can be wedged
out, a frozen section may help to make a final decision whether or not to accept the organs.
Occasionally, lungs have to be turned down during transport when an unexpected solid tumor
is found in liver or kidney after explantation. If proven to be malignant, the presence of
undetectable micrometastases in the lung may be a too high risk for the immunosuppressed
patient to receive the organs.

Every potential organ donor should be considered a potential lung donor. All efforts should
be made to check lung donor quality during multiorgan retrieval in the donor hospital. The
lungs are unique organs as they tolerate long warm ischemic periods. Therefore, even if the
retrieval of other organs is stopped prematurely because of unexpected cardiac arrest or
massive bleeding, the lungs can still be harvested with the help of simple topical cooling and
subsequent antegrade and retrograde flush in the body or on the back table.

Recommended References and Readings

Brodman RE, Goldsmith J, Veith FJ, et al. A technique for donor lung procurement and
preservation after completion of cardiac donation. Surg Gynecol Obstet. 1988;166:363366.
Casula RP, Stoica SC, Wallwork J, et al. Pulmonary vein augmentation for single lung
transplantation. Ann Thorac Surg. 2001;71:13731374.
Gamez P, Alvarez R, Hernndez H, et al. Lung transplantation: How to do the venous
anastomosis when the pulmonary graft has no auricular cuff. J Heart Lung Transplant.

Orens JB, Boehler A, de Perrot M, et al. A review of lung transplant donor acceptability
criteria. J Heart Lung Transplant. 2003; 22:11831200.
Oto T, Rabinov M, Negri J, et al. Techniques of reconstruction for inadequate donor left atrial
cuff in lung transplantation. Ann Thorac Surg. 2006;81:11991204.
Parekh K, Patterson GA. Technical considerations in adult lung transplantation. Semin Thorac
Cardiovasc Surg. 2004;16:322332.
Pasque MK. Standardizing thoracic organ procurement for transplantation. J Thorac
Cardiovasc Surg. 2010;139:1317.
Shigemura N, Bhama J, Nguyen D, et al. Pitfalls in donor lung procurements: How should the
procedure be taught to transplant trainees? J Thorac Cardiovasc Surg. 2009;138:486490.
Sundaresan S, Trachiotis GD, Aoe M, et al. Donor lung procurement: Assessment and
operative technique. Ann Thorac Surg. 1993;56:14091413.
Todd TR, Goldberg M, Koshal A, et al. Separate extraction of cardiac and pulmonary grafts
from a single organ donor. Ann Thorac Surg. 1988;46:356359.
Van Raemdonck D. Thoracic organs: Current preservation technology and future prospects;
part 1: Lung. Curr Opin Organ Transplant. 2010;15:150155.
Van Raemdonck D, Neyrinck A, Verleden GM, et al. Donor selection and management. Proc
Am Thorac Soc. 2009;6:2838.
Van Raemdonck DE, Rega FR, Neyrinck AP, et al. Non-heart-beating donors. Semin Thorac
Cardiovasc Surg. 2004;16:309321.
Yarbrough WM, Bates MJ, Deuse T, et al. Alternative technique for salvage of donor lungs
with insufficient atrial cuffs. Ann Thorac Surg. 2009;88:13741376.

2 Single Lung Transplantation

Ashok Muniappan

Single lung transplantation is suitable for the two most common causes of end-stage lung
disease, chronic obstructive pulmonary disease (COPD) and idiopathic pulmonary fibrosis
(IPF). The first successful single lung transplant was performed for IPF in 1983 at Toronto
General Hospital. Initially, patients with COPD were considered to be poor candidates for
single lung transplantation, as it was thought that preferential ventilation of the native
emphysematous lung would complicate allograft function. This concern was overstated and
only a few years later single lung transplantation for COPD was proven to be feasible. Single
lung transplantation was the most common form of pulmonary transplantation until the late
1990s, when bilateral (or double) lung transplantation became more common. In 2011, the
most recent year with available registry data, bilateral lung transplants were performed 3.8
times as often as single lung transplants.
The most significant attribute of single lung transplantation is its ability to maximize donor
supply and utilization. Presently, the donor pool for pulmonary allografts is severely
constrained, with a severe mismatch in supply and demand. Single lung transplantation
affords two recipients an opportunity to undergo transplantation from a single suitable donor,
maximizing a valuable resource.
Another attribute of single lung transplantation is that it is technically simpler and
associated with less early postoperative morbidity than bilateral lung transplantation, when
patients are selected appropriately. This is relevant for the elderly or frail patient, for whom a
prolonged anesthetic time results in increased postoperative complications.
Presently, 10% to 15% of patients listed for transplantation die on the waiting list, due to
lack of donor availability. Listing patients for both single and bilateral lung transplantation,
when appropriate, reduces waitlist deaths. This is especially relevant for a patient with IPF,
for whom disease progression can be quite rapid and a prolonged waiting time is to be
avoided. A single lung transplant may be lifesaving, if it means more prompt transplantation.
Single lung transplantation is contraindicated in patients with cystic fibrosis or other
conditions with suppurative lung disease, such as bronchiectasis. Bilateral pneumonectomy is
necessary to prevent contamination of the pulmonary allograft by native lung sepsis.
Although there are a few reports of cystic fibrosis patients undergoing single lung
transplantation and contralateral pneumonectomy (either synchronous or previously), the
vast majority of patients are best served by bilateral lung transplantation.
Severe pulmonary hypertension is another contraindication to single lung transplantation.
A single allograft may not provide enough unloading of the strained right heart. Significant
right heart dysfunction can complicate recovery from single lung transplantation. In addition,
the single lung allograft may be exposed to almost the entire cardiac output when significant
pulmonary hypertension remains in the native lung, increasing the risk of primary graft
dysfunction. Although it is uncertain what degree of pulmonary hypertension precludes safe

single lung transplantation, a mean pulmonary artery (PA) pressure greater than 50 mm Hg is
often cited as a contraindication.
Extended donor criteria including age >55 and smoking history >20 pack-years are
increasingly used to expand the donor pool. There is some uncertainty as to the
appropriateness of using marginal lungs in single lung transplantation. Both early and late
outcomes may be compromised when a single marginal lung is transplanted. There are
possibly interactions with the recipients diagnosis and condition as well and it remains to be
seen how extended criteria lungs function in both single and bilateral transplant settings.

Beyond routine preoperative assessment, a potential single lung recipient requires careful
cardiovascular evaluation. Severe pulmonary hypertension, as revealed on echocardiography
and right heart catheterization, is a contraindication to single lung transplantation. Moreover,
evidence of significant left or right heart dysfunction on echocardiography can predict the
requirement for cardiopulmonary bypass (CPB) and appropriate cannulation strategy is
selected ahead of time. A right-sided transplant may be preferable in a patient expected to
require CPB, as cannulation of the aorta and atrium is straightforward after right
thoracotomy. CPB is almost never necessary for single lung transplantation in patients with
obstructive lung disease and is necessary in about 15% to 25% of patients with fibrotic
disease. Regardless, a CPB circuit and perfusionist should be on stand-by for all single lung
A quantitative ventilationperfusion (V/Q) scan determines whether there is differential
perfusion between the native lungs. If the option is available, the less perfused lung is
transplanted, barring any other requirements for laterality (e.g., chest size, pathology in
native lung, etc.). When the recipient is suffering from obstructive lung disease, the native left
lung is less prone to hyperinflation after right lung transplant. In contrast, patients with
fibrotic lung disease may be better suited to left lung transplantation, as the liver is not a
fixed impediment to allograft expansion. In spite of these observations, there are no hard and
fast rules to guide selection of the side to transplant and reasonable outcomes can be expected
regardless of side transplanted.
Donor lung characteristics may also dictate the laterality of single lung transplantation.
When pneumonia or pulmonary contusion is severe in one lung, the contralateral lung may
still be suitable for transplantation. Thorough radiographic assessment, including liberal use
of computed tomography, helps assess donor lungs, especially when extended criteria are
used. Bronchoscopy determines whether or not hemorrhage or purulence localizes to one
lung. Even with such testing, suitability of a lung may not be determined until after donor
sternotomy. Blood gas analysis of pulmonary venous blood tests whether or not one lung has
improved function and is performed if there is any question of which side to procure.


Positioning and Incision

Single lung transplantation may be performed through either a posterolateral thoracotomy or
a muscle-sparing anteroaxillary incision. While a full lateral decubitus position is required for
posterolateral thoracotomy, an anteroaxillary approach is performed with the patient
positioned 60 degrees forward from the horizontal axis. For a posterolateral incision, the
latissmus is divided and the serratus is retracted and vice versa for an anterolateral or
anteroaxillary approach. Exposure and draping of the ipsilateral groin, especially when leftsided transplantation is performed, permits femoral cannulation for CPB. A fourth intercostal
space thoracotomy facilitates aortic cannulation and access to the pulmonary hilum.
Single lung ventilation is established through a left-sided double-lumen endotracheal tube.
Significant hypoxemia with single lung ventilation may develop, which may be an indication
for CPB. Careful anesthetic management avoids CPB in almost all patients with obstructive
lung disease and in the majority of patients with fibrotic disease undergoing single lung
transplantation. On occasion, clamping of the PA of the lung to be explanted is performed to
improve oxygenation, as this eliminates the shunt through the deflated lung.
Native lung pneumonectomy is performed with careful hilar dissection. Particular attention
is paid to preserving the phrenic nerve, as postoperative diaphragmatic paralysis complicates
recovery from transplantation. Likewise, the vagus nerve (and recurrent nerve on the left
side) should be preserved to minimize the risk of postoperative aspiration. The inferior
pulmonary ligament is completely divided and the superior and inferior pulmonary veins are
isolated extrapericardially. The PA is isolated and test clamped to determine whether the
contralateral lung permits sufficient oxygenation and reasonable hemodynamics. Right and
left heart function may severely deteriorate with PA clamping and necessitate CPB. A
reduction in cardiac output of 1 to 1.5 L/min with PA clamping suggests that CPB is
The truncus PA branch is isolated and divided (Fig. 2.1). The PA beyond this branch is also
isolated and divided with an articulating endoscopic stapler. This provides more options for
constructing the PA anastomosis and reduces size mismatches when recipient pulmonary
hypertension leads to PA enlargement. Care is taken to ensure that the PA catheter is not
within the PA before stapling. Similarly, the pulmonary veins are divided separately with the
endoscopic stapler (Fig. 2.2). With retraction on the pulmonary vein stumps, the pericardium
is opened widely and circumferentially, exposing the left atrium.

Figure 2.1 Division of right pulmonary artery. The truncus artery and the ongoing pulmonary artery are divided with an
endoscopic stapler. Seen are the divided right superior pulmonary vein and the distal right mainstem bronchus.

Figure 2.2 Preparation of the recipient left atrium. The superior and inferior pulmonary veins are stapled and divided with
an endoscopic stapler. A clamp occludes the recipient left atrium beneath the origin of the pulmonary veins. The stapled ends
are removed and the orifice of the two veins are connected, creating a cuff of left atrium suitable for anastomosis.

The mainstem bronchus is dissected at its distal aspect. The bronchus is generally divided
just proximal to the origin of the upper lobe bronchus. Division requires diligent control of
peribronchial lymphatic and bronchial artery branches with suture ligatures or
electrocautery. The recipient mainstem bronchus may be trimmed back slightly at this point,
taking care not to devascularize the terminal end. The exposure and anatomy is slightly
different after right or left pneumonectomy (Figs. 2.3 and 2.4).

Figure 2.3 The right hilum after recipient pneumonectomy. Seen are the divided bronchus, pulmonary artery, superior and
inferior pulmonary veins, phrenic nerve, and vagus nerve.

Figure 2.4 The left hlium after recipient pneumonectomy. Seen are the divided bronchus, pulmonary artery, superior and
inferior pulmonary veins, phrenic nerve, and aorta.

The donor lung is placed within the chest wrapped in gauze containing crushed ice. There
are a number of common anastomotic techniques and sequences, and familiarity and
reproducibility should dictate how the implantation is performed. Trimming of the donor
bronchus to within one ring of the origin of the upper lobe is recommended to avoid a long
ischemic segment of donor mainstem bronchus. First, the bronchial anastomosis is completed

with an interrupted anastomotic technique using absorbable 4-0 Vicryl sutures (Fig. 2.5).
When possible, the donor bronchus is intussuscepted into the recipient bronchus. Others have
recommended performing the bronchial anastomosis with a running absorbable monofilament
suture and avoid routine intussusception.
A vascular clamp is placed on the left atrium and the pulmonary vein stumps are opened to
create a cuff of recipient atrium. The donor left atrium is anastomosed to the recipient atrium
with a running 4-0 polypropylene suture using an everting technique to ensure endothelial
apposition (Fig. 2.6). The final stitch is left loose to permit flushing of the donor lung and deairing prior to release of the left atrial clamp.

Figure 2.5 Bronchial anastomosis. The anastomosis can be performed with an interrupted suture technique, using 4-0 Vicryl,
similar to that used for tracheal reconstruction. Alternatively, a running PDS suture technique is used.

Figure 2.6 Left atrium to donor atrial cuff anastomosis. The recipient left atrium is anastomosed to the donor atrial cuff with
a running 5-0 Prolene suture. An everting suture technique is used to ensure endothelium to endothelium apposition.

The PA anastomosis is constructed after placing a vascular clamp to control the proximal

recipient PA and opening the artery in a location that matches the donor PA best (Fig. 2.7).
Care is taken to appropriately trim the donor PA to avoid excessive length that may
predispose to kinking when the graft is revascularized. The anastomosis is constructed with a
running 5-0 polypropylene suture. Other centers routinely perform bronchial and PA
anastomoses before completing the atrial anastomosis.
Ventilation and reperfusion of the implanted lung is performed in a careful and deliberate
fashion. Gentle recruitment of the lung is performed before reperfusion. Appropriate
immunosuppression should be administered prior to reperfusion. The PA clamp is slowly
opened and a controlled and deliberate reperfusion and de-airing is performed. When the
graft is sufficiently de-aired, the left atrial clamp is released and the atrial anastomotic suture
is tightened. Hemostasis of the anastomoses is ensured. Once appropriate graft function is
confirmed, the chest is closed after positioning a 28-French chest tube anteriorly and a 19French soft flexible catheter posteriorly.

Figure 2.7 Pulmonary artery anastomosis. The donor pulmonary artery anastomosis to the recipient pulmonary artery is
performed with a running 5-0 Prolene suture. A vascular clamp occludes the proximal recipient pulmonary artery.

CPB or extracorporeal support may be required at various points in single lung

transplantation. Increasingly, patients present for transplantation after bridging with
extracorporeal support and familiarity with management of this circuit and how it can be
used during transplantation is necessary. CPB may also become necessary when single lung
ventilation leads to significant hypoxemia or PA clamping severely compromises
hemodynamics. It is preferable to centrally cannulate to avoid groin incisions. On the right,
the ascending aorta and right atrium are easily cannulated. On the left, the aortic arch or
descending aorta is cannulated and venous drainage is transfemoral or via the pulmonary

Early postoperative management of single lung transplantation is focused on optimizing graft
function and avoiding complications in the native lung. In patients with obstructive lung
disease, positive end-expiratory pressure is minimized (5 mm Hg) or eliminated, to

minimize risk of native lung hyperinflation. In patients with fibrotic disease and pretransplant
pulmonary hypertension, particular attention is paid to the hemodynamics in the early
postoperative period. Subtle changes in pulmonary vascular resistance of the lung allograft
can have dramatic effects on right heart function and cardiac output. The single lung
transplant may be more prone to primary graft dysfunction in fibrotic patients, making it
prudent to gently wean from paralytics, sedation, and mechanical ventilator support.

Native lung hyperinflation is a complication of single lung transplantation, in patients with
obstructive lung disease. Hyperinflation of the native lung does not always lead to allograft
dysfunction and its effect may only be apparent when the allograft is compromised, as with
acute or chronic rejection. Early postoperative difficulty with native lung hyperinflation
occurs more often when there are large bullae in the remaining lung. This complication may
be avoided by pre-emptively performing lung volume reduction in patients with very large
bullae. Occasionally, patients require lung volume reduction of the native lung in the early
postoperative period.
Lung allograft dysfunction, characterized by hypoxemia, increased pulmonary vascular
resistance, and decreased compliance may be more common after single lung transplantation.
It is more likely in patients transplanted for fibrotic lung disease and pre-existing pulmonary
hypertension. Although there are no absolute criteria for initiation of extracorporeal support,
requirement of high peak inspiratory pressure (>40 cm H2O) and 100% FiO2 are generally
recognized indications. Early initiation of extracorporeal support may protect the lung
allograft from barotrauma and oxidative damage, and protects the patient from multiorgan
dysfunction due to shock. Extracorporeal support has its own set of complications, including
increased bleeding associated with anticoagulation, cannula site complications, and stroke. In
balance, though, extracorporeal support is protective against permanent graft injury and
improves outcomes in patients with severe graft dysfunction.
Additional complications attributable to single lung transplantation include the
development of neoplasm or infection in the native lung. The risk of lung cancer developing
in the native lung is approximately 10% and is higher in the older recipient with a significant
smoking history.

It is widely espoused that bilateral lung transplantation for both IPF and COPD leads to
improved long-term survival compared with single lung transplantation. However, the benefit
is diminished or absent in elderly patients, in whom bilateral transplantation is associated
with increased early morbidity and mortality. When confounding variables are controlled
during analysis of retrospective registry data, the benefit of bilateral transplantation
disappears. Any potential benefit from bilateral transplantation is more likely in very specific
populations, such as young patients with IPF.

Ongoing donor organ shortage and concern about the morbidity of bilateral transplantation in
the elderly make single lung transplantation a relevant technique. Successful single lung
transplantation requires expert donor and recipient selection. Although the majority of single
lung transplants are performed without CPB, on occasion such support will be necessary for
intraoperative management, and requires familiarity with cannulation techniques when
operating in either chest. There are specific complications associated with single lung
transplantation, including native lung hyperinflation and development of lung cancer in the
native lung, which require vigilance and on occasion operative management.

Recommended References and Readings

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lung volume reduction. Proc Am Thorac Soc. 2009;6:6678.
Botha P, Trivedi D, Searl CP, et al. Differential pulmonary vein gases predict primary graft
dysfunction. Ann Thorac Surg. 2006; 82:19982003.
Botha P, Trivedi D, Weir CJ, et al. Extended donor criteria in lung transplantation: Impact on
organ allocation. J Thorac Cardiovasc Surg. 2006;131:11541160.
Brown CR, Mason DP, Pettersson GB, et al. Outcomes after single lung transplantation in
older patients with secondary pulmonary arterial hypertension. J Heart Lung Transplant.
de Perrot M, Keshavjee S. Everting mattress running suture: An improved technique of atrial
anastomosis in human lung transplantation. Ann Thorac Surg. 2002;73:16631664.
Diamond JM, Lee JC, Kawut SM, et al. Clinical risk factors for primary graft dysfunction after
lung transplantation. Am J Respir Crit Care Med. 2013;187:527534.
Force SD, Kilgo P, Neujahr DC, et al. Bilateral lung transplantation offers better long-term
survival, compared with single-lung transplantation, for younger patients with idiopathic
pulmonary fibrosis. Ann Thorac Surg. 2011;91:244249.
Hartwig MG, Walczak R, Lin SS, et al. Improved survival but marginal allograft function in
patients treated with extracorporeal membrane oxygenation after lung transplantation
invited commentary. Ann Thorac Surg. 2012;93:366371.
Low DE, Trulock EP, Kaiser LR, et al. Morbidity, mortality, and early results of single versus
bilateral lung transplantation for emphysema. J Thorac Cardiovasc Surg. 1992;103:1119
Mal H, Brugiere O, Sleiman C, et al. Morbidity and mortality related to the native lung in
single lung transplantation for emphysema. J Heart Lung Transplant. 2000;19:220223.
Nathan SD, Shlobin OA, Ahmad S, et al. Comparison of wait times and mortality for
idiopathic pulmonary fibrosis patients listed for single or bilateral lung transplantation. J
Heart Lung Transplant. 2010;29(10):11651171.
Pierre AF, Sekine Y, Hutcheon MA, et al. Marginal donor lungs: A reassessment. J Thorac
Cardiovasc Surg. 2002;123:421428.
Pochettino A, Bavaria JE. Anterior axillary muscle-sparing thoracotomy for lung
transplantation. Ann Thorac Surg. 1997;64:18461848.
Souilamas R, Mostafa A, Guillemain R, et al. Single-lung transplantation for cystic fibrosis and

metachronus pneumonectomy: Case reports. Transplant Proc. 2008;40:35943595.

Thabut G, Christie JD, Ravaud P, et al. Survival after bilateral versus single lung
transplantation for patients with chronic obstructive pulmonary disease: A retrospective
analysis of registry data. Lancet. 2008;371:744751.
Tsagkaropoulos S, Belmans A, Verleden GM, et al. Single-lung transplantation: Does side
matter? Eur J Cardiothorac Surg. 2011; 40:8392.
van Berkel V, Guthrie TJ, Puri V, et al. Impact of anastomotic techniques on airway
complications after lung transplant. Ann Thorac Surg. 2011;92:316321.
Yonan NA, El-Gamel A, Egan J, et al. Single lung transplantation for emphysema: Predictors
for native lung hyperinflation. J Heart Lung Transplant. 1998;17:192201.

3 Double Lung Transplant

Clemens Aigner, Doosang Kim, and Walter Klepetko

Lung transplantation is the established surgical treatment modality for end-stage parenchymal
and vascular nonmalignant lung diseases. The International Society for Heart and Lung
Transplantation (ISHLT) maintains the largest registry worldwide, which covers more than
3,000 transplants annually. The most common indication for lung transplantation has been
chronic obstructive pulmonary disease (COPD) for a long time and still represents 34% of the
overall worldwide transplant activity. With the introduction of new allocation algorithms
such as the Lung Allocation Score (LAS) the percentage of patients transplanted for idiopathic
pulmonary fibrosis (IPF) has risen. Cystic fibrosis is the third main indication for lung
transplantation. The number of patients with pulmonary arterial hypertension undergoing
transplantation has decreased and the preferred type of transplantation is nowadays bilateral
lung transplantation. Bronchiectasis, sarcoidosis, retransplantation, connective tissue disease,
lymphangioleiomyomatosis, and congenital heart disease are less common indications for
lung transplantation.
The percentage of bilateral procedures is constantly increasing and has reached more than
70% of all lung transplant procedures worldwide. In our own center the percentage of
bilateral procedures represent more than 90% of the overall lung transplant volume.
The background for this strategy can be found in the persistent survival benefit of bilateral
lung recipients compared to single lung recipients. Although a selection bias might play a role
in obtaining these superior results, the survival benefit is reproducible in the ISHLT database
among patients with different diagnoses and different age groups (Fig. 3.1).
Advanced operative techniques of bilateral transplantation with special importance for
pediatric recipients include lobar transplantation or split lung transplantation, which
however, should be performed in specialized centers only. In addition, living-related lung
donation can be another technical option for bilateral transplantation in selected patients.
There are few absolute contraindications, however, a number of relative contraindications,
which vary center wise according to different individual experiences and differences in the
availability of donor organs. Absolute contraindications are: Significant systemic diseases,
severe extrapulmonary organ dysfunctions, recent malignancies, HIV infection, hepatitis B or
C, pan-resistant MRSA or Burkholderia cepacia, active nicotine, and alcohol or drug abuse.

Figure 3.1 ISHLT Registry Slide showing KaplanMeier survival for single versus double lung transplantation.

The large number of relative contraindications must be individually judged from case to
case: Osteoporosis, muscular or skeletal diseases, extreme cachexy or obesity, long-time
corticosteroid therapy, infection with mycobacteria, coronary disease or left ventricular
dysfunction, significant peripheral vascular disease, renal insufficiency, severe chest wall
deformity, and psychosocial instability.
Pretransplant mechanical ventilation or extracorporeal support was initially considered a
contraindication to lung transplantation. However, nowadays new allocation policies and the
availability of innovative bridging options allow a safe bridge to lung transplantation in
selected patients. The current trend is to keep patients as ambulatory as possible on the

The optimal time for listing for lung transplantation is at a stage when survival expectancy
with lung transplantation exceeds the survival expectancy without transplantation and the
patient is still in a condition to survive the expected waiting period. This implies that the
timing of referral and listing for lung transplantation are not only based on recipient factors,
but also have to take the organ availability and the allocation system into account. Allocation
algorithms vary substantially in different countries. While algorithms based on waiting time
only uniformly led to high waiting list mortality and have been abandoned by most countries,
nowadays allocation algorithms using the LAS which takes the expected waiting list
mortality and the anticipated 1-year post-transplant survival into accountor center-based
allocation are the most common systems in use.

The patient is positioned supine for bilateral lung transplantation with abducted arms and the
chest is elevated by inflatable cushions (Fig. 3.2). The entire chest with either one or both
groins is scrubbed in the sterile field. This provides access for the thoracic incision as well as
for femoral cannulation if required. In this position no additional femoral arterial line to aid
in blood pressure monitoring is usually required.

Figure 3.2 Standard position of the recipient for bilateral lung transplantation.

Standard approach to the chest for bilateral lung transplantation is usually the so-called
clamshell incision, which combines a bilateral thoracotomy with a transverse sternotomy and
ligation of the internal thoracic vessels (Fig. 3.3) and can also be gained by two separate
thoracotomies (Fig. 3.4). Some centers also use a median sternotomy, which however, limits
access to the posterior hilum.
In patients with separate bilateral thoracotomies the standard approach on the right side is
the fourth intercostal space, which provides excellent access to all hilar structures and gives
the opportunity for central cannulation for cardiopulmonary bypass (CPB) or extracorporeal
membrane oxygenation (ECMO) whenever necessary. The serratus anterior muscle is divided,
while the latissimus dorsi can be left untouched. It is important to open the intercostal
muscles from just posterior of the internal thoracic artery to the posterior end of the rib to
allow full spreading of the intercostal space without causing rib fractures. On the left side it
can be beneficial to choose the fifth intercostal space to facilitate exposure of the left atrium.
The clamshell incision provides the best exposure to both hili and the heart, especially
when central cannulation for extracorporeal support is required. The decision whether to use
separate incisions or a clamshell incision is based on the individual anatomic situation,
especially the size of the recipient chest cavity, the extent of adhesions and whether
intraoperative extracorporeal support will be required.

Figure 3.3 Approaches for bilateral transplantationanterolateral thoracotomy.

Figure 3.4 Approaches for bilateral transplantationclamshell incision.

Intubation is routinely performed with a left-sided double-lumen tube to allow unilateral
ventilation. The choice, which lung is transplanted first depends on donor and recipient
issues. The preoperative recipient V/Q scan is an important tool in this decision process.
Usually the functionally worse side is transplanted first if the procedure is planned without
the use of extracorporeal support. In case of a quality difference between the donor lungs, for
example, due to traumatic alterations or other minor impairments, the better lung will be
transplanted first. The implantation is performed in a sequential technique.
Recipient pneumonectomy is performed in standard fashion with stapling of the pulmonary
artery and pulmonary veins. The bronchus is prepared centrally and opened with a scalpel.
Two polydioxanone 4-0 stay sutures are placed at the angles between the cartilaginous and
the membranous portion. Thereafter the lung is removed from the chest cavity and the
pericardium is opened between the superior pulmonary vein and the phrenic nerve and
circumferentially dissected to fully mobilize the left atrium. Thereafter, the pulmonary artery
is prepared intrapericardially as central as possible to provide sufficient length for the
anastomosis (Fig. 3.5). Once the intrapericardial dissection is completed the posterior
mediastinum can be closed with a running PDS 4-0 suture to prevent bleeding from lymph

nodes in this area, which is difficult to control after the lung has been implanted. Meticulous
hemostasis has to be performed before beginning with the implantation.

Figure 3.5 Right hilum after intrapericardial preparation of the vessels.

Figure 3.6 Bronchial anastomosis using the single running suture technique.

The donor lung is then unpacked and the vessels are prepared and shortened. The
pulmonary artery is carefully inspected for any intraluminal embolic material. The bronchus
is shortened with only one cartilage ring remaining after the separation of the upper lobe
bronchus and careful preservation of the peribronchial tissue. A bacteriologic swab is taken
and any residual mucus is removed from the bronchial system. Thereafter the implantation is
performed taking care of permanent topical cooling of the donor lung with ice slush. The first
step is the bronchial anastomosis, which is performed using a double-armed 4-0
polydioxanone suture, starting at one end of the cartilaginous part, going over the
membranous portion in a single running suture technique and then using the same single
running suture for the anterior cartilaginous part (Fig. 3.6). In case of a bronchial size
mismatch the imbalance is adjusted over the whole circumference. Usually the anastomosis is
not covered with any additional tissue.
Thereafter, the left atrium is clamped intrapericardially with a Satinsky clamp. A close
surveillance of the hemodynamic situation is warranted at this point. The left atrium is

opened and anastomosed at a level where myocardial muscle tissue is present, since at the
level of the veins the tissue is too fragile to allow for a safe anastomosis. Usually a 4-0
prolene running suture is used. An everting suture technique providing direct adaptation of
donor and recipient endothelium is preferable to minimize the risk of thrombosis (Fig. 3.7).
The suture is secured with a clamp but at this stage not yet knotted. The next step is clamping
and opening the pulmonary artery. The anastomosis is once more performed in a running
technique using a 5-0 prolene suture (Fig. 3.8).
After administering the initial dose of immunosuppression, retro- and antegrade flushing is
performed to flush out the preservation solution and de-air the vasculature (Fig. 3.9).
Thereafter, the sutures of the artery and atrium are knotted. Protective ventilation without
any manual recruitment maneuvers is started at this stage. If the procedure is performed
without the use of extracorporeal support, controlled reperfusion for 10 minutes with partial
manual compression of the pulmonary artery should be performed to avoid initial volume
overload of the newly implanted lung.
Finally hemostasis is performed with special attention to the donor pulmonary ligament
and pericardium, which can be the source of substantial bleeding.
After completing the implantation of the first lung the recipient pneumonectomy and
implantation of the donor lung is performed in an identical way on the contralateral side.

Figure 3.7 Left atrial anastomosis.

Figure 3.8 Pulmonary artery anastomosis.

Figure 3.9 Flushing the donor lung.

At the end of the operation 24 French drainages are placed in the costodiaphragmatic sinus
and toward the apex and the incision is closed. It is beneficial to insert an additional small
drain, which can be left in place to avoid basal fluid collection without compromising
mobilization of the patient after the standard chest drains are removed.
Extracorporeal Support
The routine use of intraoperative extracorporeal support in bilateral lung transplantation
remains an area of controversy. Some centers routinely perform all bilateral procedures on
extracorporeal support, with the intention to avoid uncontrolled reperfusion of the first
implanted lung and the advantage of intraoperative hemodynamic stability.
Other centers prefer to use extracorporeal support only when it becomes absolutely
necessary, for example, in patients with pulmonary hypertension or whenever insufficient
oxygenation on single lung ventilation or hemodynamic instability exists. Before
pneumonectomy is performed on the first side the pulmonary artery can be manually
compressed for 3 to 5 minutes to assess the cardiocirculatory situation. If hemodynamic
instability is observed or pulmonary artery pressure approaches levels of systemic pressure,
extracorporeal support is indicated. If the procedure is performed without support and the

first implanted lung shows signs of poor initial graft function or developing reperfusion
oedema immediate installation of extracorporeal support prior to pneumonectomy of the
second is warranted to avoid additional damage to the newly implanted lung, which is
otherwise exposed to the entire cardiac output during this phase.
The most common intraoperative support device still is CPB. However, an increasing
number of institutions start adopting to use heparine-coated ECMO instead of CPB, which
avoids full heparinization and therefore, leads to a reduced turnover of blood. In our
institution ECMO is the standard support device since 2001. With CPB, a bilateral
pneumonectomy can be performed prior to the implantation and both donor lungs can be
reperfused at the same time. With ECMO a sequential approach is mandatory. The flow rate
has to be chosen to maintain a pulsatile pulmonary blood flow, which can be monitored by
the pulmonary artery pressure curve and the end-tidal CO2. If the flow is too high the entire
cardiac output is bypassed by the lung, which then suffers from a second warm ischemia,
which has to be avoided. Intraoperative extracorporeal support can be provided either by
central or peripheral cannulation.
The decision whether to prolong the ECMO support in the postoperative period is taken
after an initial stabilization phase. Factors influencing this decision are the quality of the
donor organ, high-risk recipients especially with elevated pulmonary artery pressure as well
as an intraoperative situation with low or continuously decreasing oxygenation index
especially if combined with a high or rising pulmonary artery pressure. ECMO support is
gradually reduced and if the ECMO can be removed, the patient is decannulated and the
venous and arterial tubes of the ECMO are connected with each other and the ECMO system
is left sterile at the table circulating in it until the patient leaves the operating room. This
provides the possibility to reinsert the same ECMO system in the groin for prolonged support
in case of deteriorating graft function. In our center postoperative extracorporeal support is
liberally applied, especially in patients with pulmonary hypertension.
Size-reduced Lung Transplantation
In case of a pronounced size mismatch between donor and recipient or if the donor organ is
found to be unexpectedly large during the retrieval process various options are available to
downsize donor lungs to overcome size discrepancies. In case of a minor size mismatch of up
to 20% TLC nonanatomical simple wedge resections are an effective tool to tailor the donor
lung. The most accessible target areas for these resections are the middle lobe on the right
side and the lingula on the left side. In case of a more pronounced size discrepancy, lobar
transplantation becomes an option. The division of the lobes is performed at the back table
immediately prior to the implantation to allow the most accurate size matching. The
parenchyma of the donor lung is subdivided by standard stapler devices after identification of
the artery in the interlobar fissure. The arterial branches are ligated, the veins and the
bronchus are divided and after complete excision of the lobar carina, the lobes are separated
and the implantation is performed in standard fashion. Polydioxanone 5-0 instead of 4-0 is
used for the bronchial anastomosis. Lobar transplantations can be performed using all
combinations of lobes, with the exception of a right upper lobe in combination with the
middle lobe, which should be avoided since it requires leaving a bronchial stump, which is at
high risk for dehiscence.

All of these techniques can also be applied to accept oversized donor organs for urgent
pediatric or small adult recipients.

After uneventful bilateral transplantation early weaning and extubation should be the goal in
patients with parenchymal lung disease. In patients operated for vascular lung disease
weaning should not be precipitant due to the changes in the postoperative hemodynamic
situation and the risk for left ventricular failure. To avoid fluid overload, infusions should be
minimized and intravenous drips concentrated. Blood pressure is to be supported by
catecholamines at low doses rather than by volume loading.
After extubation of the patient, early mobilization is crucial. Physiotherapy plays an
important role in secretion clearance and should be started as early postoperative as possible.
Usually patients can be discharged from the ICU 1 or 2 days after successful extubation.
Bronchoscopies are performed routinely on the first postoperative day, immediately before
extubation and surveillance bronchoscopies start 1 week postoperative. Additional
bronchoscopies are performed upon clinical necessity.
Since wound healing is decelerated due to the high doses of immunosuppression required,
sutures and staples must not be removed before the 12th postoperative day. A lung function
test and a computed tomography of the chest are performed before discharge of the patient.
After uneventful postoperative course patients can usually be discharged 3 weeks
postoperative and subsequently spend 4 weeks at a rehabilitation centre.

Primary Graft Dysfunction (PGD)
PGD describes the development of a noncardiac pulmonary oedema caused by acute lung
injury within the first 72 hours after transplantation. Differential diagnoses include venous
obstruction and hyperacute rejection. The definition is based on the chest x-ray and
pulmonary gas exchange and three degrees of severity are differentiated. Donor and recipient
factors might contribute to the development of PGD, which occurs in up to 50% of patients.
In most patients it is a mild and transient form; however, it can result in severe gas exchange
impairment similar to ARDS. Treatment consists of negative fluid balance, increased positive
end-expiratory pressure, vasodilators, protective lung ventilation, and in severe cases the use
of venoarterial ECMO. Acute retransplantation for PGD has poor results and is not
Airway Complications
Airway complications are nowadays very rare due to improved surgical technique and
preservation strategies. Bronchial dehiscence is hardly seen any more in experienced centers.
Bronchial stenosis can occur due to shrinking at the anastomotic site with incidence rates
reported between 1% and more than 10%. Therapy of choice is balloon dilatation or insertion

of a stent via rigid bronchoscopy. Granulation tissue can be removed via surgical or laser
ablation. Bronchial stenosis can also be observed distal to the anastomosis, especially in the
intermediate bronchus, which is most likely due to an ischemia fostered by denudation of the
affected part of the bronchial system.
Hyperacute rejection is a rare event due to careful evaluation prior to transplantation and
crossmatching between donor and recipient. Preformed antibodies against HLA or ABO blood
group donor antigens cause a fulminate humoral reaction against the donor vascular
endothelium within minutes to hours after implantation of the graft. Hyperacute rejection has
an unfavorable prognosis concerning recipient survival.
Acute rejection episode have the highest incidence in the first 6 months postoperatively
and have a broad spectrum of clinical presentation ranging from completely asymptomatic
patients to severe dyspnea, cough, fever, and respiratory failure. Radiography is not
infrequently unspecific, though perihilar or interstitial infiltrates and pleural effusions may be
indicators. Diagnosis is usually established by transbronchial biopsy. Severity is classified into
four grades (A0 to A4) according to the Society for Heart and Lung Transplantation.
Long-term survival after lung transplantation is still mainly limited by the development of
chronic lung allograft dysfunction (CLAD). The irreversible decline in FEV1 caused by a
fibroproliferation narrowing of the lumen of the small airways has been defined as
bronchiolitis obliterans syndrome (BOS). In some patients a predominantly restrictive type of
allograft function is observed. Risk factors include prior acute rejection episodes, especially
late recurrent or refractory rejections, lymphocytic bronchitis or bronchiolitis,
cytomegalovirus infections, insufficient immunosuppression, HLA mismatches, and eventually
airway ischemia. Symptoms are unspecific, patients usually report about insidious dry or
productive cough and dyspnea. Different treatment strategies are used including
augmentation of the immunosuppression, switching from cyclosporin A to tacrolimus or
sirolimus, cytolytic therapy, and photopheresis. Treatment usually slows but does not
terminate functional decline. Retransplantation is a viable option in selected patients.
Due to the immunosuppression defense mechanisms are diminished and therefore, infections
pose a great risk to transplant recipients. The permanent exposure of the transplanted organ
to the outside environment and the impairment of cough reflex and mucociliary clearance
make lung transplant recipients especially prone to infectious problems.
Bacterial infections are the most common infections in the first 2 postoperative months.
Broad-spectrum antibiotics are applied prophylactically in the early postoperative phase.
Additional antibiotics are administered according to culture and bacterial sensitivity data.
Viral infections are almost solely from the herpes group viruses, with cytomegalovirus
(CMV) being the predominant source of infection. Infections may occur due to reactivation
of the virus or as primary infections mainly in the constellation of a CMV negative recipient
who receives a graft from a CMV positive donor. Symptoms are nonspecific and frequently
accompanied by leucopenia. Treatment of choice is currently ganciclovir or valganciclovir.

In addition, CMV hyperimmunglobulin (IgM) has been proven beneficial. All patients are
routinely screened for CMV infection at every outpatient follow-up appointment.
Fungal infections occur mainly during the first 2 months after transplantation with
Aspergillus species and Candida species being the predominant pathogens. Treatment of
manifest infection is performed by administration of IV antifungal agents according to the
underlying subtype.
Protozoan infections, especially with Pneumocystis carinii or Toxoplasma gondii are usually
prevented by lifelong administration of trimethoprim/sulfametrol.

Patients with bilateral lung transplantation show better long-term survival rates compared to
single-lung recipients across all indications in the ISHLT registry. These differences might be
influenced by a selection bias, however, are consistently reproducible. Survival statistics
provided by the ISHLT report overall 1-year, 3-year, and 5-year survival rates of 79%, 63%,
and 52% respectively. However, there has been a significant rise in survival rates in the most
recent period. In our center a perioperative 30-day survival of 95.8% can be achieved with
bilateral lung transplant procedures. Long-term survival according to the ISHLT registry is
57% for bilateral recipients at 5 years, compared to 48% for single-lung recipients. Even
better results can be achieved in high volume centers with 5-year survival rates approaching
Quality of life is markedly improved after lung transplantation. Independence from oxygen
insufflation with diminished dyspnea, improved sleep, improved mobility, and energy to
accomplish activities of everyday life all collude for improved quality of life. Three years after
transplantation according to ISHLT more than 40% of the patients are full- or part-time
employed. Yet with development of chronic lung allograft this trend reverses, though most
patients remain active despite the development of CLAD.

Significant evolvements over the last two decades have taken place in the field of lung
transplantation. Bilateral transplantation has become the procedure of choice for all
indications. The surgical technique has been standardized and is performed in a similar
fashion throughout the world with remaining variation in details of the procedure.
Despite the fact that lung transplantation remains to be a technically demanding procedure,
mortality and morbidity directly related to the surgical technique can be minimized by
meticulous surgical performance and experience. The long-term survival results of bilateral
lung transplantation are uniformly superior to those of single lung transplantation making it
the preferred approach. Technical refinements in combination with advances in organ
preservation and immunosuppression have contributed to improved long-term survival during
the last decades.

Recommended References and Readings

Aigner C, Wisser W, Taghavi S, et al. Institutional experience with extracorporeal membrane

oxygenation in lung transplantation. Eur J Cardiothorac Surg. 2007;31(3):468473.
Boasquevisque CH, Yildirim E, Waddel TK, et al. Surgical techniques: Lung transplant and
lung volume reduction. Proc Am Thorac Soc. 2009;6(1):6678.
de Perrot M, Granton JT, McRae K, et al. Outcome of patients with pulmonary arterial
hypertension referred for lung transplantation: A 14-year single-center experience. J Thorac
Cardiovasc Surg. 2012;143(4):910918.
Fuehner T, Kuehn C, Hadem J, et al. Extracorporeal membrane oxygenation in awake patients
as bridge to lung transplantation. Am J Respir Crit Care Med. 2012;185(7):763768.
Gruber S, Eiwegger T, Nachbaur E, et al. Lung transplantation in children and young adults: A
20-year single-centre experience. Eur Respir J. 2012;40(2):462469.
Lang G, Taghavi S, Aigner C, et al. Primary lung transplantation after bridge with
extracorporeal membrane oxygenation: A plea for a shift in our paradigms for indications.
Transplantation. 2012;93(7):729736.
Puri V, Patterson GA. Adult Lung Transplantation: Technical Considerations. Semin Thorac
Cardiovasc Surg. 2008;20:152164.
Thabut G, Christie JD, Ravaud P, et al. Survival after bilateral versus single lung
transplantation for patients with chronic obstructive pulmonary disease: A retrospective
analysis of registry data. Lancet. 2008;371(9614):744751.
Van De Wauwer C, Van Raemdonck D, Verleden GM, et al. Risk factors for airway
complications within the first year after lung transplantation. Eur J Cardiothorac Surg.
Verleden SE, Ruttens D, Vandermeulen E, et al. Bronchiolitis obliterans syndrome and
restrictive allograft syndrome: Do risk factors differ? Transplantation. 2013;95(9):1167
Weiss ES, Allen JG, Merlo CA, et al. Survival after single versus bilateral lung transplantation
for high-risk patients with pulmonary fibrosis. Ann Thorac Surg. 2009;88(5):16161625.

4 Heart and Lung En Bloc Transplantation

Jose P. Garcia and Ravi Shah


The first heartlung transplant (HLT) was performed at Stanford University in 1981 by Dr.
Bruce Reitz. While primary lung and heart transplantation is the mainstay of therapy in
patients with advanced cardiac or pulmonary failure, combined heartlung transplantation
remains an option for patients with severe heartlung failure. Patients with pulmonary
hypertension and RV failure (Eisenmenger syndrome), intrinsic pulmonary disease such as
cystic fibrosis, or congenital heart disease, which are etiologies that do not permit single
organ transplantation are the most common candidates for this procedure. The increased
number of transplant centers and their pool of status 1A recipients have made it increasingly
difficult to obtain quality heartlung blocs thus extending the already long waiting period.
Also, improved techniques for single- and double-lung transplantation have improved
outcomes in patients with end-stage lung disease since the 1990s. These factors have led to a
significant decline in the number of combined HLTs performed yearly. Data from the
International Society of Heart and Lung Transplantation Registry demonstrates that 4,310
adult individuals had undergone combined heartlung transplantation before 2012, with
between 60 and 100 dual organ transplants per year performed worldwide since 2000 (Fig.
4.1). Despite nearly 36% of dual organ transplants concentrated in seven hospitals (7% of
overall transplanting centers) performing 4 to 9 transplants per year, the majority of HLTs
occur in low-volume centers, impressing the need for standardized surgical technique and
postoperative management to optimize outcomes (Fig. 4.2). This emerging collection of
demographic data surrounding heartlung transplantation has revitalized medical and
surgical considerations in this area. In this chapter, we will review published indications and
outcomes in combined heartlung transplantation, and will detail the surgical approach to
dual heartlung transplantation.

Nearly 70% of transplant recipients are between 18 and 49 years old (median age 42 years),
with the major indication being congenital heart disease or pulmonary arterial hypertension
in adults (Table 4.1). Current cumulative survival data between 1982 and 2011 indicate a 3month survival of 71%, 1-year survival of 63%, and a 10-year survival of 31% with a 10-year
median survival for those surviving the first year after transplant (Fig. 4.3). In contrast, the
primary indication for pediatric heartlung transplantation is cystic fibrosis. Of note, data
regarding the survival benefit of heartlung transplantation for Eisenmenger syndrome
remains mixed. Although the long-term survival benefit may be debatable, there is a clear
improvement in the quality of life in this group of patients that undergo transplant. Over the
last 10 years, there has been a decline in HLTs and an increase in double-lung transplants for
cystic fibrosis. Experience shows that normalization of pulmonary pressures following lung

transplantation allows for significant recovery of the right ventricle. In patients with
noncomplex cardiac defects, repair of the defect combined with single- or double-lung
transplantation may be a viable alternative. Also, fewer adults in general are requiring HLTs
because of new and improved medical therapies. In younger patients with severe right heart
failure and severe pulmonary hypertension, combined HLT is still the best option. Combined
HLT may yet see more use as more congenital patients are living longer and reaching

Figure 4.1 Number of transplants reported by location and year.

Figure 4.2 Average center volume (transplants: January 2000 to June 2012).

TABLE 4.1 Adult HeartLung Transplant Diagnosis (Transplants: January

1982June 2012)

Figure 4.3 KaplanMeier survival for all ages (transplants: January 1982 to June 2011).

Patient Selection for HeartLung Transplant

As with any surgical procedure or intervention, patient selection is closely linked to

outcomes. HLT candidates should meet the established criteria for isolated heart or lung
transplantation. The HLT recipient is listed under both heart and lung allocation systems
through the United Network for Organ Sharing (UNOS). As in lung transplant, heartlung
candidates are stratified according to their lung allocation score (LAS) and the listing criteria
are very similar. In addition, most candidates are New York Heart Association functional class
III or IV. The UNOS LAS is meant to allow the sickest patients and the ones with the best
chance of recovery post transplant to have priority in receiving organs. The LAS is not
comparable to the stratification system used for heart transplant. The LAS also does not
clearly reflect the extent of severity of the disease in patients with pulmonary hypertension.
These patients may be best served by using the cardiac listing with a special exemption. One

criterion that is more stringent in heartlung than in isolated heart or lung is age. Most
centers have an age cut off of 50 years and only a few centers, such as Stanford University,
have transplant heartlung blocs in patients over 60 years of age. With the existing organ
shortage, we must do everything possible to ensure a good outcome and prolonged use of the
donor organs, especially since each bloc could be used to transplant three different recipients.
Another important factor that needs to be considered is recipientdonor size matching. It is
critically important not to oversize the heartlung bloc. As reported by the Papworth Hospital
transplant team, attaining predicted total lung capacity at 1 year is to be expected and if not
attained then that is suggestive of complications with the transplanted lungs. In the
perioperative period, oversizing can lead to tamponade and low cardiac output.

En Bloc HeartLung Recovery
All heart/lung recoveries begin with review of all donor data and pertinent tests, which
include serologies, blood gases, CXR, bronchoscopy, chest CT and cardiac catheterization if
available. ABO blood type and recipient compatibility should be clearly documented. The
donor is placed on the OR table in the supine position with the arms tucked at the sides. The
donor height is also rechecked for accuracy especially in an en bloc heartlung recovery, as
size matching is critical. Prior to prepping, a bronchoscopy is performed as days may have
passed since the initial examination was performed. Throughout the recovery process, it is
best to use low-dose vasoconstrictors, such as Neo-Synephrine or vasopressin for hypotension
to minimize the amount of crystalloid that is given. The FiO2 is maintained at 40%. The
donor is then prepped and draped up to the sternal notch. A midline sternotomy incision is
then performed and continued further cephalad than the usual incision for a heart operation
to allow for easier dissection and isolation of the suprainnominate proximal trachea, which is
an easier approach than between the aorta and the superior vena cava (SVC). The
pericardium is incised down the midline and then laterally down both sides at the level of the
diaphragm. Sutures are placed along the pericardial edges and a pericardial well is created
prior to entering both pleural spaces. The heart and lungs are visually inspected and palpated.
If no abnormalities are appreciated, the recipient team is notified and instructed to proceed.
The space between the aorta and pulmonary artery is then dissected with the cautery to allow
for x-clamping of the aorta. The SVC is dissected free as cephalad as possible and encircled
with a suture, which is then tied prior to x-clamping. The azygos vein is divided at this time.
The SVC is also dissected free from the underlying right pulmonary artery. The pericardial
reflection around the IVC is released to allow for mobilization. The trachea is then identified
and dissected above the innominate vein and between the innominate artery and the left
common carotid artery. The trachea is encircled with an umbilical tape. When the abdominal
team is ready for x-clamping, 300 International Unit /kg of intravenous heparin is
administered. A cardioplegia cannula is placed in the ascending aorta approximately 2.5 cm
above the aortic valve. This cannula can be left in place and used for further cardioplegia and
de-airing at the time of implantation. A pneumoplegia cannula is then placed in the
pulmonary artery at the level of the bifurcation, which is then removed at the time of PA

transection. A Satinsky clamp is then placed at the base of the left atrial appendage and the
appendage is resected. This site will serve as the venting site for the plegia. The SVC is then
ligated, making sure there are no central catheters in place. At this time, 500 mcg of PGE-1 is
directly injected into the pulmonary artery next to the cannula. The systolic blood pressure
will drop precipitously and at least 1 minute is allowed for the PGE-1 to circulate and then
the IVC can be transected. The aortic clamp is placed, the Satinsky is removed from the left
atrium, cardioplegia and pneumoplegia are initiated and ice is placed on the heart and both
pleural spaces. We prefer to administer 2 L of 4C Plegisol (Hospira, Inc., Lake Forest, IL) for
the heart. For the lungs, we administer 60 mL/kg of 4C Perfadex (Xvivo Perfusion, Inc.,
Englewood, CO) at a pressure of 10 to 15 mm Hg. The average-sized donor should receive
between 4 and 5 L of pneumoplegia. Since the left atrium is not entered, we do not
administer retrograde pneumoplegia, as is customarily done in isolated lung transplant. To
avoid over distention, lung inflation is maintained at 50% of total lung capacity, airway
pressures at less than 20 cm of H2O and FiO2 is maintained at 40%. Once the plegias have
been administered, the aorta, pulmonary artery, IVC, and SVC are transected. Inferiorly on
the right side, the pericardium is divided down to the esophagus and the dissection is carried
cephalad just anterior to the esophagus up to the azygos vein. Once the azygos vein is
transected, the dissection can be carried to the site of the umbilical tape on the proximal
trachea. This maneuver prevents injury to the right upper lobe bronchus. Similarly, this
dissection is performed on the left lung. TA 30 3.5 mm linear stapler (Ethicon, Inc.
Somerville, New Jersey) is applied across the trachea and with the lungs partially inflated,
the endotracheal tube is retracted and the stapler fired. A second line of staples is applied and
then the trachea is divided between staple lines using a knife. The trachea and lungs are
separated from the posterior ligaments and the heartlung bloc is removed from the field
(Fig. 4.4). The organs are then placed in Perfadex solution, triple bagged and transported on
ice to the recipient hospital.

Figure 4.4 Heart and lung, en bloc.

Recipient Explant
The recipient is placed in the supine position on the OR table with the arms tucked to the
side, after monitoring lines and a transesophageal echocardiography probe have been placed.
The major goals in explanting the heart and lungs are to avoid injury to the phrenic, vagi, or
the recurrent laryngeal nerves and to leave a hemostatic operative field. A midline

sternotomy or clamshell incision is made and the heart is exposed. As a significant number of
recipients have congenital disease, it is not unusual for this to be a redo sternotomy and
standard precautions should be taken. Once the heart has been mobilized, the pleural spaces
are entered and any adhesions are taken down with a cautery. The left and right phrenic
nerves are mobilized leaving a minimum of 2 cm of pericardium above and below the nerve
as a pedicle (Fig. 4.5). Heparin 300 International Unit/kg is administered and the aorta and
venae cavae are cannulated for cardiopulmonary bypass. The patient is cooled to 32C.
Tourniquets are placed around both the IVC and SVC and are snared after the initiation of
cardiopulmonary bypass. At the appropriate time, an aortic x-clamp is placed and a
cardiectomy is performed in standard fashion. The aorta, PA, IVC, and SVC are transected and
only the posterior wall of the left atrium is left behind (Fig. 4.6). Alternatively, if a right atrial
to right atrial anastomosis is to be performed, then the IVC and SVC are left intact. With the
heart removed from the field, the posterior wall of the left atrium is divided midline. The
pulmonary veins on the left side are mobilized circumferentially (Fig. 4.7) and then the PA
and bronchus are mobilized in similar fashion (Fig. 4.8). The inferior pulmonary ligament and
any remaining attachments are transected and the left lung is removed from the field. The
right hilum is dissected and removed from the field after the ligament attachments have been
transected. The trachea should be transected two rings proximal to the bifurcation of the
bronchi and the bronchial stumps resected. Lastly, the remaining pulmonary artery is
removed, leaving behind a small area adjacent to the ligamentum arteriosum to prevent
recurrent laryngeal nerve injury (Fig. 4.9). Posteriorly, care should be taken not to injure the
vagi nerves. Meticulous hemostasis should be performed prior to beginning the implantation.

Figure 4.5 Mobilization of phrenic nerves.

Recipient Implant
Once the ABO compatibility is confirmed, the donor heart and lung bloc is removed from the
transport container and brought on to a sterile back table. The trachea is transected one
cartilaginous ring above the carina. The tracheobronchial tree is irrigated and aspirated and
cultures are sent for microbiology. The bloc is then brought into the chest and with gentle

manipulation, the right lung is passed beneath the right phrenic nerve pedicle (Fig. 4.10). In
similar fashion, the left lung is passed under the left phrenic nerve pedicle. The membranous
tracheal anastomosis is performed using continuous 3-0 PDS suture. The posterior
membranous portion can be performed using a running suture or with interrupted sutures
while the cartilaginous trachea is anastomosed with interrupted sutures (Fig. 4.11). Once the
tracheal anastomosis has been completed, gentle ventilation with room air and half-normal
tidal volumes are initiated to reduce atelectasis. Topical cooling of the lungs with iced saline
is continued during this time. Next, the IVC and SVC anastomoses are performed in sequential
fashion using a continuous 4-0 polypropylene suture. Once the cavae have been anastomosed,
the patient is rewarmed to 37C. Lastly, the ascending aorta anastomosis to the donor aorta is
carried out using 4-0 polypropylene suture in end-to-end continuous fashion. Prior to
removing the clamp, the left atrium venting site must be closed with running 4-0
polypropylene suture. The aorta and pulmonary artery are then de-aired and the aortic xclamp is removed. Prior to removing the aortic cross clamp, 1,000 mg of Solu-Medrol is
administered. The heart is defibrillated as needed. The patient is then gradually separated
from cardiopulmonary bypass after an appropriate reperfusion period has passed (Fig. 4.12).

Figure 4.6 Recipient cardiectomy for bicaval implant.

Figure 4.7 Posterior left atrial wall is divided and left pulmonary veins are mobilized posteriorly and circumferentially.

Figure 4.8 Left bronchus and left PA are dissected free from attachments to allow for transection.

Figure 4.9 Remnant of main pulmonary artery is left behind in the area of ductus ligament to prevent injury to recurrent
laryngeal nerve.

Figure 4.10 Heart and lungs are placed in chest passing each lung under the phrenic nerves.

Figure 4.11 Tracheal anastomosis.

Once the patient is off bypass, the lungs are ventilated using low PEEP in the 3 to 7 cm of
H2O range and the FiO2 is set at 40%. If the heart rate is too slow, atrial and ventricular
pacing wires are placed and the heart is paced at 100 to 110 bpm. Thoracostomy tubes are
placed in both apices and over both diaphragms. The chest is closed in standard fashion, once
adequate hemostasis has been achieved. After the drapes have been removed and the patient
is hemodynamically stable, the double-lumen endotracheal tube is exchanged for a singlelumen tube. A bronchoscopy is then performed to inspect the tracheal anastomoses and to
remove any blood or mucus in the bronchial tree.

Acute postoperative complications are usually evident while the recipient is still in the
operating room. Common complications include bradycardia secondary to sinus node
dysfunction and occurs in 10% to 20% of cases, although this usually resolves within a week.
It is rare that a permanent pacemaker is required. As with isolated heart transplantation, the
use of bicaval anastomosis has been reported to reduce the incidence of sinus node
dysfunction and tricuspid regurgitation. Atrial and ventricular pacing wires should be used to
increase the heart rate to 100 to 110 bpm as cardiac output is largely dependent on heart rate
in the HLT patient. If needed, isoproterenol (0.005 to 0.01 ug/kg/min) can be used to
increase heart rate and decrease pulmonary pressures. If the myocardial function is
decreased, we either use epinephrine (1 to 3 mcg/min) and milrinone (0.1 to 0.5
mcg/kg/min) or dobutamine (1 to 5 mcg/kg/min). If the patient is vasodilated then we start
vasopressin and titrate to 0.04 units/min and then add norepinephrine (1 to 10 mcg/min) if
further vasoconstriction is needed. If hypertension is experienced, then we use Nipride (10 to
150 mcg/min) or nitroglycerin (10 to 300 mcg/min) to maintain a systolic blood pressure
between 90 and 110 mm Hg as we do with all postcardiotomy patients. If a coagulopathy
persists after the protamine has been administered, it should be aggressively treated with
fresh frozen plasma, platelets, and cryoprecipitate as needed. Vitamin K (phytonadione) or
DDAVP (Desmopressin) may also be considered. The patient should not leave the operating
room if significant blood loss is ongoing.

Figure 4.12 Heartdouble-lung transplant.

Morbidity and Mortality

The most common complications after HLT are hypertension, renal dysfunction,
hyperlipidemia, diabetes, coronary artery vasculopathy, and bronchiolitis obliterans. Early
mortality (within 30 days to 1 year) after heartlung transplantation is most commonly
related to noncytomegaloviral infections, primary graft dysfunction, or surgical/technical
complications. After 1 year, infectious complications, bronchiolitis, and graft failure are the
predominant source of death. Donor age (higher), transplant center volume (lower), and
indication for transplantation remain significant predictors of 1-year mortality post dual
organ transplant. Rejection is still commonly seen during the first year post transplant
occurring in approximately 70% of recipients. Of note, rejection in the lungs is seen more
frequently than in the heart. For this reason, most centers rely on transbronchial biopsies
rather than endomyocardial biopsies (Table 4.2). Even if lung biopsies are positive,
endomyocardial biopsies remain negative. If a significant decline in heart function is noted,
then endomyocardial biopsies are warranted. The Harefield Hospital group has also reported
that improved survival is seen in retransplant patients who do not have preformed antibodies,
sputum bacteria, and are out further than 18 months post the initial transplant.
Coronary vasculopathy is still a major factor in decreasing long-term survival in HLT
recipients, although seen less commonly than in isolated heart transplant. Angina is rarely
seen in these patients because the heart is denervated but other signs and symptoms
consistent with coronary insufficiency can be seen such as myocardial infarction, impaired
left ventricular function, arrhythmias, congestive heart failure, and sudden death. The
vasculopathy has been attributed to immune-mediated injury to the coronary vascular
endothelium. Although the etiology of this vasculopathy appears to be multifactorial,
cytomegalovirus (CMV) infection may play a more dominant role. HLT recipients should
undergo coronary angiograms on a yearly basis. Also, intracoronary ultrasound can be used
as a tool in assessing diffuse disease. In the setting of discrete proximal lesions, coronary
bypass grafting and percutaneous angioplasty have both been employed.

TABLE 4.2 Adult HeartLung Transplant Cumulative Morbidity Rates in

Survivors within 1- and 5-Year Post-Transplant (FoIIow-ups: April 1994
June 2012)

TABLE 4.3 Adult HeartLung Transplant Cause of Death (Deaths: January

1992June 2012)

As with any organ transplant, infection is commonly seen and a common reason for
hospital readmission. In the Stanford University experience, approximately 80% of recipients
had some type of infection at 3 months post transplant. About half of these infections are
bacterial and only 10% to 15% were found to be fungal. CMV is the most common viral
infection and usually occurred in the first 2 months post transplant.
With regard to recipient mortality, early death is usually attributed to graft failure and
technical issues. Late death is due largely to non-CMV infection and bronchiolitis obliterans.
Acute rejection is a cause of death in less than 2% of cases whether early or late (Table 4.3).

Although significant improvements have been made in HLT outcomes, further advances must
be made if this surgical option is to be used more frequently. It is clear that for younger
patients with end-stage heart and lung disease, HLT improves greatly the quality of life.
Nonetheless, obstacles that will need to be overcome include graft rejection and a limited
donor pool. We remain hopeful that xenotransplantation will become a viable option in the

future solving the organ shortage issue. Also, improvement of immunosuppression and organ
preservation techniques may also improve outcomes. The use of ex vivo technology also
shows promise in improving organ preservation.

Recommended References and Readings

1. Adams DH, Cochrane AD, Khaghani A, et al. Retransplantation in heart-lung recipients

with obliterative bronchiolitis. J Thorac Cardiovasc Surg. 1994;107(2):450459.
2. DeMeester J, Smits JM, Persijn GG, et al. Listing for lung transplantation: Life expectancy
and transplant effect stratified by type of end-stage lung disease: The Eurotransplant
experience. J Heart Lung Transplant. 2001;20(5):518524.
3. Gammie JS, Keenan RJ, Pham SM, et al. Single versus double lung transplantation for
pulmonary hypertension. J Thorac Cardiovasc Surg. 1998;115(2):397402.
4. Ganesh JS, Rogers CA, Bonser RS, et al. Outcome of heart-lung and bilateral sequential
lung transplantation for cystic fibrosis: A UK national study. Eur Respir J. 2005;25(6):964
5. Grarran MT, Moreno-Cabral CE, Starnes VA, et al. Cytomegalovirus infection is associated
with cardiac allograft rejection and atherosclerosis. JAMA. 1989;261(24):35613566.
6. Guihaire J, Mercier O, Flecher E, et al. Comparison of cardiac allograft vasculopathy in
heart and heart-lung transplantations: A 15-year retrospective study. J Heart Lung
Transplant. 2014; 33(6):636643.
7. Harjula AL, Baldwin JC, Glanville AR, et al. Human leukocyte antigen compatibility in
heart-lung transplantation. J Heart Transplant. 1987;6(3):162166.
8. Hayes D, Galantowicz M, Hoffman T. Combined heart-lung transplantation: A perspective
on the past and the future. Pediatr Cardiol. 2013;34:207212.
9. Higgenbotham T, Hutter JA, Stewart S, et al. Transbronchial biopsy has eliminated the
need for endomyocardial biopsy in heart-lung recipients. J Heart Lung Transplant.
10. Kapoor A, Laks H. Atlas of Heart-Lung Transplantation. New York, NY: McGraw Hill; 1994.
11. Kramer MR, Marshall SE, Starnes VA, et al. Infectious complications in heart-lung
transplantation. Analysis of 200 episodes. Arch Intern Med. 1993;153(17):20102016.
12. Lurie KG, Bristow MR, Reitz BA. Increased beta-adrenergic receptor density in an
experimental model of cardiac transplantation. J Thorac Cardiovasc Surg. 1983;86(2):195
13. Marshall SE, Kramer MR, Lewiston NJ, et al. Selection and evaluation of recipients for
heart-lung and lung transplantation. Chest. 1990;98(6):14881494.
14. Reichart B, Jamieson S. Heart and HeartLung Transplantation. Munich: Verlag R.S. Schulz;
15. Reitz BA, Pennock JL, Shumway NE. Simplified operative method for heart and lung
transplantation. J Surg Res. 1981; 31(1):15.
16. Sarris GE, Smith JA, Shumway NE, et al. Long term results of combined heart-lung
transplantation: The Stanford experience. J Heart Lung Transplant. 1994;13(6):940949.
17. Sibley RK, Berry GJ, Tazelaar HD, et al. The role of transbronchial biopsies in the
management of lung transplant recipients. J Heart Lung Transplant. 1993;12(2):308324.
18. Stoica SC,McNeil KD, Perreas K, et al. Heart-lung transplantation for Eisenmengers

syndrome: Early and long term results. Ann Thorac Surg. 2001;72(6):18871991.
19. Weiss ES, Allen JG, Meguid RA, et al. The impact of center volume on survival in lung
transplantation: An analysis of more than 10,000 cases. Ann Thorac Surg. 2009;88(4):1062
20. Yusen RD, Christie JD, Edwards LB, et al. The registry of the international society for
heart and lung transplantation: Thirtieth adult lung and heart-lung transplant report2013;
focus theme: Age. J Heart Lung Transplant. 2013;32:965978.

5 ECMO and Lung Transplantation

Nathalie Roy and Joshua N. Baker


In recent years there has been a trend toward the increasing use of ECMO prior to lung
transplantation, with increased survival in the recent era. However, survival post
transplantation remains lower than the non-ECMO patient cohort. The prevalence of
utilization of this technology and results vary across centers in the United States. In the
patient with acute respiratory failure, it can be used as bridge to transplantation, bridge to
decision, and bridge to recovery. Its best indication in the setting of lung transplantation
reside in patient optimization for transplantation rather than patient salvage.
Many modes and cannulation strategies for ECMO have been described in recent years.
Venovenous cannulation is the more prevalent in the transplantation population and can be
performed with a double-lumen cannula, multiple venous cannulas, or right atrial to
pulmonary artery cannulation. Venoarterial cannulation has also been described pre-lung
transplantation although it is rarely our approach. In the context of ECMO for lung
transplantation, ambulatory ECMO, if achievable, is preferable.


Acute or rapidly progressing respiratory failure in a patient listed for lung transplantation
Chronic respiratory failure leading to deconditioning and malnutrition in a patient listed for
lung transplantation
Impending intubation or short time intubated
Systemic sepsis
Advanced age
Serious comorbidities precluding lung transplantation
Time spent on the ventilator >7 days

Figure 5.1 ECMO circuit for patient ambulation. The various components are mounted on an IV infusion pole. C, centrifugal
pump; O, oxygenator; M, monitoring console; T, oxygen tank with gas blender.

ECMO circuit components and ambulatory setup (Fig. 5.1)
Deoxygenated blood is removed from a central vein (femoral or internal jugular vein),
pumped through a membrane leading to CO2 removal and oxygenation and returned pre-lung
(central vein, right atrium, pulmonary artery) in the case of venovenous (VV) ECMO. In the
case of venoarterial (VA) ECMO, blood can be returned to the femoral or axillary artery, left
atrium, and the aorta. The carotid artery is usually used for VA ECMO in neonates and
1. Cannulas: Double-lumen flow directed (Avalon Elite; Maquet, San Jose, CA), drainage and
perfusion cannulae inserted percutaneously or centrally.
Cannula size, mainly of the drainage cannula or component, is the major determining
factor in total pump flow. Factors taken in consideration for selection are patient size and

2. Heparin-bonded (Carmeda; Medtronic, Minneapolis, MN) 3/8 tubing.
3. Centrifugal pump (CentriMag; Thoratec, Pleasanton, CA or RotaFlow; Maquet, San Jose,
Connected to monitoring console.
4. Oxygenator (Quadrox: Maquet, San Jose, CA).
Comprising two chambers (gas and blood) divided by a semipermeable hollow fiber
membrane, allowing for carbon dioxide (CO2) and oxygen (O2) diffusion. CO2 is more
soluble than O2 and diffuses easily through the membrane. CO2 clearance is, therefore, a
result of gas flow (sweep gas) across the membrane. Oxygenation will be determined by
pump flow and gas blender (O2/air); pump flow relative to the patients cardiac output
will be the major determinant of the patients PO2.
Connected to heater/cooler for temperature management.

Venovenous (VV) ECMO
Venovenous (VV) dual cannulation strategy (Fig. 5.2)
Primarily for the patient with respiratory failure as a bridge to recovery or bridge to
Advantages and Disadvantages
The advantages are: The technique is performed rapidly, often at the bedside, and does not
require fluoroscopy or Transesophageal echo (TEE).
However, there is a higher incidence of recirculation, and as a result, it is difficult to
extubate, or mobilize and exercise these patients. For patients in whom the decision is
made to list for lung transplantation after the initiation of ECMO, this strategy can be used
as a bridge to a different cannulation arrangement.

Figure 5.2 Venovenous dual site cannulation. The drainage and perfusor cannulas have to be distanced to prevent

Concept: Blood Recirculation Fraction

With this cannulation arrangement, the inflow and outflow cannulas have to be separated
by as much distance as possible to reduce the blood recirculation fraction.
The right neck and femoral areas are prepped in the sterile field, and the ECMO lines are
divided and brought up. Right internal jugular access and femoral venous access (just above
the inguinal ligament) are obtained using a 4-Fr micropuncture needle (Cook, Bloomington,
IN), Seldinger technique, and 4-Fr introducer.
100 IU/kg of heparin is administered to the patient
The femoral vein is usually the site of the drainage cannula. We often choose a long (no. 23
to 25) multistage cannula.
The right internal jugular vein is usually the preferred site for the insertion of the perfusor
cannula. We opt for an arterial no. 19 perfusor cannula.
Alternate sites for cannulation are the left internal jugular vein and and the subclavian vein,
but we recommend that fluoroscopy be used during cannula insertion to prevent vascular
injury if these alternate sites are considered.
After femoral access is obtained, a super-stiff Amplatz (Cook, Bloomington, IN) 0.038
guidewire advanced to the level of the inferior vena cava (IVC) and right atrial (RA)
junction. Successful venous dilatations are performed, followed by the insertion of the
venous multistage cannula to the level of the diaphragm to prevent. The cannula is de-aired
and connected to the inflow limb of the circuit.

Using the same technique, the perfusor is inserted and positioned to the level of the SVC-RA
junction. Once de-aired and connected to the outflow limb of the ECMO circuit, time-out is
performed to verify (1) the flow direction, (2) the absence of air entrapped in the circuit,
and (3) adequate anticoagulation with an activated clotting time (ACT). Only then ECMO is
Recirculation can be significant with this strategy. It can be suspected when a low
arteriovenous O2 difference between the inflow and outflow limbs of the circuit. It worsens
when pump flows are increased on ECMO. If the patient remains desaturated, it often
requires a change in cannulation strategy.
Single cannula (Fig. 5.3): Dual-lumen flow directed cannula (Avalon Elite: Maquet, San
Jose, CA)
A single cannula provides inflow and outflow. The inflow has an IVC and SVC port, and the
outflow is flow directed and aimed at the tricuspid valve.
The best use of this technology is patient optimization prior to lung transplantation.
Advantages and Disadvantages
Single cannula in the upper body favors early extubation, mobilization, and ambulation.
Disadvantage is limitation of flow.

Figure 5.3 Dual-lumen flow directed cannula. The cannula is positioned with the drainage ports in the IVC and SVC. The
reinfusion port and cannula flow is directed toward the tricuspid valve orifice under TEE guidance.

Patent right superior vena cava (SVC).
Near-normal right ventricular (RV) function and no significant pulmonary hypertension
(PH). However, the presence of a PFO (naturally occurring or catheter-created) may allow
the support of a patient with pH with this cannulation strategy.
Cannula Selection
Based on ideal bodyweight for height. If possible, we aim to insert a no. 27-Fr or no. 31-Fr
cannula in all patients to obtain adequate flows.
The patients vessels are assessed with a bedside ultrasound in the ICU.
OR Setup and Patient Positioning
Central lines are moved away from the right neck vessels.
We use both fluoroscopy and transesophageal echo during cannula insertion.
The patient is positioned supine on the OR table (reversed), with the head slightly turned to
the right. The neck, chest, and abdomen to the level of the umbilicus are prepped into the
operative field.
A scrubbed assistant is useful for wire control, and limiting the blood loss in between
sequential dilatations and cannula insertion.
Using ultrasound guidance, the right internal jugular vein is accessed in the inferior third of
the neck using a 4-Fr micropuncture needle (Cook, Bloomington, IN). Using a Seldinger

technique, a 4-Fr introducer catheter is placed in the SVC.

One hundred International Units per kilogram (100 IU/kg) of unfractionated heparin is
administered to the patient and the ECMO circuit lines are divided, brought up to the
operative field, and secured in place.
Under fluoroscopic guidance, a super-stiff Amplatz 0.038 guidewire (Cook, Bloomington,
IN) is carefully positioned into the IVC.
A small incision is made in the neck, and the tract is sequentially dilated.
The Avalon cannula is then positioned on the wire and inserted with the outflow port
directed toward the tricuspid valve orifice (critical step).
The cannula is positioned under fluoroscopic guidance with the tip of the catheter in the
IVC, and the superior inflow port in the SVC. Once inserted, the cannula is difficult to
rotate on its axis; therefore, orientation of the outflow port is critical as the cannula is
being inserted.
The wire and dilator are removed, and the cannula is clamped in its inflow (inferior) and
outflow (superior). De-airing is performed, followed by connection to the corresponding
limbs of the ECMO circuit. An ECMO time-out is performed as previously described.
The cannula is then secured at the skin in multiple areas and is maintained to the patients
head using a bandana. Certain groups have described a tunneled approach to provide
additional stability to the cannula. The exiting site can be infra- or supraclavicular though
the caveat is potential kinking of the cannula.
Central right atrial to pulmonary artery (RA-PA) ECMO (Fig. 5.4AC)
Patient with PH and/or mild RV dysfunction.
Bridge to transplantation, to decision, or to recovery.
Prolonged anticipated need for ECMO support.
Patient Position
The operative table is reversed should a need for fluoroscopy guidance arise.
The patient is supine with the arms tucked in on the operative table.
Skin is prepped from the chin to the knees.
Very careful hemostasis is critical to the success of this procedure.
An upper midline incision is performed, and an upper hemisternotomy off the right edge is
performed. Very careful hemostasis of the bone edges is performed and the marrow is
controlled using Gelfoam. This approach is conducive to a subsequent lung transplantation
via a midline sternotomy or a clamshell incision in the fifth intercostal space.
A Finochietto or Squarehole retractor is used and is expanded carefully.
The thymus is split and retracted, and the pericardium is opened and retracted with deep
sutures to bring the heart into view, with extra care not to injure the phrenic nerve.
One hundred IU/kg unfractionated IV heparin is administered to the patient and the ECMO
lines are divided and brought up to the field.

Two purse-string sutures are placed on the right atrium with pledgetted (pericardial or felt)
3-0 prolene. With gentle traction on the tourniquets, this helps bring the pulmonary artery
into view. Two diamond-shaped purse strings are placed in the proximal main pulmonary
artery (MPA), with great care taken to avoid the pulmonary valve.
Incisions for the cannulas are made at the inferior right costal margin (Fig. 5.4B). The
lateral cannula will be the venous inflow, and the medial cannula, the arterial outflow in
the pulmonary artery. Very carefully, tracts are made to reach the level of the upper
sternotomy, avoiding the right pleural space if possible. A straight chest tube is used to
bring the cannulas through the skin to avoid fatty deposition inside the cannulas.
The RA cannula (venous cannula no. 28 to 32) is inserted to 5 to 7 cm with an attempt to
position the end at the IVC-RA junction to minimize suction events and flow interruption. It
is de-aired and connected to the inflow limb of the circuit, as described.

Figure 5.4 A: Venovenous RA-PA surgical approach. B: The cannulas are tunneled from the right costal margin inside a
straight thoracostomy tube. Right atrial and main pulmonary cannulations are performed. C: Final result and planning
approach for bilateral lung transplantation.

The arterial cannula (no. 23 arterial) is inserted 2 to 3 cm with care to have the tip in the
MPA. It is de-aired and connected to the outflow limb of the circuit, as described, and
ECMO is initiated.
Two flexible drains (no. 19 Fr) are positioned in the pericardial space and will remain in
place for the duration of ECMO.
The sternal edges are reapproximated with four (4) wires: One for the horizontal segment
and three for the vertical portion.
Venoarterial (VA) ECMO
In the setting of PH and hypoxemia, some centers have advocated the use of VA ECMO as a
bridge to transplantation. The cannulation strategy consists of using a venous drainage
cannula inserted percutaneously via the right internal jugular vein, and an arterial outflow
placed via a graft in the right axillary artery. This has allowed teams using this approach to
mobilize the patients. However, the caveats of this technique are the higher incidence of
upper extremity edema, brachial plexus injury, and bleeding in view of the need to keep the
ACT in higher ranges than for VV ECMO (180 to 220 seconds). Historically, the patients
transplanted after VA ECMO have had reduced survival though this data does not reflect the
current early mobilization strategy.

Management of the Patient on ECMO
ECMO for BTT requires an experienced and dedicated multidisciplinary team to be successful.
The team should comprise cardiothoracic surgeons, intensivists, neuropsychiatrists, ECMO
bedside specialists (perfusionists, respiratory therapists, and nurses), ECMO-trained bedside
nurses, physiotherapists, nutritionists, and social workers.
ECMO flow is targeted to maintain the SaO2 >90%, and the sweep is adjusted to normalize
PCO2 progressively. In terms of anticoagulation maintenance, we use an ACT target for 160 to
180 seconds for VV ECMO. Our goal is early extubation, management of anxiety and
delirium, early mobilization and exercise program, and optimization of nutrition. The
hemoglobin target >10 and platelet transfusion threshold is <20 K unless there is active
bleeding. Antibiotherapy is directed at treating the active infections.

Delirium: Most patients on ECMO experience delirium at some stage. Often, they are
intubated and heavily sedated at the time of ECMO initiation. Severe hypoxemia as a
trigger to delirium causes neuropsychiatric states that are very challenging to control.
Stroke: Hemorrhagic, or embolic in the setting of a PFO or an atrial septostomy.
RV dysfunction: Often a result of severe PH, it results in hypoxemia and hypotension in
patients with single or dual percutaneous approaches.

Hypoxemia: More often related to cannula malposition in percutaneous approaches. It can

also be observed when the patients cardiac output increases. Some centers have reported
little need to change flows during exercise. This has not been our experience; we have
noted some desaturation with ambulation, even in our centrally cannulated patients. This
can be ameliorated by increasing pump flows during exercise and keeping the hemoglobin
at higher targets (>10 to 12).
Pericardial tamponade: From guidewire perforation during insertion of percutaneous
cannulae, or as a result from mediastinal bleed when central cannulation is used. To reduce
the incidence of this latter complication, we leave soft pericardial drains in place.
Stress gastritis, ulceration, GI bleeding: Often as a result of anticoagulation and platelet
dysfunction. Our supported patients are kept on IV esomeprazole.
Platelet dysfunction: We have noticed a high incidence of platelet dysfunction in our
patients supported on ECMO long term, often resulting in bleeding from venopunctures,
nasoenteric tube insertion, etc. DDAVP can be administered in this setting and ameliorates
the bleeding diathesis.
Transfusions: May result in increased patient sensitization prior to transplantation.
Thrombosis: Clot formation in circuit and around cannulae, requiring replacement of
individual components, ECMO circuit and occasionally surgical intervention such as
pulmonary embolectomy.
HIT and HITT: Requires the use of an alternate agent for anticoagulation such a Bivalirudin,
and a non-heparin bounded circuit.
Component failure
Infection: It is important to avoid the excess use of antibiotics. Consultation with a
transplantation ID specialist is often warranted.

In the context of acute respiratory failure, ECMO can be used as bridge to recovery, bridge to
decision, or bridge to transplantation. In the recent era, the survival of patients transplanted
after ECMO has significantly improved, possibly reflecting the new paradigm of patient
optimization rather than salvage. Although controversy remains as ECMO results in
reprioritization of patients in the lung allocation score (LAS) era, and lung donors are scarce.
Thus, ECMO is carefully employed pre-lung transplantation with a goal to achieve correction
of hypoxemia and acidosis, permit early patient extubation, mobilization and adherence to an
exercise program, as well as optimization of their nutritional status prior to lung

Recommended References and Readings

Abrams D, Brodie D, Javidfar J, et al. Insertion of bicaval dual-lumen cannula via the left
internal jugular vein for extracorporeal membrane oxygenation. ASAIO J. 2012;58(6):636
Abrams D, Javidfar J, Farrand E, et al. Early mobilization of patients receiving extracorporeal
membrane oxygenation: A retrospective cohort study. Crit Care. 2014;18(1):R38. [Epub

ahead of print]
Abrams DC, Brodie D, Rosenzweig EB, et al. Upper-body extracorporeal membrane
oxygenation as a strategy in decompensated pulmonary arterial hypertension. Pulm Circ.
Agerstrand CL, Bacchetta MD, Brodie D. ECMO for adult respiratory failure: Current use and
evolving applications. ASAIO J. 2014;60(3):255262.
Diaz-Guzman E, Hoopes CW, Zwischenberger JB. The evolution of extracorporeal life support
as a bridge to lung transplantation. ASAIO J. 2013;59(1):310.
Garcia JP, Iacono A, Kon ZN, et al. Ambulatory extracorporeal membrane oxygenation: A new
approach for bridge-to-lung transplantation. J Thorac Cardiovasc Surg. 2010;139(6):e137
Garcia JP, Kon ZN, Evans C, et al. Ambulatory veno-venous extracorporeal membrane
oxygenation: Innovation and pitfalls. J Thorac Cardiovasc Surg. 2011;142(4):755761.
Hoopes CW, Kukreja J, Golden J, et al. Extracorporeal membrane oxygenation as a bridge to
pulmonary transplantation. J Thorac Cardiovasc Surg. 2013;145(3):862867; discussion
Javidfar J, Bacchetta M. Bridge to lung transplantation with extracorporeal membrane
oxygenation support. Curr Opin Organ Transplant. 2012;17(5):496502.
Javidfar J, Brodie D, Iribarne A, et al. Extracorporeal membrane oxygenation as a bridge to
lung transplantation and recovery. J Thorac Cardiovasc Surg. 2012;144(3):716721.
Toyoda Y, Bhama JK, Shigemura N, et al. Efficacy of extracorporeal membrane oxygenation
as a bridge to lung transplantation. J Thorac Cardiovasc Surg. 2013;145(4):10651070;
discussion 10701071.

6 Lung Volume Reduction: Transsternal

Thomas K. Varghese Jr.


Chronic obstructive pulmonary disease (COPD) is a significant cause of morbidity and

mortality, affecting 13 million adults in the United States, with over 134,000 deaths annually
making it the third leading cause of death. Emphysema, a form of COPD defined by abnormal
and permanent enlargement of the airspaces distal to the terminal bronchioles associated
with destruction of the alveolar wall, limits airflow and decreases functional area for gas
exchange. Lung volume reduction surgery (LVRS) or reduction pneumoplasty aims to reduce
nonfunctional lung volume by wedge excision of emphysematous tissue. By reducing the
volume of hyperinflated lung, underlying compressed lung is allowed to expand, thus
establishing improved respiratory function. Typically the amount of tissue removed is 20% to
35% of each lung during the procedure, targeting the most diseased portions.
There are two approaches to LVRSvia median sternotomy (transsternal approach) and
video-assisted thoracoscopic surgery or VATS. Although surgeons may prefer one approach to
the other, to date there has not been any demonstrated benefit with respect to mortality with
either of the approaches as compared to the other. LVRS using the VATS approach typically
takes longer secondary time needed to reposition the patient. To date, both approaches have
offered equivalent results in pulmonary function improvement. Surgeon expertise and patient
preference often have the heaviest influences for use of one technique over the other.

Indications for LVRS in the modern era are derived from the results of the National
Emphysema Treatment Trial (NETT). The largest randomized clinical trial (RCT) dealing with
LVRS, the goals of NETT were to identify the effects of treatment as well as the optimal
candidates for intervention. NETT involved 17 centers and enrolled 1,218 patients with endstage emphysema. The first publication from the study occurred after noting a specific highrisk subset of patientsthose with FEV1 <20% with homogenous disease or a diffusing
capacity or transfer factor of the lung for carbon monoxide (DLCO) <20%at the 6-month
follow-up had high mortality with surgery, with minimal improvement. After this high-risk
group was excluded, the major findings were derived from the remaining 1,078 patients. Midterm and long-term results demonstrated clinically significant improvements in spirometry,
lung volumes, diffusing parameters, oxygenation, quality of life, dyspnea, exercise capacity,
and long-term survival. Two key predictive factors were identified in NETT: Distribution of
emphysema and the level of baseline exercise capacity. Bilateral LVRS provides clinically
significant improvements in quality of life for patients with heterogenous upper lobe
predominant emphysema, with additional survival benefit in the low exercise capacity subset
of these patients.
The Centers for Medicare & Medicaid Services (CMS) has based its reimbursement policies

wholly on the results of NETT and thus will pay for bilateral LVRS in patients with advanced
upper lobe predominant emphysema that meet NETT criteria. They will not pay for the
procedure in those with lower lobe disease, alpha-1 antitrypsin deficiency, homogenous
disease, extremely advanced disease (both FEV1 <20% and DLCO <20% predicted) and
those with a contraindication for bilateral procedures (asymmetric unilateral disease or those
with bilateral disease and a history of thoracotomy). CMS recommends that procedures be
performed at facilities that fulfill one of the following criteria:
Certified by the Joint Commission on Accreditation of Healthcare Organizations (JCAHO)
under the LVRS disease-specific care certification program
Or approved as Medicare lung or heart-lung transplantation hospitals
In addition, Medicare-covered LVRS approaches are limited to bilateral resections. The
procedure is reimbursed if all of their criteria are met (Table 6.1) in the setting of severe
upper lobe predominant emphysema (on CT scan), or severe nonupper lobe emphysema with
low exercise capacity. Patients with low exercise capacity are those with maximal exercise
capacity at or below 25 W for women and 40 W for men after completion of the preoperative
therapeutic program in preparation for LVRS. Exercise capacity is measured by incremental,
maximal, symptom-limited exercise with a cycle ergometer utilizing 5 or 10 watts/minute
ramp on 30% oxygen after 3 minutes of unloaded pedaling.

TABLE 6.1 Indications for LVRS (CMS Criteria for Coverage)


LVRS is not indicated in any of the following circumstances:

Patient characteristics carry a high risk for perioperative morbidity and/or mortality.
Disease is unsuitable for LVRS (i.e., homogenous disease).
Patient is unable to complete the preoperative and postoperative pulmonary diagnostic and
therapeutic program required for surgery.
FEV1 20% predicted + homogenous distribution of emphysema on CT scan, or DLCO
20% predicted (high-risk group identified in NETT).
Severe, nonupper lobe emphysema with high exercise capacity. High exercise capacity is
defined as maximal workload at the completion of the preoperative diagnostic and
therapeutic program that is above 25 W for women and 40 W for men.

The surgery must be preceded and followed by a program of diagnostic and therapeutic
services consistent with those outlined in NETT. These programs are designed to optimize
patients health before surgery and improve the chance for successful recovery. Elements of
the preoperative program include:
Six- to ten-week series of at least 16, and not more than 20, preoperative sessions each
lasting a minimum of 2 hours. The focus of the rehabilitation program is to optimize
exercise capacity, achieve physical fitness to affect early postoperative mobilization and
provide a baseline of optimized preoperative exercise capacity or comparison with
postoperative exercise capacity.
Components of the pulmonary rehabilitation program include:
Comprehensive evaluation of medical, psychosocial, and nutritional needs
Setting of goals for education and exercise training
Exercise training (lower extremity, flexibility, strengthening, and upper extremity)
Education about emphysema and medical treatments
Psychosocial counseling
Nutritional counseling
The program should be arranged, monitored, and performed under the coordination of the
facility where the surgery will take place.
Common elements of preoperative pulmonary rehabilitation programs include controlled
breathing and cough techniques, instructions in incentive spirometry exercises, and
peripheral muscle exercise training consisting of aerobic work. Bronchodilator therapy may
be used without steroids.

Those who advocate for median sternotomy cite the shorter operative times (as repositioning
during the case is not needed) and avoiding injury to chest wall muscles and intercostal
nerves both from the operative approach and from chest tubes brought out below the costal

Working IV lines, an arterial line, and a thoracic epidural are often placed at the beginning
of the procedure. A working thoracic epidural is used to ensure adequate pain control thus
allowing for adequate pulmonary toilet in the immediate postoperative period.
After induction of general anesthesia, the patient is first intubated with a single-lumen
endotracheal tube to allow for bronchoscopy. Flexible bronchoscopy is used to suction
secretions and obtain a specimen for STAT gram stain and cultures. In addition to pulmonary
toilet, bronchoscopy allows for assessment of airway anatomy and to rule out any
endoluminal abnormalities. The single-lumen endotracheal tube is then exchanged for a leftsided double-lumen endotracheal tube, with bronchoscopic confirmation of its position.

Figure 6.1 Positioning of patient for Transsternal LVRS.

The patient is positioned with arms tucked, a shoulder roll to gently extend the neck, and
pressure points appropriately padded (Fig. 6.1). The neck, chest and upper abdomen are
prepped and draped in standard surgical fashion.
Sternotomy and Right LVRS
A midline incision is made from the sternal notch to the xiphisternum (Fig. 6.2). Adequate
clearance of pleura away from the retrosternal area is performed by sweeping from the
suprasternal and subxiphoid areas. A rolled sponge can help with the same. Ventilation to
both lungs is briefly suspended just before division of the sternum with the sternal saw.
Ventilation is restarted. The right mediastinal pleura is sharply incised taking care to avoid
injury to the phrenic nerve located at the apex of the chest. The right lung is visualized while
still ventilating to assess the degree of damage caused by emphysema to the various portions
of the lung, as well as the location of the fissures. Single-lung ventilation is initiated to allow
for decompression of the right lung. Care is taken to avoid hyperinflating the left lung, and
airway pressures are maintained at 15 to 20 cm H2O pressure.

Figure 6.2 Median sternotomy.

Figure 6.3 Right upper lobe LVRS. Resection is begun just above the hilum and extended straight back to an area just above
the fissure. Care is taken to avoid crossing the fissure and compromising the superior segment of the right lower lobe.

Upper lobe predominant disease is the most common indication for LVRS. Hence the right
middle and lower lobes are usually well-deflated soon after initiation of single-lung
ventilation. The inferior pulmonary ligament is located and taken down to the level of the
inferior pulmonary vein. Adhesions are taken down with a combination of sharp and
electrocautery dissection under direct vision. For upper lobe disease, removal of around 75%
of the right upper lung is typical. Ring forceps are introduced to help in mobilizing the lung.
Precompression of the lungs at the area of planned resection line with the aid of ring forceps
can help with application of the stapler. Selective use of cautery can be done to puncture

hyperinflated areas of lung to be removed. Traditional GIA linear staplers were used in early
series. Endoscopic staplers allow for increased maneuverability and now come in specialized
forms for use with thick tissues such as the Endo GIA Tri-Staple and Echelon Endopath
staplers. Buttress reinforcement of the staple line can be done, such as use of bovine
pericardium. Staple lengths encompassing 4.8-mm thickness are used for lung resection.
(Black load [4 to 4.5 to 5 mm] for the Endo GIA Tri-Staple and Green load [4.8 mm] for
Echelon Endopath staplers). Multiple firings of the stapler are performed, typically straight
across the upper lobe beginning medially above the hilum and ending just above the upper
extent of the oblique fissure (Fig. 6.3). Stapling across the fissure is avoided to avoid
compromising the ability of remaining middle and lower lobes to fully re-expand. If the apex
of the lung is densely adherent to the chest wall, it is often easier to divide the lung first and
then lyse the adhesions. After resection has been completed, the specimen is removed and
submitted to pathology. Warm saline is used to fill the chest, and the remaining lung
reinflated to search for any air leaks. Irrigation fluid is removed. Some have advocated for the
use of biologic sealants over the staple lines, but this should not be an attempt to make up for
poor surgical technique or technical failure. Two chest tubes are placed into the pleural
space, anteriorly and posteriorly and brought out near the midline via subcostal incisions.
Chest tubes are secured to the chest wall and connected to Pleur-Evacs.
The procedure is now repeated on the left side. The mediastinal pleura is sharply incised,
taking care to visualize and avoid injury to the phrenic nerve. Taking down the inferior
pulmonary ligament on the left side can be tricky due to the position of the heart, and this
step may need to be skipped if it is too difficult to perform. For upper lobe predominant
disease, the lingula is left intact. The upper 2/3 of the left upper lobe is removed with
multiple applications of the stapler as before. The line of excision is parallel to the oblique
fissure separating the upper and lower lobes (Fig. 6.4). Care is taken to avoid crossing the
fissure into the superior segment of the lower lobe, as this will compromise its ability to reexpand at the completion of the procedure. The specimen is removed, the lung is reinflated
and inspected for air leaks, and two chest tubes are placed into the left pleural space similar
to what was done on the contralateral side.

Figure 6.4 Left upper lobe LVRS. The lingula is spared, and the upper 2/3 of the left upper lobe is resected with the line of
excision parallel to the oblique fissure. Care is taken to avoid crossing the fissure.

The mediastinal pleura is closed on both sides, leaving a small window open inferiorly to
allow for drainage of any mediastinal fluid. A separate mediastinal drain is not needed if this
is done, as any mediastinal fluid collection should drain into the pleural space.
Sternal Closure
As most patients are on steroids before surgery, bone quality of the sternum is a concern.
Figure-of-eight stainless steel wires are the norm during closure to minimize the occurrence of
wound dehiscence. In especially brittle bone, consideration is given to use 2.4-mm thickness
titanium plates for additional support.
After completion of bilateral LVRS, the patient is returned to the supine position. A chest xray can be performed prior to extubation, or shortly after arrival to the recovery room. If
postop chest x-ray demonstrates full re-expansion, the chest tubes can be put on water seal.

Principles of standard thoracic postoperative management are followed including:
Early ambulation.
Transition from epidural analgesia to oral pain medications in 48 to 72 hours that provide
adequate analgesia.
Pulmonary toilet measures (which had begun preoperatively) such as deep breathing,
coughing, use of incentive spirometry, and handling of secretions.
Nebulized bronchodilator therapy is initiated in the early postoperative period to minimize
airway reactivity and transitioned to inhalers as needed.
Nutritional assessment and intervention is important, as it aids in healing.
Systemic steroids may be needed in the perioperative period.

Unlike other thoracic surgical procedures, early water seal is the norm and can be started
with expansion of the lung even in the presence of an air leak. Chest tubes are removed once
air leaks resolve and output has minimized, in the standard fashion. Those with persistent air
leaks in the postoperative period may be transitioned to Heimlich valve as long as the lung
remains expanded on water seal, output is minimal, and the patient is able to care for the
drain in the postdischarge setting.

LVRS is a procedure performed on a patient population with significant comorbidities.
Avoiding complications is the best path toward functional recovery. Patient selection is key
for the same.
In NETT, the operative mortality was 6%, major pulmonary morbidity was 30%, and major
cardiovascular morbidity was 20%. The most common complications were reintubation
(22%), arrhythmias (19%), pneumonia (18%), mechanical ventilation for more than 2 days
(13%), and persistent air leak for 30 days (12%). Myocardial infarction, deep venous
thrombosis (DVT), pulmonary embolism (PE), and wound infection occurred less frequently.
Most patients have an initial air leak that seal, but prolonged air leaks can be a source of
significant morbidity. Gentle handling of tissues, use of buttressed or specially designed
staplers for lung tissue and avoiding crossing of staple lines can help minimize postoperative
air leaks. Suction is selectively used for those patients with large symptomatic air leaks.
Pleurodesis and reoperations are rarely done but may be needed in situations where one
needs to revise the staple line or excise the source of the leak.
Pneumonia is avoided by aggressive pulmonary toilet measures, early ambulation, and
management of secretions. Sputum collected by bronchoscopy can be used to tailor antibiotic
therapy if infiltrates develop in the postoperative period. Pleural effusions may require
additional drainage tubes. Development of empyema will require surgical intervention, as
well as any development of mediastinitis.
Mucus plugging and respiratory complications can occur in the LVRS population. Patients
with copious sputum production should be carefully screened during the preoperative
evaluation period. If after induction of general anesthesia, bronchoscopy demonstrates
purulent sputum or copious secretions, it is better to cancel the procedure and reassess after
appropriate antibiotic therapy and evaluation.
There have been reports of association of LVRS and gastrointestinal complications such as
ileus, intestinal ischemia, and perforation. Bowel function should be carefully monitored in
the early postoperative period.

NETT mid-term and long-term results of demonstrated clinically significant improvements in
spirometry (FEV1, FVC), lung volumes, diffusing parameters (DLCO, PCO2), oxygenation
(PO2, O2 utilization), quality of life (SF-36, Quality of Well-being survey), dyspnea (St.

Georges Respiratory Quotient), exercise capacity (6-minute walk, treadmill exercise test), and
long-term survival. Several institutional case series have reported remarkably consistent
results irrespective of surgical approach. This is likely secondary to rigid criteria used for
patient selection, methodical preoperative preparation, and vigilance in the postoperative
period. Most series report a postoperative length of stay ranging from 8 to 14 days, with air
leaks being the most common reason for prolonged length of stay. Reported benefits have
included gains in exercise tolerance, freedom from oxygen use, freedom from steroid use, and
improvement in subjective quality of life scores.
Relief of dyspnea has been examined in nonrandomized series and in the NETT as a
secondary endpoint. Ciconne et al. reported in a series of 250 patients from Washington
University that 79% of patients at 1 year, and 40% of patients at 5 years had improved
dyspnea scores over baseline. In a follow-up of the NETT, quality of life scores for those with
upper lobe predominant disease and preoperative low exercise tolerance lasted through 5
years of follow-up.
Both LVRS and transplantation can be considered in end-stage emphysema. In a
retrospective series comparing LVRS, single-lung transplantation, and double-lung
transplantation findings included the following:
FEV1 improved by 79% at 6 months and 82% at 12 months for LVRS patients, 231% and
212% for single-lung ventilation patients, and 498% and 518% for double-lung ventilation
Six-minute walk test distance at 6 months improved 28% for LVRS, 47% for single-lung
transplants, and 79% for double-lung transplant recipients.
LVRS patients and transplant patients needed oxygen therapy before surgery. While all the
transplant patients did not require supplemental oxygen after surgery, 5.5% of LVRS
patients needed supplemental oxygen during exercise after surgery while none needed it at
Thus, though LVRS can be beneficial, it is a palliative procedure whereas lung
transplantation can result in superior lung function. Limitations of the study were its
retrospective nature, and baseline differences in age between the groups.

LVRS is a surgical technique that involves selective reduction of lung volume by excision of
tissue in areas where the emphysematous changes are pronounced. The choice between
transsternal and VATS approaches is most commonly a result of surgeon expertise and
patient preference.
The amount of tissue resected is 20% to 35% of each lung, which for upper lobe
predominant disease is 75% of the right upper lobe, and 2/3 of the left upper lobe.
LVRS can lead to modest improvement in spirometry, lung volumes, diffusing parameters,
oxygenation, quality of life, dyspnea, exercise capacity, and long-term survival. Key to
success is strict patient selection criteria, optimizing patients preoperatively, and aggressive
postoperative management to minimize the occurrence of complications.
Complications postoperatively include persistent air leak, reintubation, prolonged

mechanical ventilation, pneumonia, wound infection, arrhythmias, and less commonly

myocardial infarction, DVT, PE, and death.
Majority of patients are extubated in the operating room. Effective management of pain,
pulmonary toilet, early ambulation, and management of secretions are key steps in
minimizing complications.

Recommended References and Readings

Brantigan OC, Mueller E. Surgical treatment of pulmonary emphysema. Am Surg.

Centers for Medicare & Medicaid Services (CMS). National Coverage Determination (NCD) for
119&ncdver=3&bc=AgAAQAAAAAAAAA%3D%3D&. Accessed on April 20, 2014.
Cetinag IB, Boley TM, Magee MJ, et al. Postoperative gastrointestinal complications after lung
volume reduction operations. Ann Thorac Surg. 1999;68:10291033.
Centers for Disease Control and Prevention (CDC). Chronic Obstructive Pulmonary Disease
(COPD). Accessed on April 20, 2014.
Ciccone AM, Meyers BM, Guthrie TJ, et al. Long-term outcome of bilateral lung volume
reduction in 250 consecutive patients with emphysema. J Thorac Cardiovasc Surg.
Joint Commission Lung Volume Reduction Surgery (LVRS) Certification.
NCDId=119&ncdver=3&bc=AgAAQAAAAAAAAA%3D%3D&. Accessed on April 20,
McKenna RJ Jr, Brenner M, Fischel RJ, et al. Patient selection criteria for lung volume
reduction surgery. J Thorac Cardiovasc Surg. 1997;114:957964.
Fishman A, Martinez F, Naunheim K, et al.; National Emphysema Treatment Trial Research
Group. A randomized trial comparing lung-volume-reduction surgery with medical therapy
for severe emphysema. N Engl J Med. 2003;348:20592073.
National Emphysema Treatment Trial Research Group. Patients at high risk of death after
lung-volume-reduction surgery. N Engl J Med. 2001;345:10751083.
Naunheim KS, Wood DE, Mohsenifar Z, et al.; National Emphysema Treatment Trial Research
Group. Long-term follow-up of patients receiving lung-volume-reduction surgery versus
medical therapy for severe emphysema by the National Emphysema Treatment Trial
Research Group. Ann Thorac Surg. 2006;82:431443.
Naunheim KS. Chapter 20: For whom is lung volume reduction surgery effective? In:
Ferguson M, ed. Difficult Decisions in Thoracic Surgery. 2nd ed. New York, NY: Springer;

7 Lung Volume Reduction: VATS

Thomas K. Varghese Jr.


Among the 17 participating centers in the National Emphysema Treatment Trial (NETT) lung
volume reduction surgery (LVRS) was performed by median sternotomy only at eight centers
and VATS only at three. There were six centers that randomized the approach to LVRS, and
among this subgroup results were comparable with respect to morbidity, mortality, and
functional results. Costs were less for the VATS group as the median hospital length of stay
was 1 day shorter (9 vs. 10 days). Further large-scale randomized clinical trials (RCTs) have
not been performed directly comparing the two techniques, and hence surgeon expertise has
become the major factor in use of VATS.

Indications, contraindications, and preoperative planning are the same as for transsternal
LVRS and are detailed in the previous chapter.

Working IV lines, an arterial line, and a thoracic epidural are often placed at the beginning of
the procedure. A working thoracic epidural is used to ensure adequate pain control thus
allowing for adequate pulmonary toilet in the immediate postoperative period.
After induction of general anesthesia, the patient is first intubated with a single-lumen
endotracheal tube to allow for bronchoscopy. Bronchoscopy in these cases can be used for
pulmonary toilet, to assess airway anatomy and rule out any endoluminal abnormalities. The
single-lumen endotracheal tube is then exchanged for a left-sided double-lumen endotracheal
tube, with bronchoscopic confirmation of its position. Single-lung ventilation is a necessity for
VATS approach. Both sides are operated upon sequentially under the same anesthetic.
The traditional bilateral VATS approach consists of positioning the patient in either the right
or left lateral decubitus position, performance of the procedure, and then repositioning for
the contralateral side. Advantage to this method is clear visualization of the target areas,
while the disadvantage is time needed for repositioning, re-prepping, and draping for the
contralateral side.
The alternative approach is to position the patient supine on a bean bag rolled under the
back and arms that are tucked at its side, and then having the table roll to one side for

performance of the procedure, and then rolling to the other. Advantage to this method is
access to both sides of the chest without changing position. Disadvantages to this method
include the need for larger working incisions, and possible diminished view as flexion of the
bed is not used to open up the intercostal spaces. Our preference is bilateral positioning, but
either method can be used.
The patient is positioned in the full left lateral decubitus position with full flexion of the
operating table to 30 degrees between the nipples and anterior-inferior iliac spine, to open up
the intercostal spaces for introduction of thoracoscopic instruments and the thoracoscope.
Thoracoscopic Port Placement
The chest is prepped and draped in standard surgical fashion. Strategies in VATS cases that
can assist in minimizing chest wall trauma and postoperative pain are utilized, including:
Avoiding use of trocar ports (except for the camera) by introducing instruments directly
through the wound to avoid intercostal nerve compression.
Utilizing an angled 30-degree scope for visualization to avoid torque in the inferior port
Using smaller telescopes (5 mm) when possible.
Intercostal nerve blocks in addition to infiltration with local anesthetic at planned areas of
port sites.
Delivering specimen through the anterior port as the anterior intercostal spaces are wider.
Soft tissues of the incision can be spread with a Weitlaner retractor, but rib spreading is
avoided during the VATS approach.
One-lung ventilation is initiated. The anesthesia team if at all possible should avoid using
PEEP on the down lung if desaturation occurs during the procedure, as this can worsen
ventilation-perfusion mismatch, subject hyperinflated lungs on the down side to barotrauma
with risk of pneumothorax, and obscure view with shift in mediastinum into the field. Ideally
discussion of strategies to deal with desaturation should be done with the anesthesia team
before the start of the procedure.
The anterior port site is placed in the fifth or sixth intercostal space at the anterior axillary
line. A 2 to 3 cm incision is made after infiltration of local anesthetic and intercostal nerve
block. The incision is deepened through the soft tissue and muscle layers, and controlled
entry into the thoracic cavity is made. A gentle sweep is made to confirm absence of any
adhesions in the area. Either the thoracoscope can be inserted at this time to place the
inferior port site under direct vision, or if adequately free, the inferior port can be placed in
similar fashion. Placing a plastic Yankeur through the anterior port site to assess the location
of the diaphragm can help with placement of the inferior port site. Depending on the size of
the 30-degree angled scope used, either a 5 mm or 1 cm incision is made. The inferior port
site is placed in the seventh or eighth intercostal space at the midaxillary line. An additional
posterior port site is placed a fingerbreadth below the tip of the scapula (Fig. 7.1). Additional
ports may be placed if needed for lung retraction, but are rarely necessary. Thoracoscopic
port sites should be at a suitable distance from the target lung area (most often the apex) to
provide space for manipulation. Visualizing a baseball diamond can helpanterior and

posterior ports at first and third base with the camera port at home plate and the target
area of the lung at second base. In female patients, an attempt should be made to
strategically place the ports away from breast tissue to improve cosmesis.

Figure 7.1 VATS LVRS port placement.

Exploration and Mobilization of the Lung

After introduction of the thoracoscopic port and thoracoscope through the inferior port site,
the entire hemithorax is visualized and the target region of emphysematous lung is visualized.
Thoracoscopic ring forceps (Forresters) are introduced to help mobilize the lung. Adhesions
between the lung and adjacent chest wall and mediastinum are carefully lysed with a
combination of sharp and electrocautery dissection. Careful mobilization is performed to
minimize lung injury and subsequent air leak. Larger bulla in target areas that are obscuring
the view can be punctured and collapsed to improve the thoracoscopic view. Care should be
done in these situations if diathermy is utilized for puncturing, to make sure that oxygen is
not being passively introduced into the deflated lung by the anesthesia team to counteract
any desaturation episode.
The inferior pulmonary ligament can be taken down to the level of the inferior pulmonary
vein to help with re-expansion of the lung after resection and filling up of the intrathoracic
Resection of the Target Lung Area
Goals of intervention are to remove areas of lung that are especially damaged by emphysema,
allowing the remaining good lung to expand and work better. When using devices such as
surgical staplers, it is important to always keep in mind the principles of surgeryimportance
of hemostasis, gentle handling of tissue, and application of appropriate tissue compression.
Thoracoscopic forceps can help precompress the lung at the area of planned stapler resection
line (Fig. 7.2). As described in the previous chapter, for upper lobe predominant disease,
about 70% of the right upper lobe, and 2/3 of the left upper lobe are removed during the

The endoscopic stapler is introduced through the anterior port site (Fig. 7.3). Endoscopic
stapler options include use of staplers with buttress reinforcement (such as bovine pericardial
strips), or utilization of staplers adapted for use with thick tissues such as the Endo GIA TriStaple and Echelon Endopath staplers. Staple lengths encompassing 4.8 mm thickness are
used for lung resection. (Black load [4 to 4.5 to 5 mm] for the Endo GIA Tri-Staple and Green
load [4.8 mm] for Echelon Endopath staplers.) Care should be taken to not cross staple lines,
as this will lead to staple malfunctioning and air leaks. For the right lung, multiple firings of
the stapler are performed, typically straight across the upper lobe beginning medially above
the hilum and ending just above the upper extent of the oblique fissure. Care is taken not to
cross the staple lines so as to avoid compromise of the remaining middle and lower lobes.

Figure 7.2 Compression of the lung along the planned resection line with the aid of thoracoscopic ring forceps.

Inspection of Staple Lines and Completion of Procedure

Staple lines, areas where adhesiolysis were performed and port sites are inspected for
hemostasis. Some have advocated for the use of biologic sealants over the staple lines, but
this should not be an attempt to make up for poor surgical technique or technical failure. The
thoracoscope is removed from the inferior port site and introduced through the posterior port.
An anterior apical chest tube (24 or 28 French) is introduced through the anterior port and
directed anteriorly and apically. A 28-French chest tube is introduced through the old inferior
port and directed posteriorly and apically. Chest tubes are secured to the chest wall, and
connected to Pleur-Evacs. The lung is re-expanded under direct vision confirming adequate
re-expansion of the remaining lobes. The thoracoscope is removed. Remaining thoracoscopic
port sites are closed in layers, sterile dressings are placed.

Figure 7.3 Right VATS LVRS. Endoscopic stapler is introduced through the anterior port site.

Figure 7.4 Left VATS LVRS.

The patient is then repositioned in the contralateral right lateral decubitus position, taking
care to appropriately pad all the pressure points. The chest is prepped and draped, and the
procedure is repeated on the contralateral side in the same manner as described above. For
upper lobe predominant disease of the left lung, the lingula is spared, and the upper 2/3 of
the lung is resected with the line of excision parallel to the oblique fissure (Fig. 7.4). Care is
taken to avoid crossing the fissure into the superior segment of the lower lobe, as this will
lead to compromise in ability to re-expand at the completion of the procedure.
After completion of bilateral LVRS, the patient is returned to the supine position. A chest xray can be performed prior to extubation, or shortly after arrival to the recovery room. If
postop chest x-ray demonstrates full re-expansion, the chest tubes can be put on water seal.

Principles of standard thoracic postoperative management are followed including:
Early ambulation.
Transition from epidural analgesia to oral pain medications in 48 to 72 hours that provide
adequate analgesia.
Pulmonary toilet measures (which had begun preoperatively) such as deep breathing,
coughing, use of incentive spirometry, and handling of secretions.
Nebulized bronchodilator therapy is initiated in the early postoperative period to minimize
airway reactivity, and transitioned to inhalers as needed.
Nutritional assessment and intervention is important, as it aids in healing.
Systemic steroids may be needed in the perioperative period.
Unlike other thoracic surgical procedures, early water seal is the norm, and can be started
with expansion of the lung even in the presence of an air leak. Chest tubes are removed once
air leaks resolve and output has minimized, in the standard fashion. Those with persistent air
leaks in the postoperative period may be transitioned to Heimlich valve as long as the lung
remains expanded on water seal, output is minimal, and the patient is able to care for the
drain in the postdischarge setting.

Complications are similar for both transsternal and VATS LVRS, and are described in the
previous chapter.

Mid-term and long-term results of NETT demonstrated clinically significant improvements in
spirometry, lung volumes, diffusing parameters, oxygenation, quality of life, dyspnea, exercise
capacity, and long-term survival. Results are similar for both the VATS and Transsternal
techniques, and are detailed in the previous chapter.

LVRS is a surgical technique that involves selective reduction of lung volume by excision of
tissue in areas where the emphysematous changes are pronounced. The choice between
transsternal and VATS approaches is most commonly a result of surgeon expertise and
patient preference. For both techniques a thoracic epidural is placed to enable adequate
postoperative analgesia, thus facilitating deep breathing, coughing, early mobilization, and
adequate pulmonary toilet.
The amount of tissue resected is 20% to 35% of each lung, which for upper lobe

predominant disease is 75% of the right upper lobe, and 2/3 of the left upper lobe.
LVRS can lead to modest improvement in spirometry, lung volumes, diffusing parameters,
oxygenation, quality of life, dyspnea, exercise capacity, and long-term survival. Key to
success is strict patient selection criteria, optimizing patients preoperatively, and aggressive
postoperative management to minimize the occurrence of complications.
Complications postoperatively include persistent air leak, reintubation, prolonged
mechanical ventilation, pneumonia, wound infection, arrhythmias, and less commonly
myocardial infarction, DVT, PE, and death.
Majority of patients are extubated in the operating room. Effective management of pain,
pulmonary toilet, early ambulation, and management of secretions are key steps in
minimizing complications.

Recommended References and Readings

Brantigan OC, Mueller E. Surgical treatment of pulmonary emphysema. Am Surg.

Cetinag IB, Boley TM, Magee MJ, et al. Postoperative gastrointestinal complications after lung
volume reduction operations. Ann Thorac Surg. 1999;68:10291033.
Ciccone AM, Meyers BM, Guthrie TJ, et al. Long-term outcome of bilateral lung volume
reduction in 250 consecutive patients with emphysema. J Thorac Cardiovasc Surg.
Joint Commission Lung Volume Reduction Surgery (LVRS). Certification
McKenna RJ Jr, Brenner M, Fischel RJ, et al. Patient selection criteria for lung volume
reduction surgery. J Thorac Cardiovasc Surg. 1997;114:957964.
National Emphysema Treatment Trial Research Group. A randomized trial comparing lungvolume-reduction surgery with medical therapy for severe emphysema. N Engl J Med. 2003;
National Emphysema Treatment Trial Research Group. Patients at high risk of death after
lung-volume-reduction surgery. N Engl J Med. 2001;345:10751083.
Naunheim KS. Chapter 20: For whom is lung volume reduction surgery effective? In:
Ferguson M, ed. Difficult Decisions in Thoracic Surgery. 2nd ed. New York, NY: Springer;
Naunheim KS, Kaiser LR, Bavaria JE, et al. Long-term survival after thoracoscopic lung
volume reduction: A multi-institutional review. Ann Thorac Surg. 1999;68:20262031.
Naunheim KS, Wood DE, Mohsenifar Z, et al. Long-term follow-up of patients receiving lungvolume-reduction surgery versus medical therapy for severe emphysema by the National
Emphysema Treatment Trial Research Group. Ann Thorac Surg. 2006; 82:431443.

8 Monaldi Procedure

Tad Kim and Pierre de Delva

Bullous emphysema is characterized by cystic degeneration of the lung parenchyma. The

distribution of bullous emphysema can be focal or diffuse. These cystic airspaces can expand
to occupy a significant portion of the pleural cavity and, in the case of focal disease, restrict
ventilation of adjacent functional lung tissue. Giant bullae occupy greater than 30% of the
chest cavity and can cause significant dyspnea and hypoxia due to compression of functional
adjacent lung, air trapping, loss of airway elastic recoil, and impaired diaphragmatic function.
It has long been recognized that resection or decompression of giant bulla can improve
respiratory mechanics and symptoms in selected patients with giant bullous emphysema.
Bullectomy, performed by thoracoscopy, thoracotomy or sternotomy, is an accepted
method of management in patients with significant symptoms. Some patients with giant
bullae have limited pulmonary reserve and will not tolerate either single lung ventilation
required for thoracoscopy or the pulmonary compromise associated with a transthoracic
resection. Furthermore, bullectomy often sacrifices some functional lung tissue and, despite
buttressed staple lines, can be complicated by prolonged air leak. In certain situations,
drainage of the bulla can achieve similar improvements in respiratory mechanics without the
disadvantages of bullectomy.
Intracavitary intubation and suction drainage was initially described by Monaldi in 1938
for decompression of pulmonary abscess cavities with post-tuberculous infection. The
procedure was designed as a minimally invasive alternative for patients who would not
tolerate resection, thoracoplasty, plombage, or pneumothorax therapy. Monaldi recognized
that a pulmonary cavity originates from the destruction of lung tissue, resulting in the
formation of the initial pathologic space. The driving force behind the persistence and
expansion of the cavity can be due to biologic factors such as persistent infection or, as in the
case of giant bullae, mechanical expansion due to the weakened wall of the cyst and
pressurization by the communicating bronchus. Crucial to the permanent closure of cystic
cavities of the lung by drainage requires control of the infected space, collapse of the cyst,
obliteration of the feeding bronchi, and the creation of pleural adhesions to prevent
pneumothorax. The original Monaldi procedure and several modified techniques were
designed to achieve these goals.
Details of the current technique are to follow, but the original Monaldi procedure was a
staged operation designed to manage infected cyst. The cavity was localized by radiographs,
needle decompression, and exploration. A small incision was made over the cyst. A limited
segment of rib was resected, and the pleura was opened. The wound was packed to induce
pleural adhesions. One to two weeks later, a catheter was placed within the cavity for
drainage. Monaldi employed a mixture of charcoal, keratin, and collodion to achieve
obliteration of the cavity and feeding bronchus. The small bronchocutaneous fistula created
by the drainage catheter invariably healed after removal of the catheter.
Several authors have applied the principles of the Monaldi procedure to the management of
symptomatic giant bullae. The advantages of intracavitary drainage include a limited incision,
short anesthetic time, preservation of lung tissue, and low risk of persistent air leak.

Goldstraw and colleagues from the Brompton Hospital in the United Kingdom reported the
modification of the Monaldi technique into a single-stage procedure for the management of
symptomatic giant bullae. Their results demonstrate subjective symptomatic relief, objective
improvement in pulmonary function testing, and reasonable operative mortality. The
Brompton technique with slight modifications by other authors represents the modern
approach for intracavitary drainage of giant symptomatic bullae.

Historical indications for the Monaldi procedure include decompression of post-tuberculous
and pyogenic pulmonary abscess cavities. Image-guided percutaneous drainage has become
the treatment of choice for pulmonary abscesses that do not resolve with systemic antibiotics.
The modified Monaldi procedure for giant bullous emphysema (Brompton technique) is
currently indicated for patients meeting the following criteria:
1. Dominant, discrete bullous lung disease encompassing 30% or more of the pleural space
and with functional surrounding lung parenchyma.
a. The cyst should have a small number of septations to ensure complete drainage with one
or two drainage catheters.
2. Disabling dyspnea.
Absolute contraindications for a modified Monaldi procedure include:
1. No viable or functional lung surrounding the bulla.
2. Diffuse, nonparaseptal emphysema.
Relative contraindications include:
1. Mild symptoms
2. FEV1 less than 350 mL (due to higher mortality risk)

Evaluation includes history and physical examination, documentation of severity of dyspnea
and pulmonary impairment and smoking cessation. Pulmonary rehabilitation for up to 6
weeks with deep breathing exercises, coughing exercises, incentive spirometry, and out-ofbed activity has been shown to be beneficial in preoperative patients with advanced
Preoperative workup includes:
1. Chest radiograph
2. CT scan of the chest
3. Pulmonary function tests (including lung volumes by whole body plethysmography,
spirometry, and diffusion capacity)
4. Arterial blood gas
The most important aspect of the preoperative plan is selecting the appropriate patients

based on severity of symptoms and CT imaging. Patients with dominant giant bulla with
limited septations and compressed functional lung tissue are the ideal candidates for this
procedure (Fig. 8.1).

Figure 8.1 Sagittal and coronal computed tomography images of the chest demonstrating a giant bulla compressing the right
lower lobe and flattening the diaphragm.

The airway strategy is flexible with the modified Monaldi procedure and depends on the
ability of the patient to tolerate single lung ventilation. Airway management strategies
1. Spontaneous breathing with local anesthetic
2. Double lung ventilation via single-lumen tube
3. Double lung ventilation via single-lumen tube with intermittent apnea
4. Single lung ventilation via double-lumen tube or bronchial blocker
Fiberoptic bronchoscopy may be performed to assess the anatomy of the tracheobronchial
tree and obtain cultures.


The patient is placed in the optimal position to provide access to the bulla. The location of
the incision is based on CT imaging and can be landmarked by the specific interspace or rib
overlying the bulla.
Technique of the Modified Monaldi Procedure
The operative steps for the single-stage modified Monaldi procedure for decompression of

giant bullae are:

1. A small incision is made directly over the most dependent portion of the bulla as
determined by preoperative imaging or with assistance of thoracoscopy (Fig. 8.2).
a. Thoracoscopy of the pleural space can aid in selecting a site for drainage of the incision
and free up the lung from pleural adhesions.

Figure 8.2 Sagittal view of the chest wall demonstrating localization of the incision based on a rib overlying a dependent
portion of the giant bulla (light gray).

2. Subperiosteal excision of a limited segment of rib to allow visualization and adequate

exposure of the underlying pleura (Fig. 8.3).
3. The parietal pleura and bulla are incised.
4. A 3-0 polypropylene purse-string suture is placed in the bleb itself or, if the tissue is too
friable, reinforced by incorporating the parietal pleura in the purse-string suture (Fig. 8.4).
5. A finger may be inserted to lyse septations within the dominant bulla.
b. Insertion of a 5-mm thoracoscope into the cyst cavity can aid in full exploration of the
bulla. This can be accomplished by securing a thoracoport through the purse-string
incision and inserting the camera inside the cavity. Thin thoracoscopic instruments can
be used to lyse intracavitary septations.
6. A 32-Fr Foley catheter (the intracavitary drain) is inserted and the cavity insufflated with
talc via the Foley, and then the purse string is secured down with the balloon of the Foley
flush against the chest wall (Fig. 8.5).
7. A dependent intrapleural tube thoracostomy is placed to decompress the pleural space (Fig.
8.6). Talc may be applied to the pleural space intraoperatively or in the postoperative
period if there is concern for the total dosage of talc given to the patient in one setting.
8. The Foley catheter may be brought out through the incision or through a short tunnel
adjacent to the incision.
9. Both the intracavitary drain and the pleural chest tube are placed to suction.

Figure 8.3 Skin incision and subperiosteal excision of a small portion of the rib overlying the bulla.

Figure 8.4 Placement of the purse-string suture and incision of the bulla.

Figure 8.5 Intracavitary Foley catheter inserted into the bulla and secured with the purse-string suture.

Figure 8.6 Sagittal view of the chest wall demonstrates placement of the intracavitary and pleural drains.

Postoperatively, the intrapleural drain is kept on 20 cm suction for 2 days and then removed
when the air leak has stopped. The intracavitary drain is kept on suction for 2 days but may
be water sealed with a persistent air leak if the cavity is collapsed on imaging. Once the
patient is ambulating with adequate pain control, the patient can be discharged with the
intracavitary drain (Foley) on a one-way valve container (i.e., Heimlich valve) for 1 to 2
weeksallowing for formation of a controlled bronchocutaneous fistula. The intracavitary
drain can be removed after 7 to 14 days, irrespective of residual air leak. The
bronchocutaneous fistula usually closes within 24 to 48 hours.


Complications of the Monaldi procedure include mortality (due to the high-risk nature of
these patients with such poor preoperative pulmonary function), pulmonary complications
such as pneumonia or pleural space infection, and recurrence of pneumothorax due to
additional bullae. Future pneumothoraces due to residual bullae can be managed with
percutaneous pigtail catheter drainage, as the intrapleural talc administration at the index
operation should promote adhesion formation and decrease the likelihood of lung collapse.

Operative mortality with the modified Monaldi procedure ranges from 6.5% to 15%.
This procedure is associated with radiographic improvement in 97%. Objective
improvement in pulmonary function (FEV1 and vital capacity) has been observed in 83% of
cases. More importantly, symptomatic relief can be expected in well-selected patients. Shah et
al. updated the results with the Brompton technique in 1994 and reported symptomatic relief
in 90% of patients; average FEV1 increased by 28%, and average total lung capacity increased
by 12%. Venn et al. demonstrated operative mortality of 3 of 20 (15%) due primarily to low
preoperative FEV1 (median 350 mL). Symptomatic improvement was reported in 16 of the
remaining 17 surviving patients (94%) with 22% median improvement in FEV1, 11% median
reduction in total lung capacity, and 26% median reduction in residual volume.

Due to the high morbidity (up to 50%) with bullectomy or resectional procedures in patients
with poor pulmonary reserve, the Monaldi procedure is an excellent minimally invasive
option for patients with large, dominant bulla and disabling dyspnea. The current Brompton
modification of the Monaldi procedure is a safe and effective alternative to achieve successful
and complete decompression of giant bullous cavities with subsequent expansion of adjacent
lung and symptomatic improvement.

Recommended References and Readings

Cope JH. Monaldi procedure. Calif Med. 1950;73:563564.

Froeschle P, Krishnadas R, Berrisford R. Video-assisted approach combined with the open
Brompton technique for intracavitary drainage of giant bullae. Thorac Cardiovasc Surg.
Greenberg JA, Singhal S, Kaiser LR. Giant bullous lung disease: Evaluation, selection,
techniques, and outcomes. Chest Surg Clin N Am. 2003;13:631649.
Head JR. Intracavitary (Monaldi) suction. J Thorac Surg. 1946;15:153161.
Kelley WO, Pecora DV. The Monaldi procedure; a report of thirty cases. Am Rev Tuberc.
MacArthur AM, Fountain SW. Intracavitary suction and drainage in the treatment of
emphysematous bullae. Thorax. 1977;32:668672.
Monaldi V. Endocavitary aspiration; its practical application. Tubercle. 1946;28:223228.

Monaldi V. Endocavitary aspiration in the treatment of lung abscess. Dis Chest. 1956;29:193
Shah SS, Goldstraw P. Surgical treatment of bullous emphysema: Experience with the
Brompton technique. Ann Thorac Surg. 1994;58:14521456.
Suzuki C. Treatment of pulmonary tuberculosis by Monaldi transthoracic cavity suction
drainage with thoracoplasty. Tohoku J Exp Med. 1950;52:7786.
Venn GE, Williams PR, Goldstraw P. Intracavitary drainage for bullous, emphysematous lung
disease: Experience with the Brompton technique. Thorax. 1988;43:9981002.
Vergeret J, Dabadie P, Dupon M, et al. Endocavitary drainage (Monaldis technique) in the
treatment of pulmonary abscess. Rev Fr Mal Respir. 1983;11:201207.
Wang H, Xu Z, Gao W. A modified Brompton technique for the treatment of giant bulla in
patients with diffuse emphysema. Thorac Cardiovasc Surg. 2012;60:161163.

9 Cavernostomy (Aspergilloma)
Francis C. Nichols

Aspergillus encompasses over 350 known species including Aspergillus fumigatus, Aspergillus
flavus, Aspergillus niger, and Aspergillus terreus which are the most common pathogenic species.
With increasing frequency, Aspergillus species are being recognized as an important cause of
life-threatening infections in immunocompromised patients. The ever expanding population
of immunocompromised patients includes patients with prolonged neutropenia, advanced
human immunodeficiency virus (HIV) infection, and inherited immunodeficiency; patients
having undergone hematopoietic stem cell transplantation and lung transplantation.
Aspergillosis is now the third most common systemic fungal infection requiring
hospitalization in the United States. Pulmonary aspergillosis was classified into allergic,
invasive, and saprophytic infections in 1952 by Hinson et al. Clinical manifestations of
pulmonary Aspergillus infection include:
1. A localized form, aspergilloma, which is an opportunistic infection most commonly found
in individuals with pre-existing lung disease
2. Allergic bronchopulmonary aspergillosis, which is secondary to a complex immunologic
response to exposure to noninvasive Aspergillus species
3. Disseminated aspergillosis, which occurs in immunosuppressed individuals
Pulmonary aspergilloma is the most common form of Aspergillus infection. Aspergilloma
occurs when a pre-existing pulmonary cavity is colonized by the fungus producing a complex
mass of septate hyphae, blood elements, and debris commonly referred to as a mycetoma or
fungus ball. While the true incidence of aspergilloma is unknown, various cavitary lung
diseases including bullous emphysema, fibrotic lung disease, histoplasmosis, sarcoidosis, and
tuberculosis can be a predisposing factor in their formation.
It is generally believed that systemic antifungal agents are ineffective for aspergilloma.
Surgical intervention for aspergillosis occurs in two distinct circumstances: Lung biopsy for
the diagnosis of invasive aspergillosis in an immunocompromised patient and resection for
complications of aspergilloma. There are no randomized controlled trials addressing the best
treatment of aspergilloma. Literature focusing on aspergilloma treatment consists primarily of
isolated case reports and retrospective case series. The major surgical indication for patients
with aspergilloma is severe or recurring hemoptysis. Thirty percent of patients with even
minor hemoptysis can progress to massive life-threatening hemoptysis with an associated
25% mortality. Daly et al. from our group in 1986 reported on the results of surgical
treatment for pulmonary aspergilloma. Underlying chronic lung disease or immunologic risk
factors were present in 92% of patients. The most common indication for operation was an
indeterminate mass, hemoptysis, or chronic cough. In Dalys series, all aspergillomas were

classified as either simple or complex. Simple aspergillomas had thin-walled cysts with little
surrounding lung disease. Complex aspergillomas had thick-walled cavities usually greater
than 3 mm, with substantial surrounding lung disease and/or associated infiltrates. While in
our series, the most common procedures performed were lobectomy (45%), pneumonectomy
(17%), wedge excision (15%), and segmentectomy (11%); cavernostomy with muscle
transposition was performed in six patients (11%). Postoperative complications were more
common in patients with complex aspergilloma than among those with simple. It was noted
that to reduce operative complications in some of our patients with complex aspergillomas,
six were treated with cavernostomy and obliteration of the cavity with intrathoracic
transposition of extrathoracic skeletal muscle. Others too have advocated cavernostomy with
or without muscle flap transposition in patients with limited respiratory function or poor
general condition as a safe method to effectively treat aspergilloma and prevent recurrence of
The goal of aspergilloma surgery is limited resection resulting in removal of all diseased
tissue sparing more normal lung parenchyma. For simple aspergilloma in patients with
reasonable performance status and adequate pulmonary reserve, resection (e.g., wedge,
segmental, lobectomy, rarely pneumonectomy) of the aspergilloma is the procedure of choice.
Cavernostomy is an option for the management of peripheral complex aspergilloma in highrisk patients. The principal contraindications to cavernostomy are technical and relate to the
location of the aspergilloma or the amount of afflicted lung. For example, very medially
situated aspergillomas or those central within the lung far removed from the visceral pleural
surface are not good candidates for cavernostomy.

The natural history of aspergilloma may be highly variable; therefore, the initial management
of a patient depends on the clinical presentation. While surgical resection is the preferred
curative treatment for aspergilloma, cavernostomy with muscle transposition may be the best
option for the most challenging higher-risk patients. Among these patients are those with
severe hemoptysis and severe lung destruction with a high risk of morbidity. Cavernostomy
may also be the most reasonable alternative in patients with more isolated peripheral
aspergilloma but poor performance status and limited pulmonary reserve. Depending on the
patients presentation, appropriate resuscitation is undertaken and respiratory support
provided as needed. When a patient presents with mild nonlife-threatening hemoptysis or
cough, initial management can be conservative including humidified oxygen, cough
suppression, and postural drainage. These patients require close follow-up. Flexible
bronchoscopy should be performed to rule out more serious causes of airway bleeding or
cough. In cases of severe hemoptysis, bronchoscopy should quickly be performed to identify
the bleeding site. Intrabronchial instillation of iced saline with or without epinephrine may
temporarily stop the bleeding. If the bleeding is massive, balloon occlusion of the bleeding
airway may be helpful. Alternatively, double-lumen endotracheal tube intubation may be

necessary for isolation of the bleeding lung and to protect the contralateral lung from
aspiration of blood. Bronchial artery embolization may be helpful in initially stopping most
bleeding. We often consider embolization a temporizing measure. Bleeding can recur in
greater than 50% of cases due to the existence of an extensive array of collateral vessels.
Embolization, however, may obviate the need for emergent surgical intervention in this highrisk population.
Mandatory prerequisites to successful cavernostomy command adequate lung debridement,
closure of all bronchial openings, avoidance of contamination of the surrounding pleural
space, and the ability to dependably transpose extraskeletal muscle intrathoracically. It is our
strong belief that these essential items are most safely accomplished by the collaborative
efforts of a thoracic and plastic surgeon. Intrathoracic muscle transposition requires the
consideration of several factors: Location and size of the exposed cavity, general condition of
the patient, condition of the transposed muscle (e.g., previous radiation or surgery), patients
lifestyle, and type of work. The serratus anterior, latissimus dorsi, and pectoralis major
muscles are all ideally suited for intrathoracic transposition. These muscles all have one
major dominant vascular pedicle high in the thoracic inlet and of sufficient length to reach
most intrathoracic locations. Furthermore, these muscles are of sufficient size to obliterate
most pleural spaces. While not common, pectoralis minor and trapezius have also been
utilized. Knowing which chest wall muscles are available at the time of cavernostomy and
appropriately protecting these muscles during cavernostomy is important.
Nutritional status is important in this group of patients who are often debilitated and
malnourished from chronic infection. If necessary, nutritional supplementation including
liberal use of enteral feedings should be considered in all of these patients.

There are four basic principles for cavernostomy: (1) adequate lung debridement, (2)
avoidance of contamination of the remaining pleural cavity, (3) closure of all bronchial
openings, and (4) obliteration of the residual pleural space. Our most common approach is
two-staged. The first stage consists of limited chest wall resection, cavernostomy and removal
of the fungus ball, suture closure of any bronchial openings followed by a series of wound
pack changes. Only after successful completion of the first stage is the second stage
undertaken, which specifically includes transposition of a muscle flap to obliterate the
exposed cavity, an additional series of pack changes, and eventual definitive closure of the
chest wall. Gebitekin et al. have reported on a small series of patients with complex
aspergilloma successfully treated with single-stage cavernostomy and myoplasty.
All procedures begin with a team briefing. Surgeons, anesthesiologists, and operating room
personnel are in attendance. Details of the airway management individualized for each
specific patient are a major focus of the briefing. Patient identification, site marking,
procedure verification, and final anesthetic evaluation are completed. Appropriate
intravenous access is established. Epidural catheters are not utilized because of the risk of
contamination. Instead, postoperative pain management most commonly is via a patientcontrolled analgesia (PCA) pump. At least for the initial procedure isolation of the lungs is
achieved by using a double-lumen endotracheal tube. Following intubation, a urinary

catheter and lower extremity sequential compression devices are placed. Subcutaneous
injection of 5,000 units of unfractionated heparin is administered to reduce the risk of deep
venous thrombosis (DVT) and pulmonary embolism. All procedures are done in an open
fashion, in a lateral decubitus position with the affected lungs side up.
First Stage
Rib Resection, Cavernostomy, Closure of Bronchial Fistulae, Wound Packing
The patient is positioned keeping in mind both the location of the aspergilloma and the
extraskeletal muscle that will be transposed to eventually obliterate the cavernostomy
(Figs. 9.1 and 9.2A,B).

Figure 9.1 Chest CT scan of peripheral right upper lobe complex aspergilloma in patient with diffuse emphysematous lung

Figure 9.2 A,B: The three most common extrathoracic muscles transposed intrathoracically are the latissimus dorsi, serratus
anterior, and pectoralis major muscles. All are ideally suited for intrathoracic transposition. A: The latissimus dorsi and
serratus anterior muscles are transposed based on arterial branches arising from the common thoracodorsal pedicle. These
muscles can be used separately or combined on their common vascular pedicle if greater soft tissue volume is necessary to
obliterate the cavity. B: The pectoralis major muscle can be transposed laterally based on the thoracoacromial artery or more
medially when based on perforators from the ipsilateral internal mammary artery.

Figure 9.3 The latissimus dorsi muscle has been divided. The serratus anterior muscle injected with 100 units of botulinum
toxin and then mobilized with the muscles blood supply based on the crossing branch of the thoracodorsal artery. Note the
cavity with aspergilloma immediately beneath the second and third ribs.

The ipsilateral hemithorax is prepared and draped.

Most commonly a transverse incision is utilized. Hundred units of botulinum toxin is
reconstituted with 20 cc of normal saline. In this case the serratus anterior muscle will be
transposed. The latissimus dorsi muscle has been divided low in the incision. The serratus
anterior muscle is injected with 20 cc of botulinum toxin, which temporarily paralyzes the
muscle keeping it flaccid for several weeks. The serratus anterior is mobilized (Fig. 9.3).
The rib over the aspergilloma resected. The cavernostomy performed and the fungus ball
and other debris removed. Appropriate specimens are sent for microbiologic and
histopathologic testing. The length of rib resected must be sufficient for debridement of the
aspergilloma cavity, adequate visualization of the cavity, and wide enough for eventual

muscle transposition. The visceral and parietal pleura around the perimeter of the
cavernostomy site are often tightly fused. Care is taken to avoid separating them thus
preventing contamination of the adjacent pleural cavity. To further aid in visualization and
debridement, an additional segment of rib either immediately above or below can be
removed; nevertheless, avoidance of contamination of the adjacent pleural cavity is
essential (Fig. 9.4).
Any visible vessels are oversewn with 4-0 nonabsorbable monofilament suture. Due to the
often fragile tissue surrounding the vessels, small pieces of extraskeletal muscle or biologic
mesh may be used as pledgets to buttress the vessel closures.
Small bronchial fistulas are looked for by filling the cavernostomy site with saline, applying
positive pressure ventilation, and observing for escape of air bubbles from the surrounding
lung parenchyma. This testing requires appropriate adjustment of the double-lumen tube.
All bronchial fistulas are closed using interrupted 3-0 or 4-0 nonabsorbable monofilament
sutures. Due to the often fragile tissue surrounding the fistula, small pieces of extraskeletal
muscle or biologic mesh may be used as pledgets to buttress the fistula closures (Fig. 9.4).

Figure 9.4 Portions of the second and third ribs have been resected and the aspergilloma cavity immediately beneath those
ribs opened. The fungus ball and debris removed and the cavity sharply debrided. Several small bronchial openings are seen,
which need to be closed with 4-0 nonabsorbable monofilament suture. The cavity is then gently pulse irrigated with normal
saline and then irrigated with amphotericin B. If a two-stage approach is being utilized, the wound is packed with DABS and
amphotericin Bdampened gauze. If a single-stage cavernostomy and myoplasty is done, the serratus muscle is placed into
the cavity at this time obliterating the space.

The cavernostomy site is gently pulsatile irrigated with normal saline followed by irrigation
with amphotericin B. It is important that all bronchial fistulas are closed before irrigating
with amphotericin B, which is a sclerosant. After assuring hemostasis, the cavernostomy
cavity is then packed with gauze rolls damply moistened with debridement antibiotic
solution (DABS) (20 mg gentamicin and 500,000 units of polymixin B per liter of 0.9%
sodium chloride solution) and amphotericin B. The mobilized serratus anterior muscle is
placed back into its anatomic position and loosely covered with additional antibioticsoaked gauze.
The patient is returned to the operating room in 48 hours. The cavernostomy cavity again
assessed for open bronchial fistulas, which if found are further repaired, sharply debrided,

and hand-held pulse irrigated. The site is again assessed for open bronchial fistulas, which
if found are repaired. The cavernostomy site is oftentimes clean enough for muscle
transposition at this point. If the site is not adequately clean, it is again packed with gauze
rolls lightly saturated with DABS and amphotericin B. The ultimate goal for this first stage
is a clean cavernostomy site, with closed bronchial fistulas, and granulation tissue
beginning to form.
Second Stage
Obliteration of the Cavernostomy and Closure of the Chest Wound
Once the cavernostomy site appears clean enough, the previously mobilized muscle flap is
placed into the cavernostomy cavity effectively obliterating that space. To prevent
displacement, the muscle flap may be secured to the surrounding ribs and soft tissue with
interrupted 3-0 nonabsorbable monofilament (Fig. 9.5).
The patient then undergoes over a period of 1 to 1.5 weeks a series of sharp wound
debridements, hand-held pulsatile irrigations, and dressing changes with gauze rolls lightly
saturated in DABS and amphotericin B.
The debridements and dressing changes take place in the operating room every 48 hours
until the transposed muscle is sufficiently adherent after which the pack changes can often
take place in the patients hospital room utilizing if necessary monitored conscious
The wound is ready for definitive closure when there is no evidence of bronchial air
leakage, the muscle flap is adherent and growing into place, and the wound is clean and
covered with healthy granulation tissue. Final wound tissue cultures are not used to
determine the timing of wound closure, but may be obtained to guide postclosure systemic
antibiotic therapy.

Figure 9.5 The serratus anterior has been placed into the cavity effectively obliterating the space. If a two-stage approach is
being utilized the wound is packed with DABS and amphotericin Bdampened gauze. If a single-stage cavernostomy and
myoplasty is being done, a large drain placed and the skin closed.

Figure 9.6 The wound is closed over a large drain utilizing interrupted 3-0 or 4-0 nonabsorbable monofilament vertical
mattress sutures evenly spaced along the wound.

The wound is closed over a large drain utilizing interrupted 3-0 or 4-0 nonabsorbable
monofilament vertical mattress sutures evenly spaced along the wound (Fig. 9.6).
The wound is then covered with large gauze pads held loosely in place with paper tape, and
finally with a long wide elastic wrap, which keeps the dressings atraumatically in place.
Single-Stage Cavernostomy and Myoplasty
Cavernostomy, Muscle Transposition, and Wound Closure in One Procedure
The patient is positioned keeping in mind both the location of the aspergilloma and the
extraskeletal muscle, that will be transposed to eventually obliterate the cavernostomy
(Figs. 9.1 and 9.2A,B).
The ipsilateral hemithorax is prepared and draped.
Most commonly a transverse incision is utilized. 100 units of botulinum toxin is
reconstituted with 20 cc of normal saline. In this case the serratus anterior muscle will be
transposed. The latissimus dorsi muscle has been divided low in the incision. The serratus
anterior muscle is injected with 20 cc of botulinum toxin, which temporarily paralyzes the
muscle keeping it flaccid for several weeks. The serratus anterior is mobilized (Fig. 9.3).
The rib over the aspergilloma is resected. The cavernostomy is performed and the fungus
ball and other debris removed. Appropriate specimens are sent for microbiologic and
histopathologic testing. The length of rib resected must be sufficient for debridement of the
aspergilloma cavity, adequate visualization of the cavity, and wide enough for eventual
muscle transposition. The visceral and parietal pleura around the perimeter of the
cavernostomy site are often tightly fused. Care is taken to avoid separating them thus
preventing contamination of the adjacent pleural cavity. To further aid in visualization and
debridement, an additional segment of rib either immediately above or below can be
removed; however, avoidance of contamination of the adjacent pleural cavity is essential
(Fig. 9.4).
Any visible vessels are oversewn with 4-0 nonabsorbable monofilament suture. Due to the

often fragile tissue surrounding the vessels, small pieces of extraskeletal muscle or biologic
mesh may be used as pledgets to buttress the vessel closures.
Small bronchial fistulas are looked for by filling the cavernostomy site with saline, applying
positive pressure ventilation, and observing for escape of air bubbles from the surrounding
lung parenchyma. This testing requires appropriate adjustment of the double-lumen tube.
All bronchial fistulas are closed using interrupted 3-0 or 4-0 nonabsorbable monofilament
sutures. Due to the often fragile tissue surrounding the fistula, small pieces of extraskeletal
muscle or biologic mesh may be used as pledgets to buttress the fistula closures (Fig. 9.4).
The cavernostomy site is gently pulsatile irrigated with at least 3 L of normal saline
followed by irrigation with amphotericin B. It is important that all bronchial fistulas are
closed before irrigating with amphotericin B, which is a sclerosant.
The previously mobilized muscle flap is placed into the cavernostomy cavity effectively
obliterating that space. To prevent displacement, the muscle flap may be secured to the
surrounding ribs and soft tissue with interrupted 3-0 nonabsorbable monofilament (Fig.
The wound is closed over a large drain utilizing interrupted 3-0 or 4-0 nonabsorbable
monofilament vertical mattress sutures evenly spaced along the wound (Fig. 9.6).
The wound is then covered with large gauze pads held loosely in place with paper tape, and
finally with a long wide elastic wrap, which keeps the dressings atraumatically in place.

Cavernostomy patients should go to a unit skilled in the management of patients who have
undergone complex general thoracic surgery. Following the initial procedure, the majority of
these patients are successfully extubated. Most of our patients following the initial first-stage
procedure are successfully managed in our general thoracic surgical progressive care unit
(PCU). Only rarely are these patients kept intubated and managed in our general thoracic
surgical intensive care unit (ICU). Following subsequent first-stage procedures, depending on
patient-specific circumstances, the patients are managed in the PCU or on the general
thoracic surgical floor. Standard orders should not be routinely implemented without
consideration of specific individualized patient needs; nevertheless, we strive to follow unit
specific care pathways. These pathways routinely contain patient monitoring, supplemental
oxygen therapy, intravenous fluids, medications including appropriate pain management,
wound care, chest physiotherapy by trained respiratory therapists, physical therapy, diet,
patient and family education, social services, and when appropriate discharge planning.
Following second-stage definitive chest closure, the care pathway is continued and adjusted
accordingly. Wound care most commonly involves daily drain care and adjustments to the
elastic wrap. The large gauze pads are changed every 24 to 48 hours and along with the
elastic wrap continued for several weeks. The patient may shower starting in 5 days. Removal
of the monofilament sutures is individualized to the patients wound status and they routinely
remain for several weeks. The large drain is removed when there is no evidence of air leakage
and drainage is less than 20 cc per day for 2 consecutive days. In general, the 3-0 sutures
remain for at least 2 to 3 weeks and the 4-0 sutures are removed after 4 to 5 weeks.
Oral antifungal agents are begun in the perioperative period and commonly continued for 3

to 6 months. Over the past decade there has been a considerable expansion in the number of
antifungal medications available for clinical use. Specific antifungal medications and use of
other antimicrobial agents may be influenced by intraoperative cultures and consultation
with infectious disease specialists for these oftentimes immunocompromised and debilitated

Literature focusing on cavernostomy as treatment for aspergilloma consists primarily of
isolated case reports and retrospective case series often reported as subsets of more
encompassing retrospective reviews on the surgical management of aspergilloma. Specific
data related to complications is sparse and one must keep in mind that cavernostomy is
reserved for patients with poor overall performance. Nonetheless, it seems that intraoperative
complications during cavernostomy are rare. Regnard et al. reported on 17 patients having
cavernostomy. Complications included postoperative significant hemorrhage and prolonged
ventilation (>48 hours) in one patient (5.8%) each. There were no deaths in the
cavernostomy patients. Babatasi et al., in eight cavernostomy patients, reported postoperative
hemorrhage and prolonged air leakage in 12% and 50% of patients, respectively.
Perioperative mortality occurred in one patient (12.5%). Finally Daly from our institution
reported no deaths in six cavernostomy patients. Gebitekin et al. reported on nine patients
with complex aspergilloma treated with single-stage cavernostomy and muscle transposition,
and found two patients who required re-exploration for massive air leak from occult
bronchial fistulas. They reported no perioperative deaths.

Daly et al. from our institution in 1986 reported on 53 patients having surgery for
aspergilloma. Twenty-one patients (31%) had simple aspergilloma and thirty-two (47%)
complex aspergilloma. Complications occurred in 78% of patients with complex aspergilloma
and in 33% with simple aspergilloma (p = 0.002). Operative mortality was 5% (1 death) in
patients with simple aspergilloma and 34% (11 deaths) in patients with complex
aspergilloma. In an effort to reduce complications in patients with complex aspergilloma,
cavernostomy with obliteration of the cavity and intrathoracic extraskeletal muscle
transposition was utilized in six patients. There were no deaths in the cavernostomy patients
and long-term results were reported as good. Similar results have been reported by others.
Cesar et al. reported on 208 patients with surgically treated aspergilloma over a 32-year
period. One hundred and eleven patients had cavernostomy and 97 pulmonary resections. For
cavernostomy, the cavity was initially packed with gauze containing no antifungal substance.
The cavity was left to spontaneously close and muscle transposition was only performed if the
cavity failed to close after 90 days. The number of muscle transpositions was not reported.
Ten patients (9%) with cavernostomy ultimately required pulmonary resection because of
recurrence. Ten patients (10.3%) with pulmonary resection had a residual space. Infectious
complications were more frequent in pulmonary resection patients 25% versus cavernostomy

patients 7.2%. Recurrence, however, was only seen in cavernostomy patients 8.1%.
Hemorrhagic complications were more common in cavernostomy patients 45% versus
pulmonary resection patients 12%, but hemoptysis was far more frequent preoperatively in
cavernostomy patients 96% compared with 59% of pulmonary resection patients. Patient
progression, which was defined as death and cure were similar between the two groups. Cesar
et al. concluded that older patients with severe preoperative respiratory insufficiency and
peripheral aspergilloma are best served by cavernostomy and the remaining patients best
treated by pulmonary resection.
The results of Gebitekin and colleagues single-stage cavernostomy and myoplasty for
complex aspergilloma are intriguing. There were no perioperative deaths and median hospital
stay was 9 days (range 6 to 15). Eight patients were alive and well without symptoms or
recurrence at mean follow-up of 57.2 months (range: 18 to 83 months). However, this report
only included 9 patients over a 7.5-year timeframe. Worrisome is that two patients (22%)
required re-exploration for massive air leakage.

Cavernostomy with extraskeletal muscle transposition (most commonly latissimus dorsi,
pectoralis major, and serratus anterior) is an alternative treatment to pulmonary resection for
patients with aspergilloma. Patients whose overall medical condition and pulmonary function
are poor with peripheral complex pulmonary aspergilloma may be best treated with
cavernostomy and muscle transposition. Morbidity and mortality of this procedure are low
and long-term results are good.

Recommended References and Readings

Babatasi G, Massetti M, Chapelier A, et al. Surgical treatment of pulmonary aspergilloma:

Current outcome. J Thorac Cardiovasc Surg. 2000;119:906912.
Cesar JM, Resende JS, Amaral NF, et al. Cavernostomy x resection for pulmonary
aspergilloma: A 32-year history. J Cardiothorac Surg. 2011;6:129.
Daly RC, Pairolero PC, Piehler JM, et al. Pulmonary aspergilloma. Results of surgical
treatment. J Thorac Cardiovasc Surg. 1986;92:981988.
Gebitekin C, Sami Bayram A, Akin S. Complex pulmonary aspergilloma treated with single
stage cavernostomy and myoplasty. Eur J Cardiothorac Surg. 2005;27:737740.
Meland NB, Arnold PG, Pairolero PC, et al. Refinements in intrathoracic use of muscle flaps.
Clin Plast Surg. 1990;17:697703.
Regnard JF, Icard P, Nicolosi M, et al. Aspergilloma: A series of 89 surgical cases. Ann Thorac
Surg. 2000;69:898903.
Rergkliang C, Chetpaophan A, Chittithavorn V, et al. Surgical management of pulmonary
cavity associated with fungus ball. Asian Cardiovasc Thorac Ann. 2004;12:246249.
Walsh TJ, Anaissie EJ, Denning DW, et al. Treatment of aspergillosis: Clinical practice
guidelines of the Infectious Diseases Society of America. Clin Infect Dis. 2008;46:327360.

Part II
Chest Wall/Pleural Space/Diaphragm:

10 Chest Wall/Pleural Space/Diaphragm: Thoracic Outlet

SyndromeSupraclavicular Thoracic Outlet
Robert W. Thompson and Chandu Vemuri

Thoracic outlet syndrome (TOS) is a group of relatively uncommon, anatomically related,
conditions caused by compression of neurovascular structures that serve the upper extremity.
The most frequent form is neurogenic TOS (NTOS), which occurs in 85% to 90% of patients,
most typically between the ages of 15 and 40. NTOS is characterized by symptoms arising
from extrinsic compression and irritation of the brachial plexus nerves within the
supraclavicular scalene triangle or within the infraclavicular subcoracoid space beneath the
pectoralis minor muscle tendon (Fig. 10.1). NTOS results in neck and upper extremity pain,
paresthesias, and functional limitations. Clinical recognition and appropriate treatment of
NTOS are crucial to prevent disability in young active individuals (Table 10.1).
NTOS is caused by a combination of two factors: Predisposing anatomical variations and
previous neck or upper extremity injury. The anatomical variations that may predispose to
NTOS include anomalous scalene musculature, aberrant fibrofascial bands, and/or cervical
ribs. Injury superimposed on this anatomical area can subsequently result in
scalene/pectoralis muscle spasm, fibrosis, and other pathologic changes, which in turn lead to
compression and irritation of the adjacent brachial plexus nerves. While the types of injury
precipitating NTOS can include a motor vehicle collision with whiplash-type cervical strain or
a fall on the outstretched arm, NTOS can also arise as a consequence of repetitive strain
associated with frequent heavy lifting, poor posture, overhead use of the arm, or prolonged
work at a computer keyboard. Although the presence of a cervical rib is often considered a
prerequisite to the development of NTOS, only a small proportion of patients (approximately
10%) exhibit a definable cervical rib on radiographic studies, and in the absence of some
form of additional injury, development of symptoms of NTOS remains rare even in patients
with cervical ribs.

Figure 10.1 Anatomy of the thoracic outlet, with emphasis on the supraclavicular scalene triangle and the infraclavicular
subcoracoid space.

Other forms of TOS include compression of the subclavian vein (venous TOS), most often
presenting with the axillarysubclavian vein effort thrombosis (PagetSchroetter)
syndrome. This condition is readily differentiated from NTOS, as it results in marked arm
swelling, cyanotic discoloration, and distention of subcutaneous veins around the shoulder
and chest wall and is not usually associated with pain and paresthesia. The least frequent
form of TOS arises from compression of the subclavian artery with pathologic changes
(arterial TOS), usually in patients with a bony anatomical anomaly (e.g., cervical rib).
Arterial TOS can result in fixed subclavian artery obstruction, resulting in cramping muscular
fatigue with arm use similar to intermittent claudication. More frequently, it leads to
poststenotic subclavian artery aneurysm formation and thromboembolism, hand ischemia,
rest pain, and/or digital ulceration and necrosis. This clinical presentation is also readily
differentiated from that of NTOS. It is important to recognize that positional compression of
the subclavian artery during elevation of the arm is a frequent finding on physical
examination in a substantial number of asymptomatic individuals and should not be
considered evidence for arterial TOS in the absence of established arterial pathology.

TABLE 10.1 Differential Diagnosis of NTOS

Surgical treatment for NTOS can be accomplished effectively by several different

approaches, including transaxillary first rib resection and anterior (supraclavicular)
decompression, with each approach having its advantages and disadvantages. Supraclavicular
decompression for NTOS most frequently involves complete anterior and middle
scalenectomy, first rib resection, and brachial plexus neurolysis. This operation provides
superb surgical exposure, a high degree of safety in experienced hands, and the most
definitive means to address the relevant neurovascular structures, as well as flexibility in
managing the entire spectrum of circumstances that may be encountered.
Supraclavicular decompression is a recommended treatment option for NTOS when the
clinical diagnosis is considered to be sound and the patient has had substantial disability,
with symptoms that interfere with daily activities and/or work. A third criterion for surgical
treatment is that the patient has had an insufficient response to a course of physical therapy
that has been appropriately targeted toward NTOS. Use of the supraclavicular approach to
thoracic outlet decompression is also recommended when there has been no response to
appropriate conservative measures in patients with persistent or recurrent symptoms of NTOS
following a previous operation.1
For individuals with symptoms of disabling NTOS that are referable on physical
examination to the subcoracoid space, the inclusion of pectoralis minor tenotomy is an
important consideration as part of supraclavicular thoracic outlet decompression. In patients
with NTOS in whom nerve compression symptoms appear confined to the subcoracoid space,
pectoralis minor tenotomy may be performed as an isolated procedure.

In the preoperative holding area, the supraclavicular surgical site is confirmed and marked.
The subcoracoid space is included if concomitant pectoralis minor tenotomy is planned.
Prophylactic antibiotics are administered within an hour of the planned procedure.


After general endotracheal anesthesia is induced, the patient is positioned supine with the
head of the operating table elevated approximately 30 degrees. The neck is extended and
turned to the opposite side, and a small inflatable pillow is placed behind the shoulders. The
neck, chest, and affected upper extremity are prepped into the sterile field, and the arm is
wrapped in stockinette to permit free range of movement during the operation (Fig. 10.2).
Lower extremity sequential compression devices are placed for prophylaxis against
A transverse neck incision is made parallel to and just above the clavicle. This begins at the
lateral edge of the sternocleidomastoid muscle and extends to the anterior edge of the
trapezius muscle. The incision is carried through the subcutaneous layer and the platysma
muscle is divided, then subplatysmal flaps are developed to expose the scalene fat pad. The
sternocleidomastoid muscle is retracted medially, but it is not divided (Fig. 10.3).

Figure 10.2 Patient position and planned incisions for left-sided supraclavicular thoracic outlet decompression with
pectoralis minor tenotomy.

Figure 10.3 The skin incision is made just above and parallel to the clavicle, extending from the lateral border of the
sternocleidomastoid muscle to the anterior border of the trapezius muscle (A). Subplatysmal flaps are created to expose the
underlying scalene fat pad (B). The scalene fat pad is mobilized, beginning with its medial attachments to the internal
jugular vein (IJV) (C), and the omohyoid muscle is divided (D).

Mobilization of the Scalene Fat Pad

One of the keys to simplifying the supraclavicular exposure is proper mobilization and lateral
reflection of the scalene fat pad.
The scalene fat pad is initially detached with the electrocautery along the lateral edge of the
internal jugular vein and along the superior edge of the clavicle, while ligating small blood
vessels and lymphatics. The omohyoid muscle is routinely divided. The thoracic duct is
usually identified near the junction of the internal jugular and subclavian veins (this is
more prominent on the left side, but a prominent accessory thoracic duct may also be
found on the right side), and it may be ligated and divided (Fig. 10.3).
Using gentle fingertip dissection, the scalene fat pad is progressively elevated by moving in
a medial to lateral direction, over the surface of the anterior scalene muscle. The phrenic
nerve is identified as it descends along the muscle surface, passing in a lateral to medial
direction, with a dartle (diaphragmatic startle) response elicited by gentle manipulation.

With further lateral mobilization of the scalene fat pad, the brachial plexus nerve roots
(posterior and lateral to the anterior scalene muscle), and the middle scalene muscle
(behind the brachial plexus) are gradually brought into view. The lateral aspect of the first
rib may also be palpated and visualized at this stage. The long thoracic nerve is observed
where it emerges from the body of the middle scalene muscle and passes beyond the lateral
part of the first rib. The mobilized scalene fat pad is then held in position with several silk
retraction sutures. The exposure is further maintained with a Henley self-retaining
retractor, using the third arm to hold the edge of the sternocleidomastoid muscle. This
exposure represents the first and most important of six critical views that should be
obtained during supraclavicular decompression (Table 10.2) (Fig. 10.4).
Anterior Scalenectomy
Attention is next turned to detachment of the anterior scalene muscle from its insertion on
the top of the first rib and subsequent resection of the muscle up to the apex of the scalene
The lower lateral edge of the anterior scalene muscle is dissected where it attaches to the
first rib. The subclavian artery and brachial plexus are carefully mobilized away from the
muscle, until a fingertip can be easily passed behind the muscle just above the first rib to
displace the neurovascular structures posterolaterally. Blunt fingertip dissection is then
continued in front of and behind the muscle to its medial edge, taking care to avoid the
phrenic nerve by gentle medial retraction. Once the insertion of the anterior scalene muscle
onto the top of the first rib has been completely isolated under direct vision, it is sharply
divided from the top of the bone with scissors (Fig. 10.5).

TABLE 10.2 Critical Views Obtained During Supraclavicular Thoracic

Outlet Decompression

Figure 10.4 Following lateral reflection of the scalene fat pad, direct visualization is obtained of the internal jugular vein
(IJV), anterior scalene muscle (ASM), phrenic nerve (PhN), brachial plexus (BP), subclavian artery (SCA), middle scalene
muscle (MSM), and long thoracic nerve (LTN).

The end of the divided anterior scalene muscle is elevated and its attachments to the
underlying extrapleural fascia are sharply divided, avoiding electrocautery to prevent
inadvertent nerve injury. Any muscle fibers extending from the posterior aspect of the
muscle to the subclavian artery are divided to fully release the artery, and any scalene
minimus muscle fibers (which pass between the roots of the brachial plexus) are divided.
The anterior scalene muscle is then passed underneath and medial to the phrenic nerve, to
better visualize and protect the upper brachial plexus nerve roots. The origin of the anterior
scalene muscle on the C6 transverse process is palpated in the upper aspect of the operative
field (the apex of the scalene triangle) and the muscle is divided with scissors under
direct vision. The entire anterior scalene muscle is removed with a typical specimen
weighing 5 to 10 g. Minor bleeding from the edge of the divided muscle origin should be
controlled with a small polypropylene suture rather than electrocautery, given the
proximity of the nerve roots (Fig. 10.5).
Middle Scalenectomy
The brachial plexus nerve roots are next approached at the edge of the middle scalene
muscle. Using blunt fingertip dissection along the lateral aspect of the nerves, the exposure
is extended deeper to the inner curve of the first rib and the extrapleural space. A small
malleable retractor is placed between the brachial plexus nerves and the middle scalene
muscle and with gentle medial retraction of the brachial plexus, each nerve root from C5 to
T1 is sequentially identified (Fig. 10.6).
The transverse cervical artery and vein are usually identified where they pass through the
brachial plexus and middle scalene muscle and should be ligated and divided to avoid

The long thoracic nerve is gently retracted posteriorly, using a second malleable retractor
placed lateral to the middle scalene muscle and the first rib. The attachment of the middle
scalene muscle to the top of the first rib is then clearly exposed and carefully divided with
the electrocautery. A periosteal elevator may be used as the dissection proceeds posteriorly,
to a point parallel with the underlying T1 nerve root. The middle scalene muscle lying
anterior to the long thoracic nerve is sharply excised, with a typical specimen weight of 3
to 8 g (Fig. 10.7). One to two figure-of-eight silk sutures are used along the edge of the
middle scalene muscle to control minor bleeding, avoiding the electrocautery to avoid
thermal injury to the C8 nerve root or long thoracic nerve.

Figure 10.5 The anterior scalene muscle (ASM) insertion is isolated by displacing the underlying subclavian artery (SCA)
and brachial plexus (BP), using blunt fingertip dissection behind the muscle, and the subclavian vein (SCV) from in front of
the muscle, and the muscle is sharply divided from the top of the first rib (ER) (A). The end of the divided ASM is lifted and
sharply dissected free of structures lying behind the muscle, including the SCA (B). As it is mobilized, the ASM is passed
underneath and to the medial side of the phrenic nerve (PhN) (C). The dissection is carried up to the level of the C6
transverse process, where the ASM can be safely divided from its origin and removed (D).

First Rib Resection

Maintaining the exposure used for middle scalenectomy, intercostal muscle attaching to the
lateral edge of the first rib is separated from the bone with the electrocautery. The
posterior first rib is fully exposed where the T1 nerve root emerges from underneath it, to
join the C8 nerve root in forming the lower trunk of the brachial plexus. A right-angle
clamp is passed underneath the posterior neck of the first rib and the instrument is gently
spread to detach additional intercostal tissue, and a modified Giertz-Stille rib cutter is
inserted around the neck of the first rib. After ensuring that the C8 and T1 nerve roots are
well protected the bone is sharply divided, and a Kerrison bone rongeur is used to smooth
the posterior end of the bone. The end of the bone is then sealed with bone wax (Fig. 10.7).

Figure 10.6 The brachial plexus is separated from the anteromedial border of the middle scalene muscle down to the level of
the first rib and extrapleural fascia, and gently retracted medially to visualize all five nerve roots (C5 to T1).

Using blunt fingertip dissection, the remaining extrapleural fascia and intercostal muscle
are separated from the undersurface of the rib, progressing anteriorly to the level of the
scalene tubercle. It is not necessary to avoid opening the pleura during this portion of first
rib resection, as any such opening will promote drainage of postoperative fluids away from
the brachial plexus and thereby help to diminish perineural adhesions.
The subclavian vein and other soft tissues underneath the clavicle are elevated with a small
Richardson retractor. Fingertip pressure is used to displace the posterior part of the first rib
inferiorly, to open the anterior costoclavicular space. The subclavian artery and brachial
plexus are then displaced laterally with a small malleable retractor, and the Giertz-Stille rib
cutter is placed around the anterior first rib (Fig. 10.8). The first rib is then divided under
direct vision immediately medial to the scalene tubercle, and the intact specimen is
extracted from the operative field (Fig. 10.9). A Kerrison bone rongeur is used to remodel
the remaining anterior edge of the first rib to a smooth surface, to a level well underneath

the clavicle. Oxidized cellulose fabric (Surgicel, Ethicon, Inc.) is placed within the bed of
the resected first rib as a topical hemostatic agent.
If a cervical rib is present, it is readily identified within the plane of the middle scalene
muscle, posterior to the brachial plexus and subclavian artery, and anterior to the long
thoracic nerve. An incomplete cervical rib will typically have a ligamentous extension to
the first rib. Thus, the posterior cervical rib will be encountered during dissection of the
middle scalene muscle and divided in the same manner as described for the posterior first
rib. The anterior attachment of the cervical rib is subsequently divided and the bone
removed prior to first rib resection. In contrast, a complete cervical rib will be attached to
the lateral first rib in the form of a true joint. In this event, the anterior portion of the
cervical rib is left attached while the first rib resection is completed, and the two are
removed together as a single specimen (Fig. 10.9).

Figure 10.7 After detaching the middle scalene muscle (MSM) from the top of the posterolateral first rib using the
electrocautery, the muscle tissue lying anterior to the long thoracic nerve (LTN) is excised (A). Typical operative specimens
of the anterior and middle scalene muscles (B). The posterior first rib is exposed with visualization of the C8 and T1 nerve
roots, and the rib is divided with a modified Giertz-Stille rib cutter (C). The posterior edge of the first rib is further
remodeled with a Kerrison rongeur to obtain a smooth edge, immediately medial to the T1 nerve root (D).

Brachial Plexus Neurolysis

Supraclavicular decompression is completed by fully mobilizing the individual nerve roots
contributing to the brachial plexus. Each nerve root from C5 to T1 is meticulously dissected
free of any adherent perineural fibrous scar tissue (external neurolysis). In particular, there is
often a small fibrofascial band overlying the most proximal aspect of the C8 and T1 nerve
roots, which should be specifically sought out and resected (Fig. 10.10).

Figure 10.8 With the posterior end of the first rib pushed downward to open the anterior costoclavicular space, the anterior
portion of the first rib is exposed underneath the clavicle and the subclavian vein (A). The subclavian artery (SCA) and
brachial plexus (BP) are protected, and the anterior first rib is divided with a rib cutter immediately medial to the scalene
tubercle (B).

Pectoralis Minor Tenotomy

Beginning at the level of the coracoid process, a short vertical incision is made in the
deltopectoral groove. The deltoid and pectoralis major muscles are gently separated and
the plane of dissection is carried deeper, medial to the cephalic vein. Using a small Deaver
retractor, the lateral edge of the pectoralis major muscle is gently lifted. The tissue plane
between the pectoralis major and minor muscles is separated by blunt fingertip dissection.
The pectoralis minor muscle is palpated and the overlying fascia is exposed (Fig. 10.11).
The pectoralis minor muscle tendon is identified near its attachment to the coracoid
process. The fascia along its medial and lateral borders is opened and the muscle is
encircled using blunt fingertip dissection, taking care to avoid the short head of the biceps
muscle, which also inserts on the coracoid process. With the underlying neurovascular
bundle well protected, the pectoralis minor tendon is then elevated and its insertion on the
coracoid process is divided with the electrocautery. After the lower edge of the divided
pectoralis minor muscle has retracted inferiorly, releasing any compression of the
neurovascular bundle, it is oversewn with a running silk suture to ensure hemostasis (Fig.

Figure 10.9 Operative specimens following first rib resection (A) and following combined resection of a cervical rib and first
rib (B).

Figure 10.10 Fibrous scar tissue is removed from each of the brachial plexus (BP) nerve roots by external neurolysis (AC).

No further dissection of the brachial plexus nerves or axillary vessels is performed, but the
remaining clavipectoral fascia is incised to the level of the clavicle, along with any other
anomalous fascial bands that might be present over the brachial plexus. The wound is
closed in layers without a drain after infiltrating the edge of the pectoralis major muscle
with a long-acting local anesthetic.
Drain Placement and Closure
At the end of supraclavicular decompression, the pleural apex membrane is opened to
promote postoperative drainage of fluid away from the brachial plexus into the chest cavity.
A closed suction drain is placed into the operative field through a separate stab wound where
it passes posterior to the brachial plexus with its tip extending into the posterior pleural
space. Two multihole perfusion catheters are placed within the wound and connected to an
osmotic pump for continuous postoperative infusion of local anesthetic (0.5% bupivacaine for
3 days). The brachial plexus nerves are wrapped with a bioresorbable polylactide film
(SurgiWrap; Mast Biosurgery) to suppress postoperative perineural fibrosis. After restoring the
scalene fat pad to its anatomic position overlying the brachial plexus, it is held in place with
several silk sutures to the back of the sternocleidomastoid muscle and the periclavicular
fascia. The platysma muscle layer is closed with interrupted sutures and the skin edges are

reapproximated with an absorbable subcuticular stitch.

Figure 10.11 Pectoralis minor tenotomy is performed through a short vertical incision in the deltopectoral groove, just
below the coracoid process (A). The plane of dissection is carried medial to the cephalic vein, and the pectoralis major
muscle is lifted to expose the fascia over the pectoralis minor muscle (B).

Figure 10.12 The pectoralis minor muscle is encircled near its insertion on the coracoid process and then divided with the
electrocautery (A). The retracted edge of the divided pectoralis minor muscle is oversewn with a continuous suture (B).

An upright chest radiograph is performed in the recovery room. Any small air or pleural
fluid collections are observed with the expectation of spontaneous resolution. Continuous-

infusion perineural local anesthesia is used for pain control until postoperative day 3, along
with patient-controlled intravenous opiates. The expected postoperative hospital stay is 3 to
4 days and at hospital discharge, an oral opioid, muscle relaxant, and nonsteroidal antiinflammatory agent are routinely prescribed and continued for several weeks. The closed
suction drain is typically removed in the outpatient office 5 to 7 days after surgery when its
output is less than 50 mL per day.
The day after surgery, physical therapy is resumed to maintain range of motion and limit
muscle spasm. No sling or other restraint is used on the upper extremity and the patient is
allowed to use the extremity as tolerated. After hospital discharge, physical therapy is
continued and the patient is advised to avoid excessive reaching overhead, heavy lifting
with the affected upper extremity, and other activities that might result in muscle strain,
spasm, and significant pain. Beginning 3 to 4 weeks after surgery, further rehabilitation is
overseen by a physical therapist with expertise in the management of TOS in conjunction
with a physical therapist located near the patient. A gradual, steady, return to normal use
of the upper extremity is emphasized.
Most patients are permitted cautious light-duty work activity by 4 to 6 weeks after surgery,
with progressively diminished restrictions on upper extremity activity. Recovery from
surgery is typically considered to be complete between 6 and 12 weeks after operation.
Follow-up visits are continued every 3 months in the first year to assess long-term results,
and physical therapy and other aspects of care are continued as long as necessary to
achieve an optimal level of function.

Persistent pain, numbness, and/or paresthesias.
Postoperative bleeding, localized hematoma, or hemothorax.
Wound infection (cellulitis or abscess).
Pleural effusion (serosanguinous).
Persistent lymph leak, chylothorax.
Brachial plexus nerve dysfunction (temporary or sustained).
Phrenic nerve dysfunction (temporary or sustained).
Long thoracic nerve dysfunction (temporary or sustained).
Recurrent NTOS.

Within several months of supraclavicular decompression for disabling NTOS, approximately
80% to 85% of patients can expect a substantial improvement in symptoms and increased
functional use of the upper extremity compared to their condition prior to surgery. This rises
to approximately 90% to 95% for patients who have had a positive anterior
scalene/pectoralis minor muscle block prior to treatment.5 Other factors that are associated
with less responsiveness to treatment include extremely debilitating and longstanding
symptoms (often >5 years); pain syndromes with a widespread distribution; those who have

had previous operations on the cervical spine, shoulder, or peripheral nerves for the same
symptoms; age over 50 years; depression; and previous or ongoing use of opiate pain
medications prior to surgery.
It is important to emphasize that patients with longstanding symptoms of NTOS may have
some degree of residual symptoms despite appropriate thoracic outlet decompression, as
surgical treatment cannot be assured to completely eliminate all symptoms. Such residual
symptoms may still be quite tolerable compared to those present prior to surgery and most
patients can expect to gradually improve further over time. The surgeon undertaking
thoracic outlet decompression should recognize the need to provide continuing support and
reassurance to the patient during the prolonged period of recovery and rehabilitation.
It has been shown that adolescent patients with NTOS have enhanced outcomes after
surgical treatment compared to adults over 21 years of age, including assessment based on
patient-reported survey instruments and use of opiate pain medications. Recent reports also
indicate that the early outcomes for surgery in patients selected for isolated pectoralis
minor tenotomy are similar to patients who have undergone combined supraclavicular
decompression and pectoralis minor tenotomy, but these patients should be closely
followed for development of recurrent symptoms, which may warrant subsequent
supraclavicular decompression.
Recurrent NTOS occurs in approximately 2% to 5% of patients undergoing surgical
treatment, usually within the first 2 years after operation. Development of recurrence in a
patient who has previously had good results after surgery is often associated with a
secondary injury, likely as the result of perineural inflammation and accelerated fibrosis.
The supraclavicular approach is optimal for reoperations for NTOS, providing the most
complete exposure of the relevant anatomy with the greatest degree of safety.1 In these
procedures, the scalene fat pad is reflected in the same manner as in a primary operation
and the brachial plexus nerve roots are carefully exposed and mobilized. Given the dense
fibrous scar tissue that is usually present within the operative field, it is especially
important to avoid nerve and blood vessel injury during this dissection. If any of the
pertinent anatomic structures were retained at the initial operation, such as the anterior
and middle scalene muscles, anomalous fibrofascial bands, and/or the first rib, these are
removed. An extended and complete brachial plexus neurolysis is then performed. Prior to
closure, the brachial plexus is encircled with a bioabsorbable film and covered by
reapproximating the scalene fat pad.

The surgical treatment of NTOS is founded on a sound clinical diagnosis, the presence of
disabling symptoms, and failure of these symptoms to improve with a suitable trial of
physical therapy management. Imaging studies, electrophysiologic tests, and vascular
laboratory examinations may be useful in the exclusion of other conditions, but they add
little in the specific diagnosis of NTOS. Clinical findings leading to a diagnosis of NTOS
may be strongly supported by a positive anterior scalene/pectoralis minor muscle block,
which also demonstrates the likelihood of a favorable response to surgical treatment. In

addition to findings referable to the scalene triangle, the potential contribution of brachial
plexus compression at the level of the subcoracoid (pectoralis minor) space should always
be assessed and included in surgical treatment if present.
Proper mobilization and lateral reflection of the scalene fat pad is a key step in simplifying
supraclavicular exposure for thoracic outlet decompression. This permits the critical view
to be obtained in which all of the relevant structures can be visualized in the same
operative field: The internal jugular vein, phrenic nerve, anterior scalene muscle, brachial
plexus, middle scalene muscle, first rib, and long thoracic nerve. The thoracic duct should
be ligated and divided, if necessary, to prevent postoperative lymph leak.
During anterior scalenectomy, all fibers passing from the posterior aspect of the anterior
scalene muscle to the subclavian artery and the extrapleural fascia should be divided, along
with any scalene minimus muscle encountered. Once divided from the first rib and
elevated, the anterior scalene muscle should be passed underneath and medial to the
phrenic nerve, to facilitate dissection of the muscle to its origin on the C6 transverse
During mobilization of the brachial plexus, all five nerve roots should be well visualized
and only gently retracted. The transverse cervical vessels should be ligated and divided
where they pass through the brachial plexus and middle scalene muscle. During division of
the middle scalene muscle from the top of the first rib, the long thoracic nerve should be
visualized and protected. Any cervical rib present should be resected before resection of the
first rib. Prior to division of the posterior first rib, the T1 and C8 nerve roots should be well
visualized and protected from injury, and any small fibrofascial bands present over the
proximal aspect of the C8 and T1 nerve roots should be resected. A small segment of the
divided posterior first rib should be removed to facilitate fingertip dissection underneath
the remaining lateral and anterior portions of the bone. It is not necessary to avoid opening
the pleura during dissection of the first rib. The anterior first rib is divided underneath the
clavicle and subclavian vein, at a level medial to the scalene tubercle, while protecting the
subclavian artery and brachial plexus. Any fibrous scar tissue should be thoroughly
removed from around each nerve root of the brachial plexus (C5 to T1), to maximize nerve
mobility and to avoid one of the principal causes of persistent symptoms. The brachial
plexus is subsequently wrapped with a bioresorbable film to minimize perineural fibrosis.
Pectoralis minor tenotomy is included with supraclavicular decompression if there are
concomitant symptoms of NTOS referable to the subcoracoid space.
A closed suction drain is placed into the supraclavicular space behind the brachial plexus,
with its tip extending into the pleural space, to be removed approximately 6 to 7 days after
operation. Continuous postoperative infusion of a local anesthetic into the operative field
can help diminish the need for opiate pain medications.
The large majority of patients (85% to 90%) with disabling NTOS can expect a substantial
improvement in symptoms and upper extremity function within several months of
supraclavicular decompression. Diminished responsiveness to treatment tends to be
associated with extremely longstanding (>5 years) and debilitating symptoms, widespread
pain syndromes, multiple previous operations (cervical spine, shoulder, or peripheral
nerves), depression, older age (>50 years), and pre-existing use of opiate pain medications.

Recommended References and Readings

1. Ambrad-Chalela E, Thomas GI, Johansen KH. Recurrent neurogenic thoracic outlet

syndrome. Am J Surg. 2004;187(4):505510.
2. Caputo FJ, Wittenberg AM, Vemuri C, et al. Supraclavicular decompression for neurogenic
thoracic outlet syndrome in adolescent and adult populations. J Vasc Surg. 2013;57(1):149
3. Emery VB, Rastogi R, Driskill MR, et al. Diagnosis of neurogenic thoracic outlet syndrome.
In: Eskandari MK, Morasch MD, Pearce WH, et al., eds. Vascular Surgery: Therapeutic
Strategies. Shelton, CT: Peoples Medical Publishing House-USA; 2010:129148.
4. Illig KA, Thompson RW, Freischlag JA, et al. Thoracic Outlet Syndrome. 1st ed. London:
Springer-Verlag; 2013.
5. Jordan SE, Ahn SS, Gelabert HA. Differentiation of thoracic outlet syndrome from
treatment-resistant cervical brachial pain syndromes: Development and utilization of a
questionnaire, clinical examination and ultrasound evaluation. Pain Physician.
6. Povlsen B, Belzberg A, Hansson T, et al. Treatment for thoracic outlet syndrome. Cochrane
Database Syst Rev. 2010;20:CD007218.
7. Reilly LM, Stoney RJ. Supraclavicular approach for thoracic outlet decompression. J Vasc
Surg. 1988;8:329334.
8. Sanders RJ, Hammond SL, Rao NM. Diagnosis of thoracic outlet syndrome. J Vasc Surg.
9. Sanders RJ, Hammond SL. Management of cervical ribs and anomalous first ribs causing
neurogenic thoracic outlet syndrome. J Vasc Surg. 2002;36(1):5156.
10. Sanders RJ, Hammond SL. Supraclavicular first rib resection and total scalenectomy:
Technique and results. Hand Clin. 2004; 20:6170.
11. Sanders RJ, Rao NM. The forgotten pectoralis minor syndrome: 100 operations for
pectoralis minor syndrome alone or accompanied by neurogenic thoracic outlet syndrome.
Ann Vasc Surg. 2010;24:701708.
12. Sanders RJ, Raymer S. The supraclavicular approach to scalenectomy and first rib
resection: Description of technique. J Vasc Surg. 1985;2:751756.
13. Sanders RJ. Thoracic Outlet Syndrome: A Common Sequelae of Neck Injuries. Philadelphia,
PA: J. B. Lippincott Company; 1991.
14. Thompson RW, Driskill M. Thoracic outlet syndrome: Neurogenic. In: Cronenwett JL,
Johnston KW, eds. Rutherfords Vascular Surgery, 7th ed. Philadelphia, PA: Elsevier;
15. Thompson RW, Petrinec D, Toursarkissian B. Surgical treatment of thoracic outlet
compression syndromes. II. Supraclavicular exploration and vascular reconstruction. Ann
Vasc Surg. 1997; 11(4):442451.
16. Thompson RW. Comprehensive management of subclavian vein effort thrombosis. Semin
Intervent Radiol. 2012;29(1):4451.
17. Vemuri C, Wittenberg AM, Caputo FJ, et al. Early effectiveness of isolated pectoralis
minor tenotomy in selected patients with neurogenic thoracic outlet syndrome. J Vasc Surg.

11 Thoracic Outlet Syndrome Requiring Vascular

Reconstruction: Vein, Artery
Dean M. Donahue

Vascular reconstruction techniques are required in the management of patients with thoracic
outlet syndrome (TOS) when a vascular injury has occurred to either the subclavian vein or
artery. Neurogenic TOS (NTOS) accounts for between 90% and 95% of clinical cases and is
caused by compression or irritation of the brachial plexus. The remainder of cases is venous
TOS (VTOS), which results from stenosis of the subclavian vein. Arterial TOS (ATOS) only
occurs when compression of the subclavian artery results in arterial thrombosis and/or an
aneurysm formation. This is very uncommon and accounts for less than 1% of all cases.
VTOS frequently presents with symptoms of upper extremity swelling with or without skin
discoloration. Patients may report a heavy sensation or a feeling of pressure in the upper
extremity. For suspected cases of VTOS, the initial management is immediate anticoagulation
with subcutaneous lowmolecular-weight or intravenous heparin. Venous ultrasound studies
are often used in the initial diagnosis, but the high degree of false-negative studies limits its
usefulness. A contrast venogram has much greater diagnostic accuracy and a therapeutic
capability as well. Catheter-delivered chemical thrombolysis, and possibly mechanical
thrombectomy may be used, the authors preference is to avoid balloon venoplasty at the
initial presentation. If balloon venoplasty is felt to be necessary, limiting this to an 8 mm or
less balloon is preferable. The use of intravascular stents as a management for VTOS should
be strictly avoided.
Some cases of VTOS may be treated nonoperatively. Patients who present in their mid-30s
or older, have minimal or no narrowing of the subclavian vein after lytic therapy and remain
asymptomatic may be treated with 3 to 6 months of anticoagulation and observed. This is a
fairly small percentage of patients presenting with VTOS. The majority of patients will require
surgical thoracic outlet decompression with or without vein reconstruction.
Patients with ATOS from a subclavian or axillosubclavian artery aneurysm represent an
absolute indication for surgery, even if asymptomatic at the time of presentation.

The surgical treatment of TOS requiring vascular reconstruction involves resection of the first
thoracic rib through a supraclavicular or paraclavicular (combined supra- and infraclavicular)
approach. The surgeon and the assistant would benefit from the use of surgical telescopes and
a headlight to improve visualization. During the procedure, the degree of retraction on the
spinal nerves, phrenic nerve, and brachial plexus trunks must be minimized to avoid a nerve
traction injury. The author uses bipolar cautery for much of the procedure to avoid
transmitting electrical current to the nerves in this area.

General anesthesia is administered and the patient is intubated with the endotracheal tube
taped to the side of the patients mouth opposite to the side of the procedure. The use of
neuromuscular blocking agents is avoided following intubation so an electrical nerve
stimulator can be used to assist in identifying and confirming the function of nerves.
The patient is placed in a modified semi-Fowler position with the head on a padded roll,
rotated 45 degrees away from the operative side. Both arms are tucked to the side if possible.
Otherwise, the operative side arm is tucked to the patients side and an arm board is placed
on the nonoperative side as far down on the bed as possible to allow the assistant to stand
close to the table. A roll of gauze is placed into the patients hands for padding. The
operative-side shoulder is elevated off of the bed by placing a stack of folded surgical towels
behind the shoulder to pivot the shoulder and lateral clavicle anteriorly and open the
costoclavicular space. The field is draped so that a sternotomy can be performed in the
unlikely event that additional exposure is needed.
Supraclavicular Exposure
A 5 cm long incision is made beginning at the lateral border of the sternocleidomastoid
muscle (SCM). The incision extends laterally 1 to 2 cm above the clavicle. The subcutaneous
tissue and platysma muscle are divided, and flaps are raised under this muscle with
electrocautery. A Weitlaner retractor is placed below the level of the platysma and the
scalene fat pad is mobilized off of the lateral border of the SCM using electrocautery. Small
sensory nerve branches and anterior jugular veins are identified running approximately
perpendicular to the incision. These structures are identified and mobilized laterally without
tension. Another self-retaining retractor can be placed between the lateral wound edge and
the SCM muscle to retract it medially. The scalene fat pad is now mobilized laterally. The
omohyoid muscle is identified running approximately parallel to the incision. This is
encircled with a vessel loop to allow for its retraction. Deep to the omohyoid muscle will lie
the anterior scalene muscle.
Dissection through the deep part of the fat pad is done with bipolar cautery to protect the
phrenic nerve and brachial plexus. The suprascapular and transverse cervical arteries are
identified and preserved. They typically run parallel to the incision, with the suprascapular
artery below the level of the incision, and the transverse cervical artery above it. The
dissection continues with bipolar cautery until the scalene muscle is identified deep and
slightly medial to the lateral edge of the SCM muscle. Mobilization of the scalene fat pad
continues from medial to lateral exposing the upper and middle trunks of the brachial plexus,
as well as the subclavian artery. The lower trunk is deeper to these structures, and not usually
identified at this point. The suprascapular artery is dissected off of the scalene fat pad
laterally to complete the mobilization. A 2-0 silk traction suture is placed on the tip of the fat
pad, which is retracted laterally.
The phrenic nerve is then identified on the surface of the anterior scalene muscle running
from lateral to medial. A nerve stimulator (current setting 0.5 to 1 mA, frequency setting 30

Hz) is used to confirm the location and function of the nerve. The areolar plane between the
surface of the scalene muscle and the phrenic nerve is developed, and tissue adjacent to the
nerve is grasped and gently retracted to mobilize the nerve medially. Occasionally, an
accessory phrenic nerve branch located at the lateral edge of the anterior scalene muscle is
preserved if present. Near the cephalad portion of the scalene muscle, the phrenic nerve
receives a contribution from the C5 spinal nerve, which limits the degree that the phrenic
nerve can be mobilized. After mobilization, the nerve stimulator is used to confirm intact
phrenic nerve function. Once the phrenic nerve is mobilized off of the anterior surface of the
scalene muscle, the plane along the medial border of the muscle is developed using bipolar
cautery. The subclavian artery is identified medially, and the dissection around the anterior
scalene is continued down to the scalene tubercle of the first rib. A Richardson or Cloward
retractor placed below the clavicle facilitates exposure. There may be muscle fibers running
between the anterior and middle scalene muscles that must be divided to facilitate
mobilization of the brachial plexus trunks.
The lower portion of the anterior scalene muscle is partially divided medially and laterally
directly on the scalene tubercle exposing part of the first rib. The central part of the muscle is
preserved at this time to facilitate the division of the cephalad portion of the anterior scalene
muscle. The scalene muscle is then divided with bipolar cautery as far cephalad as possible
while protecting the phrenic nerve and its C5 spinal nerve. Once the cephalad border of the
muscle is divided, the remaining muscle attachments to the first rib are divided and the
muscle is removed.
The brachial plexus trunks and the subclavian artery are then dissected. The upper trunk
and subclavian artery are often the first two structures identified. The middle scalene muscle
is deep to the brachial plexus trunks, and is easiest to identify cephalad and deep to the upper
trunk. The subclavian artery is then mobilized to improve the exposure of the lateral aspect of
the first rib. The dorsal scapular artery originating along the cephalad border of the
subclavian artery is identified and preserved. This branch is typically 1 to 2 cm lateral to the
lateral border of the anterior scalene muscle. It is important to remember that the brachial
plexus trunks are oriented obliquely, with the middle trunk lying more dorsal (or deeper) to
the upper trunk, and the lower trunk lying further dorsal to the middle trunk. While not
consistently present in cases of vascular TOS, there may be scar tissue around the brachial
plexus, which is removed to increase nerve mobility for the remainder of the dissection.
Removal of this scar tissue is frequently done sharply, with fine-tip bipolar cautery forceps
used for hemostasis. Identification of the proper plane can be difficult, but the goal is to not
disrupt the epineurium layer containing the blood supply to each nerve. Tissue adjacent to
each nerve is grasped with atraumatic forceps and gently retracted to assist in identifying the
proper dissection plane. Occasionally, blunt dissection with a no. 4 Penfield elevator is done
to gently peel scar tissue away from the epineurium. During the dissection of the upper trunk,
the dorsal scapular nerve may be identified originating from the cephalad border. This
initially runs parallel to upper trunk before turning dorsally toward the suprascapular notch.
Circumferential dissection of the middle and lower trunks are performed in a similar manner.
It is important to completely remove any remaining scalene muscle fibers around the nerve
trunks and artery.
After the brachial plexus trunks are mobilized, modified Love nerve root retractors are used

to work between the trunks to identify the middle scalene muscle lying immediately deep to
the brachial plexus. It is important to minimize the degree of retraction on the nerves to
avoid injury. By palpating above and below the middle trunk, the posterior aspect of the first
rib can be identified. This is exposed by dividing the attached middle scalene fibers above the
rib with bipolar cautery. Because of individual anatomic variability, there is no consistent
plane to the posterior first rib. Typically, this is approached by working between the upper
and middle trunks, but occasionally this is accomplished between the middle and lower
trunks. If a cervical rib or an elongated C7 transverse process is to be removed, then the best
approach is often by working above and below the upper trunk. The dorsal scapular nerve
(from the C5 spinal nerve) and the long thoracic nerve (from the C5, C6, and C7 spinal
nerves) run dorsally and laterally to penetrate the middle scalene muscle. It is, therefore,
important to divide the posterior middle scalene fibers inserting on the first rib less than 1 to
2 cm away from the upper surface of the rib to avoid injuring these nerves. The inner edge of
the posterior first rib is then exposed, and dense tissue bands are divided off of this part of
the rib using bipolar cautery to avoid injury to the T1 spinal nerve as it arises from below the
first rib. The costotransverse ligaments between the neck of the first rib and the transverse
process are then divided with bipolar cautery to separate the rib from the transverse process
of the first thoracic vertebrae.
Muscle fibers are divided off of the cephalad and dorsal surfaces of the first rib working
from medial to lateral. The exposure of the lateral aspect of the rib is facilitated by working
both above and below the lower trunk with minimal traction on this nerve. The middle
scalene muscle and fibers from the upper part of the serratus anterior muscle are divided off
of the rib posterior to the subclavian artery.
Once the muscle tissue completely divides off of the cephalad surface of the first rib, the
plane along the undersurface of the rib is developed. This is started with either sharp
dissection or with bipolar cautery, and then continued under the rib with blunt dissection of
Sibsons fascia using a small sponge or the surgeons finger. The goal is to avoid entry into the
pleural space, but there is little consequence if it is entered. The remaining attachments to the
first rib are now the intercostal muscle fibers between the first and second ribs. These are
divided with electrocautery using an insulated extended tip with a slight angle created by
bending the tip with a snap. Ventilation should be held intermittently during the division of
this muscle to avoid cautery injury to the lung. If exposure of the remaining soft tissue
attachments is limited, then dividing the first rib allows it to be mobilized to improve this
The rib is divided at its neck medial to the end of the T1 transverse process using a straight
Kerrison rongeur ranging from 3 to 5 mm. The smooth synovial joint between the transverse
process of the T1 vertebrae and the angle of the first rib is exposed during this maneuver.
Infraclavicular Exposure for VTOS
Division of the medial portion of the anterior rib may be difficult because of limited exposure
from the supraclavicular approach. In cases where a vascular reconstruction is necessary, an
infraclavicular incision will be required for vascular exposure and control. This also greatly
facilitates exposure to the anterior rib. For VTOS cases, a 5- to 6-cm incision is made 1 to 2
cm below the clavicle beginning at the lateral border of the manubrium. The underlying soft

tissues are divided with electrocautery exposing the pectoralis major muscle. These muscle
fibers run obliquely, and are split between the upper and middle portions of this muscle. The
underlying intercostal muscle fibers between the first and second rib are divided, and the
subclavius muscle and tendon are partially resected off of the anterior surface of the rib
preserving the costoclavicular ligaments. The cartilage of the first rib is then divided close to
the manubrium with an angled duckbill rongeur or a Kerrison rongeur being careful to avoid
the internal mammary vessels. With the rib completely free of soft tissue attachments, it is
removed intact while avoiding any traction on the brachial plexus or subclavian artery. The
subclavian vein is now exposed above and below the clavicle. A circumferential removal of
surrounding tissue is then performed with sharp dissection and electrocautery. Following this,
the vein is inspected and palpated to evaluate the extent of residual narrowing due to
intrinsic vein injury. If the vein appears contracted and fibrotic, and is palpably thickened, a
vascular reconstruction is indicated.
Infraclavicular Exposure for ATOS
For ATOS cases, exposure of the axillary artery for distal vascular control requires that the
incision begin at the medial third of the clavicle and continue laterally to the deltopectoral
groove. The exposure through the pectoralis major muscle is similar to the VTOS approach,
but the underlying pectoralis minor muscle is frequently divided off of the coracoid process.
The underlying axillary sheath is opened exposing the axillary vein. This is gently dissected
away to expose the artery lying deep to the vein.
Vascular Reconstruction for VTOS
Once it is determined that a vein reconstruction is required, the patient is anticoagulated with
a 5,000 unit bolus of intravenous heparin. Proximal venous control is achieved at two
locations. One clamp is placed across the innominate vein from the infraclavicular incision
using a Satinsky or other curved vascular clamp. Attention must be paid to the location of the
phrenic nerve during this maneuver. A second curved vascular clamp is used medial at the
internal jugular vein medial to its junction with the subclavian vein. A DeBakey clamp is then
used to control the vein distally.
There are two options for vein reconstruction: Vein patch angioplasty, or vein replacement
with an interposition bypass graft. To determine which option is appropriate, a longitudinal
venotomy is made in the cephalad portion of the vein through the supraclavicular incision.
The lumen of the vein is evaluated, and if the degree of intimal scar is not excessive, then a
vein patch angioplasty is appropriate. The patch material can either be from the patients
saphenous vein harvested from the thigh, or a piece of cryopreserved femoral vein. This is
secured to the subclavian vein with running 5-0 or 6-0 polypropylene suture (Ethicon Inc.
Sommerville, NJ).
If the lumen of the subclavian vein is densely fibrotic, then the segment is excised and a 10to 14-mm conduit of cryopreserved femoral vein is inserted. A proximal end-to-side
anastomosis is constructed between the conduit and the junction between the jugular and
innominate veins using running 5-0 or 6-0 polypropylene suture. The conduit is then passed
under the clavicle, and a beveled distal end-to-end anastomosis between the conduit and the
subclavian vein is performed through the infraclavicular incision laterally.

Vascular Reconstruction for ATOS

Through the supraclavicular incision the subclavian artery is mobilized proximally to the
level of the vertebral artery. A silastic vessel loop is passed around the artery at this level.
Through the infraclavicular incision the distal subclavian artery is mobilized by releasing a
tight fascial band often found around the outer portion of the artery. Small arterial branches
may need to be divided and ligated with 5-0 polypropylene suture ligatures. Distally the
axillary artery is controlled with a silastic vessel loop. The patient is then systemically
heparinized with 5,000 units of intravenous heparin, which is allowed to circulate for 5
minutes. Vascular clamps are then placed on the proximal subclavian and axillary arteries.
The artery is transected distal to the subclavian clamp, allowing an adequate cuff for creation
of the proximal anastomosis. The artery including the aneurysm is then dissected out and
removed from underneath the clavicle. The specimen is transected distally and removed. This
is opened on the back table to inspect the aneurysm for signs of ulceration and thrombus.
The conduit of choice for replacement of the subclavian artery is ring-reinforced
polytetrafluoroethylene (PTFE). Size of the conduit varies with the patient, but most
commonly a 6-mm graft is used, which is passed through the infraclavicular tunnel. There
may be bands of tissue that need to be divided to allow easy passage of the graft. A proximal
end-to-end anastomosis to the subclavian artery is performed with two 5-0 polypropylene
sutures, with one placed at the heel and one at the toe of the anastomosis. These sutures run
in a nonlocking continuous fashion to complete the anastomosis. An antegrade flushing
maneuver is then performed. Distally the graft is precisely trimmed to prevent both tension
and kinking of the conduit. A distal end-to-end anastomosis between the axillary artery and
the ringed PTFE graft is then performed in a similar fashion to the proximal one. Antegrade
and retrograde flushing maneuvers are each performed, and the graft is flushed with
heparinized saline. The clamps are then removed to re-establish flow to the axillary artery.
The graft pulse is palpated, and flow in the distal artery is evaluated by Doppler signal.
Wound Closure
The surgical field is inspected, and hemostasis is achieved with bipolar cautery. This is
critical, as a postoperative hematoma can lead to nerve irritation and potentially increased
scar formation. The function of the phrenic nerve is again confirmed with a nerve stimulator.
A no. 15 round closed suction drain is placed through a separate stab wound laterally to the
supraclavicular incision, and positioned in the bed of the resected first rib. A second Blake
drain can be used laterally to the infraclavicular incision if necessary. If there is an entry into
the pleural space, a no. 14 red rubber catheter is placed through this entry into the pleural
After a final inspection for hemostasis, the omohyoid muscle and scalene fat pad are
returned to their normal positions. The infraclavicular wound is closed by reapproximating
the pectoralis major muscle fibers with running 3-0 Vicryl suture (Ethicon Inc. Sommerville,
NJ). This is followed with a second layer of subcutaneous tissue closed in a similar fashion.
The platysma muscle at the supraclavicular incision is reapproximated from medially to
laterally with a running 3-0 Vicryl suture. Before tying this suture, the pleural space is
evacuated by providing a sustained positive-pressure breath while suction is intermittently
applied to the red rubber catheter. This catheter is then withdrawn from the wound. Suction

is then applied to the wound drain via a vacuum bulb. The stitch for the platysma is then
tied, and the skin of both incisions is closed with a subcuticular 4-0 Vicryl suture. A sterile
dressing is then applied, which remains on for 24 hours.

VTOS patients who have undergone vascular reconstruction require the initiation of
anticoagulation once the risk of surgical bleeding has abated. Therapy with warfarin is
typically started on the third or fourth postoperative day. Lowmolecular-weight heparin is
started at the same time and continued until the patient is in therapeutic range from the
warfarin. ATOS patients are typically placed on an adult dose aspirin in this same time frame.
Patients with VTOS will undergo a venogram within the first few weeks postoperatively.
During that procedure, a diagnostic venogram is performed on the contralateral side. While it
is uncommon that significant disease is identified on the contralateral side, it occurs often
enough to justify the mild inconvenience of this additional procedure. Immediate
postoperative imaging is not required for ATOS patients, but the authors practice has been to
obtain a CT angiogram of the chest every 1 to 2 years.

Complications following surgical treatment of TOS are fortunately uncommon. Infections
inherent to all surgical procedures such as bleeding and wound infection occur less than 2%
of all cases. The more dreaded complication of nerve injury, from either traction injury or less
commonly nerve transection, is reported to occur in 1% to 3% of all cases. This can involve
the phrenic nerve (reportedly more common following supraclavicular approach) or the
brachial plexus. A postoperative pneumothorax can occur regardless of approach, and is
treated with either observation or tube decompression depending upon the size and clinical
progression. An uncommon complication includes increased lymphatic drainage from either
disruption of a small lymphatic branch or the thoracic duct. Low-volume lymphatic drainage
(less than 200 mL) may be treated with a low-fat diet and continued observation. Outputs
greater than 200 mL on a low-fat diet may require neck re-exploration for ligation of the
leaking channel.

For VTOS, vein patency and freedom from symptoms occur in greater than 80% of cases, with
most series approaching 100%. The cumulative experience for surgical treatment of ATOS
also shows primary and secondary patency rates in the 90% to 100% range.


Familiarity with vascular reconstruction techniques is critical in the management of complex

cases of VTOS and all cases of ATOS. Particularly for VTOS, where there may be uncertainty
regarding the need for such techniques, preoperative awareness and preparation are
mandatory in achieving a successful outcome.

Recommended References and Readings

1. Criado E, Berguer R, Greenfield L. The spectrum of arterial compression at the thoracic

outlet. J Vasc Surg. 2010;52:406411.
2. De Leon R, Chang DC, Busse C, et al. First rib resection and scalenectomy for chronically
occluded subclavian veins: What Does It Really Do? Ann Vasc Surg. 2008;22:395401.
3. Donahue DM. Supraclavicular 1 st rib resection. Operative Techniques in Thoracic and
Cardiovascular Surgery. 2011;16(4):252266.
4. Illig KI, Doyle AJ. A comprehensive review of Paget-Schroetter syndrome. J Vasc Surg.
5. Lee JT, Karwowski JK, Harris EJ, et al. Long-term thrombotic recurrence after
nonoperative management of Paget-Schroetter syndrome. J Vasc Surg. 2006;43:12361243.
6. Melby SJ, Vedantham S, Narra VR, et al. Comprehensive surgical management of the
competitive athlete with effort thrombosis of the subclavian vein (Paget-Schroetter
syndrome). J Vasc Surg. 2008;47(4):809820.
7. Molina JE, Hunter DW, Dietz CA. Protocols for Paget-Schroetter syndrome and late
treatment of chronic subclavian vein obstruction. Ann Thorac Surg. 2009;87(2):416422.
8. Singh MJ, Fanciullo DJ. Surgical techniques: Approach to the axillosubclavian artery. In:
Illig KA, Thompson RW, Freischlag JA, et al., eds. Thoracic Outlet Syndrome. New York, NY:
Springer Science; 2013:597603.
9. Thompson RW. Surgical techniques: Operative decompression using the paraclavicular
approach for VTOS. Illig KA, Thompson RW, Freischlag JA, et al., eds. Thoracic Outlet
Syndrome. New York, NY: Springer Science; 2013:433445.

12 Thoracic Outlet Syndrome: Transaxillary Approach

Julie Freischlag and Natalia Glebova

Thoracic outlet syndrome (TOS) is a spectrum of disorders resulting from compression of the
neurovascular structures within the thoracic outlet. The three subtypes of TOS are identified
based on the structures affected: The brachial plexus which is compressed in the most
common subtype, neurogenic TOS; the subclavian vein which may be thrombosed in the
second most common subtype, venous TOS; and the subclavian artery which may become
stenotic or aneurysmal in arterial TOS. Transaxillary approach to first rib resection and
anterior scalenectomy is indicated in all three subtypes of TOS unless the subclavian artery
needs to be resected and replaced.
The initial treatment of neurogenic TOS is nonoperative with physical therapy, avoidance
of inciting activities, and image-guided neuromuscular blockade of the anterior scalene
muscle with lidocaine of Botulinum toxin A (Botox). Ample time is allowed for work with
physical therapists, at least several months. If no improvement occurs with physical therapy,
if the anterior scalene block is positive (the patient obtains temporary symptomatic relief
with local anesthetic injection), and if symptoms are truly significant, then an operation is
Transaxillary first rib resection and scalenectomy is indicated for both venous and arterial
TOSs as symptoms will recur without this definitive operation even if thrombus is removed
via thrombolysis or thrombectomy. Reoperation for residual symptoms after prior
supraclavicular first rib resection is also best performed with a transaxillary approach as this
avoids scar tissue from the prior operation.
Another indication for this operation is the symptomatic presence of a cervical rib. Cervical
ribs, defined as anomalous ribs originating from the seventh cervical vertebrae, are frequently
fused to the first rib and may cause symptomatic arterial compression, thrombosis, aneurysm
formation, and embolization. Those patients with symptomatic cervical ribs who do not
require vascular reconstruction should undergo transaxillary first rib resection, anterior
scalenectomy, and cervical rib resection. Patients with this syndrome who require arterial
bypass are best served by a supraclavicular approach that allows arterial reconstruction at the
time of rib resection.
A contraindication to the transaxillary approach is first rib resection in patients with
arterial TOS in whom replacement of the subclavian artery is planned due to aneurysmal
changes. These patients are best served with a supraclavicular approach (with sometimes an
infraclavicular counterincision) which allows direct arterial reconstruction. Also, preoperative
first rib resection in a patient who has had a transaxillary approach should be done using the
supraclavicular technique.


Preoperative planning and evaluation vary depending on the type of TOS with which the
patient presents.
Patients with suspected neurogenic TOS often present with vague symptoms of arm pain,
weakness, or paresthesias. These nonspecific symptoms may result from many other
conditions, and thus it is imperative to determine whether such patient have TOS and may
benefit from first rib resection. A reliable approach to confirming the diagnosis is
neuromuscular blockade of the anterior scalene muscle. The diagnosis is confirmed if an
injection of lidocaine into the anterior scalene under ultrasound or computed tomography
(CT) guidance produces relief. Nonoperative management should then be attempted, with
physical therapy and careful attention to activities that incite symptoms. Botulinum toxin A
may also be injected into the anterior scalene muscle for longer duration of relief. If
nonoperative management is unsuccessful, first rib resection and anterior scalenectomy is
Venous TOS typically presents with arm swelling and subclavian vein thrombosis in the
setting of exercise or overuse. Thrombosis may be acute or chronic. This disease entity is also
known as effort-induced thrombosis of the subclavian vein or PagettSchroetter syndrome.
Historically, these patients underwent thrombolysis and percutaneous venoplasty. Recent data
indicate that preoperative thrombolysis and percutaneous venoplasty are of no benefit for
patients with TOS manifested by subacute or chronic venous thrombosis. Preoperatively,
these patients should undergo laboratory evaluation for the presence of hypercoagulable
disorders such as Factor V Leiden mutation, protein C or S deficiency, antithrombin III
deficiency, prothrombin gene mutations, homocysteinemia, activated protein C (APC)
resistance, antiphospholipid antibodies, and lupus anticoagulant. Patients with venous TOS
should also be anticoagulated, preferably with therapeutic dosing of Lovenox of 1 mg/kg
twice a day, which is continued until the operation.
Arterial TOS is characterized by chronic thrombosis manifesting as arm claudication, or in
the acute form by potentially limb-threatening hand and digit ischemia due to
thromboembolism from the subclavian artery secondary to compression. These patients often
have a bony abnormality such as a cervical rib. Poststenotic dilatation and aneurysm
formation may occur in the subclavian artery in the chronic form of the syndrome.
Preoperative planning may include urgent thrombolysis or thrombectomy in the presence of
clinically significant distal ischemia. Hypercoagulability studies are conducted as for venous
TOS. A plain chest radiograph should be obtained to evaluate for the presence of a cervical
rib and other bony abnormalities. A duplex ultrasound should also be performed to evaluate
for arterial stenosis and dilatation, as well as to measure arterial velocities. An arteriogram
may be helpful in delineating thrombosis or aneurysm formation. It is imperative to
determine whether the patient requires arterial reconstruction in addition to first rib resection
and scalenectomy, as the transaxillary approach should be reserved for patients not
undergoing arterial bypass. The supraclavicular approach is best for patients who require
replacement of the subclavian artery.

The operation of first rib resection and anterior scalenectomy is performed under general

endotracheal anesthesia. Short acting paralytics are used at the start of the operation, so that
their effects wear off and do not interfere with nerve identification during the operation.

Figure 12.1 A: Patient positioning with the operative side facing up and the arm circumferentially prepped (photo courtesy
of Holly Grunebach, PA-C). B: Operative side arm is secured in the Machleder retractor prior to incision (photo courtesy of
Holly Grunebach, PA-C). C: Incision at inferior aspect of hairline between the borders of pectoralis major and latissimus dorsi
muscles. D: Arm raised in the Machleder retractor allowing visualization of axillary structures with supplemental lighting.

The patient is positioned on a beanbag in the lateral position with the operative side facing
up (Fig. 12.1A). The beanbag is inflated, and ample amounts of padding are used to protect
pressure points. The lower leg is slightly bent, and the upper leg is straight and padded with
pillows. The axilla is prepped in the standard fashion, and the arm on the operative side is
prepped circumferentially. Once the patient is draped, a Machleder retractor is placed on the
bed, and the operative arm is extensively padded with Kerlix and towels, and then secured
with CoBand to the retractor (Fig. 12.1B).

The operation commences with an incision in the inferior aspect of the hairline between the
posterior border of the pectoralis major muscle and the anterior border of the latissimus dorsi
muscle (Fig. 12.1C). The subcutaneous space is entered, and electrocautery is used to dissect
down to the chest wall. Lymphatics may be encountered, and if so they are tied. Once the
chest wall comes into view, blunt dissection is utilized to sweep the remainder of adipose
tissue off the chest wall.
A self-retaining retractor is now placed at the skin level, and the arm is elevated by raising
the Machleder retractor (Fig. 12.1D). In order to aid in visualization of deep axillary
structures, a Deaver retractor is placed on one side of the incision, and a lighted retractor
such as a St. Marks retractor on the other side. As the operation proceeds, frequent breaks are
taken and the arm is relaxed into a more neutral position while the wound is packed in order
to minimize the amount of stretch on the brachial plexus.
At this time, it is imperative to identify the subclavian vein and artery in order to find the
first rib. The artery is revealed by its pulsation. The vein may be difficult to find in patients
with venous TOS as it may be quite fibrotic. Nonetheless, the vein is anterior to the artery.
Blunt dissection is used to sweep away tissues around these structures in order to identify
them and the anterior scalene muscle that lies between them and attaches inferiorly to the
first rib. This is done carefully so as not to avulse any small arterial branches. These branches
are tied when encountered. The brachial plexus is visible posteriorly to the subclavian artery,
and does not need to be dissected (Figs. 12.2A,B).
Once these structures are identified, dissection of the first rib begins. A sharp periosteal
elevator is used to clear intercostal muscles off the inferior aspect of the first rib. One is
careful to push precisely along the rib edge so as not to enter the pleural space or injure
intercostal vessels. Once the inferior edge of the first rib is freed of intercostal muscle
attachments both anteriorly and posteriorly, a small blunt periosteal elevator is used
underneath the first rib to push pleura off the rib inferiorly. One is careful not to enter the
pleural space at this point. The first rib is mobilized from the subclavian vein anteriorly to the
brachial plexus posteriorly.
Next, the subclavius muscle located at the anterior aspect of the first rib next to the
subclavian vein is sharply divided. Care is taken to divide the muscle right on top of the rib
edge, without injuring the vein. The anterior scalene muscle between the artery and the vein
is then divided sharply. A right angle clamp is used to lift muscle fibers up and away from the
subclavian artery, and the muscle is divided with scissors leaving as much muscle as possible
on the first rib (Fig. 12.2C). This is done in stages, by lifting subsequent portions of the
anterior scalene muscle, so that one does not cut the artery.
A right angle clamp is then placed underneath the first rib to check the extent of
mobilization. The middle scalene muscle may at this time be pushed away from the first rib if
necessary. This is done with a periosteal elevator hugging the rib so as not to injure the long
thoracic nerve. With the first rib sufficiently mobilized, a bone cutter is placed anteriorly, and
the first rib divided next to the subclavian vein. The first rib is then divided posteriorly, with
great care taken not to injure the brachial plexus. Due to the extensive mobilization described
above, one can pull the rib inferiorly to visualize the nerve root. The rib is divided anterior to
the plexus and removed from the field (Fig. 12.2D).

A rongeur is then used to remove any remaining bony edges until they are smooth and
appear to be away from the neurovascular structures. The field is then inspected for
hemostasis and pleural tears. Next, the axillary space is filled with saline, and the patient is
given several positive pressure breaths to evaluate for a pneumothorax manifested as air
bubbles in the saline. If a pneumothorax is present, a 12-French chest tube is placed in the
second intercostal space through a separate incision. The wound is then closed in layers and a
sterile dressing is applied. The chest tube is connected to a Pleuravac at 20 cm water.

Figure 12.2 A: Axillary structures prior to rib resection. B: Schematic depiction of axillary structures. C: Anterior scalene
muscle being presented between tines of a right angle clamp for division. D: Appearance of the axilla after rib removal.
Please note the empty space between the borders of the removed rib.

Postoperatively, the patient is admitted overnight for observation. A plain chest radiograph is
obtained in the postoperative recovery area to evaluate for pneumothorax or confirm position

of the chest tube. If a pneumothorax is present, it is usually small and does not require
placement of a chest tube postoperatively. Pain is controlled with PCA overnight, and diet is
advanced as tolerated. No toradol or NSAIDs are given due to risk of bleeding. An arm sling is
used for comfort. On postoperative day 1, intravenous pain control is discontinued and
parenteral narcotics and muscle relaxants such as soma are started. Most patients are
discharged home on postoperative day 1.
Patients with venous TOS restart anticoagulation with Lovenox 72 hours after surgery.
They undergo a venogram 2 weeks after rib resection. If no stenosis is present at this time,
anticoagulation is stopped. If there is persistent subclavian vein stenosis, the patient
undergoes gentle percutaneous venoplasty, and anticoagulation is continued for 1 to 2
months, at which time vein patency is checked with duplex ultrasound. If there is vein
occlusion, anticoagulation is continued for a maximum of 6 months. These patients are
checked with serial ultrasounds every 2 months to evaluate vein patency. Once the vein is
patent, anticoagulation is stopped. It is stopped regardless of patency at 6 months. Patients
with arterial TOS undergo duplex evaluation at 6 months and 1 year after operation. All
patients receive physical therapy starting 2 weeks after the operation, focusing on posture
training and muscles in the shoulder, chest, and neck area, and eventually progressing to
mimicking work-related activities.

The complication rate of transaxillary first rib resection and scalenectomy is low. The most
common complication is pneumothorax, occurring at a rate of approximately 10%. Bleeding
and infection of the wound are rare. Injuries to nerves such as the brachial plexus or the long
thoracic nerve occur in less than 1% of cases. Symptom recurrence or failure of symptom
resolution occurs in about 10% of patients with neurogenic TOS, and management of these
patients presents several challenges beyond the scope of this chapter.
If significant bleeding is encountered during the operation, the imperative is to obtain
timely proximal and distal control. One may be able to repair venous injury without further
exposure by applying pressure proximally and distally on the vein to allow time for repair.
With arterial injury, distal control is obtainable via the existing exposure. Proximal control
will likely require additional exposure. A supraclavicular incision will allow proximal
subclavian control rapidly and without the need for patient repositioning. One must keep in
mind the important structures with this approach, including the phrenic nerve and the
thoracic duct (on the left side). Packing of the operative field to temporize bleeding will allow
time for systematic exposure. Arterial repair is accomplished once proximal and distal control
is obtained. Postoperative bleeding, namely significant hematoma, is usually managed via the
existing axillary incision.

The results of transaxillary first rib resection and scalenectomy are best measured by
resolution of symptoms, return to work and daily activities, and effects on quality of life. In

neurogenic TOS, this operation has been shown to result in significant improvements in
patients quality of life. Furthermore, long-term follow-up (mean 44.7 months) of patients
after surgical decompression for neurogenic TOS reveals that the improvement in quality of
life continues over time. Poorer outcomes are associated with coexisting chronic pain
syndromes, neck and/or shoulder disease, other systemic diseases, smoking, age >40 years,
and opioid use. Successful symptom resolution has also been shown in patients with venous
TOS who undergo transaxillary first rib resection and scalenectomy with close postoperative
follow-up based on several algorithms.

Transaxillary first rib resection and scalenectomy is a safe and effective operation for
neurogenic, venous, and arterial TOSs. With careful patient selection, meticulous surgical
technique, and attention to postoperative management, this operation improves the quality of
life in patients with TOS.

Recommended References and Readings

Call D, Grunebach HL, Freischlag JA. Role of the Noninvasive Vascular Laboratory in
Thoracic Outlet Syndrome. AbuRahma AF, eds. Noninvasive Vascular Diagnosis. London:
Springer-Verlag; 2013:499504.
Chang DC, Lidor AO, Matsen SL, et al. Reported in-hospital complications following rib
resections for neurogenic thoracic outlet syndrome. Abb Vasc Surg. 2007;21(5):564570.
Chang DC, Rotellini-Coltvet LA, Mukherjee D, et al. Surgical interventions for thoracic outlet
syndrome improves patients quality of live. J Vasc Surg. 2009;49:630635.
Chang KZ, Likes K, Demos J, et al. Routine venography following transaxillary first rib
resection and scalenectomy (FRRS) for chronic subclavian vein thrombosis ensures
excellent outcomes and vein patency. Vasc Endovascular Surg. 2012;46(1):1520.
Chang KZ, Likes K, Demos J, et al. The significance of cervical ribs in thoracic outlet
syndrome. J Vasc Surg. 2013;57(3):771775.
Christo PJ, Christo DK, Carinci AJ, et al. Single CT-guided chemodenervation of the anterior
scalene muscle with botulinum toxin for neurogenic thoracic outlet syndrome. Pain Med.
2010; 11(4):504511.
DeLeon RA, Chang DC, Hassoun HT, et al. Multiple treatment algorithms for successful
outcomesin venous thoracic outlet syndrome. Surgery. 2009;145:500507.
Guzzo JL, Chang K, Demos J, et al. Preoperative thrombolysis and venoplasty affords no
benefit in patency following first rib resection and scalenectomy for subacute and chronic
subclavian vein thrombosis. J Vasc Surg. 2010;52(3):658662.
Lum YW, Brooke BS, Likes K, et al. Impact of anterior scalene lidocaine blocks on predicting
surgical success in older patients with neurogenic thoracic outlet syndrome. J Vasc Surg.
2012; 55(5):13701375.
Rochlin DH, Gilson MM, Likes KC, et al. Quality-of-life scores in neurogenic thoracic outlet
syndrome in patients undergoing first rib resection and scalenectomy. J Vasc Surg.

Rochlin DH, Likes KC, Gilson MM, et al. Management of unresolved, recurrent, and/or
contralateral neurogenic symptoms in patients following first rib resection and
scalenectomy. J Vasc Surg. 2012;56(4):10611067.

Part III
Chest Wall/Pleural Space/Diaphragm:
Pectus Repair

13 Pectus Excavatum: The Nuss Repair

Daniel P. Doody


Pectus excavatum, depression of the sternum and parasternal cartilages, is the most common
congenital chest wall abnormality, accounting for approximately 90% of chest wall defects.
The second most common abnormality, pectus carinatum, accounts for 5% to 6% of chest
wall anomalies where more complex abnormalities including Poland syndrome, Silverman
Currarino syndrome, sternal cleft, and asphyxiating thoracic chondrodystrophy (Jeune
syndrome) are rare chest wall abnormalities.
Pectus excavatum occurs in approximately 1 in 300 to 400 births. There is a definite male
predominance with a male to female ratio of 3:1 to 4:1. In addition, an ethnic predisposition
is seen as Caucasian children and adolescents have a much higher incidence of pectus
excavatum as compared to children of African American or East Asian descent.
In approximately half of the children who present for evaluation of pectus excavatum, some
sternal depression may be noted in early childhood, with some parents dating the
abnormality to infancy. However, many families will report the new appearance of the sternal
depression in the preadolescent or early adolescent age period when somatic growth
Approximately 25% to 35% of children who present for evaluation of the chest wall defect
will identify other family members as having a chest wall abnormality, either pectus
carinatum or pectus excavatum. Approximately 5% of children will have identifiable genetic
or connective tissue disorders such as Noonan syndrome or Marfan syndrome. In particular,
children with Marfan syndrome have a much higher incidence of failure of repair following
surgical correction of the pectus excavatum defect, which needs to be considered when
recommending repair to the family.
There is no question that the chest wall abnormality often affects the childs perception of
his/her body image and exercise capacity. Controversy exists regarding the physiologic
consequences of pectus excavatum although more recent data support that there is a
physiologic impairment because of abnormality in chest wall motion, particularly with
exercise, as well as compression and impingement on the right side of the heart with more
severe defects. Many children will have a mild restrictive defect on static pulmonary function
tests and typically will fall in the lownormal range during exercise stress test. The incidence
of mitral valve prolapse is much greater in patients with pectus excavatum as compared to
the general population.
The Nuss repair can be used in repair of adults who present with pectus excavatum defect.
The repair with a stiffer anterior chest wall may be associated with a greater degree of pain
and discomfort in the postoperative period. Moreover, the repair in the adult patient often
requires two or even three pectus bars to support and reshape the adult thorax. Although
minor, some series report a higher incidence of bar displacement, likely related to the more
rigid and less compliant chest wall.
Finally, the Nuss repair can be used successfully in reoperative pectus excavatum surgeries

whether the initial surgery was the minimally invasive repair or the open repair as described
by Ravitch and Welch. As with the adult repair, there does appear a higher incidence of bar
displacement and complications. In addition, the current thought argues that a more severe
defect, as measured by the Haller pectus index, is needed before reoperative surgery is
recommended. While there appears to be consensus that a Haller index of greater than 3.25
with symptoms is an indication for surgical correction of a pectus excavatum defect,
experienced authors have argued that a Haller index greater 3.7 should be seen and the
patient should be suffering symptoms (dyspnea, chest wall pain) before recommending repair
for retrusion following a previous pectus excavatum repair.

A variety of symptoms may occur in the patient with the pectus excavatum defect, or the
patient may have no symptoms but a clinically apparent anterior wall depression. In our
practice, it is infrequent that preschool-aged or early school-aged children are evaluated.
However, children in the early school years with a clinically apparent pectus excavatum may
present for evaluation. These younger children frequently have few complaints in terms of
exercise intolerance or chest wall pain.
The more typical patient is the preadolescent or a child in the early teenage years,
frequently with the new appearance and progression of symptoms that may be associated
with the chest wall abnormality. Most, but not all, patients will report some increasing
dyspnea on exertion, particularly with low-intensity, long-duration exercise such as distance
running, swimming, rowing, or bicycle riding as compared to anaerobic exercises where highintensity, short-duration muscle activity is needed, such as sprinting or weightlifting. Often,
the patient will report that they can sprint without problem but middle distance running will
often lead to early fatigue and exhaustion. Shortness of breath at rest is very atypical in this
age group and may need additional cardiac and pulmonary evaluation.
Chest wall pain is commonly noted, particularly in the area of the parasternal cartilages
and sternum. Young women may note unilateral breast hypoplasia, particularly with
asymmetrical chest wall defects.
Finally, body image issues in this particular teenage and young adult age group should not
be ignored and the psychosocial pressures can be significant to the point that it is often life
altering (I wont take off my shirt.; I am considering not having children.; I have stopped
playing sports.) to infrequent, but worrisomely life-threatening, concerns (I cant live like
A past history of known metal allergy or adverse reaction to jewelry should alert the
clinician that a nickel allergy may be present. Nickel is a component of the stainless steel
pectus bar and has been identified as an allergen. The potential adverse effects include an
erythematous macular rash, the development of excessive granulation tissue at the surgical
sites, wound separation, and pleural effusions. For patients with known nickel allergy,
individualized preshaped titanium pectus bars can be manufactured for correction of the
symptomatic chest wall defect but must be ordered before surgery can be scheduled. These
titanium bars are more brittle and should not be reshaped at the time of the operation.
Physical examination often demonstrates typical findings including the posterior deflection

of the sternum that may involve the lower sternum or involve the entire sternal body below
the manubrium. Many times, the defect is asymmetrical, typically with the greater depression
seen on the right side. There is often some costal flaring, which needs to be pointed out to the
patient and family as that may become more prominent after surgical correction using the
Nuss technique. The shoulders are frequently inturned. The surgeon should listen carefully for
a systolic click, which may indicate mitral valve prolapse. Additional skeletal abnormalities
including scoliosis or kyphosis should be noted. Other clinical signs including a high-arched
palate, crowded teeth, poor vision, abnormal long arms, joint laxity, or striae without recent
weight gain or loss with an associated chest wall defect may be seen with Marfan syndrome.
Measurement from the midaxillary line to midaxillary line at the point of greatest chest
depression should be recorded as that measurement helps to determine the length of the
pectus bar used during the surgical correction. The pectus bar length is often 2 to 3 cm less
than the midaxillary to midaxillary line measurement.

Figure 13.1 Axial CT imaging at point of greatest sternal depression to determine Haller index. The internal transverse
measurement is divided by the internal anteroposterior measurement from the sternum or parasternal tissue to the anterior
border of the vertebral body.

Imaging studies have proven the most helpful in determining whether surgical correction
should be recommended. The Haller index, a CT-derived measure, is generally accepted as the
most accurate measurement of the severity of the chest wall defect. This CT scan of the chest
without contrast allows the surgeon and radiologist to determine the internal transverse
diameter of the chest at the point of greatest depression as well as the anteroposterior
distance from the retrosternal or parasternal point of greatest depression to the anterior
vertebral body (Fig. 13.1). The general population without a chest wall defect will have a
Haller index of 2.5. Although authors vary at the Haller index value where they would
recommend surgical correction, an index greater than 3.25 is used in our institution. In the
asymptomatic patient, an abnormal Haller index alone is not an indication for surgical repair.
However, most patients are experiencing symptoms before presenting to the pediatric surgeon
or thoracic surgeon for evaluation of the chest wall defect.
If the Haller index is greater than 3.25, an echocardiogram is performed to look for aortic
root dilatation or mitral valve prolapse. The presence of mitral valve prolapse is an indication
for surgery, as this valvular abnormality may disappear following correction. If aortic root
dilatation is found, evaluation by cardiology and genetics is performed before we recommend
surgical correction. Significant compression of the heart chambers by the pectus defect is also

considered an indication for surgery.

Exercise pulmonary function tests are performed, which we feel more accurately reflect the
cardiopulmonary effects associated with the pectus excavatum defect. The vast majority of
children will show low, normal, or below normal values, particularly in oxygen delivery and
cardiac output with exercise. Below normal values on the exercise stress test makes a strong
argument that correction of the chest wall defect is indicated.
A similar preoperative evaluation will be performed for adult patients or patients with
recurrent pectus excavatum defects who are being considered for repair.
Generally, we do not recommend repair of a pectus excavatum defect in the preschooler or
elementary school-aged child. The classic open repair in this age group is contraindicated
because of the potential of the abnormal chest wall scarring and secondary thoracic
chondrodystrophy. While this abnormal scarring does not seem to be an issue in patients
following the Nuss repair, our concern for retrusion during the adolescent growth spurt leads
us to recommend repair at the beginning of the growth spurt (ages 8 to 12) with the
expectation that correction and stabilization of the chest wall during the growth spurt would
be ideal. However, a more typical patient who first presents to our practice would be a
teenager who has completed his/her growth spurt and noted either new appearance of the
pectus defect or significant worsening of the chest wall depression.

Figure 13.2 SilvermanCurrarino defect with broad superior pectus carinatum defect often associated with a lower sternal
pectus excavatum anomaly and congenital heart defects.

For some chest wall defects, the Nuss repair without removal of parasternal cartilages may
result in unsatisfactory outcome. The SilvermanCurrarino syndrome, or pouter pigeon chest
wall deformity (Fig. 13.2), is a rare anomaly, often associated with congenital cardiac defects
that requires an open correction of the superior pectus carinatum portion of the mixed chest
wall defect while the Nuss repair can be used to support the lower sternal pectus excavatum

defect. The etiologic cause of the sternal abnormality is believed to be related to premature
fusion of the manubrialsternal junction in addition to early fusion of other sternal elements
that may result in a foreshortened sternum.
The severe, broad-based upper carinatum defect typically does not respond to orthotic
bracing, and these young patients will not have significant chest wall remodeling with
correction of the lower pectus excavatum defect alone. A combined repair to address the
mixed pectus carinatumpectus excavatum abnormality should be recommended. We have
used the Nuss repair to correct the lower sternal pectus excavatum defect while removing the
parasternal cartilages as one would with an open correction of the pectus carinatum defect.
Often, several sternal osteotomies, or even wedge resection of the sternum with osteotomies,
are necessary to address the severe anterior angulation of the upper sternum to have the best

In most patients, an epidural catheter is placed for intraoperative and postoperative pain
management. The patient is returned to the supine position and induced with general
endotracheal anesthesia. While other centers prefer the patient in a simple shoulder abducted
position on boards, our preferred position for a standard repair is with the arms elevated and
flexed over the head, placed either in an arm cradle or attached to a padded ether screen.
After an appropriate patient position has been obtained, the chest and lateral chest walls are
sterilely prepped and draped from above the sternal notch to below the costal margins. We
use an iodophor-impregnated adhesive drape to cover this wide surgical field and hold the
underlying sterile towels in place.
Before the procedure begins, the surgical team selects the intercostal spaces for the planned
bar placement close to the point of greatest sternal depression. If a single bar is planned, 4- to
6-cm lateral chest wall incisions from the anterior axillary line to the midaxillary line are
made simultaneously at the point of greatest depression. It has been our practice to use a twoteam approach with surgeons working on both sides of the thorax simultaneously. This lateral
chest wall dissection typically brings us directly onto the serratus anterior muscles while
being anterior to the latissimus dorsi muscles. Subcutaneous pockets are created above the
fascia of the serratus muscles, extending in a cephalocaudad (vertical) direction for the later
placement of the stabilizing bars. Once the lateral pockets are of adequate size, we dissect
anteriorly in the subcutaneous plane above the muscular fascia to the tip of the pectus ridge.
In most cases, this dissection is at the inferior margins of the pectoralis major and pectoralis
minor muscles.
Although we have used bilateral thoracoscopic guidance, particularly with severe pectus
excavatum defects, in most cases we will place a single right-sided 5-mm Thoracoport for
thoracoscopic visualization of the anterior mediastinal dissection and placement of the pectus

bar. The right side port placement is chosen to direct the dissection as the depressed left
sternal border is obscured by the heart and pericardium. This right-sided port is introduced
inferior to the right-sided subcutaneous pocket, typically in the eighth intercostal space. A 5mm 30-degree-angled thoracoscope placed into the right chest provides good field
visualization for the procedure (Fig. 13.3).
We do use carbon dioxide insufflation during our dissection with the settings at 6 to 8 mm
Hg and 2 L of flow. This additional intrathoracic positive pressure helps to prevent loss of
visual field during the mediastinal dissection with expansion of the native lung from positive
pressure ventilation with general anesthesia.
Under vision, the pectus introducer is placed into the right hemithorax. With the tip of the
pectus introducer at the junction of the sternum and the anterior pleura, a cephalocaudad
rubbing/abrasion is used to bluntly create a space in the right-sided pleura and begin the
dissection in the anterior mediastinum. Once a small space is created, the surgeon uses the
pectus introducer to displace the pericardium in a posterior direction and away from the
sternum by moving the tip of the instrument in an anteriorposterior direction (Fig. 13.4).
Moving slowly and cautiously across the sternum with the tip of the pectus introducer firmly
pressed anteriorly against the posterior sternum, the surgeon enters through the contralateral
left pleural space above the pericardium and into the left hemithorax.

Figure 13.3 Right-sided thoracoscopic view of pectus excavatum defect.

Figure 13.4 Retrosternal dissection using the pectus introducer with posterior deflection of the adjacent pericardium.

Once the tip of the pectus introducer is palpated at the previously marked left-sided
intercostal space, the pectus introducer is forcibly directed anteriorly to exit the left
hemithorax at the most superior portion of the left-sided pectus ridge. A small retractor is
placed to lift the anterior margin of the left lateral chest wall incision, so that the left-sided
surgical team can visualize the tip coming through the intercostal muscles (Fig. 13.5). The
pectus introducer can most frequently be introduced bluntly through the intercostal muscles.
In some instances, the tough pericardium will be caught by the tip of the pectus introducer
and brought to the surface even through the intercostal muscles. The surgical team should be
aware that if this white fibrous pericardial tissue is seen, the pectus introducer needs to be
withdrawn and placed again after extending the dissection into the left hemithorax and
displacing the pericardium posteriorly.
If the depression is so severe that the surgeon cannot keep the tip of the pectus introducer
in view during the retrosternal dissection, a second bar should be placed one to two
intercostal spaces superior to the point of greatest depression. Elevating the more superior
sternum almost invariably improves the sight lines for the lower bar to be placed safely.

Figure 13.5 View from the head of the operating table: Pectus introducer exiting the left chest at the pectus ridge just lateral
to the retractor.

Figure 13.6 Orange aluminum templates contoured to the patients chest wall for planned shaping of pectus bar. The
template helps to determine the bar length that would be appropriate for the patient. Cotton cloth cord has been divided and
separated for the planned bar placement.

Once the pectus introducer has been placed across the anterior mediastinum and brought
out onto the anterior surface of the left chest, the pectus introducer is forcibly lifted in an
anterior direction, often several times, almost to the point that the pectus excavatum defect
appears and corrected by the pectus introducer. This maneuver may help to prevent
intercostal muscle injury when the bar is flipped.
A long length of cloth cord tape (approximately 100 to 110 cm) is introduced to the eyelet
at the tip of the pectus introducer, and then the pectus introducer is withdrawn under vision
from the left hemithorax, through the anterior mediastinum, and back out through the rightsided chest wall incision. The cloth cord tape is divided at its midpoint, with one cord to
guide the pectus bar through the dissection plane while the other cord is reserved as a safety
measure in the event there is a problem with the introduction of the pectus bar, and the
initial cloth cord tape breaks or unties from the pectus bar.
We use the orange aluminum template to determine the approximate length and shape of
our planned correction (Fig. 13.6). As with the pectus bars, the templates are serially sized
from lengths of 7 to 17 in in 1-in increments.
Using the tabletop bar bender and the hand-held bar bender, the pectus bar is individually
shaped to the patients corrected chest wall contour. Once shaped, one of the cloth cord
tapes is tied through the opening at the end of the pectus bar. The bar with the convex side
directed posteriorly is then introduced from the left hemithorax, underneath the sternum
through the anterior mediastinum (Fig. 13.7), and out through the right hemithorax under
vision. When first placed, the convexity of the pectus bar is facing posteriorly toward the
heart, and the ends of the bar will be facing anteriorly and above the anterior chest (Fig.

Figure 13.7 Thoracoscopic view from the right chest showing pectus bar exiting the mediastinum.

Figure 13.8 Pectus bar after placement with convex side positioned posteriorly.

The thoracoscope is removed from the chest as the rotation of the bar may catch the
telescope and break it. The bar flippers are then placed at the end of the bars and rotated
simultaneously (Fig. 13.9). The bars may be rotated in a superiorinferior direction or in an
inferiorsuperior direction. Occasionally, if we are concerned that after the initial rotation the
bar placement is not stable on the anterior chest when we check thoracoscopically (the bar
appears angled rather than lying flat against the sternum), we will rotate the bar in the
opposite direction to see if the bar appears more stable and flat against the anterior
musculoskeletal wall.
If the correction does not appear to be sufficient, the bar may need to be withdrawn and
reshaped using the bar benders. With an inadequate correction, we first check to determine if
there has been posterior displacement of the bar, typically seen by tears in the intercostal
muscle posteriorly. This intercostal tearing is a particular problem for the adult patient and in
those patients who are having repair of a recurrent pectus excavatum defect. If the intercostal
muscles cannot support the bars, the use of an additional pectus bar is almost certainly
needed. If there is no tear in the intercostal muscles, the bar is removed and can be reshaped
to ensure an adequate correction.
Once satisfied with the correction, the stabilizing bars are placed over the ends of the bar

and secured with a 22-gauge wire to prevent pectus bar rotation. The stabilizing bars and the
pectus bar itself are then secured to the muscular chest wall using a series of interrupted 0
Vicryl sutures. We prefer the UR-6 needle as the 5/8 needle curve passes easily from the
muscular chest wall and through the eyelet of the stabilizing bars and pectus bar.

Figure 13.9 Pectus bar flipped 180 degrees into position with immediate correction of the chest wall deformity.

While the surgical teams are securing the pectus bar and stabilizing bars to the muscular
chest wall, the thoracoscope is removed and a 16-French chest tube is passed through the
Thoracoport and directed superiorly. The Thoracoport is slid backward over the chest tube
and removed from the right hemithorax. The chest tube is then placed to Pleur-evac drainage
at 20 cm of water during the closure. We previously used red rubber catheters passed
through the Thoracoport, aspirating the pleural spaces with 60 mL irrigation syringes but
found that several patients had moderate, often bilateral, pneumothoraces identified on their
postoperative x-rays. The use of the chest tube and Pleur-evac suction during closure has
essentially eliminated that problem. After the surgical sites are closed, the patient is placed in
Trendelenburg position and airplaned with the left side down, and several large, positive
pressure inspiratory breaths are given by the anesthesia team to help evacuate any residual
intrathoracic carbon dioxide. Once the Pleur-evac shows that there is no additional carbon
dioxide to be evacuated, a U-suture is placed at the chest tube site, and the chest tube is
If two bars are needed for the repair, we typically make separate incisions for each bar
placement. The superior bar is also positioned over the serratus anterior muscle, but we will
then tunnel the superior bar under the pectoralis major and minor muscles when we create
our tunnel for bar placement. If there is definite need for two bar placements because of the
length of the pectus excavatum defect or because it is a second repair, placing and turning the
initial bar at the less severe portion of the defect often facilitates instrumentation and bar
placement at the more severely depressed portion.

A postoperative chest x-ray is obtained. As mentioned in techniques, the placement of a chest
tube through the Thoracoport site placed to negative suction drainage at the end of the

operative procedure has minimized the risk of postoperative pneumothoraces of significance.

If there is a persistent air leak seen in the operating room (almost only seen in repair of a
recurrent chest wall defect), the chest tube will remain in place and to suction until the air
leak is no longer seen.
Most postoperative care is primarily directed at pain management, and it can be a
challenge. Our own pain management is the use of an anestheticnarcotic mix (bupivacaine
hydromorphone; bupivacainefentanyl) delivered by epidural via a patient-controlled
epidural pump and regular administration of nonsteroidal anti-inflammatories. As many of
our patients have anorexia in the early postoperative period, intravenous ketorolac is
typically given in the first 48 hours. We continue regular dosing of naproxen or ibuprofen
once the patients appetite improves. As the patient tolerates diet, we transition to oral pain
medications including oxycodone or hydromorphone and continue the oral nonsteroidal antiinflammatories. Once the pain is controlled with oral medication, the patient is ready for
discharge, typically on the fourth to sixth hospital day.
Before discharge, standard posteroanterior and lateral chest x-rays are obtained. In
particular, the lateral chest x-ray helps to determine the baseline position of the bar. This
baseline position is an important comparison point to determine if bar rotation has occurred,
particularly if there are complaints of chest pain or bar movement at any point in the
postoperative recovery.
As many patients are discharged home with oral opioids for continued pain management,
the bowel management program begins in the hospital with the initiation of diet, using
polyethylene glycol and docusate sodium. These medications continue until the patient is
evacuating regularly and without discomfort. If the patient has not been able to evacuate
before discharge, we strongly encourage them to accept an enema as severe constipation at
home has been an issue for some patients.
There is no restriction in sleeping position although most patients will sleep in the supine
position in the early recovery. Many patients report that they are more comfortable with a
slight head up position, and a reclining cushioned chair is often reported as the most
comfortable sleeping platform.
The patients ambulate with assistance on the first postoperative day and are encouraged to
sit for short periods of time (15 to 30 minutes) in their room. As the postoperative pain
abates, further activity is encouraged. At home, a walking program is initiated and
recommended to continue at discharge. The program should gradually advance the distance
that is covered over the first 7 to 14 days at home. Weightlifting of moderate to heavy
weights is not allowed in the first month after the surgery. As the patient becomes more
comfortable, aerobic activity such as running or swimming can resume, even in the first
month. Activity that is associated with torso rotational motion is not allowed for the first 2
postoperative months. This includes most sports, particularly tennis, golf, baseball batting,
hockey, and soccer. After 2 months, we allow our patients to resume sports, including contact
At the first postoperative visit, it is our practice to give the families a letter for airplane
travel, explaining that metal hardware has been surgically placed, and we encourage our
patients to obtain a medical alert bracelet to identify the pectus bar in the chest in the event
of an emergency.

Bar Removal

Although the bars may remain in place without the need for removal, most patients report
vague chronic pain and discomfort at the chest wall site and removal of the bars would be
indicated. For the best long-term result and to minimize the risk of recurrence, the bars need
to remain in place for at least 2 years. In our own experience with older patients, we typically
recommend leaving the bar in place for a longer period of time, typically 3 to 4 years. In
these late teenage patients and young adults, we may see chest wall remodeling into the third
and fourth year. An examination is performed, and we do perform CT imaging of the chest to
check surgical anatomy, location of the bar, and to determine if there is heterotopic
calcification around the bar before removal.
Unlike bar placement, the bar removal is typically performed as a day surgery operation.
As it has been our practice to place stabilizing bars, if possible, on both ends of the pectus
bar, the surgery begins by opening through the previous incisions and dissecting down to the
fibrous capsule that surrounds the pectus bar and the stabilizing bars. These capsules are
embedded in the serratus anterior muscle. The stabilizing bars are removed after removing
the wires used for fixation. The pectus bar is straightened using bar benders and then
withdrawn through either the left or right chest. Thoracoscopy is not required for bar
With dissection into the muscles, there is discomfort although this postoperative pain is
typically managed easily by oral analgesics. The procedure is performed as an outpatient
surgery, and the patient is discharged home after awakening in the recovery room. A
postoperative chest x-ray is obtained to exclude a pneumothorax.
Six months following bar removal, exercise pulmonary tests are performed as a baseline to
determine if exercise tolerance has remained stable, worsened, or improved. In our
experience, we almost invariably find that the values are stable or slightly improved.

Early Complications
Early complications are problems commonly associated with chest surgery. In our own
experience, we have not had to place a chest tube for a pneumothorax, pleural effusion, or
hemothorax in the typical preteen or teenager who presents for an initial repair. Patients
undergoing repair of recurrent pectus excavatum defect do have a higher incidence of pleural
adhesions and are at greater risk for postoperative air leaks. In those cases, if an air leak is
found when the chest tube is placed to evacuate the carbon dioxide following the Nuss
procedure, the chest tube is left in place until the air leak ceases, typically within 48 to 72
Our practice is to continue antibiotics for 48 hours following the hardware implantation.
Infection is unusual but has occurred once. Suture reactions will occur in rare patients and
reports with a larger population suggest that this problem is present in approximately 1% of
their cases.
With postoperative chest wall pain, atelectasis is common on follow-up x-rays although

clinical symptoms associated with atelectasis (cough and fever) are infrequent as our practice
is to encourage early mobilization and incentive spirometry is started on the afternoon of the
operative day. On occasion, pleural effusions complicating the procedure are identified
although the need to drain a pleural effusion has not occurred in our practice, and a large
pleural effusion requiring drainage would be considered a rare complication in larger series
(less than 1%).
Late Complications
Identification of technical problems that occurred in the initial Nuss repair experience led to
compositional changes in the pectus bar as well as development of hardware and techniques
to stabilize the pectus bar. During that early experience, bar displacement or rotation was
considered a common problem, occurring in up to 15% of cases. More recent experience
would suggest that the incidence of bar rotation or displacement is low but may occur in 2%
to 5% of cases following an initial repair. This rate of displacement is higher in an adult
patient and in patients undergoing repair of a recurrent pectus excavatum defect.
In the current era, the risk of retrusion (recurrent sternal depression) after bar removal
appears to be in the range of 1% to 2%, a risk that appears to be lower than the risk of
recurrence that has been previously reported with the open repair of the pectus excavatum
Even after screening for a nickel allergy, a macular, erythematous rash, typically limited to
the distribution of the bar may appear early or late in the postoperative course. This rash may
be along the entire path of the pectus bar or limited to one or both surgical sites. Other skin
and soft tissue problems, including the sudden appearance of granulation tissue and swelling
at the lateral chest wall incisions, may be the first manifestation of a nickel or metal allergy.
Interestingly, some children, who develop the subcutaneous and soft tissue signs after pectus
bar implantation, are not positive for a nickel allergy on subsequent testing. Persistent pleural
effusions have also been associated with the placement of the pectus bar in a child with a
known metal allergy. At many centers performing the Nuss procedure, testing for a metal
allergy has become part of the routine preoperative screening and should be considered
postoperatively in patients who have patchy erythema around the location of the pectus bar.
If a nickel allergy is discovered after bar placement, a short course of systemic steroids may
avoid the need for bar removal. In those rare patients who recently have had corrective
surgery but had serious cutaneous manifestations including skin breakdown, replacement of
the bar with a titanium pectus bar has been shown to resolve the allergic response while
preserving the pectus correction.
Rare patients have chronic severe pain that is poorly explained by the operative repair and
appears to be neuropathic. In our own experience, one patient had the bar removed at 7
months because of the severity of the chest wall discomfort. However, an additional 1% to
2% of patients in our experience have had additional consultation by the pain service to try
to address this chronic neuropathic pain. In some instances, additional psychiatric
consultation may help design a program of behavioral modification, meditation, or guided
visualization, and occasionally prescribe medication that can help with anxiety that may be
associated with chronic pain.

Figure 13.10 A: CT imaging of a patient with a Haller index of 11.2 before surgical correction. B: Haller index of 2.6 in the
preoperative evaluation before bar removal, 4 years following the Nuss repair.

Unfortunately, catastrophic cardiac injury has occurred with placement and removal of the
bar and needs to be considered as a potential risk that is seen with the Nuss repair and
unlikely to occur with the more classic Ravitch repair. In some centers, a sternotomy
operating room surgical setup is immediately available as part of their practice with bar
placement and/or removal.

The reports of improvement in the physiologic parameters following the Nuss pectus
excavatum repair are mixed. Studies vary with some showing an improvement in static
pulmonary function although other reports show stable but unimproved pulmonary function
in postoperative testing. Most authors agree that with successful correction of the pectus
defect using the Nuss repair, exercise stress test does show improvement in cardiac function
with improved cardiac filling and an increased stroke volume with exercise, possibly related
to relief of right-sided cardiac compression (Fig. 13.10).
Studies evaluating both quality of life and overall patient satisfaction show that the patients
and their families perceive a significant improvement in the appearance of the chest wall
(Fig. 13.11). Most report that the surgical correction is good to excellent in greater than 90%
of cases. This perceived improvement often is associated with improved psychosocial scores
on standardized testing.

Figure 13.11 Preoperative and immediate postoperative appearance of the chest wall following Nuss repair of a moderate
pectus excavatum defect.

Modifications and improvement of hardware and technique have led many pediatric surgeons
and some thoracic surgeons to use the Nuss repair as their preferred technique for pectus
excavatum repair. As experience has been gained, the length of time the hardware needs to
be in place has been elucidated, the importance and technique of stabilization has minimized
the early risk of bar rotation, and modifications of the composition of the hardware has
resulted in less malleable bars that are able to withstand posteriorly directed forces of the
pectus defect. In our own practice, placing a chest tube through the Thoracoport site at the
end of the procedure has essentially eliminated postoperative pneumothoraces.
Overall, our experience with the Nuss repair of pectus excavatum defects has been
rewarding. Like many groups, our initial experience was with the pediatric patient. We
gradually extended the use of this minimally invasive surgical correction to adults for a
primary repair, as well as pediatric and adult patients with recurrence of the pectus
excavatum defect following open or previous Nuss repairs. The patient satisfaction following
repair is generally excellent, with improved appearance of the chest, the subjective feeling
that exercise tolerance is better, and the psychosocial benefits of an improved body image.

Recommended References and Readings

Brichon PY, Wihlm JM. Correction of a severe pouter pigeon breast by triple sternal
osteotomy with a novel titanium rib bridge fixation. Ann Thorac Surg. 2010;90:e97e99.
Croitoru DP, Kelly RE Jr, Goretsky MJ, et al. The minimally invasive Nuss technique for
recurrent or failed pectus excavatum repair in 50 patients. J Pediatr Surg. 2005;40:181187.
Haller JA Jr, Kramer SS, Lietman SA. Use of CT scans in selection of patients for pectus
excavatum surgery: A preliminary report. J Pediatr Surg. 1987;22:904906.
Hebra A. Minimally invasive repair of pectus excavatum. Semin Thorac Cardiovasc Surg.
Hebra A, Jacobs JP, Feliz A, et al. Minimally invasive repair of pectus excavatum in adult
patients. Am Surg. 2006;72:837842.
Kelly RE Jr, Cash TF, Shamberger RC, et al. Surgical repair of pectus excavatum markedly

improves body image and perceived ability for physical activity: Multicenter study.
Pediatrics. 2008;122:12181222.
Kelly RE, Goretsky MJ, Obermeyer R, et al. Twenty-one years of experience with minimally
invasive repair of pectus excavatum by the Nuss procedure in 1215 patients. Ann Surg.
Kelly RE Jr, Mellins RB, Shamberger RC, et al. Multicenter study of pectus excavatum, final
report: Complications, static/exercise pulmonary function, and anatomic outcomes. J Am
Coll Surg. 2013;217:10801089.
Kelly RE Jr, Shamberger RC, Mellins RB, et al. Prospective multicenter study of surgical
correction of pectus excavatum: Design, perioperative complications, pain, and baseline
pulmonary function facilitated by internet-based data collection. J Am Coll Surg.
Lawson ML, Mellins RB, Tabangin M, et al. Impact of pectus excavatum on pulmonary
function before and after repair with the Nuss procedure. J Pediatr Surg. 2005;40:174180.
Nuss D. Minimally invasive surgical repair of pectus excavatum. Semin Pediatr Surg.
Nuss D, Croitoru DP, Kelly RE Jr, et al. Review and discussion of the complications of
minimally invasive pectus excavatum repair. Eur J Pediatr Surg. 2002;12:230234.
Nuss D, Kelly RE Jr. Minimally invasive surgical correction of chest wall deformities in
children (Nuss procedure). Adv Pediatr. 2008; 55:395410.
Nuss D, Kelly RE Jr. Indications and technique of Nuss procedure for pectus excavatum.
Thorac Surg Clin. 2010;20:583597.
Nuss D, Kelly RE Jr, Croitoru DP, et al. A 10-year review of a minimally invasive technique
for the correction of pectus excavatum. J Pediatr Surg. 1998;33:545552.
Redlinger RE Jr, Kelly RE Jr, Nuss D, et al. One hundred patients with recurrent pectus
excavatum repaired via the minimally invasive Nuss techniqueeffective in most regardless
of initial operative approach. J Pediatr Surg. 2011;46:11771181.
Redlinger RE Jr, Rushing GD, Moskowitz AD, et al. Minimally invasive repair of pectus
excavatum in patients with Marfan syndrome and marfanoid features. J Pediatr Surg.
Rushing GD, Goretsky MJ, Gustin T, et al. When it is not an infection: Metal allergy after the
Nuss procedure for repair of pectus excavatum. J Pediatr Surg. 2007;42:9397.
Yoon YS, Kim HK, Choi YS, et al. A modified Nuss procedure for late adolescent and adult
pectus excavatum. World J Surg. 2010; 34:14751480.

14 Pectus RepairRavitch

Konstantinos Papadakis and Robert C. Shamberger

Pectus excavatum is the most common chest wall deformity in infants, children, and
adolescents. Its incidence is estimated between 1 in 400 live births and 7.9 per 1,000 births.
There is a male to female ratio of 3:1. The etiology of pectus excavatum is unknown. There is
a positive family history of chest wall abnormalities in 37% of cases.
The sternal deformity in pectus excavatum may be either symmetrical or asymmetrical. In
the asymmetric deformity, the more severe depression is typically on the right side. In up to
90% of cases, the deformity can be seen within the first year of life.
Children with pectus excavatum may present with symptoms of shortness of breath,
dyspnea on exertion, and fatigue. Symptomatic improvement is frequently noted after repair.
However, consistent improvement in pulmonary function tests does not follow the repair. Due
to the restrictive nature of the defect, symptomatic improvement may be due to the relief of
anterior compression of the heart, especially on the right ventricle, as well as the release of
pulmonary compression. In addition to the physiologic components of the deformity, affected
children also can have adverse psychological consequences.
Indications for surgery include both assessments of physiologic and psychological
implications of the condition. Parents and patients must both be counseled on the risks and
expected benefits of surgical correction.

The most important factor in preoperative consideration is the severity of the deformity,
usually quantified by the Haller index. It can be determined from a standard AP and lateral
chest radiograph. It is defined as the ratio of the transverse diameter (the horizontal distance
of the inside of the thorax) and the anteroposterior diameter (the shortest distance between
the anterior aspect of the vertebrae and the posterior aspect of the sternum). A normal Haller
index should be about 2.5. Depression of the sternum will increase the index. A Haller index
of 3.25 or greater is the usual cutoff for consideration of surgery.
Additional evaluation can include an electrocardiogram, echocardiogram, and/or
pulmonary function tests, at the surgeons discretion. These evaluations may be required to
define the extent of the physiologic abnormality and to exclude other pathologic processes.
Another factor that must be considered is patient age. This may impact both physical and
psychological concerns. Correction of pectus excavatum at a young age, before relative
skeletal maturity, may lead either to a recurrence of the deformity during the pubertal growth
spurt or development of a constricting deformity of the chest wall resulting from impaired
chest wall growth. It is recommended to proceed with repair after the onset of puberty to
avoid these problems. Psychological maturity must also be evaluated to ensure that the rigors

of postoperative pain management, hospital stay, and activity restrictions are understood and
adhered to.

The Open Ravitch Procedure
The current standard open repair is attributed to Ravitch although his initial description
included the resection of the costal cartilage and the perichondrium with anterior fixation of
the sternum with Kirschner wires. Welch and Baronofsky in subsequent reports stressed the
vital importance of preservation of the perichondrium to achieve optimal regeneration of the
costal cartilage after repair.
The patient is placed supine on a well-padded table. Lower body Bair Huggers are used to
help maintain normothermia.
A transverse incision is made below and between the nipple lines. In females, particular
attention is taken to place the incision within the projected inframammary crease thus
avoiding complications of breast deformity and development. The pectoralis major muscle
is elevated from the sternum along with portions of the pectoralis minor and serratus
anterior bundles (Fig. 14.1).

Figure 14.1 Location of the incision and initial mobilization of the pectoral muscle flaps.

Figure 14.2 Creation of a plane between the pectoral muscle flaps and the chest wall.

The correct plane of dissection of the pectoralis muscle flap is defined by passing an empty
knife handle directly anterior to a costal cartilage after the medial aspect of the muscle has
been elevated with electrocautery. The knife handle is then replaced with a right-angle
retractor, which is pulled anteriorly. The process is then repeated anterior to an adjoining

costal cartilage. Anterior distraction of the pectoral muscle during the dissection facilitates
identification of the avascular areolar plane and avoids entry into the intercostal muscle
bundles (Fig. 14.2).
Elevation of the pectoral muscle flaps is extended bilaterally to the costochondral junctions
of the third to fifth ribs and a comparable distance for ribs six and seven or to the lateral
extent of the deformity.
Subperichondrial resection of the costal cartilage. The objective of this step is the removal
of the costal cartilage connecting the ribs to the sternum, while leaving the perichondrial
sheath in place. The cartilage removal will allow mobilization of the sternum, and the
remaining sheath will act as a conduit for rib regeneration after the repair. The resection is
achieved by incising the perichondrium anteriorly between the intercostal muscles (Fig.
14.3). The perichondrium is then dissected away from the costal cartilages in the bloodless
plane between perichondrium and the costal cartilage. Cutting back the perichondrium 90
degrees in each direction at its junction with the sternum facilitates visualization of the
back wall of the costal cartilage (Fig. 14.3).
The cartilages are sharply divided at their junction with the sternum as a Welch
perichondrial elevator is held posteriorly to elevate the cartilage and protect the
mediastinum (Fig. 14.4). The divided cartilage can then be held with an Allis clamp and
elevated. The costochondral junction is preserved by leaving a segment of costal cartilage
on the osseous ribs by incising the cartilage with a scalpel. Costal cartilages three through
seven are generally resected, but occasionally the second cartilages must be removed as
well. Segments of the sixth and seventh costal cartilages are resected to the point where
they flatten to join the costal arch. Familiarity with the cross-sectional shape of the medial
ends of the costal cartilages facilitates their removal. The second and third cartilages are
broad and flat, the fourth and fifth are circular, and the sixth and seventh are narrow and
Once the costal cartilages are all separated from the sternum, a sternal osteotomy is created
at the level of the posterior angulation of the sternum (Fig. 14.5). Generally, this is at the
level of the third cartilage. Two transverse sternal osteotomies are created through the
anterior cortex with a Hall air drill 3 to 5 mm apart, and the wedge of bone is partially
mobilized. The base of the sternum and the rectus muscle are elevated with two towel clips
and the posterior plate of the sternum at the osteotomy is fractured. The xiphoid can be
divided from the sternum if its anterior angulation produces an unsightly bump below the
sternum when it is elevated into its corrected position. The insertion of the rectus muscle
into the sternum can generally be preserved by dividing the xiphoid with electrocautery
through a lateral approach. Preservation of the attachment of the perichondrial sheaths and
xiphoid to the sternum, avoids an unsightly depression that can occur below it.

Figure 14.3 Omission of the perichondrial for resection of the costal cartilages.

A retrosternal strut is placed behind the sternum and is secured to the rib ends laterally to
prevent migration (Fig. 14.6).
The perichondrial sheath to either the fourth or fifth rib is divided from its junction with
the sternum to allow passage of the strut behind the sternum. It is secured with two
pericostal sutures at each end to prevent migration (Fig. 14.6). The wound is then flooded
with warm saline and antibiotic solution to remove clots and inspect for pleural entry. A
single-limb medium Hemovac drain is brought through the inferior skin flap and placed in
a parasternal position.

Figure 14.4 Division of the medial and lateral extent of the costal cartilages.

Figure 14.5 Creation of sternal osteotomy to allow anterior displacement of the sternum.

The pectoral muscle flaps are secured to the midline of the sternum, advancing the flaps
inferiorly to obtain complete coverage of the entire sternum (Fig. 14.7). The rectus muscle
fascia is then joined to the pectoral muscle flaps, closing the mediastinum.
The incision is meticulously closed in layers to prevent traction on the wound. Steri-strips
and an occlusive dressing are applied.

Figure 14.6 Location of the retrosternal strut which is passed through a tunnel created posterior to the anterior and anterior
to the pericardium.

Figure 14.7 Closure of the pectoral muscle flaps which are advanced inferiorly to cover the previously bone sternum. The
flaps are secured to both the sternum and to the rectus sheath.

Postoperative antibiotics are given for one dose. Pain control is managed by a variety of
techniques, which may include an epidural catheter, transpleural catheters, or intravenous
narcotics in the immediate postoperative period. A multidisciplinary strategy to optimize
postoperative pain may be very beneficial to the patient. Postoperative care should also
include a bowel regimen, pulmonary toilet, and early ambulation. The Hemovac drain is
removed when there is less than 15 mL drainage for an 8-hour shift. The average length of
stay for the Ravitch procedure is 3 to 5 days. Retrosternal struts are removed a minimum of 6
months after repair to allow solid fusion of the sternum fracture and complete regeneration of
the costal cartilages. The retrosternal struts are removed via a small incision over one end of
the strut as an ambulatory procedure.

Complications of the procedure include wound infection and pneumothorax. Wound infection
can be treated with oral or intravenous antibiotics, in severe cases. Most patients with
pneumothorax can be observed unless the pneumothorax is large enough to cause pulmonary
impairment. Excessive blood loss that requires transfusion is rare.
Recurrence of the defect is a well-documented occurrence. The use of strut fixation
optimizes early results. Delay of the repair until the patient has begun the pubertal growth
spurt and achieved much of the ultimate chest wall size will decrease the amount of chest
remodeling that occurs with continued growth. The risk of recurrence in large series with
adequate follow-up is approximately 5% to 15%. There can be progressive deterioration of
the repair over time, but once full stature is achieved, chest wall configuration is generally

quite stable. Rigid strut fixation is commonly applied to patients with Marfan syndrome
because of their well-recognized high risk of recurrence.
Limited postoperative rib growth has been noted to occur in children after operative repair
at an early age. It results in limited growth of the ribs after resection of the costal cartilages,
and produces a band-like narrowing of the midchest. This may be related to a growth plate
injury at the costochondral junction, which is the longitudinal growth center for the ribs.
Serious complications regarding strut bar migration have been identified. Intracardiac
migration, with resultant aorto-ventricular fistula, has been reported. Strut migration is more
common in struts that have been left in place for a prolonged postoperative period. Close
postoperative follow-up and routine bar removal is recommended to prevent this type of
serious, yet remote complication.

Deformity of the chest wall led many early authors to attribute the symptomatic improvement
in patients after pectus surgery to improvement in pulmonary function. Brown and Cook
performed respiratory studies on patients before and after surgical repair. Vital capacity was
normal in these patients, but maximal breathing capacity (MBC) was markedly diminished in
the majority of cases. MBC increased an average of 31% after surgical repair. Orzalesi and
Cook performed studies in 12 children with severe pectus excavatum. The group showed a
significant decrease in vital capacity, total lung capacity, and MBC from height-matched
normal children. When lung volumes were measured, absolute lung volumes increased only in
postoperative patients who had grown in height after surgery.
Cahill et al. performed preoperative and postoperative studies in pectus excavatum
patients. The pectus excavatum patients demonstrated low normal vital capacities unchanged
by operation, but a small improvement in their total lung capacity and a significant
improvement in the maximal voluntary ventilation. Exercise tolerance was also improved in
patients after surgery as determined by both total exercise time and the maximal oxygen
consumption although both of these factors would clearly be effort related.
Derveaux et al. studied pre- and postoperative PFTs in cases that involved extensive chest
wall dissection. The postoperative values for FEV1 and vital capacity were decreased in all
groups when expressed as a percent of predicted. Those with less than 75% of predicted
function had improved function after surgery whereas results were worse after surgery if the
preoperative values were greater than 75% of predicted. These physiologic results were in
contrast to the subjective improvement in symptoms from the subjects and the improved
chest wall configuration. The decline in pulmonary function in postoperative studies was
attributed to the surgery because the defect appeared stable regardless of the age of the initial
repair. Further studies suggested that the increased restrictive defect was produced by
extrapulmonary rather than pulmonary factors or that surgery produced increased rigidity of
the chest wall.
Wynn et al. showed that cardiac output and stroke volume increased appropriately with
exercise before and after operation in both groups, and operation was thought to have
produced no physiologically significant effect on the response to exercise.

Kelly et al. in a large prospective, multicenter study, reviewed pre- and postoperative
pulmonary function tests after surgical pectus correction using both the open and Nuss
technique. A separate cohort was subjected to both static and exercise pulmonary function
testing after 1 year. All groups demonstrated a significant improvement in lung function at
rest in VO2 max and O2 pulse following surgical correction. However, the cohorts who
underwent exercise testing early and at 1-year post correction, failed to show significant
improvement after repair. There is significant improvement in CT index following surgery,
but there is no significant improvement in exercise pulmonary functions when measured.
Overall, the studies of pulmonary function have failed to document consistent improvement
in pulmonary function resulting from surgical repair. Studies have indeed demonstrated
deterioration in pulmonary function at long-term evaluation attributable to increased chest
wall rigidity after surgery. Despite these findings, studies have shown improvement in
exercise tolerance after repair.
Depression of the sternum can deform the underlying heart, particularly producing anterior
indentation of the right ventricle. Exercise studies have shown that increased cardiac output
can be achieved primarily by increased heart rate as the stroke volume is limited. Intracardiac
pressures are normal at rest and with exercise despite the apparent limitation of ventricular
volume. Postoperative studies have shown an increase in cardiac index on average of 38%.
An enhanced stroke volume response was responsible for this increase as heart rate at
maximal exercise was not higher after surgery.
The degree of symptoms cannot be correlated with the severity of the anatomic defect.
Peterson et al. documented a marked decrease in symptoms after surgical correction of pectus
excavatum in a regulated exercise protocol, substantiating anecdotal reports regarding
symptomatic improvement after repair.

The open Ravitch procedure for pectus excavatum is well tolerated.
It has excellent structural results.
It has a low complication rate.
For optimal results, it should be performed after the patient has begun or completed their
pubertal growth spurt.
In cases of patients with connective tissue disorders, the struts will need to be left in for a
longer period of time to minimize the risk for recurrence.
Preoperative severity of the defect does not correlate with functional limitations.
Surgical correction of the pectus excavatum often leads to subjective improvement in
exercise tolerance.
Cardiac function may improve after repair with improvement in oxygen consumption and
cardiac index.
Objective recurrence rate is low.

Recommended References and Readings

Aydemir B, Sokullo O, Hastaoglu O, et al. Aorto-to-right ventricular fistula due to pectus

migration. Thorac Cardiovasc Surg. 2011;59:5152.

Bevegard S. Postural circulatory changes at rest and during exercise in patients with funnel
chest, with special reference to factory affecting the stroke volume. Acta Med Scand.
Borgeskov S, Raahove D. Long-term result after operative correction of funnel chest. Thorax.
Brown AL, Cook O. Cardio-respiratory studies in pre and post operative funnel chest (pectus
excavatum). Dis Chest. 1951;20:378391.
Cahill JL, Lees GM, Robertson HT. A summary of preoperative and postoperative
cardiorespiratory performance in patients undergoing pectus excavatum and carinatum
repair. J Pediatr Surg. 1984;19:430433.
Colborn GL, Weidman TA, Mirilas P, et al. Chapter 2. Thoracic wall and pleurae. In:
Skandalakis JE, ed. Surgical Anatomy: The Embryologic and Anatomic Basis of Modern Surgery.
Athens, Greece: PMP; 2004:117146.
Derveaux L, Clarysse I, Ivanoff I, et al. Preoperative and postoperative abnormalities in chest
x-ray indices and in lung function in pectus deformities. Chest. 1989;95;850856.
Derveaux L, Ivanoff I, Rochette F, et al. Mechanism of pulmonary function changes after
surgical correction for funnel chest. Eur Respir J. 1988;1:823825.
Haller JA, Kramer SS, Lietman A. Use of CT scans in selection of patients for pectus
excavatum surgery: A preliminary report. J Pediatr Surg. 1987;22:904906.
Humphreys GH II, Jaretzki A III. Pectus excavatum: Late results with and without operation. J
Thoracic Cardiovasc Surg. 1980; 80:686695.
Kelly RE Jr, Mellins RB, Shamberger RC, et al. Multicenter study of pectus excavatum, final
report: Complications, static/exercise pulmonary function, and anatomic outcomes. J Am
Coll Surg. 2013;217(6):10801089.
Morshuis WJ, Mulder H, Wapperom G, et al. Pectus excavatum: A clinical study with longterm postoperative follow-up. Eur J Cardiothoracic Surg. 1992;6:318329.
Orzalesi MM, Cook CD. Pulmonary function in children with pectus excavatum. J Pediatr.
Papadakis K, Shamberger RC. Congenital thoracic deformities. In: Prem Puri, ed. Newborn
Surgery. 3rd ed. London, Great Britain: Hodder Arnold; 2011:297304.
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function before and after pectus excavatum repair. J Thorac Cardiovasc Surg. 1985;90:251
Prevot J. Treatment of sternocostal wall malformations of the child: A series of 210 surgical
correnctions since 1975. Eur J Pediatr Surg. 1994;4:131136.
Ravitch MM. Operative treatment of congenital deformities of the chest. Am J Surg.
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Shamberger RC, Welch KJ. Surgical repair of pectus excavatum. J Pediatr Surg. 1988;23:615
Shamberger RC. Congenital chest wall deformities. Curr Probl Surg. 1996;33:469542.
Scherer LR, Arn PH, Dressel DA, et al. Surgical management of children and young adults
with Marfan syndrome and pectus excavatum. J Pediatr Surg. 1988;23:11691172.

Wynn SR, Driscoll DJ, Ostrom NK, et al. Exercise cardiorespiratory function in adolescents
with pectus excavatum. J Thorac Cardiovasc Surg. 1990;99:4147.
Zhang R, Hagl C, Bobylev D, et al. Intrapericardial migration of dislodged sternal struts as
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Part IV
Chest Wall/Pleural Space/Diaphragm:
Chest Wall

15 Open Reduction and Internal Fixation of Chest Wall


Hon Chi Suen

Annually, 350,000 people in the United States suffer from rib or sternal fractures. These
injuries are associated with a lot of morbidity and mortality. Chest wall fractures result in
severe pain, which results in shallow breathing and ineffective coughing, which in turn leads
to sputum retention, atelectasis, pneumonia, and respiratory failure. Severe pain in the chest
also affects the function of the whole body. The sharp edges of fracture can lacerate thoracic
and abdominal organs and cause bleeding and pneumothorax. Displaced chest wall fractures
result in chest wall deformities causing compromised lung function and unsightly cosmetic
result. The severe physiologic compromise due to flail chest has been well established in
Flail chest is established when two or more ribs are fractured at two places on each rib. It
results in paradoxical movement of the flail segment and ineffective respiration. There are
long-term consequences. Twenty five percent of these patients are permanently disabled. Only
40% eventually return to work. Forty nine percent have chronic pain, 63% dyspnea, and 57%
abnormal spirometry.
Traditionally, chest wall fractures have been treated conservatively with the use of
analgesics (oral, parenteral, intercostal nerve block, or epidural) or traditional stabilization
methods (chest wall binder, Kirschner wire, Judet staple, or internal pneumatic stabilization
with the use of the ventilator and positive pressure ventilation). However, these methods are
slow in pain control and not very effective in addressing the residual deformity. The use of
ventilator increases the risk of pneumonia and prolongs ICU and hospital stay. Return to work
or normal life is delayed or denied.
In recent years, open reduction and internal fixation (ORIF) of chest wall fractures have
evolved into a good strategy to treat chest wall fractures when indicated. ORIF of chest wall
fractures results in rapid pain relief, correction of chest wall deformity, preservation of lung
function, shortened ICU and hospital stay, and rapid return of body function and rapid return
to work.
Althausen et al. (2011) compared 22 operatively managed patients and 28 case-matched
controls. Patients who had undergone ORIF of rib fractures had shorter ICU stays, decreased
ventilator requirements, shorter hospital stays, fewer tracheostomies, less pneumonia, less
need for re-intubation, and decreased home oxygen requirements. In a Best Evidence Topic
review article, Girsowicz et al. (2011) concluded that surgical stabilization improved
outcomes in patients with isolated multiple distracted and painful nonflail rib fractures by
reducing pain, improving respiratory function, improving quality of life, and reducing socioprofessional disability.

ORIF of chest wall fractures can be carried out during the acute trauma phase or in the
latent phase when patients present with symptomatic fracture nonunion.
Current indications for ORIF of chest wall fractures include:
1. Severe pain not relieved by traditional analgesic approaches.
2. Fractures resulting in ineffective respiratory physiology.
3. Chest wall deformity.
4. Fracture nonunion especially with pain.
ORIF of chest wall fractures is contraindicated when the patient is unstable, involved in other
more severe life-threatening injuries, or when the patient is septic.

In the evaluation of the trauma patient, basic ATLS principles should be followed. When the
patient is stabilized, priority in the management of the multiple-trauma patient is established.
The patient is carefully examined and the CT chest of the patient is thoroughly studied to
identify the number and sites of chest wall fractures and plan is made regarding how many
and which fractures to fix. In the presence of multiple chest wall fractures, ORIF of different
fractures can be staged.
Not all fractures require ORIF. In general, the most painful or displaced fractures require
ORIF. The less painful and nondisplaced fractures can heal conservatively once the major
ones are fixed.

The author has experience in the use of MatrixRIB system and sternal fixation system from
Synthes. The systems use titanium locking plates.
Advantages of titanium include:
1. Very stable and can remain in the body indefinitely
2. Good pliability allows precise adaptation to the contour of the chest wall
3. Minimal rebound after bending
4. Rare allergic reaction
5. Minimal interference with CT or MRI
The locking rib plates come precontoured to fit an average rib shape and minimize
intraoperative bending. They are also color coded to distinguish left and right designs (Fig.
15.1). However, the eight-hole universal plate featured in the operative photos of this chapter
is the authors favorite. It can be bent to fit almost any fracture anywhere.
These systems employ orthopedic AO principles of anatomic reduction, stable fixation,
preservation of blood supply, and early, active mobilization. The locking plate/screw system
allows the screw to be fixed to the bone and to the plate so that the whole system will be

stable without requiring every bit of the plate touching the bone.

Figure 15.1 Color-coded pre-contoured rib plates. DePuy Synthes CMF, a division of DOI 2013. All rights reserved.

ORIF of Fracture Ribs
Patient could lay supine, full lateral or semi-lateral depending on which rib(s) and which part
of the rib(s) need to fix. After receiving the preoperative antibiotic, an incision is made over
the fractures to be fixed. Muscle division is minimized to preserve respiratory function. The
fractures are exposed and nonviable bone removed. The periosteum is left intact. The
fractures are reduced and the broken rib segments are re-approximated. The thickness of the
rib is measured with a caliper. The length of the screw is chosen by adding 2 mm (accounting
for the plate thickness) to the rib thickness. The appropriate rib plate is chosen and bent
according to the contour of the rib. The plate is then positioned on the rib straddling the
fracture with holes for at least three screws on each side of the fracture. The drill guide is
attached to the plate and the appropriate drill bit is used to create holes in the rib. The drill
guide is then removed and the appropriate screw is inserted with the help of an electric
screwdriver. Preferably, at least three screws are applied on each side of the fracture. Figure
15.2 is a diagrammatic representation of the steps provided by Synthes. Video 15.1
demonstrates the application of drill guide, drilling, and application of a screw.
If the wound does not expose part of the plate well, separate holes may need to be created
in the skin to insert the drill or screw to avoid excessively enlarging the incision. The screws
are finally hand tightened to ensure secure application.
Other procedures such as bronchoscopy, drainage of pneumothorax, drainage of
hemothorax, or decortication may need to be done concomitant with the rib fracture fixation.
Figures 15.3 and 15.4 describe two representative patients and their excellent results.

ORIF of Fracture Sternum

The patient is positioned supine with arms tucked along the sides. The sternum is exposed
through a vertical incision. Debridement of necrotic bone is performed. Bone graft may be
needed to fill the gap. Bone graft can be obtained from the iliac crest or a rib.

Figure 15.2 Steps of ORIF of rib fracture (AM). DePuy Synthes CMF, a division of DOI 2013. All rights reserved.

For transverse fractures, one or two straight plates are used with preferably at least four
screws on each side of the fracture.
For vertical fractures (such as repair of median sternotomy dehiscence), an assortment of
manubrium plates, sternal body plates or straight plates can be used depending on the
After measuring the thickness of the sternum, 3 mm is added to account for the plate
thickness and then the appropriate screw is chosen and applied.
Figure 15.5 illustrates ORIF of transverse sternal fracture. Videos 15.215.5 demonstrate
the trimming of plate, bending of plate, applying the screw, and tightening of the screws.
Figure 15.6 showed repair of median sternotomy dehiscence using an assortment of plates.

Figure 15.3 A: A 29-year-old man had displaced fracture of right sixth to tenth ribs after a motor vehicle accident and
developed hemopneumothorax. B: There was instability of chest wall and tapes were applied in the emergency room to
reduce it. C: The intercostal muscles were also lacerated. D: The fractures were grossly displaced. E: The three most severely
displaced rib fractures (seventh to ninth) were fixed by ORIF using the eight-hole universal plates. F: PA and lateral chest xrays 3 months after ORIF showed absence of deformity and good alignment of all the ribs.

Figure 15.4 A: A 52-year-old man had 10 rib displaced fractures on the right after a motor vehicle accident associated with
hemopneumothorax. The right chest cavity had markedly diminished in size due to overlapping of the ribs from severe
displacement. There would be severe compromise of respiratory function if the severe deformity was not fixed. B: Severe
right chest wall deformity before surgery was corrected after ORIF of 5 of the 10 rib fractures. C: PA and lateral chest x-rays
4 months after ORIF showed re-expansion of right chest cavity, absence of deformity, and good alignment of all the ribs.

Figure 15.5 A: 53-year-old lady presented 14 months after a motor vehicle accident with painful nonunion of sternal
fracture. B: The necrotic bone at the site of nonunion was debrided. C: A bone graft harvested from the iliac crest was
inserted into the sternal defect. D: Two straight sternal plates were applied for internal fixation.

Figure 15.6 Repair of median sternotomy dehiscence with an assortment of sternal plates.

Patients in general are extubated in the operating room and they usually feel that the chest
wall pain is immediately improved. Postoperative management is according to the routine
management of a post-thoracotomy patient: perioperative antibiotic, management of chest
tube(s) if present, pain control, incentive spirometry, and early ambulation. In general, they
can be discharged home within a few days (range outpatient procedure to 4 days after
surgery) unless there are other indications to keep the patient in the hospital.

Complications in general are uncommon but include bleeding, hardware fracture, hardware
infection, and hardware migration. The last three complications are usually treated with
hardware removal. In my patient who had hardware fracture 2 years after implantation, the
sternal fracture had completely healed and there was no problem in removing the fractured

Almost all patients experienced immediate and dramatic improvement of the pain and their
ability of deep breathing and moving around. They are very happy with their cosmetic and
functional results and have no trouble recommending the procedure to the next patient.
Videos 15.6 and 15.7 demonstrate the good functional result after two-stage ORIF of
multiple right rib fractures.

In selected patients with chest wall fractures, especially those with severe pain not relieved
by conventional analgesic techniques, respiratory compromise, chest wall deformity, or
nonunion, ORIF has been proven to dramatically reduce the pain, improve the respiratory
physiology, reduce ICU and hospital stay, and result in early return to society and work.

Recommended References and Readings

Althausen PL, Shannon S, Watts C, et al. Early surgical stabilization of flail chest with locked
plate fixation. J Orthop Trauma. 2011; 25:641647.
Bhatnagar A, Mayberry J, Nirula R. Rib fracture fixation for flail chest: What is the benefit? J
Am Coll Surg. 2012;215:201205.
Bille A, Okiror L, Campbell A, et al. Evaluation of long-term results and quality of life in
patients who underwent rib fixation with titanium devices after trauma. Gen Thorac
Cardiovasc Surg. 2013; 61:345349.
Campbell N, Conaglen P, Martin K, et al. Surgical stabilization of rib fractures using inion

OTPS wraps-techniques and quality of life follow-up. J Trauma. 2009;67:596601.

Fabricant L, Ham B, Mullins R, et al. Prolonged pain and disability are common after rib
fractures. Am J Surg. 2013;205:511515.
Girsowicz E, Falcoz P, Santelmo N, et al. Does surgical stabilization improve outcomes in
patients with isolated multiple distracted and painful non-flail rib fractures? Interac
Cardiovasc Thorac Surg. 2012;14:312315.
Lafferty M, Anavian J, Will RE, et al. Operative treatment of chest wall injuries: Indications,
technique, and outcomes. J Bone Joint Surg Am. 2011;93:97110.
Leinicke JA, Elmore L, Freeman BD, et al. Operative management of rib fractures in the
setting of flail chest: A systematic review and meta-analysis. Ann Surg. 2013;258(6):914
921. [Epub ahead of print]
Marasco SF, Davies AR, Cooper J, et al. Prospective randomized controlled trial of operative
rib fixation in traumatic flail chest. J Am Coll Surg. 2013;216:924932.
Mayberry JC, Ham LB, Schipper PH, et al. Surveyed opinion of American trauma, orthopedic,
and thoracic surgeons on rib and sternal fracture repair. J Trauma. 2009;66:875879.
Nirula R, Diaz JJ Jr, Trunkey DD, et al. Rib fracture repair: Indications, technical issues, and
future directions. World J Surg. 2009; 33:1422.
Richardson JD, Franklin GA, Heffley S, et al. Operative fixation of chest wall fractures: An
underused procedure? Am Surg. 2007;73: 591597.
Slobogean GP, MacPherson CA, Sun T, et al. Surgical fixation vs nonoperative management of
flail chest: A meta-analysis. J Am Coll Surg. 2013;216:302311.

16 Chest Wall Resection/Reconstruction for Tumors

Francesco Puma and Jacopo Vannucci

Chest wall reconstruction is indicated in widely different clinical situations, such as resection
of tumors, infected or irradiated wounds, congenital deformities, and posttraumatic injuries.
In this section we will analyze the various technical options for reconstruction in the
oncologic setting.
Chest wall resection and reconstruction for neoplastic disease can be carried out in three
different clinical circumstances:
1. primary chest wall tumors;
2. chest wall metastasis or direct infiltration from other malignancies;
3. direct invasion from non-small cell lung cancer (NSCLC).
Such classification is necessary because extent of resection is actually different according to
indications: It usually involves some ribs, in the treatment of NSCLC; it often entails a large
excision of soft tissues and bony thorax for primary chest wall tumors; it is widely variable in
the other possible conditions. Reconstruction may be delegated only to the thoracic surgeon,
but in the case of extensive skin and soft tissue resection, repair should include teamwork
with plastic surgeons. A multidisciplinary approach is often required.
Primary Chest Wall Tumors
The majority of benign chest wall tumors requiring a thoracectomy arises from the bony
thorax (osteochondroma, chondroma), followed by soft tissue tumors (fibrous dysplasia,
desmoid tumors, etc.) and by tumors of neural origin (neurofibroma, neurilemmoma). These
lesions are often, but not always, slow-growing tumors and are usually asymptomatic, rarely
being painful, as in case of osteochondroma or fibrous dysplasia when complicated by
pathologic fractures. Chondroma is another common benign tumor, which can easily create
problems of differential diagnosis with the corresponding well-differentiated malignant
Primary malignant chest wall tumors are mainly represented by sarcomas. The most
common is chondrosarcoma, a chemo- and radioresistant tumor, its prognosis is related to its
grade, dimension, and width of resection. Other malignancies are Ewings sarcoma,
osteosarcoma, synovial sarcoma, fibrous histiocytoma, plasmacytoma, and a variety of soft
tissue sarcomas. Ewings sarcoma and plasmacytoma are responsive to chemotherapy.
Different biology can grade these tumors from indolent to rapidly aggressive and occasionally
related to latent or manifest systemic disease. Multifocal tumor is a possible entity that
heavily limits the surgical indication.
Metastatic Chest Wall Tumors
Bloodstream metastases to the chest wall infrequently occur from epithelial tumors such as

carcinomas of the thyroid, breast, and kidney, but also from other primaries. Palliation is
generally obtained by radiation therapy and resection is rarely indicated.
Surgery might be considered in selected cases: (a) As part of a multidisciplinary treatment
program (e.g., differentiated thyroid tumors); (b) as a treatment of a local complication such
as radiation or infected wound (occasional in breast cancers); (c) for a bleeding lesion (typical
of renal cell carcinoma); (d) for the sole palliation, generally for pain relief (occasional in
every histology).
Chest Wall Involvement by Lung Cancer
Peripheral NSCLC sometimes infiltrates the parietal pleura or the chest wall and this
condition is defined as T3 tumor; invasion of the vertebral body is defined as T4. In patients
with vertebral body involvement surgery is rarely indicated and the related techniques will
not be analyzed in this chapter. Surgical indication is disputed in T3N2 disease, but cT3N01
can undergo en-bloc chest wall and lung resection with satisfactory oncologic outcome. Many
experiences encourage the role of surgery but there are some peculiar aspects that define the
indication to surgery as part of a possible multimodality treatment. Prognostic factors are
multiple and mainly dependent on complete resection, N status and depth of infiltration; the
latter is also a key factor to assess the correct technique. Currently there are some
uncertainties on the extent of resection. When the tumor clearly infiltrates ribs and/or soft
tissues, the only radical operation is the concomitant chest wall and lung en-bloc resection. If
the parietal pleura is marginally infiltrated, extrapleural lobectomy without chest wall
resection could be performed, provided that the extrapleural plane is easily achieved and the
outer surface of the detached parietal pleura is left absolutely intact (however, only the final
pathologic examination can definitely rule out the possible full-thickness parietal pleural
involvement). It is important to interrupt the extrapleural dissection in case of resistance to
the maneuver. If the procedure goes smoothly, a full-thickness chest wall resection could be
an overtreatment because the tumor can be fixed to the parietal pleura only by inflammatory
adhesions, or be confined just to the pleural plane. The decision must be made
intraoperatively and requires an experienced surgeon.
If the parietal pleura is invaded, many authors deem extrapleural lobectomy a not surely
radical operation because of the higher probability of local recurrence. In fact, although data
are not definitive, in T3 tumors, chest wall and lung en-bloc resection should lead to better
long-term outcome than extrapleural lobectomy. Anyhow, concomitant chest wall and lung
resection is unquestionably required if the patient complains chest pain or if parietal pleura
infiltration is not minimal.

Evaluation of the Patient
Functional Assessment
Analysis of preoperative functional studies is beyond the scope of this chapter. Synthetically,
we should consider adequate for a major chest wall resection the same functional respiratory,

metabolic, and cardiovascular parameters used to judge a patient eligible for a pulmonary
lobectomy. If a large thoracectomy en-bloc with a major pulmonary resection has been
scheduled, the patient should be functionally fit for pneumonectomy.
Clinical Data of the Patient
Chest wall resection should be undertaken after a meticulous treatment plan resulting from
deep knowledge of the disease and adequate assessment of the patient. Clinical history and
physical examination are fundamental both for correct diagnosis and therapeutic plan.
Multiple factors influence the technique of resection and reconstruction of the chest wall:
Some of them are related to the patient and to his clinical history, others are linked to the
The most important patient-related factors to be considered are: Comorbidities,
performance status, symptoms, lifestyle, occupation, age, previous radiation therapy, previous
surgery or chemotherapy, body habitus, infection, skeletal muscle function, body mass, and
nourishment. Chest pain should be carefully investigated because it is the most important
sign of local invasion. The growth rate of the tumor, when detectable, is a critical prognostic
factor. Thorough physical examination is essential for surgical planning: The characteristics of
the mass, its relationship with both the superficial and deep layers, and any local sign of
infection must be carefully examined.
Tumor biology, prognosis, and possible multimodal treatment planning represent the most
important disease-related factors, influencing the presumed extent of resection and the kind
of reconstruction.
Instrumental Evaluation of the Disease
Contrast-enhanced computed tomography (CT) is the imaging test of choice to define size,
localization, radiodensity, shape, contour, margins, boundaries, homogeneity/heterogeneity,
calcifications, necrosis, vascularity, patterns of contrast enhancement, and distant metastasis;
cleavage planes and possible infiltration into adjacent structures may be not definitively
determined in all patients.
Magnetic resonance imaging (MRI) is to be considered complementary and not alternative
to CT scan. It is recommended in selected cases to evaluate soft tissue planes and to better
assess neural, spinal, and vascular involvement.
Even though advances in imaging techniques can make biopsy unnecessary in very selected
cases, tissue diagnosis is essential for a correct treatment strategy. In fact, only when the
benign or malignant nature of the chest wall tumor has been established, surgical planning
can be correctly drawn up. Furthermore, some diseases such as chest wall metastases, Ewings
sarcoma, and plasmacytomas require chemotherapy and surgery should be only considered as
part of a multimodal approach.
Biopsy options include fine-needle aspiration, core-needle biopsy, incisional biopsy, and
excisional biopsy. Fine-needle aspiration has a poor diagnostic yield in primary chest wall
tumors and should be performed only if chest wall invasion from lung cancer or from other

malignancies is suspected. Conversely, the very high diagnostic accuracy of core-needle

biopsy makes incisional biopsy rarely needed in the diagnosis of primary tumors. Excisional
biopsy is mandatory in case of a chondromatous lesion but can be a reasonable alternative to
minimal biopsies also for other tumors, providing that the resulting chest wall defect is small.
In conclusion, the choice between the different options for biopsy must be essentially
individualized on the basis of the features of the lesion.
Nuclear Imaging Tests
Both 18FDG-positron emission tomography and bone scan may be useful in selected cases to
assess the extent of the disease.

The correct approach comes from the analysis of three different points:
a. Resection
b. Restoration of skeletal stability
c. Soft tissue coverage
The extent of resection varies depending upon the indications.
Benign chest wall tumors: The correct treatment is tumor removal with clear margin. As a
rule, resection should not be extended to the skin and the adjacent musculature if not
clearly required, but care must be taken to avoid an incomplete resection. In selected
cases a wider excision is recommended for the risk of an undiagnosed malignant tumor
(chondrosarcoma), or for the possible high local recurrence rate (Desmoid tumors).
Primary malignant chest wall tumors: Wide en-bloc resection is the key for a successful
management. It is generally defined as wide en-bloc resection of a tumor excision with 4cm free resection margins, including the involved skin and soft tissues, ribs and/or
sternum, and any other structure invaded by the disease. If a previous surgical biopsy has
been done, en-bloc resection of the entire biopsy site must be performed, to avoid the
high risk of tumor seeding during the procedure. Radical surgery is often the only real
therapeutic chance and the extent of resection should not be limited by anticipated
difficulties in reconstruction.
Chest wall direct invasion by lung cancer: Chest wall and lung en-bloc resection is the
standard of care. There is no unanimous agreement about the security margin:
Theoretically one rib above and below the macroscopic tumor should be recommended
with a lateral margin of 3 to 4 cm. Some authors deem 1 cm of free margin in all
directions sufficient to balance the surgery-related morbidity, being complete resection
the goal to be achieved.1 We think that the security margin must be possibly wide: A
minimum resection margin, even if microscopically negative, should be categorized as a
compromise solution, to be reserved for those patients in whom the other technical
solutions would result in an excessive surgical trauma. In this context, the most common
situation is chest wall invasion near the paravertebral sulcus without direct spine

involvement, where a minimum histologically negative resection margin could be

considered acceptable, making a balanced assessment between risk of local recurrence
and trauma related to the vertebral bodies resection.
Chest wall metastasis or direct invasion from other malignancies: A minimum resection
margin is generally considered satisfactory. Surgery is rarely indicated, if any, always in
the context of a multimodal treatment. If resection is required for a radiation wound or
for an ulcerated, infected tumor, wide resection should be performed: Despite extensive
resection and apparent removal of any residual infected tissue, the use of synthetic
prosthetic material is contraindicated and the resulting dead space must be obliterated by
well-vascularized flaps, preferably by a pedicled omental flap.
Resection of primary or secondary chest wall tumors must be performed en-bloc with the
adjacent involved tissues, to avoid tumor seeding. Only few tips and tricks may be provided:
The procedure is not technically demanding but a precise method is required. When dealing
with lung cancer infiltrating the chest wall, thoracectomy should be performed first, going
ahead with en-bloc lobectomy only when the involved chest wall has been freed into the
pleural cavity. The chest should be approached well distant from the involved area, to
properly assess the local extent of disease, without risks of tumor seeding. Chest wall
resection should start with the easier side to expose (i.e., from back to front, for anterior
thoracectomies; from front to back, for posterior resection; from below to above, for resection
of the first five ribs and vice versa for lower rib resections). In selected lung cancer patients
requiring extended thoracectomy, a preliminary atypical lung resection with linear staplers
may be useful, provided that a macroscopically free resection margin has been achieved.
Subsequently, thoracectomy en-bloc with sublobar resection is carried out. Completion
lobectomy and mediastinal lymph node dissection can be performed at the end of the
demolitive phase, without any technical obstacles. This surgical strategy facilitates both chest
wall and lung resection; in fact, lung adhesion to the chest wall may preclude adequate
exposure of the opposite side of the ribs to be removed and a large segment of resected chest
wall, dropped into the pleural cavity, can hinder hilar dissection and prevent the lung to be
moved inside the chest. However, in most cases requiring an extended thoracectomy, a wide
wedge resection is not feasible with a safe margin and the above described technique may be
In posterior thoracectomies, resection of the vertebral transverse process must be carried
out with caution. In fact, control of bleeding near the intervertebral foramen is extremely
delicate due to the adjacent spinal cord; moreover, the dura mater can be torn during
paravertebral sulcus dissection, with possible cerebrospinal fluid leak. For such reasons, the
vertebral transverse process should be resected only if the head of the rib is dorsally
infiltrated by the tumor; in the other conditions, if necessary, the ribs can be completely
disarticulated with a precise technique. Ribs are strongly connected to the spine by a peculiar
kind of articulation. Rib head articulates with the body of the thoracic vertebrae and the rib
tubercle with the transverse process, with a relatively long overlapping of the bone segments.
This type of articulation is categorized as arthrodial joint and is characterized by tight joint
capsules, strengthened by multiple and tough ligaments. To achieve complete rib
disarticulation, anterior costal interruption is performed first, to allow a higher mobility of

the posterior segment of the chest wall to be resected. The erector spinae muscles are then
incised to expose the costotransverse joint. The tubercular ligament is cauterized and a
curved heavy periosteal elevator is inserted between the transverse process and the rib (Fig.
16.1). To release the neck of the rib it is necessary to divide the costotransverse ligament,
which is generally very strong, so much so that rib neck fracture may be easily produced. The
cautious use of a light hammer can be helpful to facilitate insertion of the periosteal elevator.
The rib neck is dislocated anteriorly by the periosteal elevator, wedged forward with a
progressive lever action, until the costal head has been detached from the vertebral body; at
the end of the procedure the residual costovertebral ligaments are divided by scissors.

Figure 16.1 The periosteal elevator is wedged forward between rib tubercular facet and vertebral transverse process.
Vigorous, active pendulum movement (arrow) achieves disarticulation without fracture.

Figure 16.2 PET-CT scan of a cT3 left upper lobe lung cancer, suitable for double-step anterior resection and reconstruction.

For lung cancer invading very anteriorly the chest wall and requiring en-bloc thoracectomy

with division of costal cartilages, an anterolateral thoracotomy is the most intuitive choice
because surgical dissection of the costochondral joints is hampered by lung infiltration, if
approached posteriorly (Fig. 16.2). On the other hand an anterior approach may have two
drawbacks: (1) It does not allow the ideal surgical exposure of the chest wall, posteriorly to
the midaxillary line; (2) the resected thoracic wall segment, released within the pleural
cavity, is cumbersome and can hamper hilar dissection. In such circumstance, we found
advantageous a preliminary short longitudinal parasternal incision to cut the invaded costal
cartilages close to the sternum, easily achieving the appropriate resection margin. Before
wound closure, a variable number of heavy nonabsorbable stitches are placed on the
remaining healthy tissues and/or through the sternum, to medially anchor the future
prosthesis: The needles are removed and the stitches knotted distally and temporarily
abandoned inside the chest. Then a posterolateral thoracotomy is performed to conclude the
en-bloc pulmonary resection facing the easier lateral side of the thoracectomy. The
reconstructive phase is facilitated by fixing the prosthesis to the far anterior border of the
defect, collecting the anterior stitches previously placed, which are secured to the prosthetic
mesh by free needle (Fig. 16.3).
Restoration of Skeletal Stability
The reconstructive technique should ensure early return to normal breathing, protection of
intrathoracic organs, restoration of physiologic volume of the rib cage, and satisfactory
cosmetic result.
Return to efficient ventilation and protection of intrathoracic viscera are the fundamental
targets. A multidisciplinary team, including plastic surgeons, is recommended if an extensive
soft tissue and skin resection has been scheduled: It is worth underlining that correct surgical
planning constantly requires soft tissue coverage and skin closure, while rigid stabilization of
the bony thorax is not always necessary and represents a controversial issue. Reconstruction
of the bony thorax is unnecessary for small defects not overlying cardiac structures, which do
not significantly impair breathing. In fact, soft tissues reconstruction may provide normal
respiratory mechanics in patients with a small chest wall defect and good baseline lung
function. Large full-thickness defects not adequately stabilized may act as a sort of traumatic
flail chest. However, the two conditions are not exactly comparable: Paradoxical movement
of the chest wall after multiple ribs resection is usually not a life-threatening condition as
severe traumatic flail chest could be. Probably for these reasons, some surgeons do not
usually repair the bony defect, thus underestimating the problem of paradoxical breathing.2
We do not agree with this behavior, although there is no conclusive evidence to support the
necessity for bony reconstruction of a large chest wall defect. First of all, an inadequate bony
reconstruction after wide thoracectomy may have serious pathophysiologic consequences,
affecting both postoperative course and pulmonary status of the patient. Secondly, progress
currently achieved in the field of chest wall prostheses allows an easy and safe stabilization of
the bony thorax, with minimal morbidity related to the reconstructive procedure. A
significant paradox impairs ventilatory mechanics, weakens cough effectiveness, causes
mucus retention, increases the risk of pneumonia, and often leads to prolonged postoperative
mechanical ventilation, which in itself increases the risk of infection. Respiratory failure is
the possible final outcome of these pathophysiologic events. The high incidence of respiratory

complications reported after chest wall resection has been correlated to the residual
paradoxical movement, resulting from an inadequate reconstruction. In fact, a lower
incidence of respiratory complications has been reported by those authors who systematically
use skeletal stabilization for large defects.3 For such reasons we believe that any chest wall
defect that has the potential for paradox, requires restoration of the skeletal stability.
Regardless of the adequacy of soft tissue coverage, prevention of the paradoxical chest wall
movements should represent a fundamental goal in surgical planning.

Figure 16.3 A: Preliminary limited longitudinal left parasternal incision: The sternocostal joints of the second, third, and
fourth ribs are interrupted and nonabsorbable stitches are placed on the peristernal tissues and temporarily abandoned inside
the chest cavity. B: Posterolateral thoracotomy allows to easily complete the posterior section of the involved ribs and the
pulmonary resection. Chest wall reconstruction is facilitated by fixing the prosthesis to the far parasternal border of the
defect, collecting the anterior stitches previously placed.

Size and location of the defect are the two interdependent factors mainly influencing the
likelihood of occurrence and the entity of a postoperative paradox.
Size of the defect. Number, length of rib resection and width of skin soft tissues excision are
to be taken into account. There is not a definite threshold that, per se, makes rigid
stabilization of a chest wall defect mandatory, even though, roughly, it would be
preferable to reconstruct every large bone defect. It has been reported that the >5-cm
resection of two consecutive ribs should require rigid stabilization but actually, even a
larger defect may be left unreconstructed, thus proving that location more than size of
the defect is the basic factor in the decision-making process.
Location of the defect. To guide the decision whether bony chest wall reconstruction is
necessary or not, the hemithorax can be topographically divided into noncritical and
critical areas. The latter usually require skeleton reconstruction after full-thickness
Noncritical areas are the apical and the posterior regions; critical areas are the basal, the

lateral, and the anterior regions.

The apical region (including first, second, and third ribs) is frequently involved by chest wall
resection for the treatment of Pancoast tumors. Resection of the posterior half of the first
three ribs does not require bony reconstruction, because the defect lies beneath the
scapula. Even if complete resection of the first three ribs is performed, stabilization is not
required since the resulting defect works as a thoracoplasty, causing reduction in size of
the chest cavity with obliteration of the apical pleural space.
The posterior region is located between the posterior spinal line and the posterior axillary
line. Chest wall instability is rarely significant in this area for the following reasons: It is
well protected by a thick layer of muscles (latissimus dorsi, trapezius muscle); the supine
decubitus of the patient reduces the paradoxical movement of the chest wall. Bony
reconstruction is required if the tip of the scapula can fall within the defect and get
trapped during movements of the arm (such event must be anticipated if the defect
includes the fifth rib). In case of extended soft tissue resection, reconstruction of the
posterior thorax is usually achievable by a variety of pedicled flaps.
The lateral region (including fourth, fifth, and sixth ribs between the anterior and posterior
axillary lines). Bony reconstruction is recommended after large thoracectomy involving
this area, because it is relatively protected only by the serratus anterior and the cranial
digitations of the external oblique muscle. Serratus anterior, pectoralis major, and
latissimus dorsi muscle flaps can be used for closure of an axillary defect.
The basal region includes the ribs from seventh to tenth, whose resection is followed by an
important paradox. In fact, during the breathing cycle, these ribs undergo a significant
excursion, since they move laterally when are elevated (the so-called bucket-handle
movement). Latissimus dorsi muscle flap may reliably cover large defect of this area.
Also the diaphragm can be used, suturing it to the lower untouched rib. If the
peritoneum has been opened, omental flap can be considered the first choice to cover
prosthetic material.
The anterior region has the following boundaries: (a) laterally: anterior axillary lines; (b)
cranially: jugular notch and subclavicular fossa; (c) caudally: costal margin. Sternum and
costal cartilages are the skeletal structures of the anterior region, forming a rigid
protection to the heart and mediastinum, providing the fulcrum for rib cage movements.
The sternal manubrium articulates with the clavicles and participates to the shoulder
girdle function. Pectoralis major muscles are the principal muscular layers covering the
anterior region. The reconstruction technique of this area should restore the skeletal wall
stability and also protect the heart with a solid and rigid support. A regional flap for
wound coverage is always needed if the pectoralis major muscles are involved in the
Restoration of normal volume of the rib cage and limitation of thoracic deformity could be
considered relatively minor goals to achieve, but are anyway significant. The loss of about
50% in volume of a hemithorax results in a restrictive ventilatory deficit, which usually does
not produce dramatic effects in patients without preoperative pulmonary impairment.
However, in patients with poor baseline lung function, the physiologic rib cage configuration
must be restored to avoid postoperative respiratory failure.
Limitation of chest wall deformity must be considered both from a cosmetic and functional

point of view. Resection of long segments of at least three consecutive ribs in critical areas
may result in significant deformity and volume reduction of the hemithorax. The use of a
large nonrigid prosthesis can alter the anatomical shape of the chest because the mesh must
be placed under tension, stretched between the ribs bordering the defect; the result is
equivalent to a straight line drawn between the rib stumps. The possible technical solutions
will be discussed later.
Prosthetic Material for Chest Wall Stabilization
The ideal prosthetic material should be:
strong enough to withstand physiologic stresses;
elastic and flexible, to avoid progressive limitation of the pulmonary function;
light and smooth, unable to induce decubitus ulcers and pain;
easy to mold;
incorporable into the host tissue;
solid, to ensure protection to the visceral structures;
securely fixable;
biocompatible, unable to induce allergic or adverse foreign body reactions;
durable and not subject to deterioration over time;
resistant to infection and to radiation;
not dangerous in case of blunt trauma;
radiolucent and nonmagnetic;
readily available.
No single material fulfills all these features, even though significant improvements have
been achieved in the field of prosthetic substitutes for the chest wall. The different techniques
currently available for restoration of the chest wall stability will be briefly discussed.
Grid of Nonabsorbable Sutures
It is a simple way to reduce chest wall paradoxical movement. Multiple heavy nonabsorbable
sutures can be utilized, placed between the superior and inferior untouched ribs, delimiting
the defect. When the sutures are tightened in tension, the final result is a semirigid grid,
which will act as a support to the overlying myoplasty.
Indications. This method can be considered as a compromise solution to be used when the
reconstruction of the bony thorax is not certainly required. Small defects can be
effectively bridged by this method, which is also very useful for skeletal stabilization in
contaminated or irradiated fields, where any prosthetic material should be avoided. The
procedure can also be effectively used in combination with mesh prosthesis, to increase
the strength of the reconstruction.
Pros. Suture grid is an undemanding and cheap procedure, useful to create a semirigid
support for the overlying muscular layers. The primary advantage is avoidance of any
prosthetic material. A possible mild wound infection could be well tolerated with no risk
of rejection of the used material and no loss of solidity of the reconstructed chest wall.
The chest tubes through the large meshes of the grid easily drain the wound.

Cons. It is a rough technique. The problem of postoperative paradox is attenuated, but not
abolished. The method does not provide a rigid plate for protection of visceral structures.
Prolonged postoperative pain may occur, if a subcostal nerve is trapped by the suture.
We generally use no. 2 braided polyester suture, placed approximately 3 cm from each other,
to encircle the costal edges. A Langenbeck periosteal elevator is used to carefully free the
subcostal neurovascular bundle from the costal groove, in order not to entrap the nerve in the
suture, thus decreasing postoperative pain. The use of a drill to perform transcostal sutures is
not recommended, since after multiple holes the bone becomes too fragile, as the stitches
must be tightened in tension.
Mesh and Soft Patch ReconstructionBioabsorbable Material
The long-term stability of any chest wall reconstruction with prosthetic meshes is due to
repair by tissues incorporating the employed material. The mesh acts as a scaffold for scar
tissue growth. Basically this is the rationale in the use of reabsorbable materials.
Bioabsorbable material has been experimented alone or in combination with a nonabsorbable
suture grid, but it did not find widespread clinical application, because no significant
advantages were demonstrated over the use of nonreabsorbable mesh. Recent technologic
advances in biomaterials, mainly developed for tissue reinforcement in ventral hernias
repair, renewed interest in the use of absorbable materials for chest wall reconstruction.
Synthetic and biologic absorbable materials are available. In our preliminary experience we
achieved good results with the use of GORE BIO-A Tissue Reinforcement, (W. L. Gore &
Associates, Flagstaff, AZ). This is a synthetic bioabsorbable prosthesis, characterized by a
web-like structure, similar to collagen fiber network, that is substituted within a 6-month
period by scar tissues of the same thickness. Among biologic material, the acellular bovine
pericardium (Veritas Collagen Matrix, Synovis Surgical Innovations, St Paul, MN, USA) and
the acellular porcine collagen (Permacol, Covidien, Mansfield, MA) proved to be highly
resistant to infection in complicated abdominal hernias repair and have occasionally been
experimented for chest wall reconstruction, in combination with other prosthetic materials.
Indications. The sole use of absorbable material has probably little significance, since the
indication should be limited to stabilization of small defects. Indeed reabsorbable
implants are useful in combination with other techniques, especially in potentially
contaminated fields, or if postoperative irradiation is contemplated.
Pros. Complete integration of the prosthesis into the host tissues. Efficient scaffold for tissue
regeneration. Slow reabsorption time. Better resistance to infection than nonabsorbable
mesh. Excellent biocompatibility.
Cons. Unsuitable method to repair large defects if the material is utilized alone. Visceral
protection unsatisfactory.
Mesh and Soft Patch ReconstructionNonabsorbable Synthetic Material
Nonabsorbable synthetic tissues are the most commonly used products for chest wall
reconstruction. A variety of meshes are available, basically categorized by weight
(heavyweight; lightweight) and pore size (macropore, micropore). Heavyweight meshes are

specially designed to ensure long-term mechanical stability and are therefore, suited for chest
wall reconstruction. Conversely, lightweight meshes are appropriate for ventral hernia
repair because they are woven with thin fibers and are mainly designed to improve flexibility
rather than stability of the reparative process. The mesh can be woven with monofilament or
multifilament fibers with a different design that specifically affects the pores size between
the fibers. Pores size is very important as it is directly related to ability of the prosthesis to be
incorporated or not into the surrounding tissues.
Macropore tissues, such as polypropylene mesh, (Prolene, Ethicon, Cincinnati, OH, USA;
Marlex, Bard, Billerica, MA, USA) facilitate the tissues growth inside, eliciting dense scar
formation and ensure good mechanical strength until the conclusion of the biologic processes
of incorporation. During the incorporation process, the macropore meshes may cause foreign
body reaction, variable inflammatory response, and always induce adhesions to the
neighboring tissues. Before incorporation, the mesh is permeable to air and liquids and, for
such reason, is unsuitable in case of pneumonectomy. After long-term implantation the
macropore mesh undergoes shrinkage and thickening. Micropore meshes, such as expanded
polytetrafluoroethylene (PTFE soft patch) (Gore-Tex, W. L. Gore & Associates, Flagstaff, AZ,
USA) are poorly integrated into the host tissue, because the very small size of the pores (less
than 10 m) prevents cell growth within the fabric. On the other hand, such mesh is
impermeable, does not undergo significant shrinkage and causes less intense foreign body
reaction and inflammatory response than macropore meshes.
Indications. Nonabsorbable synthetic meshes are suitable for reconstruction of smallmoderate defects in critical areas. For reconstruction of wider defects, such material can
be favorably used in combination with others techniques: Grid of sutures, titanium
plates, methyl methacrylate (MMA).
Pros. Both macropore and micropore meshes display excellent mechanical strength, if
correctly positioned. The better incorporation into the host tissue achieved by the
macropore meshes is a value in chest wall surgery, since thickening and possible
adhesion formation are not a problem, as opposed to abdominal wall surgery. However,
complete mesh incorporation does not seem essential because no significant differences
in outcomes and complications were found between the use of micropore and macropore
meshes in chest wall surgery.4 Micropore mesh is preferable if impermeability is required
(i.e., chest wall reconstruction after pneumonectomy, prosthetic reconstruction of the
diaphragm) and/or when visceral adhesions should be minimized.
Cons. Nonabsorbable synthetic mesh is inadequate to reconstruct very large chest wall
defects because it does not warrant satisfactory mechanical stability, reliable visceral
protection, and chest wall shape restoration. The mesh must be placed under tension
with interrupted suture around the defects margins and consequently, chest wall contour
is altered if long rib segments have been resected. Pericostal suture may cause
neuropathic pain. Infection, although infrequent, is a serious complication, and this
material should not be used in contaminated or irradiated fields.
A paper template of the defect is useful to customize the prosthetic material. The trimmed
mesh should be sutured in a radial fashion to the chest wall under tension. Multiple heavy

permanent sutures are placed through the superior and inferior untouched ribs and possibly
to bone stumps delimiting the defect. The mesh should be also fixed to the soft tissues all
around the defect to obtain a tight fixation. It is advisable to pass only few stitches around
the inferior rib, taking care not to injure the intercostal nerve; interrupted transverse sutures
to the intercostal muscles can complete anchoring to the lower edge of the defect. When the
nonabsorbable mesh is used in combination with other material, its position in the context of
the prosthesis is variable: We experienced the association of grid of sutures with
nonabsorbable meshes placing the mesh above, underneath, or within the grid. The last
method seems to be the most reliable and we use to tie the grid of sutures at the end of the
procedure, so as to control the tension of the implanted prosthesis (Figs. 16.4 and 16.5).
Titanium plates and omentum must always be positioned over the mesh (Figs. 16.6, 16.7 and

Figure 16.4 Wide thoracectomy of sixth, seventh, and eighth ribs (A); reconstruction by grid of sutures and mesh (B).

Figure 16.5 Preoperative image of a primary chest wall tumor (A); surgical specimen of full-thickness chest wall resection
(B); resulting thoracic defect (C); prosthetic reconstruction by polypropylenePTFE and nonabsorbable sutures grid (D).

Figure 16.6 A: Titanium repair by Stratos system for left anterolateral defect. B: Chest x-ray shows the contralateral rib
anchorage of the medical agrafes.

Figure 16.7 Right anterior chest wall schwannoma. A: Specimen. B: Intraoperative image after PTFE mesh and triple
titanium bars placement (Synthes system). C: Postoperative chest x-ray shows a valuable recontruction. D: Rib fracture and
lower bar rotation after mild trauma, occurred 2 years after surgery. The patient remained asymptomatic.

Biologic Bone Graft

Bone grafts have been almost exclusively used for reconstruction after sternal resection; the
isolated use of biologic soft tissue graft has little role in chest wall reconstruction, as
discussed above.
Biologic bone substitutes are: Autograft (obtained from the patients own tissues); allograft
(cadaveric human graft, received from a bone bank); xenograft (obtained from a species other
than human). The latter two materials need to be processed to achieve complete sterility and
to lose any antigenic power and infectivity. If adequately vascularized, only autografts may
have osteogenic properties, contributing to new bone formation. For allografts and xenografts
the concept is roughly the same described for synthetic tissues: The graft provides a scaffold
that is slowly reabsorbed and replaced by new native tissue. However, unlike the absorbable
material, the biologic bone graft is capable to maintain an absolute mechanical strength

during the whole process of host tissues restoration. Autografts are unsuitable for
reconstruction of large chest wall defects because of the additional trauma, related to bone
harvesting. Bovine bone xenograft has been completely abandoned. Conversely, the current
possibility of sternal reconstruction with sternochondral allograft obtained by bone banks and
fixed to the skeleton of the recipient by titanium plates and screws has raised great interest.5
Indications. Biologic bone grafts are indicated only for reconstruction of wide sternal defect.
The technique is still experimental.
Pros. The hypothetical advantage of bone autograft, represented by osteogenic potential
capacity, does not seem to be sufficient to justify its use. Bone allografts show
theoretical, mechanical, and biologic advantages, are available from bone banks and are
interesting mainly because they do not entail a heavier surgical trauma. So far biologic
and technical problems have not been reported. The allogenic sternum can be easily
tailored to obtain the geometric coverage of the entire chest wall defect; in particular the
sternoclavicular joints reconstruction is feasible, thus limiting the functional impairment
of the shoulder girdle after resection of the sternal manubrium.
Cons. Bone autografts should not be used because they entail an additional surgical trauma
that is not counterbalanced by the potential benefits. The use of bone allografts is still
investigational; only few studies have been reported and further experience is needed to
evaluate the long-term outcomes.
The allogenic sternum is trimmed to exactly match the geometric shape of the defect, like the
piece of a jigsaw puzzle. Graft measurement can be conducted directly on the surgical
specimen, or alternatively, on the defect, by using a template. Once proportions have been
optimized and chest anatomy is restored, the graft is fixed to the adjacent skeleton with a
variable number of titanium screws and bars (Synthes). Transposition of pectoralis major flap
to the midsternum is then performed bilaterally.
Methyl Methacrylate Sandwich Technique
MMA is an acrylic resin extensively used as cement in various medical fields, primarily in
orthopedic and dental surgery. The use of this material wrapped between two layers of
polypropylene mesh was described in 1981 for the reconstruction of large chest wall defects.
Since then, the sandwich technique has been widely applied in chest wall surgery with only
minor technical modifications. The meshes, enveloping the resin, are used to secure correct
positioning of the MMA plate and to anchor it to the neighboring tissues.
Indications. The sandwich prosthesis is particularly suitable for repair of wide sternal
defects and after extensive thoracectomies requiring restoration of the rounded thoracic
Pros. The prosthesis is: Malleable (suitable for restoration of the thoracic shape); rigid
(excellent for skeletal stabilization and intrathoracic organs protection); customizable
(fit for any size and shape of defect).
Cons. The main concern is risk of infection, since such prosthesis is not incorporable into
the host tissues. Other significant disadvantages can be attributed to the MMA plate,
because (a) it can undergo fragmentation and migration; (b) it is rigid and may cause

long-term pain and restrictive ventilatory deficit; (c) it has a finite lifespan and should
not be implanted in young patients with very long life expectancy; (d) it is irritating for
the human airway and inhalation exposure is dangerous during processing; (e) if
implanted during the polymerization phase it may cause thermal necrosis to the host
tissues because it produces an intense exothermic reaction.
1. A paper template of the defect is carefully modeled.
2. Two layers of the mesh are cropped 1 cm larger than the defect.
3. MMA is provided as a powder, which mixed with liquid, becomes a pliable, dense paste
that gradually hardens, resulting in thermal reaction.
4. At the beginning of processing, the paste is malleable and must be carefully spread on the
mesh to let it permeate the fabric porosity. A free rim of mesh, measuring at least a couple
of centimeters all around, should be preserved.
5. The second layer of the mesh is applied on top of the paste and pressed on it.
6. The resulting sandwich prosthesis should be shaped and rounded according to the chest
wall contour, before the cement becomes hard.
7. To prevent migration of the plate, the MMC has to be secured between the two layers of
mesh by strong nonabsorbable sutures, tied all around its edges.
8. When the prosthesis is cooled and hardened, it is fixed to the margins of the defect,
anchoring the free rim of the mesh to the bone stumps and to the intercostal muscles.
Tips. The MMA plate should be fashioned definitely smaller than the defect and must be
smoothed immediately after it has been spread between the two layers of the mesh. In such a
way the possible occurrence of long-term postoperative pain and decubitus ulcers is reduced.
Plate migration can be prevented by securing it within the meshes, by multiple sutures
around the edges. MMA fragmentation is avoided by using only strips of the material, rather
than creating a unique plate. A steel mesh added to the MMA, as described in the original
technique, is not recommended because it enhances prosthetic rigidity.
Titanium Plate and Screws
Stainless steel was rarely used in the reconstruction of chest wall defects, as no advantages of
such material were demonstrated over synthetic nonabsorbable meshes. The recent
introduction into clinical practice of titanium devices, specifically designed for chest wall
repair, provides the thoracic surgeon with new and interesting technical options. In fact,
titanium has the highest strength-to-weight ratio than any other metal alloy; it is
biocompatible, chemically inert, corrosion resistant, and stiff and tough but pliable and
moldable. Furthermore, it is compatible with CT and MRI imaging. For all these properties it
is very suitable for medical applications.
Two different titanium devices are currently available for chest wall reconstruction: The
Stratos system (Stratos, MedXpert GmbH, Germany), consisting of titanium bars, anchored by
rib clips (Fig. 16.6), and the Synthes system using titanium screws for fixation of different
plates and bars (Fig. 16.7) (Synthes, Canada Ltd.).
Indications. Titanium devices have been developed both for rib fractures fixation and for

chest wall reconstruction after wide resection; for the latter indication the material is
generally used in combination with soft patches.
Pros. The titanium devices currently available allow a light, biocompatible, well-tolerated
and reliable chest wall repair. They are suited for reconstruction of very large rib and
sternal defects. Restoration of the thoracic shape, avoidance of paradoxical chest wall
movements, and re-establishment of a rigid support for visceral protection are achievable
by a relatively simple procedure. The method allows restoration of the anatomic rib
continuity, which probably preserves more physiologic breathing mechanics after wide
thoracectomies than single-plate or mesh prosthesis.
Cons. Titanium alloy prostheses are expensive and their use should be justified only in
selected clinical situations. The fracture of titanium devices is rather unlikely, but in case
of postoperative blunt trauma, the adjacent bones could be particularly liable to
fractures, especially at the level of prosthetic anchoring (Fig. 16.7); even a violent
sneezing could be dangerous if the plates have been implanted on osteoporotic ribs. This
appears to be the main problem in using titanium devices. Chronic chest pain is possible
with the Stratos system, if the subcostal nerve has been entrapped by the rib clip clamp.
The Stratos system includes different connecting bars and rib clips with three possible
angulations, customizable to the variable anatomical situations. Special bending instruments
have been developed to individualize the prosthesis. First, the clips must be firmly secured to
the rib stumps by apposite pliers, avoiding to entrap the subcostal nerve and to fix the clip to
the costal cartilages. To achieve a tight fixation of the rib clips, the superior and inferior
edges of both costal stumps must be adequately exposed, for at least the length of the rib clip.
The connecting bars are then cut and bent to obtain the appropriate size and shape, suited to
the chest contour. The bars are tightened to facilitate their final fixation to the rib clips, by
means of appropriate crimping pliers (Fig. 16.6).
The Synthes system consists of precontoured plates and screws, mainly designed for rib
fractures fixation, but also suited for chest reconstruction after thoracectomy. The Synthes
plates are to be modeled on the anatomic thoracic defect using the provided malleable
template: The titanium plate is cut to the appropriate length, longer than the defect to allow
the placement of at least three screws on each bone stump for an adequate fixation. Dedicated
pliers are used to achieve the required longitudinal and axial twist of the plate. The screw
length is carefully calculated to secure the prosthesis to the posterior cortex, without
protruding excessively toward the chest cavity: Drill bits with stops at the desired length are
provided to prevent overdrilling. Without removing the periosteum, the plate is secured to
the bone by three consecutive screws on each bone stump. Stable fixation is guaranteed by
perfect screw length and by screw heads firmly locked into the threaded holes of the titanium
plate (Fig. 16.7).
Tips. We have experienced both devices with satisfactory results. The Stratos system offers an
easy to learn and quick procedure because fixation to the adjacent bones is simply achieved
by the rib clips. However, direct anchoring of the bar to the sternum is impossible and
surgical exposure of the contralateral rib cage may be required in case of an anterior defect
(Fig. 16.6). Stratos clips are not indicated even for repair of posterior defects, when at least a
6-cm dorsal rib stump is not available. The Synthes system requires a learning curve. Perfect

alignment of the drill hole with the plate hole is necessary; any dead space between struts
and bone should be carefully avoided; the rib stump must be drilled in the center and at the
defined depth; customizing the bars is complicated, since the bars holes must be strictly
aligned to the axis of the rib stump. For all these reasons the Synthes technique might be
considered a tedious and time-consuming method, but in our experience, it seems to be more
versatile than the Stratos technique.
Soft Tissue Coverage
Adequate soft tissue coverage is the main purpose and can be accomplished by various
technical solutions, chosen on the basis of multiple factors.
Correct surgical planning is the key to successful outcome. Width and depth of the
presumed defect must be predicted to evaluate if a multidisciplinary approach, generally
involving plastic surgeons, is required. In such a case surgical strategy should be accurately
planned together. Even though the best soft tissue reconstruction is always the simplest
possible, coverage of large full-thickness chest wall defects is not a simple procedure, and
should not be underestimated from a technical point of view, especially if a very large skin
resection is expected.
Regardless of the method of rigid stabilization performed, consistent, viable, and possibly
bulky soft tissues should be rebuilt over the skeletal reconstruction, avoiding the closure of
skin and subcutaneous tissues directly above bare prosthetic material. In major defects this
goal is achieved by flaps: Adequate vascularization is the prerequisite of any flap and
understanding of the blood supply of the tissues to transpose is the key factor.
Flap Classifications
A variety of criteria can be adopted for flaps classification. The simplest categorization
divides flaps into local and distant. Local flaps include tissues transferred from a neighboring
area. Distant flaps are tissues transposed from a remote location. A distant flap is called
pedicled flap if it is transposed preserving (entirely or partially) its original blood supply; a
free flap is a distant flap, transposed detaching its vascular pedicle, which should be
subsequently connected to the local vessels by vascular anastomosis.

Figure 16.8 Type III muscle flap according to Mathes and Nahai classification. A: Serratus anterior. B: Rectus abdominis.

According to the tissues transposed, the flap can be divided into simple, if it is composed by
one type of tissue and composite, when it is constituted by multiple tissues (in chest wall
reconstruction the latter are mostly myocutaneous flaps).
According to the vascularization, the flaps can be divided into: Random flap (when a
precise anatomical vascularization is not identifiable) and Axial flaps (when the vascular
supply derives from anatomically recognizable vessel/s). The patterns of axial blood supply of
the muscle flaps have been accurately classified by Mathes and Nahai into five types: Type I
one vascular pedicle. Type II dominant pedicle/s and minor pedicle/s. Type III two
dominant pedicles. Type IV segmental vascular pedicles. Type V one dominant pedicle
and secondary segmental pedicles (Figs. 16.8 and 16.9).6
Pectoralis major muscle flap is the first choice for upper sternal defects.
Insertion. Intertubercular groove of the humerus.
Origin. Outer surface of the sternum. Ribs and costal cartilages (second to sixth).
Clavicle. Aponeurosis of external abdominal oblique muscle on the midline.
Blood supply. Thoracoacromial vessels (dominant pedicle). Perforators vessels from the
internal thoracic artery and from intercostal arteries (secondary pedicles).
Innervation. Medial pectoral nerve and lateral anterior thoracic nerve.
Mathes and Nahai flap classification. Type V (One dominant pedicle and secondary

segmental pedicles) (Fig. 16.9).

Type of flap. Muscle flap. Myocutaneous flap.
Sites of use. Upper sternum. Upper ventral chest wall defect. Upper dorsal chest wall
defects. Axillary defects. Neck.

Figure 16.9 Type V muscle flap according to Mathes and Nahai classification. A: Pectoralis major. B: Latissimus dorsi.

Advancement flap. The muscle is elevated off the chest wall starting from the midline to the
lateral side. The flap should be based on the dominant vascular pedicle and the
secondary perforator branches from the internal mammary artery must be carefully
ligated. Dissection is carried out to obtain the sliding of the muscle to the desired site
without any tension. Additional length can be obtained by dissection of the clavicular
insertions of the muscle. Advancement pectoralis major flap is an easy procedure, widely
used, mainly in the treatment of deep sternal wound infection.
Rotation flap. This muscle flap or myocutaneous flap is also based on the thoracoacromial
vessels. It is mainly used to provide coverage of head and neck areas but, since a wide
arc of rotation is possible, the flap has been also used to cover axillary, shoulder and
upper dorsal chest wall defects. Rotation pectoralis major flap requires cooperation with
plastic surgeons to minimize the morbidity rate, primarily represented by possible flap
Turnover flap. It is obtained by basing the flap on the internal mammary perforator arteries.
Division of the dominant vascular supply and humeral and clavicular insertion are
Advantages. Large muscle readily available for one-stage reconstruction of anterior defects.
No change of surgical position is generally required.
Disadvantages. The pectoralis major flap can be inadequate to fill the inferior third of the
anterior chest wall; it does not always provide sufficient bulk to fill wide defects,

especially in female and in debilitated patients. Detachment of the muscle from its
insertion on the humeral bone may cause functional sequelae.
Latissimus dorsi muscle flap is one of the most commonly used flaps in reconstructive
surgery because of the muscle broadness and its long and reliable vascular pedicle.
Insertion. Intertubercular groove of humerus.
Origin. Iliac crest, spines of lower six thoracic vertebrae, lumbar vertebrae, sacral vertebrae,
lower four ribs.
Blood supply. The thoracodorsal artery (dominant pedicle): It is the terminal branch of the
subscapular artery, which originates from the axillary artery. The secondary segmental
pedicles are the perforating branches of the intercostal and lumbar arteries, which
constitute the blood supply for the medial and inferior edge of the muscle.
Innervation. Thoracodorsal nerve.
Mathes and Nahai flap classification. Type V (One dominant pedicle and secondary
segmental pedicles) (Fig. 16.9).
Type of flap. Muscle flap. Myocutaneous flap.
Sites of use. Lateral, midposterior, midlateral, anterior regions.
Techniques. A muscle-sparing thoracotomy must be obviously planned. Considering the
blood supply coming from above, the flap has to be fashioned by cutting the
inferoposterior part of the muscle. This muscle provides a great spectrum of flap size that
is of maximal dimension when the dissection is carried out along the rachis. If a
myocutaneous flap is required, the skin surface can overlap the muscle perimeter. If any
cut had been previously performed on the muscle, the distal portion cannot be used.
Latissimus dorsi can be posteriorly or anteriorly rotated after dissection of the three sides
rising to the neck (posteriorly) and sternum (anteriorly); if the flap is well prepared,
tension and rotation impairment should not be encountered due to the possible flap size.
Advantages. Latissimus dorsi has a valuable rotation degree that provides a great space for
rotation flap although translational advancement for anterior defect can be performed.
The use of this flap can provide coverage to the largest thoracectomies suitable for soft
tissue reconstruction. The regional blood supply allows consistent myocutaneous flap.
Disadvantages. In case of large myocutaneous flap, the primitive posterior muscle site can
require skin grafting. The dorsal primary pedicle can be damaged by previous upper
chest radiation. In case of posterolateral thoracotomy the muscle part to be rotated can
be consistently reduced.
Serratus anterior muscle flap is generally adopted for intrathoracic use.
Insertion. Scapula (medial margin and inferior angle)
Origin. Rib surface (first to eighth)
Blood supply. Serratus branch of thoracodorsal vessels and long thoracic artery and vein
Innervation. Bells nerve
Mathes and Nahai flap classification. Type III (two dominant pedicles) (Fig. 16.8).
Type of flap. Muscle flap, myocutaneos flap if used with pectoralis major or latissimus dorsi.
Sites of use. Lateral region if used alone. Lateral posterior if used with latissimus dorsi,
lateral anterior if used with pectoralis major. Intrathoracic use is the main indication.
Techniques. If thoracotomy encompasses muscles incision, the serratus anterior can be the
best solution because usually preserved by common thoracotomies. The pedicle is cranial

and posterior coming from the subscapular artery. The need of preservation of the
dominant blood supply is basic and allows complete detachment from the ribs.
Introduction into the pleural space is usually carried out through the second intercostal
space and fashioned for mediastinal or parietal purposes.
Advantages. The main anatomical feature is that it can be used as an adjunctive flap to
pectoralis major and latissumus dorsi. Suitable for lateral plasty. Very easy to use as an
intrathoracic flap.
Disadvantages. Limited surface, limited translational potentials if used alone.
Rectus abdominis muscle flap is very useful for the repair of anteroinferior chest wall
Insertion. Costal cartilages (fifth to eighth)
Origin. Pubis cresta
Blood supply. Internal mammary and inferior epigastric vessels
Innervation. Intercostal nerves (seventh to twelfth)
Mathes and Nahai flap classification. Type III (two dominant pedicles) (Fig. 16.8).
Type of flap. Muscle flap, myocutaneos flap
Sites of use. Lower sternum, anterior lower chest wall.
Techniques. The technique is based on flap preparation on the mammary artery pedicle
because the inferior epigastric is divided for the thoracic surgery procedure. The possible
rotation is both vertical and horizontal. After a longitudinal skin incision, the ipsilateral
rectus abdominis is dissected and rotated to the defect. Accurate measurement from the
vascular pedicle and the defect must be obtained to create a fitting flap. The flap can
sometimes be prepared by saving the skin between the donor site and the defect. It can
be achieved with a subcutaneous bridge where the flap can be slided to the defect.
Advantages. This flap is really useful in reconstruction of the anterior chest wall especially
the lower sternum. It potentially provides very long graft to be placed with a
considerable rotation degree. It can be the flap of choice if other possible tissues have
been irradiated.
Disadvantages. Vascular patency of the internal mammary artery must be quantified and
maintained after the axial rotation.
Omentum. Muscle flaps are undoubtedly the first choice for soft tissue coverage after
extensive full-thickness chest wall resection. Omentum is to be considered a precious
alternative in very selected cases, especially in infected or irradiated wound, when retrieval
of a well-vascularized replacement tissue is the primary issue. In fact it has been proved as a
very valuable option in the treatment of deep sternal wound infection (Fig. 16.10).

Figure 16.10 Large sternal defect after infectious disease (A), laparoscopically prepared omental flap (B) is brought to the
defect (C). View of the laparoscopic operating field; the omentum is transposed to the chest through a small diaphragmatic
incision (D).

Blood supply. Most of the blood supply of the omentum is derived by the gastroepiploic
arcade, which is formed on the side of the greater curvature of the stomach by
anastomosis between the right and left gastroepiploic vessels. At least three omental
arteries branch off from the gastroepiploic arcade, forming a constant peripheral vascular
connection called Barkows arcade, characterized by an extensive anastomotic network.
Type of flap. Simple, pedicled flap.
Sites of use. Sternal defects are suited for omental flap, because deep sternal wound
infection is the most frequent indication for such type of repair. However the omental
flap can reach every site of the thorax, if necessary. Also wide basal defects appear to be
suitable for omental reconstruction, especially if the diaphragm has been involved by the
resection and the abdominal cavity has been opened (Fig. 16.11).
Techniques. Thoracic transposition of pedicled omentum can be achieved with an open
procedure or by laparoscopy (Figs. 16.10 and 16.11). The latter technique is now to be
considered the first choice. The patient is placed in the supine position with both arms
adducted with an inflating bag positioned under the shoulders. A 10-mm Hasson trocar is
placed through a 2-cm midline vertical incision, just above the umbilicus; a 30-degree
telescope is then inserted and the pneumoperitoneum is established. Three operative
ports with 5-mm trocars are sufficient to obtain a good surgical maneuverability. In our
experience, the use of ultrasound scissors has been helpful (Harmonic Scalpel;

UltraCision: Ethicon Endo-Surgery, Inc, Cincinnati, Ohio) to divide possible adhesions

and separate omentum from the transverse colon, if necessary. Through a right or left
subcostal port the gastric wall is grasped to facilitate dissection. If a long and bulky flap
is needed, complete mobilization of the omentum based on the right gastroepiploic artery
is performed. Alternatively, for lower sternal defect in a suitable anatomy, the
gastroepiploic arcade may be left untouched and the omental flap may be simply
developed at the expense of Barkows arcade, dividing some of the anastomosing arteries.
The decision is made on the basis of required flap bulk and length and the individual
anatomical variability, which is remarkable in this area. Thoracic transposition of the
mobilized omentum is achieved through a 5-cm substernal diaphragmatic incision, if the
flap has been developed to obliterate the space of an anterior defect; if the omental flap
has been designed to cover defects located elsewhere, the site of transdiaphragmatic
thoracic transposition is chosen on the basis of the target location of the pedicled tissue
flap. Great care must be used to control the correct position of the stomachs greater
curvature, which could have been stretched cranially during the omental transposition.7

Figure 16.11 Operative field of infected sternal metastasis of mammary cancer (A), intraoperative view of the large defect
after resection of skin, pectoralis muscles, sternum, and thymus gland (B), omental flap completely fills the anterior gap after
resection (C), soft tissue coverage has been achieved by the ipsilateral mammary gland (D).

Advantages. This flap is seldom required for chest wall reconstruction but the technique
must belong to the thoracic surgeons armamentarium, because the possible fields of
application of the omentum are multiple and potentially extremely useful. Omentum has
a very rich blood supply, induces neovascularity and can survive in highly contaminated
fields, where it aids to eradicate infection; it conforms to every recess and its possible
large size makes it suitable to cover wide prosthetic reconstruction in different thoracic
Disadvantages. Omentum has no structural support and should be placed on a rigid base.
When harvested by laparotomy the thoracic omental transposition entails multiple
drawbacks: Heavier surgical trauma, increased postoperative pain, oral nutrition delay,
and possible abdominal hernia. All these disadvantages are avoided by laparoscopic
Diaphragm. Phrenoplasty is a possible method of chest wall reconstruction, even if it should

not be classified within the soft tissues coverage procedures. Phrenoplasty is an old technique
developed in the tuberculosis era, for the management of dead space after lobectomy. The
application of this procedure for chest wall reconstruction has not been adequately reported
in the literature.
Sites of use. Defects in the basal area are very well reconstructed by the diaphragm,
regardless of whether the muscle was partially involved in the resection: In particular the
technique of phrenoplasty is suited for repair of defects resulting from resection of the
seventh, eighth, ninth, and tenth ribs.
Techniques. The concept is simply reattaching the diaphragm at a higher level (Fig. 16.12).
The phrenic nerve innervates the diaphragm from the center outward and it is possible to
preserve the main branches of the nerve, by peripheral incision of the muscle. Muscle
incision at the level of the costodiaphragmatic recess gets a large flap that is secured by
heavy nonabsorbable pericostal sutures to the lower uninvolved rib. Even if the
diaphragm has been partially resected, the flap can be elevated at the desired level, at
the expense of the phrenic dome. The technique allows transformation of a thoracic
defect into an abdominal defect, with fewer pathophysiologic consequences;
reconstruction of the gap is as well required to prevent an abdominal hernia
development. A variety of methods can be used for such purpose. Titanium bars and
omentum covering a synthetic mesh are reasonable choices (Fig. 16.13).

Figure 16.12 Lower chest wall defect, suitable for reconstruction with the diaphragm. The diaphragm has been radially
incised and fixed to the lowest uninvolved rib. A: Anterior view. B: Lateral view.

Figure 16.13 A: Intraoperative image of diaphragmatic reconstruction after left eighth, ninth, and tenth ribs resection. B,C:
Abdominal defect reconstruction by PTFE prosthesis, covered by omental flap and single titanium bar placement. D:
Postoperative chest x-ray shows a linear diaphragmatic profile.

Advantages. The pathophysiologic consequences of the defect are strongly limited, in

particular those of respiratory type because no paradoxical movements of the wall can
Disadvantages. A mild reduction of the pleural cavity volume is the only drawback of this

Chest wall surgery is a fascinating topic due to its multiple pathophysiologic implications, the
continuous improvement of techniques and materials, and the variety of the possible surgical


Special thanks to Elisa Scarnecchia for pictures and artworks. The authors also acknowledge
Beatrice Sensi and Mark Ragusa for the editing support.

Recommended References and Readings

1. Riquet M, Arame A, Le Pimpec Barthes F. Non-small cell lung cancer invading the chest
wall. Thorac Surg Clin. 2010;20(4):519527
2. Facciolo F, Cardillo G, Lopergolo M, et al. Chest wall invasion in non-small cell lung
carcinoma: A rationale for en bloc resection. J Thorac Cardiovasc Surg. 2001;121(4):649
3. Weyant MJ, Bains MS, Venkatraman E, et al. Results of chest wall resection and
reconstruction with and without rigid prosthesis. Ann Thorac Surg. 2006;81(1):279285.
4. Deschamps C, Tirnaksiz BM, Darbandi R, et al. Early and long-term results of prosthetic
chest wall reconstruction. J Thorac Cardiovasc Surg. 1999;117(3):588591
5. Marulli G, Hamad AM, Cogliati E, et al. Allograft sternochondral replacement after
resection of large sternal chondrosarcoma. J Thorac Cardiovasc Surg. 2010;139(4):e69e70.
6. Mathes SJ, Nahai F. Classification of the vascular anatomy of muscles: Experimental and
clinical correlation. Plast Reconstr Surg. 1981;67(2):177187
7. Puma F, Fedeli C, Ottavi P, et al. Laparoscopic omental flap for the treatment of major
sternal wound infection after cardiac surgery. J Thorac Cardiovasc Surg. 2003;126(6):1998

17 Sternal Resection/Reconstruction
Eric N. Feins and Christopher R. Morse

Resection and reconstruction of the sternum comprises a wide spectrum of surgical
techniques applied to a range of clinical conditions. As methods have evolved for skeletal and
soft tissue reconstruction, the ability to manage sternal pathology has greatly improved. The
main conditions requiring sternal resection and reconstruction are infectious or neoplastic
although radiation-induced necrosis of the anterior chest wall, as well as trauma, may also
require surgical intervention.
Infection represents the most common indication for resection/reconstruction of the
sternum. Sternal infections are typically a postoperative occurrence following median
sternotomy for cardiac surgery although sternal osteomyelitis from IV drug use can also
occur. Several patient- and surgically related factors predispose to postoperative sternal
wound infections, including obesity, diabetes, recent tobacco use, urgent surgery, use of
internal mammary arterial grafts (especially bilateral), and postoperative bleeding. Superficial
sternal wound infections generally do not require surgical intervention and can be managed
with IV antibiotics and local wound care. Deep sternal wound infections, however, require
urgent surgical intervention to widely resect all infected and/or nonviable tissue. The extent
of infection obviously dictates the degree of bony and soft tissue debridement, which in turn
dictates the reconstructive technique. Partial sternectomy is preferred so long as the surgeon
is able to debride to healthy, solid bone and soft tissue with bleeding margins. In the case of
extensive sternal osteomyelitis with widely necrotic bone that is soft and/or oozing pus, a
total sternectomy must be performed. The implantation of prosthetic material for skeletal
reconstruction in the setting of active infection is contraindicated. Reconstructive techniques
for sternal wound infections, therefore, rely on soft tissue coverage with muscle or
myocutaneous flaps or omentum, typically done in collaboration with a plastic/reconstructive
Sternal neoplasms are rare but represent another major indication for sternal
resection/reconstruction. Primary sternal tumors, which are most commonly sarcomas
(especially chondrosarcoma), are a clear indication for sternectomy and reconstruction
because radical resection may permanently eradicate the tumor and improve long-term
survival. The extent of resection follows oncologic principles. A 3- to 5-cm macroscopic
margin is the goal. Depending on the extent of tumor invasion, the following sternal
resections are indicated.
Total Sternectomy (sternal body, manubrium, medial 1/3 of clavicles): Large tumors
involving the manubrium + sternal body, primary neuroendocrine tumors
Subtotal Sternectomy (sternal body with sparing of manubrium/clavicles): Tumors confined
to the sternal body
Partial Sternectomy: Tumors limited to the manubrium or lower 1/3 of the sternal body

In cases where tumor invades deeper to involve underlying mediastinal structures, such as
the pericardium or major vessels, the involved structures must be resected en block with the
sternum, and appropriate reconstruction (e.g., caval reconstruction) performed.
The indication for resection of secondary sternal tumors (e.g., locally recurrent breast
cancer, metastatic lung cancer, renal cell carcinoma) is more controversial given the poorer
oncologic outcomes. In this setting, resection/reconstruction is often indicated for palliative
purposes to relieve pain, inflammation, or bleeding related to the tumor.
Sternal reconstruction following oncologic resection takes a variety of forms, and there is
some debate as to the proper approach. Because of the sternums important role in chest wall
stability and respiratory mechanics, large bony defects that put a patient at risk for
paradoxical chest wall motion (e.g., following total sternectomy) typically undergo rigid
fixation with a prosthesis followed by soft tissue coverage using muscle or myocutaneous
flaps. Small bony defects (i.e., <5 cm in greatest diameter), however, do not require skeletal

Preoperative evaluation and management depend upon the surgical indication. Regardless of
indication, the surgeon must be aware of any prior thoracic and/or cardiac procedures that
will impact the surgical approach. This includes knowledge of prior internal mammary artery
harvest for coronary artery bypass procedures, which will affect the choice of muscle flaps for
reconstruction. In addition, it is critical to know the patients underlying cardiopulmonary
status. Given that sternal resection can leave people with altered respiratory mechanics, it can
be particularly morbid for those with pre-existing pulmonary disease.
For deep sternal wound infections, physical examination, standard blood work, wound
cultures, blood cultures, and imaging are necessary. Clinical findings suggestive of sternal
osteomyelitis include fevers/chills, wound drainage, and sternal instability upon palpation.
Computed tomography (CT) is the most useful modality for assessing the extent of sternal
infection. CT findings consistent with deep sternal wound infection include changes to bone
configuration, fat stranding, and substernal fluid collection(s)/abscess(es). Importantly, after
cardiac surgery the mediastinum will have standard postoperative changes that can make the
radiographic assessment for infection more challenging. Plain films of the chest are of limited
value but will show late bony findings consistent with osteomyelitis. Preoperative
management should include prompt initiation of broad-spectrum IV antibiotics, as well as
resuscitation in the setting of sepsis.
In patients with a sternal neoplasm, preoperative evaluation includes standard blood work
and imaging. While CT is the most informative for assessing the tumor size and location, MRI
can provide additional information about tumor invasion and involvement of underlying
mediastinal structures. Bone scan or PET-CT is performed to rule out extrathoracic metastasis.
Tissue biopsy should be obtained prior to definitive surgery to determine tumor type and
grade. This is important given that sarcoma grade dictates management: Patients with highgrade tumors may require neoadjuvant therapy prior to operative resection.

Prior to surgery, the patient should receive standard prophylactic IV antibiotics within 1 hour
of incision. For patients with deep sternal wound infections who are already receiving
antibiotics, the surgeon must ensure with anesthesia that antibiotics are continued and dosed
The patient is placed in the supine position and is prepped and draped with sterile
towels/sheets. If a single-stage procedure is planned with immediate sternal reconstruction
the sterile field must be wide enough to accommodate flap preparation, including the
abdomen if a rectus flap or omentum will be used.
Sternal Debridement for Infection
For deep sternal wound infections, the prior midline sternotomy incision is reopened and
dissection is performed down to the sternum. Deep sternal wound cultures are obtained. A
combination of cold dissection and electrocautery is used to completely debride the presternal
soft tissue, until healthy, viable bleeding tissue surfaces are reached. The surgeon may have
to extend the initial incision laterally on either side at the superior and/or inferior aspects of
the midline incision in order to gain adequate exposure.
The sternal wires must be cut and removed, and the sternum reopened. Sternal
debridement is carried out using a curette and/or rongeur to remove all necrotic/infected
bone from the cut edge of the sternum until healthy, bleeding surfaces are reached. Sharp
bone edges should be filed down to prevent injury to the heart. Importantly, if the sternum is
widely involved then total or subtotal sternectomy must be performed (see below).
After debridement is completed the surgeon performs pulse lavage of the wound bed with
antibiotic solution. There have been no randomized controlled trials proving the effectiveness
of antibiotic pulse lavage, but it is a standard step in sternal debridement. Once the surgeon is
satisfied with the debridement, and after confirming hemostasis, a vacuum-assisted closure
device is placed in the wound. Negative pressure therapy has become an increasingly popular
method of wound management following sternal debridement and serves as an effective
bridge to definitive closure.
Reconstructive procedures are not performed at the time of sternal debridement in the
setting of active infection, unless the surgeon (in consultation with a plastic/reconstructive
surgeon) is extremely confident that the debridement was complete and there would be no
benefit to an interval period of wound care. Interval flap reconstruction is typically performed
in collaboration with a plastic/reconstructive surgeon once it is certain that the infection has
been completely controlled.
When resecting a sternal tumor, an elliptical skin incision is made over the sternum to include
the prior biopsy incision. The incision extends from the manubrium to the xiphoid. Dissection

is carried down to the sternum with electrocautery. In cases where there is tumor
involvement of the skin and/or presternal soft tissue then the incision must be extended out
laterally to normal tissue with a 3-cm macroscopic margin, and subsequent dissection down
to sternum must remain wide to fully encompass the tumor (Fig. 17.1).
Once down to sternum, the medial attachments of the pectoralis major are divided to raise
each muscle off the sternum and costal cartilage (Fig. 17.2). This exposes the lateral extent of
the sternum. If the tumor clearly involves the pectoralis major then these muscles should be
left in place and resected with the specimen.

Figure 17.1 An elliptical incision is made for sternectomy in the setting of neoplasm. The incision includes the prior biopsy
incision. Macroscopic margins should be at least 3 cm if the tumor involves the presternal soft tissue and/or skin. Incision
may have to be extended laterally at the superior aspect overlying the clavicles (dashed lines) in cases where resection of the
manubrium and clavicles is necessary.

The sternal notch is dissected and the superior retrosternal space is developed. The xiphoid
is also fully dissected up to the costal cartilages, and the inferior retrosternal space is
developed. The degree of tumor invasion is assessed to define the extent of resection. The
intercostal spaces are dissected out with electrocautery, and the internal thoracic arteries are
identified, suture ligated, and divided.
The perichondrium is removed at each intercostal level, and the costal cartilages are
divided with a sternal saw (Fig. 17.3). Division of the costal cartilage should begin on the side
that has less tumor involvement and should extend to one intercostal space above the
superior aspect of the tumor. Laterally the point of division is dictated by tumor invasion,
with care taken to attain adequate margins (3 cm or more). Special care should be taken to
identify and isolate the intercostal vascular bundle at each level and divide the vessels
between clamps.
The posterior perichondrium is divided at each level to free the sternum from the ribs. The
sternum is gently suspended upward to expose the underlying retrosternal tissue. The soft
tissue between the pericardial fat and the undersurface of the sternum is divided with
electrocautery, which gradually frees the specimen (Fig. 17.4). If the manubrium is free of
disease and an adequate margin can be accomplished, then the sternum is divided with the
sternal saw just above the second interspace, separating the specimen from the manubrium.

Figure 17.2 Dissection of the pectoralis major muscles off from their medial attachments to the sternum and chostochondral

Figure 17.3 The sternum is fully exposed, with complete dissection of the intercostal spaces. The internal mammary arteries
have been ligated. Division of the costochondral cartilage is performed with a sternal saw.

If the tumor involves the manubrium, then the dissection is carried superiorly to the first
costochondral cartilage and laterally over the clavicles. This may require lateral extension of
the skin incision. When dissecting the manubrium and clavicles, care is taken to stay directly
on bone, to separate the underlying vessels from the eventual specimen. Division of the
clavicles is performed lateral enough to attain adequate margins, and the whole specimen is
taken en bloc.

Figure 17.4 Superior retraction of the specimen with dissection of the underlying adhesions between the endothoracic fascia
and the underlying pericardial fat. The specimen is removed en bloc.

Skeletal Reconstruction
After removal of the specimen the sternal defect is assessed for reconstruction, with
rigid/bony reconstruction performed for large sternal defects. A variety of materials exist for
skeletal reconstruction, including rigid prostheses (polypropylenemethylmethacrylate
sandwiches, cryopreserved homografts [iliac crest, rib], titanium plates, or meshes), and
nonrigid prosthesis (PTFE patches, polypropylene patches).
PolypropyleneMethylmethacrylate Sandwich Reconstruction of the Sternum
A layer of polypropylene mesh is sized to the sternal defect. The sandwich is then created by
suturing two layers of mesh together using a nonabsorbable suture. Methymethacrylate is
injected in between the two mesh layers, which will lend rigidity to the prosthesis following
implantation. The prosthesis is then molded to the sternal defect and anchored to the chest
wall using interrupted, monofilament, nonabsorbable sutures at the corners. It is preferable to
have the sizing of the prosthesis be slightly smaller than the defect to avoid overriding and
subsequent pain. After placement of a drain behind the prosthesis, the prosthesis is fully
secured to the chest wall with more nonabsorbable sutures coupled with running
nonabsorbable sutures between the mesh and the cut rib edges or costal cartilages (Fig. 17.5).
Allograft Reconstruction of the Sternum
A cryopreserved allografttypically iliac crestcan be fitted to the defect to serve as the
neosternum (in lieu of a methylmethacrylate prosthesis). When the manubrium has been left
in place, the allograft is anchored to the manubrium using titanium screws. Laterally, the
graft can be secured to the rib edges with titanium bars, which are anchored with titanium
screws (Fig. 17.6). Alternatively, methylmethacrylate sandwiches are constructed and sutured
to the anterior chest wall on either side of the allograft and then sutured to the lateral aspect
of the allograft with interrupted, nonabsorbable sutures through holes drilled in the graft.

Figure 17.5 Sewing in the methymethacrylate prosthesis fill the poststernectomy defect.

Figure 17.6 Allograft implantation, with titanium bars/screws used to anchor the prosthesis to the chest wall.

Titanium Plating

A variety of titanium prostheses exist that can be implanted to provide rigid fixation of the
anterior chest wall. For large defects (i.e., after subtotal sternectomy), three titanium plates
are implanted across the defect. Prior to implantation they are shaped to conform to the chest
wall. They are secured to the ribs on each side with three titanium screws, which are sized to
the thickness of the patients ribs.
Soft Tissue Reconstruction
When the prostheses mentioned above are implanted, an omental flap may be performed,
with placement of the flap underneath the prosthesis to provide separation between the
prosthesis and the heart. As a highly vascular structure, the omentum also helps promote
tissue integration with the prosthesis. The omentum is secured in place with interrupted
nonabsorbable sutures.
The pectoralis muscles are then reapproximated to the costal cartilage and the presternal
fascia in the midline to cover the prosthesis. This is done over another drain, which lies
behind the pectoralis muscle layer. The presternal soft tissue is then reapproximated with a
running, absorbable suture, such as PDS. Finally the skin is closed with a running monocryl
If the soft tissue defect is large, then a muscle or myocutaneous flap reconstruction can be
performed, typically with a pectoralis major advancement flap, based on the thoracoacromial

Analgesia and aggressive pulmonary physiotherapy are critical in the immediate
postoperative period given that anterior chest wall reconstruction can leave patients with
altered respiratory mechanics. Inadequate analgesia with subsequent splinting will exacerbate
this. When operating for sternal wound infections IV antibiotics are continued for 6 to 8
weeks if there was presence of osteomyelitis, with narrowing of antibiotics based on culture
data. Standard perioperative antibiotics are appropriate after surgery for noninfectious
reasons. Drains should be left in place until outputs reach an acceptably low level
(approximately 20 to 40 cc per day) to prevent seroma formation. If patients were on
anticoagulant therapy preoperatively, resumption should be delayed for as long as possible to
minimize the risk of hematoma formation.

Respiratory and wound complications are the main concerns following sternal
resection/reconstruction. Pulmonary complications, including pneumonia, respiratory failure,
and prolonged ventilator support, are related to the altered chest wall mechanics and in some
cases paradoxical motion of the chest wall. These complications represent a major cause of
nononcologic, postoperative mortality after sternal resection/reconstruction. Wound
complications include seroma formation, hematoma formation, prosthesis infection, and
partial or complete flap loss. Small seromas typically resorb over several weeks without

intervention; however, sterile aspiration is necessary for large seromas. Hematomas, if large
enough mandate reoperation for evacuation. Prosthesis infection is a serious wound
complication that usually requires reoperation to remove the infected material.

For patients undergoing resection for sternal neoplasm, tumor type is the most important
predictor of survival. Those who undergo radical resection of a primary sternal tumor fair the
best, as demonstrated in multiple studies. In a review of 49 patients undergoing sternal
resection/reconstruction for malignancy at MD Anderson between 2001 and 2012, the
oncologic mortality rate was 49%, with a median survival of 18 months. Patients with
primary sternal tumors had a 17% oncologic mortality, compared to a 50% mortality among
those with breast cancer, and an 87% mortality in those with metastatic cancer other than
Lequaglie et al. reviewed 88 patients who underwent sternal resection for neoplasm over a
19-year period. The 10-year actuarial survival for patients with resected primary sternal
tumors was 85%. Patients undergoing resection for breast cancer relapses had a 42% 10-year
survival while none of those with other metastatic cancers were alive at 10 years.
Chapelier et al. reviewed 38 patients who underwent sternal resection/reconstruction for
primary sternal tumors over a 16-year period. Tumor grade was the primary predictor of
survival in this study. Local recurrence rates were nontrivial. Approximately 25% of patients
had a local recurrence within 1 year of surgery, most of whom underwent reresection.
Patients with radiation-induced sarcoma are at particular risk for local recurrence because the
surrounding irradiated tissue is abnormal, making it difficult to be certain of negative
The outcomes of patients who undergo debridement and flap reconstruction for deep
sternal wound infections are largely dependent on preoperative characteristics. Those with
end-stage renal disease, COPD, or poststernotomy prolonged ventilator support have an
increased mortality following sternal resection/reconstruction. Patients with sepsis
preoperatively have mortality rates as high as 25%, compared to only 3% in those without it.

Techniques for sternal resection and reconstruction play an important role in the
management of sternal wound infections as well as sternal neoplasms. The extent of sternal
resection depends entirely on the degree of diseased tissue and can range from limited
debridement or partial sternectomy to total sternectomy. Surgical techniques have evolved for
reconstructing the poststernectomy defect. Large sternal defects require rigid fixation to
prevent paradoxical chest wall motion and optimize respiratory mechanics. A range of
techniques and materials exist today, including mythymethacrylate, bone allograft, and
titanium prostheses, which can be used alone or in combination to replace the structure and
function of the sternum.

Recommended References and Readings

Butterworth JA, Garvey PB, Baumann DP, et al. Optimizing reconstruction of oncologic
sternectomy defects based on surgical outcomes. J Am Coll Surg. 2013;217(2):306316.
Chang RR. Thoracic reconstruction. In: Thorne CH, Beasley RW, Aston SJ, et al., eds. Grabb
and Smiths Plastic Surgery. Philadelphia, PA: Lippincott Williams & Wilkins; 2007:665669.
Chapelier A. Resection and reconstruction for primary sternal tumors. Thorac Surg Clin.
Chapelier AR, Missana MC, Couturaud B, et al. Sternal resection and reconstruction for
primary malignant tumors. Ann Thorac Surg. 2004;77:10011007.
Harper JG, Losken A. Sternal wound infections. In: Franco KL, Thourani VH, eds.
Cardiothoracic Surgery Review. Philadelphia, PA: Lippincott Williams & Wilkins, 2012:180
Kucharczuk JC, Kaiser LR. Chest wall resections. In: Kaiser LR, Kron IL, Spray TL, eds. Mastery
of Cardiothoracic Surgery. Philadelphia, PA: Lippincott Williams & Wilkins; 2007:222227.
Lequaglie C, Massone PB, Giudice G, et al. Gold standard for sternectomies and plastic
reconstructions after resection for primary and secondary sternal neoplasms.
LoCicero III J. Infections of the chest wall. In: Shields TW, LoCicero III J, Reed CE, Feins RH,
eds. General Thoracic Surgery. Philadelphia, PA: Lippincott Williams & Wilkins; 2009:633
Rocco G. Anterior chest wall resection and reconstruction. Operat Techn Thorac Cardiovasc
Surg. 2013;18(1):3241.
Rocco G. Overview on current and future materials for chest wall reconstruction. Thorac Surg
Clin. 2010;20:559562.

Part V
Chest Wall/Pleural Space/Diaphragm:

18 Plication/Thoracotomy/VATS

Michael H. Kwon and Christopher R. Morse

First described by Wood in 1916 and first performed successfully by Morrison in 1923,
diaphragmatic plication as a surgical treatment for diaphragmatic paralysis secondary to
phrenic nerve dysfunction remains an effective option for both pediatric and adult patients in
whom the associated mechanical effects of a paralyzed and elevated hemidiaphragm have led
to chronic symptoms of dyspnea and/or orthopnea. It is also indicated for well-selected
mechanically ventilated patients in whom chronic diaphragmatic paralysis continues to
preclude effective weaning from mechanical ventilation after other contributory factors have
been optimized. Understanding the etiology and pathophysiology of diaphragmatic paralysis
is critical in understanding the indications and contraindications of this procedure and
thereby the ability to appropriately select patients who stand to benefit from the procedure
with minimal risk.
Diaphragmatic paralysis can be congenital or acquired although in many cases it is difficult
to identify an obvious cause, many suspecting a viral etiology. Congenital paralysis or paresis
is known as diaphragmatic eventration and results from a failure of normal diaphragmatic
muscular development in the setting of normal phrenic nerve function. Plication in infants
and children with eventration is beyond the scope of this chapter, which will instead focus on
adults with acquired disease. In recent years the most common acquired etiology in adults is
iatrogenic injury to the phrenic nerve after cardiac (and to a lesser extent thoracic) surgical
procedures and usually leads to unilateral diaphragmatic parlaysis. In order of increasing
severity and chronicity of the paralysis itself, injury to the nerve in this setting results from
hypothermic injury from ice or cold packs placed in the chest (usually leading to temporary
paralysis/paresis), traction injury, thermal injury from local electrocautery, and complete
laceration (usually but not always permanent). Other etiologies include invasion of tumor,
penetrating trauma, blunt trauma, as well as other more rare conditions including neuralgic
amyotrophy. Meanwhile, bilateral diaphragmatic dysfunction usually develops gradually on a
spectrum from paresis to paralysis and is usually limited to patients with progressive
neuromuscular disorders such as amyotrophic lateral sclerosis, multiple sclerosis, and
myasthenia gravis.
When the diaphragm becomes paralyzed, normal caudal movement of the diaphragm
during inspiration becomes impaired, leading to decreased ventilation. The diaphragm takes
on a more cephalad baseline position throughout the respiratory cycle. With ongoing disuse,
the muscle fibers become atrophic, and the surface area of the diaphragm expands as the
connective tissue remodels, ultimately leading to a highly redundant and floppy overall
architecture. As this progresses, the negative intrapleural pressure created by contraction of
the accessory muscles of inspiration can lead to paradoxical motion of the diaphragm in the
cephalad direction during inspiration (reduced inspiratory capacity), and in the caudad
direction during expiration when the intrapleural pressure becomes positive (increased
functional residual capacity), thereby further limiting tidal volumes and overall ventilation.
For patients with underlying lung disease, this can create significant hypoxia as well and
exacerbate dyspnea. Furthermore, when patients are in the supine position, the

noncontractile and redundant diaphragm is unable to exert the normal tonic opposition to the
gravitational pressure exerted by the intra-abdominal viscera, leading to further cephalad
displacement of the diaphragm and the development of orthopnea as a progressive symptom.
Understanding these mechanical disadvantages, one can then appreciate that although
plication does not restore contractile function of the diaphragm per se, many, if not all of the
deleterious mechanical effects of chronic paralysis can be significantly ameliorated simply by
respositioning and surgically remodeling the diaphragm into a flat, taut, nonredundant, and
more caudally oriented planar structure by means of plication. In doing so, plication can
allow for the resolution of symptoms (namely dyspnea and orthopnea) by achieving the
following specific mechanical goals:
1. Increased total lung capacity by virtue of more caudal displacement of the diaphragm.
2. Decreased redundancy of diaphragmatic surface area and minimization of paradoxical
3. Decreased diaphragmatic compliance that allows intercostal and other accessory muscles of
respiration to more effectively create negative and positive intrapleural pressures necessary
for effective inspiration and expiration, respectively.
4. Increased opposition to cephalad displacement of abdominal viscera while in supine
position to decrease orthopnea.
However, unless patients are symptomatic, improving the respiratory mechanics in this
manner is not indicated, that is, the presence of an elevated hemidiaphragm alone does not in
and of itself warrant plication unless symptoms are present. Furthermore, depending on the
etiology, the decision to operate should be delayed to ensure that the paralysis is indeed
permanent. Several authors have suggested a 1- to 2-year period of observation for patients
with postcardiac surgery diaphragmatic paralysis if the symptoms are mild, chronic, and
stable. A much shorter period of observation may be appropriate in patients with more severe
symptoms or for patients in whom symptoms have progressed and are not attributable to
other forms of lung disease or heart failure. A significantly shorter period of 2 to 6 weeks may
be suitable for patients in whom the goal of plication is to assist in effective weaning from
mechanical ventilation.
Meanwhile, plication is typically deferred in morbidly obese patients for several reasons
including (1) overall technical difficulty due to body habitus and the potential for arriving at
suboptimal mechanical results, and (2) the possibility that with aggressive weight
loss/bariatric surgery, the associated improvement in overall chest wall compliance may be
sufficient to improve symptoms without plicating the diaphragm. Finally, those with
progressive neuromuscular disorders are usually not candidates because it is not just the
diaphragm that is dysfunctional but also the accessory muscles of respiration. The benefit of
plication is, therefore, limited, and such patients are better candidates for an eventual
transition to a tracheostomy and mechanical ventilation as palliation near the end of life.

The three critical concepts in the preoperative planning for a diaphragmatic plication are to
(1) make the diagnosis, (2) determine the presence and duration of symptoms, and (3)

medically optimize other factors that may be contributing to dyspnea.

In symptomatic patients, diagnosis is usually established by the finding of an elevated
hemidiaphragm on a chest radiograph. Portable radiographs taken in critically ill patients are
significantly less specific for the diagnosis, especially if the degree of elevation is mild (less
than 2 cm), but a high-quality film taken of a standing patient at full inspiration
demonstrating significant elevation (e.g., several rib spaces) is usually sufficient to make the
diagnosis without additional studies. When the diagnosis is in doubt, a fluoroscopic sniff test
or ultrasound can be used to demonstrate limited or paradoxical diaphragmatic movement
with full respiratory effort.
We obtain standing and supine pulmonary function tests where a restrictive pattern may
worsen when supine, evidenced by a drop in vital capacity. However, PFTs are often
nonspecific for the diagnosis and are rather used as an adjunct to a carefully taken history
and physical examination in determining how the patient will tolerate single-lung ventilation
during the planned procedure.
Ruling out and optimizing other concomitant sources of respiratory insufficiency (e.g.,
heart failure, interstitial lung disease, pneumonia, smoking, morbid obesity, reactive airway
disease, etc.) is critical in the observational period as symptoms may resolve without the need
for surgery when these factors are improved.
Standard preoperative planning otherwise includes a full chemistry panel, complete blood
count, coagulation profile, and a recent chest radiograph (assists in determining the rib space
for entry into the chest).

After intubation with a dual-lumen endotracheal tube, a nasogastric tube is placed to
decompress the stomach. The patient is then positioned in the standard decubitus position
with the break of the operating room table near the level of the xiphoid or slightly lower.
Steep Trendelenburg positioning aids in caudal displacement of the abdominal viscera and,
therefore, the diaphragm by gravity, allowing for less tension on the sutures as the operation
proceeds. In addition, placement of a thoracic epidural catheter for postoperative pain control
is recommended, especially for patients undergoing an open procedure.
Open Transthoracic Diaphragmatic Plication
A posterolateral thoracotomy is made in the sixth, seventh, or eighth intercostal space
depending on the degree of diaphragmatic elevation on preoperative imaging. The inferior
pulmonary ligament is taken down sharply to improve the working space. The standard
technique, thought to distribute tension most evenly over the diaphragm, is termed the
accordion technique, in which multiple rows of nonabsorbable, pledgeted horizontal mattress
sutures are placed in the diaphragm (Fig. 18.1). Using a double-armed suture of relatively
large caliber (e.g., size 2-0 or 0 polypropylene monofilament or braided polyester), preloaded
with a pledget midlength, multiple consecutive full-thickness bites are taken with each arm of

the suture running in a straight line from posterior to anterior along the medial aspect of the
diaphragm to create pleats, which are oriented in a medial-to-lateral axis. Once both arms of
each suture are taken all the way to the anterior aspect of the diaphragm, the needles are
placed through another pledget and the suture tied down. Additional sutures are placed
parallel to the first row, working medial to lateral with each successive suture until the
redundancy has been completely taken up and the diaphragm pleated down with an
accordion-like topography. Care is taken to prevent inadvertently taking bites into hollow
abdominal viscera and some surgeons advocate for opening the diaphragm at the central
tendon, which allows direct visualization of the abdomen. The thoracotomy is closed in layers
and a thoracostomy tube is left in place.
Alternative suturing schema for plicating the diaphragm exist including (1) interrupted
horizontal mattress sutures without the accordion technique (requires more pledgets, more
time-consuming, but sometimes necessary in an extremely thin and friable diaphragm), and
(2) continuous running stitches (baseball stitch vs. horizontal mattress). Due to the small
number of patients in even the largest case series, it is unknown whether the long-term
results are more favorable with one technique versus the other. In our anecdotal experience,
the pledgeted accordion technique described above represents the optimum balance between
efficiency and distribution of tension.

Figure 18.1 Accordion plication. A: Mattress sutures are placed with bites oriented along the posterior to anterior axis. B:
Completed repair.

Thoracoscopic Diaphragmatic Plication

Thoracosopic diaphragmatic plication is a minimally invasive method by which similar
results can be achieved in comparison to the open technique. The potential advantages
include decreased postoperative pain and decreased length of stay. The main disadvantages
are that unlike the open procedure (which, with an adequate incision and good retraction of
inflated lung, can reasonably be performed without single-lung ventilation), thoracoscopic
plication requires dual-lumen intubation and decompression of the ipsilateral lung, especially

given the limited space in which to maneuver in the setting of the elevated diaphragm. For
patients in whom pulmonary function is adequate, thoracoscopic plication is performed using
the same positioning as in the open technique. Two ports can be used if the operating port is
made into a posterolateral minithoracotomy through which standard instruments can be used.
A more standard approach is to use three ports, which typically include a 10-mm
thoracoscopic port at the midaxillary or posterior axillary line in the eighth interspace and
two operating ports in the fifth interspace, one anteriorly and one posteriorly (Fig. 18.2).
Sutures can be placed and tied intracorporeally with traditional thoracoscopic instruments or,
depending on the experience of the surgeon, the Endo Stitch (Covidien, Mansfield, MA)
device can also be used. The type of suture used is similar to that used in the open technique.
Again, as in the open technique, there are several schema for placing the plicating sutures
including (1) the pledgeted accordion technique (often technically difficult due to space and
angle constraints), (2) multiple rows of pledgeted interrupted U-stitches, and (3) one or more
continuous running sutures (Fig. 18.3). Regardless of the method, the principle of distributing
tension while taking up as much of the redundancy as possible remains the same as in open

Figure 18.2 Port site placement for thoracoscopic plication. Two ports are placed in the fifth intercostal space and a third
port in the eighth intercostal space. The thoracoscope is moved from one port to another depending on the specific location
of the diaphragm being sutured. Shown here with use of an Endo Stitch device.

Figure 18.3 Alternate schema for placement of diaphragmatic sutures for plication.

Laparoscopic Diaphragmatic Plication

Laparoscopic techniques have also gained in popularity in recent years. A full description of
the laparoscopic approach can be found in Chapter 19.

Patients are generally extubated in the operating room unless they already required
mechanical ventilation in the preoperative period. A single thoracostomy tube is left to
suction at a pressure of 20 cm H2O. Notwithstanding significant patient comorbidities and
varying levels of comfort among staff and nursing, most patients undergoing surgery
electively can be admitted to a monitored floor bed after a short stay in the postanesthesia
care unit. A portable chest radiograph is obtained immediately in recovery to assess for the
new baseline position of the diaphragm and adequate expansion of the lung. The
thoracostomy tube is usually removed on postoperative day 1 without the need for a trial on
water seal unless an air leak is present. The diet is advanced, followed by removal of the
epidural catheter and Foley catheter when patients demonstrate an ability to tolerate oral
intake. Virtually all patients experience a sensation of tightness in the lower abdominal area
after the procedure and should be counseled as such. Attention is paid to rule out signs of
peritonitis, which could represent injury to the stomach or bowel. An aggressive bowel
regimen, antiemetics, and pulmonary toilet are essential to prevent and treat problems such
as a postoperative ileus, wretching/vomiting, and coughing, all of which have the potential to
lead to undue tension on the new repair and cause tearing or failure of the stitches. Barring

these and other early complications, patients are often ready for hospital discharge in 2 to 4

All manner of complications have been described in the myriad small case series written on
both open and thoracoscopic procedures. In general the spectrum of complications is similar
to that seen in pulmonary resections (e.g., atrial fibrillation, pneumonia, pulmonary edema,
pleural effusions, acute myocardial infarction, empyema, superficial wound infection, deep
venous thrombosis, pulmonary emoblism, etc.), but with a decreased risk of persistent air
leak and/or bronchopleural fistula as the lung is not intentionally violated during plication.
Meanwhile, there is a higher overall risk of injury to the spleen, stomach, liver, colon, and
small intestine, which can occur while taking full-thickness bites of diaphragm without
adequate cephalad retraction of the local tissue. As noted above, excessive coughing or
wretching in the early postoperative period can cause early recurrence of diaphragmatic

A pooled analysis of five retrospective and one prospective case series of nonventilated adults
undergoing both open and thoracoscopic diaphragmatic plication from 1979 to 2003 (total of
71 patients, mean follow-up ranging from approximately 2 to 8.5 years) demonstrated no
operative deaths, resolution of symptoms in 96% of patients, radiologic improvement in 92%
of patients, and functional improvement in 100% of patients. Overall short-term morbidity
noninclusive of early recurrence (see complications above) occurs in about 5% to 10% of
patients. To date, there are no adequately powered studies that can comment on the longterm differences in outcomes between (1) open versus thoracoscopic plication, and (2) any
plication suturing schema versus another.

In well-selected symptomatic patients in whom other potential sources of restrictive and
obstructive pulmonary disease have been ruled out or optimized, diaphragmatic plication for
diaphragmatic paralysis is an effective surgical treatment with a high success rate and overall
low morbidity. Although the ideal operative approach for the typical patient who is able to
tolerate single-lung ventilation remains unknown, the choice between open thoracotomy and
thoracoscopic plication can be reasonably informed by the training, experience, and
preference of the surgeon.

Recommended References and Readings

Blackmon SH. Technique of video-assisted thoracoscopic surgery diaphragm plication. Oper

Tech Thorac Cardiovasc Surg. 2012; 302310.

Curtis JJ, Nawarawong W, Walls JT, et al. Elevated hemidiaphragm after cardiac operations:
Incidence, prognosis, and relationship to the use of topical ice slush. Ann Thorac Surg.
Freeman RK, Van Woerkom J, Vyverberg A, et al. Long-term follow-up of the functional and
physiologic results of diaphragm plication in adults with unilateral diaphragm paralysis.
Ann Thorac Surg. 2009;88:11121117.
Graham DR, Kaplan D, Evants CC, et al. Diphragm plication for unilateral diaphragmatic
paralysis: A 10-year experience. Ann Thorac Surg. 1990;49:248252.
Groth SS, Andrade RS. Diaphragm plication for eventration or paralysis: A review of the
literature. Ann Thorac Surg. 2010;89:S2146S2150.
Higgs SM, Hussain A, Jackson M, et al. Long term results of diaphragmatic plication for
unilateral diaphragm paralysis. Eur J Cordiothoracic Surg. 2002;21:294297.
Moroux J, Padovani B, Poirier NC, et al. Technique for the repair of diaphragmatic
eventration. Ann Thorac Surg. 1996;62:905907.
Morrison JMW. Eventration of diaphragm due to unilateral phrenic nerve paralysis. Arch
Radiol Electrother. 1923;28:7275.
Patterson GA, Cooper JD, Deslauriers J, et al, eds. Pearsons Thoracic and Esophageal Surgery.
3rd ed. Philadelphia, PA: Churchill Livingstone Elsevier; 2008:14311444.
Versteegh MI, Braun J, Voigt PG, et al. Diaphragm plication in adult patients with diaphragm
paralysis leads to long-term improvement of pulmonary function and level of dyspnea. Eur
J Cardiothorac Surg. 2007;32:449456.

19 Laparoscopic Diaphragmatic Plication

Eitan Podgaetz and Rafael S. Andrade

Laparoscopic diaphragmatic plication is a safe and effective operation in carefully selected
patients. Laparoscopic diaphragm plication was first reported by Httl et al. in three patients.
We reported our experience with laparoscopic hemidiaphragm plication in 25 patients, and
found that laparoscopic diaphragm plication significantly improves dyspnea, quality of life,
and pulmonary function tests (PFTs) in patients with unilateral diaphragm paralysis or
The approach for hemidiaphragm plication should be individualized by patient anatomy,
comorbidities, and surgeon experience. Regardless of approach, proper patient selection,
safety, and a tight imbrication of the entire hemidiaphragm are essential. A transabdominal
approach offers some theoretical advantages and disadvantages over a transthoracic approach
for diaphragmatic plication.
Supine decubitus
Ventilation with single-lumen endotracheal tube
Ample working space within abdominal cavity
Direct visualization of intra-abdominal organs to prevent injury during imbrication
Less postoperative pain
Difficulty visualizing the posterior portion of the hemidiaphragm
Potential splenic or liver laceration
Technically demanding operation in centrally obese patients
Prospective candidates for diaphragmatic plication must have dyspnea that cannot be solely
attributed to another process (i.e., poorly controlled primary lung or heart disease) and must
have an elevated hemidiaphragm on a posteroanterior and lateral (PA/LAT) chest x-ray. Since
the only goal of diaphragm plication is to treat dyspnea, operative intervention is indicated
exclusively for symptomatic patients. An elevated hemidiaphragm or paradoxical motion per se
do not merit surgery in the absence of significant dyspnea. Morbidly obese patients should be
evaluated for medical or surgical weight loss prior to diaphragmatic plication, since dyspnea
may improve after significant weight loss and plication may no longer be required.
Technically, any type of plication is challenging in the morbidly obese patient: The degree of
plication may be compromised due to technical difficulties, the relief of dyspnea may be
limited, and complications may be more common than in normal BMI patients. Patients with
neuromuscular disorders should be approached with extreme caution as their symptomatic
improvement is moderate at best, and complications are common. It is necessary to approach

patients with morbid obesity and neuromuscular disorders in an individualized

multidisciplinary fashion to decide if a plication will improve the patients condition.
Relative contraindications to a laparoscopic approach to diaphragm plication include
previous extensive abdominal surgery, BMI >35, and comorbidities that may worsen with
pneumoperitoneum (e.g., chronic renal failure, history of deep venous thrombosis). Morbidly
obese patients pose particular technical challenges due to hepatomegaly from steatosis or
excessive omental fat in the left upper quadrant.

Clinical Evaluation
The diagnosis of symptomatic hemidiaphragm paralysis or eventration is primarily clinical,
and relies mostly on history, chest x-ray, and the physicians clinical acuity.
The evaluation of a symptomatic patient with hemidiaphragmatic paralysis or eventration
should include an objective assessment of dyspnea, physical examination, PFTs, and imaging
A careful respiratory history on the duration and progression of dyspnea and orthopnea is
essential. Any potential additional causes of dyspnea (e.g., morbid obesity, primary lung
disease, heart failure, etc.) need to be investigated and corrected if possible, since dyspnea
secondary to diaphragmatic paralysis or eventration is largely a diagnosis of exclusion.
All patients with dyspnea secondary to an elevated hemidiaphragm or eventration should
fill out a standardized respiratory questionnaire to evaluate the severity of their symptoms as
objectively as possible and to assess the response to treatment.
Pulmonary Function Tests
PFTs provide relative objectivity to the assessment of dyspneic patients with an elevated
hemidiaphragm; however, PFTs are imprecise and do not correlate well with severity of
dyspnea or response to plication. Diaphragm dysfunction reduces the compliance of the chest
wall; hence, a restrictive pattern (i.e., low forced vital capacity [FVC] and low forced
expiratory volume in 1 second [FEV1]) is the norm.
The diaphragm is the principal inspiratory muscle; therefore, assessing inspiratory PFT
parameters (i.e., maximum forced inspiratory flow [FIFmax]) may be of added value.
FVC should be measured in the upright and supine position; supine FVC in healthy
individuals can decrease up to 20% from upright values, and supine lung volumes may
decrease by 20% to 50% in patients with hemidiaphragmatic eventration or paralysis.
Imaging Studies
Chest x-ray
On standard full-inspiratory PA/LAT chest x-ray, the right hemidiaphragm is normally 1 to 2
cm higher than the left. Hemidiaphragm elevation can be a sign of diaphragmatic paralysis;
however, this is nonspecific since a variety of pulmonary, pleural, and subdiaphragmatic
processes can also elevate the hemidiaphragm. As a result, further studies may be necessary if

an elevated hemidiaphragm is noted on a chest x-ray in the presence of dyspnea.

Fluoroscopic Sniff Test
During fluoroscopy, patients are instructed to sniff, and diaphragmatic excursion is evaluated.
Normally, the diaphragm moves caudally, but in patients with hemidiaphragmatic paralysis,
the diaphragm may (paradoxically) move cranially. Patients with diaphragmatic eventration,
however, may also exhibit passive upward movement of the diaphragm when sniffing.
The clinical value of a sniff test is limited in the presence of an elevated hemidiaphragm
and dyspnea. The principal role of the sniff test is to help discern the etiology of dyspnea in
when it is not entirely clear if hemidiaphragm elevation is the main cause of dyspnea.
Fluoroscopic findings should be interpreted with caution. Approximately 6% of normal
individuals exhibit paradoxical motion on fluoroscopy; to increase the specificity of this
study, at least 2 cm of paradoxical motion should be noticed. Also, a paralyzed or eventrated
hemidiaphragm may move very little or not at all, without paradoxical motion, making the
interpretation of the sniff test and the distinction between paralysis and eventration even
more difficult.
The main utility of CT scans is to rule out the presence of a cervical or intrathoracic tumor as
the cause of phrenic nerve paralysis or to evaluate the possibility of an infra- or
supradiaphragmatic process as the cause of hemidiaphragm elevation. However, a CT scan is
not routinely required if the clinical suspicion of an alternate process is low.
Other Tests
Other diagnostic tests such as ultrasonography, dynamic magnetic resonance imaging,
maximal transdiaphragmatic pressure, and phrenic nerve conduction studies are of limited or
no clinical value in the evaluation of a patient with dyspnea and an elevated hemidiaphragm
on chest x-ray.
Clinical Evaluation Summary
Potential candidates for laparoscopic diaphragm plication have an elevated hemidiaphragm
on chest x-ray and dyspnea; the minimal clinical assessment before a plication should include
history and physical examination, evaluation of the severity of dyspnea with a validated
standardized respiratory quality-of-life questionnaire, a PA and lateral chest x-ray, and PFTs.
Fluoroscopic sniff test and CT scan are of value in select patients but are not mandatory.

The procedure is performed under general anesthesia, with a single-lumen endotracheal tube;
selective ventilation is not necessary.
The patient is in the supine position with arms abducted. The abdomen and lower lateral

chest wall are prepared and draped to allow access for chest tube placement, a foot board is
essential for steep Trendelenburg positioning.
Operative Technique
1. Ports: We use four 12-mm ports; two assistant ports are placed 2 cm parallel to the midline
on the opposite site of the elevated hemidiaphragm. The two working ports are placed in
the ipsilateral upper quadrant (Fig. 19.1). We insufflate the abdomen with CO2 at a
pressure of 15 mm Hg.
2. Exposure: Steep reverse Trendelenburg positioning helps optimize exposure of the posterior
portion of the hemidiaphragm; for a right-sided plication, transection of the falciform
ligament is useful for appropriate access to the diaphragm. The thinned-out hemidiaphragm
is taut and displaced cranially as a result of pneumoperitoneum (Fig. 19.2A). We make a
small perforation at the dome of the diaphragm with electrocautery (Fig. 19.2B). The
resultant pneumothorax releases the tension on the hemidiaphragm and allows the surgeon
to easily pull the hemidiaphragm into the abdominal cavity for suturing (Figs. 19.2C,D). At
this point, we often place a 19 Blake pleural drain through an incision in the anterolateral
chest wall to vent the pneumothorax as needed.

Figure 19.1 Port placement for laparoscopic left hemidiaphragm plication. A1, A2 = assistant ports (placed about 2 cm
parallel to the midline on the right side); S1, S2 = surgeon ports (placed about 2 to 4 cm above the level of the umbilicus).
Dotted lines represent the midline and a horizontal line at about to the distance from umbilicus to xiphoid.

Figure 19.2 A: Cephalad displacement of the left hemidiaphragm following CO2 insufflation, the hemidiaphragm is taught
and difficult to handle. B: A small opening with the electrocautery induces a pneumothorax. C: Floppy hemidiaphragm after
pneumothorax. D: Easy manipulation of the floppy hemidiaphragm.

3. Stitching: We use pledgeted U-stitches (no. 2 nonabsorbable, braided suture, 31-mm curved
needle). We place the first stitch centrally and as far posteriorly as possible (Fig. 19.3A).
Traction on the first stitch facilitates exposure for two or three subsequent deeper stitches
(Fig. 19.3B) to plicate the posterior portion of the hemidiaphragm in an anteroposterior
direction (Figs. 19.3C,D). To plicate the anterior portion of the hemidiaphragm we use two
to three weaving stitches (Fig. 19.4). The diaphragm must be taught at the end of the
procedure (Fig. 19.5). Closure of the initial perforation at the dome occurs with the

Figure 19.3 A: Placement of first pledgeted U-stitch in the central portion of the diaphragm. B: Retraction on the first stitch
allows exposure for placement of two or three subsequent stitches in anteroposterior direction. C,D: Completed posterior
plication with four stitches; the posterior portion of the hemidiaphragm is taught and the anterior portion is still displaced in
cephalad direction. E: This shows U-shaped stitches with pledgets (blue rectangles) before tying them; the numbers show
the sequence of placement starting in the middle of the left half of the diaphragm and progressing toward the back. The
arrow shows the direction of placement of the stitches.

Figure 19.4 A: Placement of first of two to three weaving stitches, the arrows show the course of the U stitch in
posteroanterior direction. B: The posterior three stitches seen in this figure have now been tied. Two anterior stitches have
been placed on the anterior half of the left hemidiaphragm; they have not been tied yet.

4. Tube thoracosotmy: We leave the pleural drain in place upon completion of the procedure
and verify that it has not been caught in a stitch.
5. Intraoperative management of lower lobe atelectasis: Upon completion of the plication, we
ask the anesthesia team to ventilate the patient with high tidal volumes and a PEEP of 10
cm H2O until extubation with the intention to re-expand the lower lobe. If respiratory
secretions are copious after recruitment, a flexible bronchoscopy should be performed.

Postoperatively, we assure patients participate in intense pulmonary toilet to re-expand the
lower lobe of the ipsilateral lung. The chest drain remains in place until output is less than
200 mL per day; occasionally patients need to be discharged with the chest tube in place.
Premature removal of the chest drain can lead to symptomatic pleural effusion with recurrent
lower lobe atelectasis. The immediate postoperative chest x-ray should show that the plicated
side is lower than the opposite side with an acute costophrenic angle (Fig. 19.6), and that the
opposite side is actually elevated in comparison to the preoperative chest x-ray. One month
after surgery, both hemidiaphragms are about at the same level and should remain that way
on long-term follow-up (Fig. 19.6). We monitor patients with the St. Georges Respiratory
Questionnaire (SGRQ), PA/LAT chest x-ray, and PFTs at 1 month after discharge and yearly

Figure 19.5 Completed plication.

Figure 19.6 Sequence of chest x-rays from a patient with left hemidiaphragm paralysis. Note the acute left costophrenic
angle and the cephalad displacement of the right hemidiaphragm immediately postoperatively. At 1 month the
hemidiaphragms have settled in new positions (a small left effusion can be seen); and at 5 years both hemidiaphragms
remain unchanged from the 1-month follow-up CXR.


Complications of laparoscopic plication include prolonged chest tube drainage (>7 days) in
approximately 8%, respiratory failure (4%), gastrointestinal hemorrhage (4%), splenic
laceration requiring splenectomy (4%), stroke (4%), and atrial fibrillation (4%). The severity
of some of these complications is probably also a reflection of the severity of comorbidities in
this patient population.

TABLE 19.1 Comparison of SGRQ Score, FVC, and FEV1 before and 1 Year
after Laparoscopic Diaphragm Plication in 25 Patients

Laparoscopic diaphragmatic plication achieves a very significant improvement in dyspnea at
1 month and 1 year after surgery. The total SGRQ scores improve on average by 20 points
(4 points is considered clinically significant). PFTs improve on average by about 10%, an
indication that FVC and FEV1 do not correlate well with symptoms in patients with
hemidiaphragmatic eventration or paralysis. Table 19.1 summarizes preoperative and
postoperative (1 year) SGRQ scores and PFT in 25 patients. Figure 19.6 illustrates a
representative series of chest x-rays in a patient with 5-year follow-up. Figure 19.7
emphasizes the importance of a thorough posterior plication.

Properly selected patients with symptomatic hemidiaphragmatic paralysis or eventration
benefit significantly from laparoscopic diaphragm plication as long as the surgeon adheres to
basic principles of patient selection, safety, and tight imbrication of the entire

Figure 19.7 This series of lateral views emphasizes the importance and persistence of the posterior plication in a patient
with right hemidiaphragm paralysis.

Recommended References and Readings

Celik S, Celik M, Aydemir B, et al. Long-term results of diaphragmatic plication in adults with
unilateral diaphragm paralysis. J Cardiothorac Surg. 2010;5:111.
Freeman RK, Van Woerkom J, Vyverberg A, et al. Long-term follow-up of the functional and
physiologic results of diaphragm plication in adults with unilateral diaphragm paralysis.
Ann Thorac Surg. 2009;88(4):11121117.
Freeman RK, Wozniak TC, Fitzgerald EB. Functional and physiologic results of video-assisted
thoracoscopic diaphragm plication in adult patients with unilateral diaphragm paralysis.
Ann Thorac Surg. 2006;81(5):18531857.
Graham DR, Kaplan D, Evans CC, et al. Diaphragmatic plication for unilateral diaphragmatic
paralysis: A 10-year experience. Ann Thorac Surg. 1990;49(2):248251.
Groth SS, Andrade RS. Diaphragm plication for eventration or paralysis: A review of the
literature. Ann Thorac Surg. 2010;89(6):S2146S2150.
Groth SS, Rueth NM, Kast T, et al. Laparoscopic diaphragmatic plication for diaphragmatic
paralysis and eventration: An objective evaluation of short-term and midterm results. J
Thorac Cardiovasc Surg. 2010;139(6):14521456.
Higgs SM, Hussain A, Jackson M, et al. Long term results of diaphragmatic plication for
unilateral diaphragm paralysis. Eur J Cardiothorac Surg. 2002;21(2):294297.
Httl TP, Wichmann MW, Reichart B, et al. Laparoscopic diaphragmatic plication: Long-term
results of a novel surgical technique for postoperative phrenic nerve palsy. Surg Endosc.
Kizilcan F, Tanyel FC, Hisnmez A, et al. The long-term results of diaphragmatic plication. J
Pediatr Surg. 1993;28(1):4244.
Mouroux J, Venissac N, Leo F, et al. Surgical treatment of diaphragmatic eventration using
video-assisted thoracic surgery: A prospective study. Ann Thorac Surg. 2005;79(1):308312.
Welvaart WN, Jak PM, van de Veerdonk MC, et al. Effects of diaphragm plication on
pulmonary function and cardiopulmonary exercise parameters. Eur J Cardiothorac Surg,

Welvaart WN, Paul MA, van Hees HW, et al. Diaphragm muscle fiber function and structure
in humans with hemidiaphragm paralysis. Am J Physiol Lung Cell Mol Physiol.

20 Diaphragmatic Pacing

Scott K. Berman and Cynthia S. Chin


The diaphragm is the predominant muscle of inspiration and accounts for approximately 65%
of the vital capacity in a fully functional individual. Without its proper functioning, a patient
can experience mild-to-severe respiratory symptoms. The diaphragm is innervated by the
phrenic nerve, which is composed of nerve fibers from cervical 3, 4, and 5 nerve roots.
The majority of patients referred for diaphragmatic surgery has unilateral diaphragm
paralysis and are treated with diaphragm plication. A smaller percentage of patients have
bilateral diaphragm paralysis, which can lead to respiratory failure requiring ventilator
dependence. Diaphragmatic pacing is utilized in patients with intact phrenic nerves but
interruption of the nerve signal conduction from the respiratory center in the brainstem to the
phrenic nerve. Diaphragm pacers are most commonly placed for patients with a high cervical
spinal cord injury (SCI) or central alveolar hypoventilation. The initial reports on diaphragm
pacing were published in the late 1700s. Sarnoff was the first to show that phrenic nerve
stimulation could produce adequate ventilation. His techniques utilized transcutaneous
electrodes, which were not suitable for long-term use. It was Glenns pioneering work in the
1960s, which produced successful results by employing an implantable diaphragm pacing
device in patients with high cervical injuries or central alveolar hypoventilation. Intrinsic
motor neuron disease was considered a contraindication to placement of a diaphragm pacer;
however, recent studies have not supported this thought.

Injury to the cervical spine above the level of C1 to C2 results in quadriplegia and prevents
stimulation of the diaphragm. It is important to realize that these patients have intact phrenic
nerves but are simply unable to transmit a nerve impulse to the diaphragm. Every year, there
are approximately 12,000 new patients affected with SCI. More than 50% of this group will
develop quadriplegia with >4% requiring mechanical ventilation. The medical cost of a
mechanically ventilated patient can approach $200,000 a year. In addition to this
astronomical cost, patients with mechanical ventilation have a much poorer quality of life
and are riddled with complications. Ventilated patients can experience difficulty with speech,
inability to eat properly leading to frequent aspirations, increased production of secretions
requiring frequent suctioning, and an increase rate of ventilator-associated pneumonias. It has
been reported that the estimated life expectancy for a 20 year old with SCI requiring
mechanical ventilation, is more than 41 years shorter than a person of the same age who has
a SCI that does not require mechanical ventilation. Diaphragm pacers are placed in this
cohort of patient with the goal of decreasing ventilator dependence.
Patients with central alveolar hypoventilation do not have the normal increased respiratory
response when hypoxic or hypercapneic. The diminished response is present night and day;

however, the patient is able to make a conscious effort to breathe during the day, which is
not the case at night. This form of hypoventilation can be congenital or acquired. The
congenital form affects 1 in 50,000 live births. The diagnosis of congenital central
hypoventilation syndrome requires documentation of hypoventilation during sleep in the
absence of primary respiratory, cardiac, or neuromuscular disease or a brainstem lesion.
Once, it is diagnosed, children require nighttime positive pressure ventilation for the rest of
their lives. The acquired form can be secondary to brainstem stroke, surgical trauma, tumor,
hemorrhage, or meningoencephalitis. Implantation of a diaphragmatic pacer in these patients,
whether a child or adult, can drastically improve the patients quality of life by releasing
them from a lifelong requirement of nightly positive pressure ventilation. It is important to
differentiate between central alveolar hypoventilation and obstructive sleep apnea as the
latter does not benefit from implantation of a diaphragmatic pacer.
Contrary to initial thoughts, some recent studies have reported utility of diaphragmatic
pacing in the amyotropic lateral sclerosis (ALS or Lou Gehrig disease). ALS patients have an
idiopathic motor neuron degeneration in the cerebral cortex, brainstem, and spinal cord. This
is a progressive and ultimately fatal disease. All of the muscles utilized for respiration are
adversely affected in ALS patients resulting in progressive respiratory failure requiring
mechanical ventilation. More than 80% of deaths in ALS are attributed to pulmonary failure
and complications. It was conceptualized that in these patients, the utilization of diaphragm
pacing before the onset of respiratory failure may help maintain diaphragm strength and
provide trophic effects allowing the phrenic nerve neurons to remain viable much longer. The
goal with diaphragm pacing would be to increase the time from diagnosis to the onset of
respiratory failure requiring mechanical ventilation in ALS patients.

Diaphragmatic pacing has been proven successful in removing ventilator dependency in a
highly specific subset of patients. It is critical to select the appropriate patients for this
procedure. Only patients who have an intact phrenic nerve and functional diaphragm should
be selected for implantation. Patients with SCI have had partial and sometimes full recovery
of the phrenic nerve up to 12 months after the initial injury. Therefore, it is important to wait
12 months before assessing these patients for a diaphragm pacer. Once phrenic nerve and
diaphragmatic function is confirmed the patient can be considered for surgical placement of a
diaphragm pacer.
Standard preoperative workup includes:
History and physical examination
Particular attention needs to be paid to signs and symptoms of respiratory and neurologic
deficits. Patients with underlying intrinsic lung disease may not benefit from
diaphragmatic pacing because severe lung pathology may be the major contributor to
poor oxygenation and ventilation. In which case, a pacer may not have a dramatic
impact on the patients respiratory status. CT scans of the brain, cervical spine, neck, and
chest are important to rule out symptoms secondary to a mass lesion.
Pulmonary function tests (PFTs)

In patients with a paralyzed diaphragm, a restrictive process is seen on PFTs. There is a

loss of vital capacity, which is worse when measured in the supine position.
It is important to look for evidence of intrinsic lung disease to better select patients who
will benefit from pacing.
Chest x-ray (CXR)
A CXR is more useful in identifying patients with unilateral diaphragmatic paralysis as it
will show an elevated hemidiaphragm on the affected side compared to the normal
diaphragm on CXR. Patients with bilateral diaphragmatic paresis may not have an
obvious finding on CXR as both hemidiaphragms may elevate and thus appear in
normal position.
Fluoroscopic sniff test
When a patient takes a deep breath, intercostal and accessory muscles are the main
contributors to the respiratory excursion. Breathing through ones nose, sniffing,
ensures diaphragmatic involvement. A patient is asked to sniff while in the supine
position. Radiopaque markers are used to measure maximal diaphragmatic movement. In
a patient with normal phrenic nerves, the sniff will result in a quick downward deflection
of the diaphragm. The test is positive for diaphragmatic paralysis if there is paradoxical
upward movement of the diaphragm during inspiration.
Percutaneous cervical electrical stimulation
This is the gold standard for testing phrenic nerve function. Electrodes are placed in the
neck and electrical stimulation is performed. And intact phrenic nerve results in
hemidiaphragm stimulation and contraction.
Prolonged latency or failure to conduct indicates poor phrenic nerve conduction.
Social assessment
Patients undergoing diaphragmatic pacemakers need to be highly motivated with a solid
social and economic foundation. It is vital that the caregivers are enthusiastic as well
since postoperative manipulations of the pacer may require frequent visits with the
medical team.
Of special note, patients with congenital central hypoventilation syndrome as well as
patients with high cervical SCI, have been reported to have bradyarrhythmias requiring
cardiac pacing systems. Diaphragmatic pacers do not have sensing capabilities so there is no
risk of interference from a cardiac pacemaker. However, there is the potential for a cardiac
pacemaker to be influenced by the diaphragmatic pacemaker. In patients with cardiac
pacemakers, it is important to discuss the case with the cardiac electrophysiology service as
they may need to adjust the cardiac pacemaker settings prior to implantation of a diaphragm
pacer. Although this is a theoretical concern, Onder et al. published a report on 20 patients
with cardiac pacemakers in whom a diaphragmatic pacer was placed. None of the patients
experienced immediate or long-term device-to-device interactions.

Amyotropic Lateral Sclerosis

The preoperative forced vital capacity (FVC) must be greater than 40% in ALS patients
otherwise it is been found that there is a high risk of failure to extubate the patient at the
conclusion of the implantation procedure.

The American Academy of Neurology recommends that ALS patients with respiratory
symptoms and a FVC of less than 50% should be offered noninvasive positive pressure
ventilation (NIPPV). Patients considered for diaphragm pacing should have these masks fitted
and utilized prior to surgery so they are accustomed to them if they are needed in the
immediate postoperative period.

Currently there are four devices that are available worldwide: Vienna Phrenic Pacemaker
(Medimplant, Vienna, Austria), Astrostim (Atrotech Ltd., Tampere, Finland), the Avery Mark
IV Phrenic Pacemaker (Avery biomedical, Commack, NY, USA), and the NeuRx Diaphragm
Pacing System (DPS: Synapse Biomedical Inc., Oberlin, OH, USA). The first three systems
utilize direct phrenic nerve stimulation by directly implanting the electrodes on the phrenic
nerve. The NeuRx system places the stimulating electrode directly onto the under surface of
the diaphragm. All systems then require connection of the stimulating electrode to a receiver
usually placed in a subcutaneous pocket.
In the 1980s it was shown that direct diaphragmatic stimulation can be achieved. Mortimer
et al. were able to produce diaphragmatic contractions when they stimulated areas where the
phrenic nerve enters the diaphragm. Electrodes placed in this area, known as motor points,
were able to produce diaphragmatic contractions similar to those obtained with direct
phrenic nerve stimulation. Onders has since published extensively on the effectiveness of
laparoscopic electrode placement at motor points in patient with respiratory insufficiency.
The remainder of this chapter will discuss the Avery Mark IV and NeuRx systems.

Avery Mark IV
Electrodes surgically placed on bilateral phrenic nerves
Lead wires that connect electrodes to subcutaneous receivers
Antennae that are taped over the receivers
External transmitter
Electrodes surgically placed at motor points on bilateral diaphragms
Grounding electrode
Control unit
Cable and external battery-powered pulse generator

Anesthetic Considerations
Overall strategy should be to avoid paralytics since motor points need to be identified
during the surgery.
Rapid reversible, short-acting anesthesia is preferred.
In ALS patients, succinylcholine is contraindicated because it can trigger hyperkalemia in

these patients who have denervated muscles with increased acetylcholine receptors.
Local anesthesia should be used in all incisions to decrease pain response and minimize the
amount of general anesthesia required.

Surgical Procedure

The implantation of phrenic nerve electrodes used for diaphragmatic pacing can be
performed through a cervical, thoracic, abdominal approach.
All of these approaches first require an understanding of the path and course taken by the
right and left phrenic nerves as they exit the spinal cord and travel to the diaphragm.
While the phrenic nerve contains motor and sensory fibers, the right and left phrenic
nerves provide the only motor innervation of the diaphragm. In addition, they supply
sensation to the central tendon of the diaphragm. They originate in the neck from C3 to C5
with most of the fibers of the phrenic nerve primarily originating from the fourth cervical
nerve. See Figure 20.1.

Figure 20.1 Course of phrenic nerve in neck: Note the phrenic nerve traveling on the anterior surface of the anterior scalene
muscle as it travels from lateral to medial. The nerve is deep to the transverse cervical artery and the suprascapular artery
which can be injured in the dissection. Note the nerve entering the thoracic inlet just lateral to the junction of the internal
jugular vein and the subclavian vein.

Right Phrenic Nerve

After leaving the vertebral foramen from C3 to C5, the right phrenic nerve is identified on
the posterolateral aspect of the internal jugular vein.
The nerve exits between the middle scalene muscle posteriorly and the anterior scalene
muscle anteriorly to travel obliquely across the anterior surface of the anterior scalene
At this level on the anterior scalene muscle, the phrenic nerve is deep to the prevertebral

layer of the deep cervical fascia as well as the transverse cervical artery and the
suprascapular artery. As it descends and reaches the inferior and medial aspect of the
anterior scalene muscle, the phrenic nerve is superficial to the second portion of the right
subclavian artery and as the nerve passes medially it is deep to the right subclavian vein.
The nerve then passes deep to the under surface of the first rib and at the level of the first
costochrondral junction it will cross the innominate artery.
As it enters the right hemithorax, the phrenic nerve is found anterior to the superior vena
cava and pulmonary hilum running along the pericardium lateral to the right atrium.
The right phrenic nerve leaves the right hemithorax by passing through the vena caval
hiatus in the diaphragm at the level of T8.
The right phrenic nerve then enters the diaphragm through the tendinous portion of the
diaphragm just lateral to the inferior vena caval foramen.
Upon entering the diaphragm the right phrenic nerve will break into three branches on the
inferior undersurface of the diaphragm forming an anterior branch, a lateral branch, and a
posterior branch.
These branches will then spread out in a radial pattern to supply motor function to the right

Left Phrenic Nerve

The left phrenic nerve course through the neck is a mirror image of its right-sided
counterpart. As the left phrenic nerve enters the left hemithorax, it passes superficial from
lateral to medial on the arch of the aorta.
The left phrenic nerve then passes along the pericardium anterior to the left pulmonary
The left phrenic nerve then curves anteriorly.
It will enter the diaphragm anterior to the central tendon and just lateral to the
Upon entering the diaphragm the left phrenic nerve will break into three branches on the
inferior undersurface of the diaphragm forming an anterior branch, a lateral branch, and a
posterior branch.
These branches will then spread out in a radial pattern to supply motor function to the left

Cervical Approach Technique

The cervical approach is usually considered a minimally invasive procedure since it does not
require a formal thoracotomy, thoracoscopy, or laparoscopy and is frequently performed as
an outpatient procedure. This procedure can be performed under general anesthesia or using
local anesthesia with intravenous sedation.
The patient is placed on the operating room table with a small roll under the patients
shoulders to aid in the cervical visualization.
The patient is prepped and draped in the usual sterile fashion.
A 3- to 5-cm incision is made approximately 2 cm above and parallel to the midportion of

the clavicle.
The platysma can then be divided and the sternocleidomastoid muscle dissected and
reflected medially providing exposure of the prescalene fat pad laterally.
The prevertebral layer of the deep cervical fascia can be incised exposing the anterior
surface of the anterior scalene muscle and internal jugular vein.
The phrenic nerve is identified running superficial on the anterior surface of the anterior
scalene muscle.
If there is any question as to the identity of the phrenic nerve, a nerve test probe can be
used to test and identify the nerve.
Meticulous dissection is used to free a portion of the phrenic nerve taking care to avoid
electrical injury to the nerve.
Depending on the particular anatomy, the nerve can be exposed between the transverse
cervical artery and the suprascapular artery or it can be exposed inferior to the
suprascapular artery before the nerve dips behind the subclavian vein.
A tunnel is then created beneath the nerve lifting it off the superficial surface of the
anterior scalene muscle.
The tunnel should measure approximately 10 to 12 mm and can be created with a right
angle clamp or tonsil clamp.
The electrode is then passed under the phrenic nerve and secured to itself and sutured in
At this point remove any retractors to ensure that the nerve is not compromised or kinked.
Make an incision approximately 5 cm below the clavicle and create a pocket to create the
Using a tonsil clamp make a subcutaneous tunnel connecting the two incisions traveling
over the clavicle.
Making sure to leave slack on the electrode wire where it connects to the nerve, pull the
electrode wire through the subcutaneous tunnel so that it may be connected to the receiver
in the infraclavicular pocket.
Secure the electrode to the receiver and place the receiver in the pocket making sure that
the anode disc side is down and making good contact with the anterior chest wall.
Test the receiver function to demonstrate diaphragmatic stimulation.
Once appropriate function is demonstrated, place a nonabsorbable tie around the electrode
connector to the receiver to prevent any fluid from entering the receiver, which could
disrupt function.
Excess wire may be coiled in the subcutaneous pocket but should not be placed on top of or
beneath the receiver itself.
The incisions can then be closed in a subcuticular fashion.
Test again after skin closure for proper functioning.
Note that when both hemidiaphragms are to be paced, two receivers are implanted.

Thoracic Approaches and Technique

Thoracic approaches to the implantation of a phrenic nerve pacemaker can be divided into a
traditional or limited thoracotomy, or some form of a minimally invasive procedure.

Minimally invasive procedures can include a traditional VATS (video-assisted thoracic

surgery) approach or a robotic VATS approach.
Thoracotomy Method and Technique
Although a formal standard posterolateral thoracotomy was previously employed during the
infancy of phrenic nerve pacemaker insertions, this is rarely performed today.
More commonly, a limited anterior thoracic thoracotomy approach is now employed.
Before placing the patient on the operating room table, an I roll should be made which will
facilitate in the positioning of the patient and exposure during the surgery. This is created
by rolling a sheet that will be placed vertically under the patients spine. Two additional
sheets are rolled, which will be placed horizontally under the patients shoulders and the
small of the patients back. The three rolls are then taped together forming an I.
The upper horizontal portion of the I should be no wider than the patients shoulders.
Place the patient on the operating room table.
The I roll is placed under the patient with the vertical portion under the patients spine, the
upper horizontal portion under the patients shoulders, and the lower horizontal portion in
the small of the patients back. The patient lies supine on the operating room table. The
patients arms can either be placed over their head or at their sides with the patients
shoulders slightly externally rotated and allowed to fall slightly posterior.
Although a bronchial blocker has great utility in thoracic surgery, it is most efficient to use
a double-lumen endotracheal tube (ETT) for this procedure so lung isolation can be
achieved by adjusting clamps, which obviates the need for the intraoperative manipulation
that would be required if a blocker was used.
The patient should receive intravenous antibiotics within 60 minutes prior to incision.
After prepping and draping in the usual sterile fashion, a 5- to 7-cm transverse incision is
made over the second or third intercostal space just lateral to the sternum. The incision is
extended down to the costal cartilage and rib surface.
The intercostal space is entered. If necessary, the costal cartilage can be removed as in a
Chamberlain procedure to help facilitate exposure.
A small rib spreader is then inserted.
The lung is deflated, the pleural space entered, and the lung and can be packed off
superiorly and inferiorly.
The pericardium is visualized and the phrenic nerve is identified running anterior to the
pulmonary hilum on the anterolateral surface of the pericardium.
On the right side, the phrenic nerve location is usually chosen at the junction of the
superior vena cava and right atrium.
On the left side, the phrenic nerve is chosen at the level of the main pulmonary artery as
it leaves the pericardial reflection.
The phrenic nerve bundle is then dissected off the pericardium, taking care to avoid either
mechanical or electrical injury to the nerve.
A tunnel is made under the phrenic nerve allowing it to be elevated off the pericardium.
The tunnel should measure between 10 to 12 mm in width.
The electrode is passed under the phrenic nerve and secured to itself and the electrode is
then fixed with sutures to the pericardium.

A pocket can then be made at the inferior and lateral portion of the thoracic incision for
implantation of the receiver on the anterior chest wall.
The electrodes are brought out through the incision and connected to the receiver and the
receiver is placed in the pocket with the anode side in direct contact with the chest wall.
The receiver is then tested and the electrode function confirmed.
Nonabsorbable ties are then placed around the insertion point of the electrode into the
receiver to prevent leakage of fluid at the level of the connection, which could interfere
with proper functioning.
Excess electrode wire may be coiled and placed elsewhere in the pocket.
Is important to make sure that the anode surface of the receiver is in good contact with the
chest wall.
The incision can then be closed in a layered fashion and the skin closed in a subcuticular
The procedure is then repeated on the opposite side.
A chest tube can be placed through a separate incision.
If chest tubes are to be avoided, a red rubber catheter attached to suction, can be placed
into the chest through the incision. The incision can be closed around the catheter. Once
the incision is closed and suction is applied, ask the anesthesiologist to give a breath and
hold. The red rubber catheter can be quickly removed at this point. A CXR can then be
obtained in the operating room to determine if a chest tube is required.
Minimally Invasive Thorascopic Approach and Technique
The minimally invasive thorascopic approach can be performed in either a traditional VATS
fashion with the patient placed sequentially in the right lateral decubitus and then the left
lateral decubitus position, or the patient can be placed in a supine position similar to the
approach used for VATS mediastinal surgery. In addition, surgery can be performed as a
traditional VATS procedure or with the da Vinci robotic assistance.
The advantage of the supine position is that repositioning is not required.
If the supine position is used, then an I roll (previously described) is placed under the
patient with the patients arms either over their head with care being taken to avoid injury
to the brachial plexus, or with the arms at the patients side in a supine position with the
shoulders slightly externally rotated and posteriorly deviated.
Lung isolation is obtained using a double-lumen ETT.
CO2 insufflation may be used at the preference and discretion of the individual surgeons.
Once general anesthesia has been induced and the chest or chests prepped and draped,
thorascopic or robotic incisions can be placed which are designed to facilitate exposure of
the upper pulmonary hilum.
If the patient is in the supine position, port incisions can be made in the fourth intercostal
space, 2 cm anterior to the anterior axillary line, and in the second and sixth intercostal
spaces at the level of the anterior axillary line.
If the patient is in the lateral decubitus position, port incisions can be made at the seventh
intercostal space in the posterior axillary line, in the fifth intercostal space in the
midaxillary line, and in the ninth intercostal space in the posterior axillary line.
The phrenic nerve is usually identified at the superior aspect of the pericardium.

On the right side this is where the superior vena cava enters the right atrium.
On the left side this is just inferior to the aortic arch where the pulmonary artery exits the
pericardium to enter the left pulmonary hilum.
Care is taken to avoid directly grasping the phrenic nerve.
Incisions are made in the mediastinal pleura anterior and posterior to the phrenic nerve and
a tunnel is created beneath the phrenic nerve freeing it from the pericardium and
measuring 10 to 12 mm in width.
A small subcostal incision is made and a subcutaneous pocket created, which will house the
A 3- to 4-in length of Penrose drain is placed over the electrode connector and tied in place
with a suture.
The electrode is then fed into the chest cavity through the lowest trocar port space.
A tonsil clamp is then passed from the subcutaneous pocket, under the ribs and through the
anterolateral peripheral aspect of the diaphragm into the chest cavity under direct
The free end of the Penrose drain is grasped and the connector and excess wire is delivered
into the subcutaneous pocket.
The phrenic nerve electrode is then brought under the phrenic nerve through the tunnel
previously created below the nerve.
The electrode is sutured in position on either side of the nerve using 4-0 or 5-0
nonabsorbable sutures. See Figure 20.2.
The electrode is then connected to the receiver and the receiver is inserted into the
subcutaneous pocket with the anode disc side down making contact with the abdominal
wall musculature.
After the connection is made, the receiver and phrenic nerve electrode are tested to ensure
diaphragmatic stimulation.

Figure 20.2 Electrode placement on phrenic nerve. The Avery Mark IV system requires the attachment of an electrode to the
phrenic nerve, either in the neck or in the chest. Note the electrode is tunneled under the phrenic nerve and sutured to itself.
It is then secure here to the pericardium.

Once diaphragmatic stimulation is confirmed, a nonabsorbable tie is passed around the

connector where it enters the receiver to prevent any fluid from disrupting the connection.
It is important to have sufficient excess wire in the chest cavity to prevent any traction on
the phrenic nerve and any remaining wire can be coiled and left in the subcutaneous
If a chest tube is to be used, it can then be placed through the inferior most trocar port and
secured in place.
If a chest tube is not to be used, place a red rubber catheter, as previously described, to
remove the pneumothorax.
Port incisions are closed in layers using 2-0 absorbable sutures for the deep layer and either
3-0 or 4-0 absorbable sutures for the skin.

Laparoscopic Approach and Technique

This laparoscopic approach utilizes a standard four-port technique, which allows visualization
of the entire diaphragm.
The patient is placed in the supine position under general endotracheal anesthesia. The
patient cannot be paralyzed to evaluate the diaphragm.
In addition to the usual grounding pads, which are used with electrocoagulating
instruments, an additional grounding pad will be placed on the patient and attached to the
clinical station which will be used intraoperatively to map diaphragmatic stimulation and
record changes in intra-abdominal pressure during stimulation.
The initial port is usually placed several centimeters above the umbilicus in the midline
using either a 5- or 10-mm port depending on the laparoscope, which is employed. CO2
insufflation is then performed.
Either a 0-degree or a 30-degree laparoscope may be used.
A right and left lateral 5-mm subcostal port are placed.
These ports are frequently used to aid in the mapping of the right and left
The lateral ports are also used to completely divide the falciform ligament, which can be
accomplished either using a Bovie or harmonic scalpel.
Complete division of the falciform ligament aids in visualization of the right
A 12-mm epigastric port is then placed. This port will primarily be used for the
implantation instrument. See Figure 20.3.
After laparoscopic access is obtained, mapping of the hemidiaphragm proceeds.
Mapping identifies the area on the diaphragm where electrical stimulation causes the
greatest amount of diaphragmatic excursion.
The mapping instrument is passed through one of the lateral ports.
The mapping instrument consists of a hollow flexible tubing, which sits inside of a rigid
outer metal cannula. This is then connected to the typical operating room suction
Once the mapping instrument has been placed in the abdomen, a grasper is used through
the other lateral port and the tip of the probe is pulled out of the outer metal cannula.

The tip of the electrode is grasped with the dissector and then touched along the
undersurface of the diaphragm. It is attached to the diaphragm with suction.
Once attached, a stimulating current is then applied. See Figure 20.4.
Changes in intra-abdominal pressure are measured as well as direct observations of
diaphragmatic contractions.
The closer the testing electrode is to a diaphragmatic motor point, the stronger the observed
contraction will be and the greater the magnitude of change in measured intra-abdominal

Figure 20.3 Typical laparoscopic port placement utilizing an upper epigastric port, two lateral ports, and one supraumbilical
port for visualization and mapping of both hemidiaphragms a placement of electrodes.

When the area of maximal stimulation is identified, this area can be marked using the Bovie
as the primary electrode placement site.
More recently, some surgeons have elected to avoid formal mapping using the mapping
instrument. Instead, an alligator clip can be connected to a Maryland dissector which is
then touched to the diaphragm to evaluate diaphragmatic stimulation.
The area with the next highest level of contraction is marked as the secondary electrode
On the right hemidiaphragm, the motor point is usually noted just lateral to the central
tendon while on the left hemidiaphragm, the motor point tends to be more lateral since the
phrenic nerve enters the diaphragm from a more lateral aspect on the left.
Also note that the phrenic nerve bundles tend not to run with the vascular bundles unlike
other areas of the body.
Once the primary and secondary electrode locations have been identified in the right and
left hemidiaphragms, an empty implant instrument can be used to decide, which port
provides the best approach angle.

Figure 20.4 The NeuRx system does not attach directly to the phrenic nerve, but operates by stimulation of the
diaphragmatic motor point to directly cause diaphragm contraction. The mapping instrument demonstrated here shows the
flexible inner plastic hollow tubing protruding from the rigid metal outer cannula. Suction applied through the hollow tubing
allows for contact to the diaphragm.

Figure 20.5 In the laparoscopic NeuRx system, the electrode is delivered through the rigid delivery device and pulled
through the diaphragm, securing it in place.

The electrode is loaded into the lumen of the implant instrument so that only a small
portion of the hooked tip of the electrode and a small portion of the blue polypropylene
barb extends beyond the needle.
The most posterior diaphragmatic electrode site should be inserted first to prevent
interference with the excess lead from the placement of the other electrodes.
With the needle closed, the insertion device is passed into the abdomen.
The needle is then advanced into the diaphragm perpendicular to the muscle fibers to
increase the likelihood of capture of the barb on the muscle fibers.
After insertion of the electrode the needle is withdrawn by applying some backward
traction on the needle and counter pressure on the hemidiaphragm using a separate
dissector. The barbed electrode lodged in the diaphragm, remains behind. See Figure 20.5.
The electrode should then be tested to ensure that proper stimulation and contraction of the
hemidiaphragm is obtained.
The remaining additional electrodes are then implanted in a similar fashion until all
electrodes have been placed.
It is important to keep the right and left hemidiaphragm electrodes separate.
The electrodes wires are brought out of the epigastric port.
Excess wire can remain intra-abdominally and is frequently placed over the dome of the

An area of the chest is identified, which is easily accessible to either the patient or their
health care provider.
The electrodes are tunneled into this area of the chest by making a subcutaneous tunnel for
each electrode separately keeping the right electrodes inferior to the left electrodes.
The electrodes are again checked to ensure proper functioning.
It is also important to check that there is no capture of the patients cardiac rhythm.
The port incisions can then be closed in the usual manner.
The electrode wires are then connected to a connection block, which is inserted into the
diaphragmatic stimulator.

Diaphragmatic Pacemaker Receiver Replacement

It is occasionally necessary to replace the phrenic nerve stimulator receiver.

A CXR should be obtained before replacing the phrenic nerve receiver to identify the
location and direction of the connectors and the anode disc. This will allow for planning of
the incision and decrease the likelihood of transection of the wires.
If the new receiver is smaller than the present one, a smaller pocket must be made to ensure
good electrical contact between the bottom anode plate of the receiver and the chest wall.
Receiver replacement can frequently be performed under local anesthesia on an outpatient
Injection of the local anesthetic into the fibrous sheath that frequently forms around the
receiver may also facilitate its removal.
An incision is made directly over the receiver and carries down onto the surface of the
The fibrous sheath over the receiver can be incised and then cut in a cruciate fashion to
facilitate delivery of the receiver into the surgical wound.
The anode disc is removed.
Any previously placed sutures to secure the connectors are cut.
Disconnect the connectors by gently pulling and rolling the connector out of the receiver.
Examine the plating material on the connectors of the phrenic nerve electrodes.
If there is evidence of discoloration or oxidation then you can wipe the connectors with a
dry sponge or scrape them lightly with a scalpel.
The replacement receiver is then connected to the electrodes and tested using a sterile
Ties are then placed around the connectors where they insert into the receiver to prevent
fluid from entering and disrupting the connection.
If necessary, a new subcutaneous pocket can be made.
The receiver is then placed in the pocket making sure that the anode disc is in direct
contact with the chest wall.
The incision can then be closed and layers closing the subcutaneous tissues with absorbable
sutures and the skin with a subcuticular suture.
The pacemaker may be used immediately upon completion of surgery if necessary.

Diaphragmatic Conditioning

In individuals with diaphragm paralysis for 6 months or longer and in particular those
individuals who had a paralyzed diaphragm for 2 years or longer, a period of diaphragmatic
conditioning is required. This may last anywhere from 3 to 9 months. This is necessary to
achieve optimization of diaphragmatic functioning using a diaphragmatic pacemaker.
Throughout the day, the amount of time that the diaphragm is paced per hour is gradually
increased, followed by a 12-hour period of rest when the patient is placed back on positive
pressure ventilation.
Long-term mechanical ventilation frequently results in chronic hyperventilation and
decreased levels of CO2. Since the diaphragmatic pacing systems are designed to return the
patient to a physiologic state, patients may frequently experience the sensation of shortness
of breath or dyspnea during initiation of pacing. This can be minimized by adjusting the
CO2 levels while the patient is on the ventilator during conditioning.
Diaphragm conditioning usually proceeds in a step-by-step fashion by gradually increasing
the amount of time the patients diaphragm is able to be paced.
When the patient is sitting, higher levels of electrical stimulation may be required because
of the effects of gravity on the diaphragm.
The ultimate goal is to achieve full-time pacing without developing diaphragmatic fatigue
and loss of contractility.

Diaphragmatic pacing complications are related both to the function of pacing and to the
surgical procedure employed.
Infection, as with any surgical procedure and especially one where a foreign body is
introduced, can develop following surgery. Wound infections have been reported with a
rate of approximately 3%.
When a thoracic approach is employed, pulmonary complications can develop such as
pneumonia, pneumothorax, hemorrhage, and empyema.
When a cervical approach is employed, the patient can develop stimulation and movement
of the upper extremity due to transmission of the pacemaker impulses to the brachial
Phrenic nerve electrode malfunction or fracture can result in the loss of the ability to pace
the diaphragm.
When the laparoscopic approach is performed, a capnothorax can occur from the electrodes
being placed in a thin diaphragm with escape of carbon dioxide into the hemithorax. This
occurs in up to 50% of patients and usually resolves spontaneously over a short period of
time or can be aspirated.
Most common complication reported has been the iatrogenic injury to the phrenic nerve
itself. The incidence of this has decreased as the techniques for implantation have evolved.

Initial studies done in SCI multicenter trials showed 98% of patient gained independence for
mechanical ventilation. In addition to reporting short-term positive results with diaphragm
pacers, Glenn reported long-term follow-up in 12 patients who underwent bilateral phrenic
nerve pacemaker placement 15 to 20 years prior. The report confirms that patients with
phrenic nerve pacers were able to achieve long-term respiratory independence from
mechanical ventilation. In highly selected ventilated patients, there was been multiple reports
of improved quality of life after placement of a diaphragmatic pacer. In SCI and central
alveolar hypoventilation patients, such life-changing improvements include an improved
olfactory sense, which has been associated with increased pleasure, increased independence
from noisy machinery, which allows for better reinsertion into the community, improved
posterior lobe ventilation resulting in decreased respiratory infections, increased ability to
clear secretions leading to decreased need for suctioning, and reduced time on the ventilator
and possible complete freedom from the ventilator and decannulation of the tracheosotomy.
There have been reports in which diaphragmatic pacers were placed safely in ALS patients
under general anesthesia with no 30-day mortality. It has also been reported in a study of 38
ALS patients who had diaphragmatic pacer placed, that there was a 2-year delay for the need
of ventilatory support when compared to historical controls. Treatment of ALS patients with
diaphragm pacers is an area of active investigation.
There has not been any direct comparison of the different devices or the surgical
techniques required for their placement. The cervical placement of the Avery Mark IV had the
advantage of being able to be done under local anesthesia and, therefore, there is a decreased
risk of exposure to general anesthesia. There, however, have not been any reports of
anesthesia complications associated with either thoracic or abdominal placement of the
devices. There is a risk of injury of the phrenic nerve when placing an Avery Mark IV which
is not present when placing the NeuRx pacer. However, the incidence of this has decreased as
the surgical procedure for implantation has evolved. Diaphragm pacers placed in each of the
three locations have had excellent results with relatively minimal-associated morbidity and
mortality. The choice of surgical technique and which pacer to use should be based on
surgeon comfort.

Compared with mechanical ventilation, diaphragmatic pacing, either via phrenic nerve
pacing or direct pacing of motor end plates on the diaphragm, can have a dramatic
improvement on a patients quality of life and sense of well being. In addition to the great
physical and emotional benefits, there is a significant economical advantage to those patients
who have successful placement of a diaphragm pacer.

Recommended References and Readings

Ali A, Flageole H. Diaphragmatic pacing for the treatment of congenital central alveolar
hypoventilation syndrome. J Pediatr Surg. 2008;43(5):792796.

Chen ML, Tablizo MA, Kun S, et al. Diaphragm pacers as a treatment for congenital central
hypoventilation syndrome. Expert Rev Med Devices. 2005;2(5):577585.
Dimarco AF, Onders RP, Kowalski KE, et al. Phrenic nerve pacing in a tetraplegic patient via
intramuscular diaphragm electrodes. Am J Respire Crit Care Med. 2002;166(12):16041606.
DiMarco AF, Onders RP, Ignangi AI, et al. Phrenic nerve pacing via intramuscular diaphragm
electrodes in tetraplegic subjects. Chest. 2005;127 671677.
Ducko CT. Clinical advances in diaphragm pacing. Innovations. 2011;6(5):289297.
Elefteriades JA, Hogan JF, Handler A, Loke JS. Long-term follow-up of bilateral pacing of the
diaphragm in quadriplegia. N Engl J Med. 1992;326(21):1433.
Elefteriades JA, Quin JA, Hogan JF, et al. Long-term follow-up of pacing of the conditioned
diaphragm in quadriplegia. Pacing Clin Electrophysiol. 2002;25:897906.
Glenn WW, Holcomb WG, McLaughlin AJ, et al. Total ventilator support in a quadriplegic
patient with radiofrequency electrophrenic respiration. N Engl J Med. 1972;286:513516.
Jarosz R, Littlepage MM, Creasey G, et al. Functional electrical stimulation in spinal cord
injury respiratory care. Top Spinal Cord Inj Rehabil. 2012;18(4):315321.
Kolb C, Eicken A, Zrenner B, et al. Cardiac pacing in a patient with diaphragm pacing for
congenital central hypoventilation syndrome (Ondines curse). J Cardiovasc Electrophysiol.
2006;17: 789791.
Onders RP, DiMarco AF, Ignagni AR, et al. Mapping the phrenic nerve motor point: The key
to a successful laparoscopic diaphragm pacing system in the first human series. Surgery.
Onder RP, Carlin AM, Elmo M, et al. Amyotrophic lateral sclerosis: The midwestern surgical
experience with the diaphragm pacing stimulation system shows that general anesthesia
can be safely performed. Am J Surg. 2009;197:386390.
Onders RP, Elmo M, Khansarinia S, et al. Complete worldwide operative experience in
laparoscopic diaphragm pacing: Results and differences in spinal cord injured patients and
amyotrophic lateral sclerosis patients. Surg Endosc. 2009;23(7):14331440.
Onders RP, Khansarinia S, Weiser T, et al. Multicenter analysis of diaphragmatic pacing in
tetraplegics with cardiac pacemakers: Positive implications for ventilator weaning in
intensive care units. Surgery. 2010;148:893898.
Sarnoff SJ, Hardenbergh E, Whittenberger JL. Electrophrenic respiration. Science.
Tedde ML, Vasconcelos Filho P, Hajjar LA, et al. Diaphragmatic pacing stimulation in spinal
cord injury: Anesthetic and perioperative management. Clinics. 2012;67(11):12651269.

Part VI
Chest Wall/Pleural Space/Diaphragm:
Pleural Space

21 Decortication: Thoracotomy and VATS

Robert E. Merritt

Indications for Decortication

The most common benign condition involving the pleura is an infection involving the pleural
space or empyema. Patients who present with pneumonias often have associated pleural
effusions, which can be either parapneumonic effusions or an empyema. The pleural fluid
should be sampled with thoracentesis to determine the distinction between paraneumonic
effusion and empyema. If the fluid gram stain or culture is positive for a pathogen or the fluid
pH is less than 7.1, then an empyema is typically diagnosed. The classification of empyema is
based on the temporal evolution of the pleural space infection and dictates the optimal
management. The three phases of empyema consist of:
1. Exudative Phase: This initial phase of empyema is characterized by free-flowing purulent
fluid through the thorax and associated inflamed parietal pleura. Simple drainage with
chest tube thoracostomy and intravenous antibiotics are usually sufficient to manage the
pleural effusion.
2. Fibropurulent Phase: This phase is characterized by loculated pleural fluid and fibrinous
exudative deposits on the visceral pleural surfaces. Empyemas in this phase often require a
VATS or thoracotomy to lyse adhesions, break up loculations, and drained purulent pleural
3. Fibrous Phase: This phase is characterized by the formation of a thick, fibrous rind on the
visceral pleural surface of the lung. A thoracotomy is usually required to achieve a
complete decortication.
An early decortication with a VATS approach during the fibropurulent phase is highly
effective and can significantly decrease morbidity associated with empyema. VATS offers a
decided advantage over simple chest tube thoracostomy because of multiple factors.
1. Loculated purulent fluid can be completely drained because adhesions can be directly
visualized and lysed during VATS.
2. Atelectatic lung can be re-expanded under direct vision.
3. Chest tubes can be placed in the appropriate position for optimal drainage in the
postoperative period.
The definitive drainage of purulent fluid associated with empyema with VATS can
significantly improve patient outcomes and prevent progression to a fibrothorax, which often
requires an open thoracotomy. Other indications for decortication include chronic
hemothorax and recurrent pleural effusion.

Contraindications for Decortication

Malignant pleural disease

Endobronchial tumor with bronchial obstruction
Chronic respiratory failure and ventilation dependence
Chronically trapped lung with limited pulmonary dysfunction

Patients with empyema should have a preoperative CT scan of the thorax to identify loculated
fluid cavities that need to be drained. The location of loculated fluid pockets will assist with
the placement of VATS ports. Broad-spectrum antibiotics should be initiated to treat active
pneumonia. The antibiotic coverage can be modified after the culture and sensitivities are
completed. Large pockets of purulent fluid can be drained with a chest tube thoracostomy
prior to a planned VATS decortication. Chest tube drainage is particularly important for
patients who present with an empyema and associated signs of sepsis, such as fever,
tachycardia, leukocytosis, and hypotension.

Positioning for VATS Decortication
I routinely perform a fiberoptic flexible bronchoscopy before a VATS decortication procedure
to assess the airway anatomy and to obtain endobronchial cultures. Also, an endobronchial
tumor causing airway obstruction and postobstructive pneumonia can be identified and
treated. After the fiberoptic flexible bronchoscopy is completed with a single-lumen
endotracheal tube, the patients are reintubated with a double-lumen endotracheal tube for
selective lung ventilation. Patients are then positioned in the right or left lateral decubitus
position. All pressure points should be padded with gel pads to prevent nerve compression
and skin necrosis. A padded beanbag is used to hold the patient in position. The operating
room table is flexed with the patients anterior-superior iliac crest below the break in the bed.
The flexion opens up the rib spaces to allow placement of VATS ports. The video monitors are
placed at the head of the table and the surgeon stands in front of the patient.
Three standard VATS incisions are used to perform a VATS decortication (Fig. 21.1). The first
incision is placed in the eighth intercostal space in the posterior axillary line. A 5-mm trocar
is placed through the incision and 5-mm thoracoscope inserted in the left chest. The 5-mm
thoracoscope is lower profile and less likely place torque on the intercostal nerve. A 10-mm
incision is placed three to four fingerbreadths below the tip of scapula. A 10-mm incision is
also placed anteriorly at the level of the inframammary crease. I use low profile lung clamps
and vascular clamps, which easily pass through the VATS incisions without placing pressure
on the intercostal nerve.

Figure 21.1 The standard placement of the incisions for a VATS decortication.

VATS Decortication Technique for Fibropurulent Phase of Empyema

Once the VATS ports are placed, the 5-mm thoracoscope is placed into the chest cavity for
inspection of the free pleural space. A 10-mL syringe can be used to aspirate fluid to ensure
the VATS incision is located at a level where there is a free pleural space. The first VATS port
should be placed in a pocket of free fluid to avoid injury to the lung parenchyma. Free fluid is
aspirated with a 5-mm suction catheter and sent for gram stain and culture. Complete
mobilization of the lung should be performed by lysing adhesions between the visceral pleura
and the chest wall. The lysis of adhesions can be performed with sponge on clamp with blunt
dissection (Fig. 21.2). The blunt dissection should be carried to the hilum circumferentially.
The lung apex and the lung base should be fully mobilized as well. Dense adhesions between
the lung base and the diaphragm can be divided with the bovie electrocautery or a Ligasure
device. Injury to mediastinal structures, such as the esophagus, the trachea, aorta, and
superior vena cava should be avoided. The phrenic nerves should be identified and
persevered as well. The lung is then re-expanded by the anesthesia team to identify areas of
trapped lung that may need further decortication. I typically place a right-angle chest tube in
the costophrenic sulcus and a straight chest tube toward the apex for postoperative drainage.

Figure 21.2 The sponge stick is used to bluntly dissect the plane between the visceral pleura and rind.

Figure 21.3 The pleural rind is being mobilized bluntly.

Open Decortication Technique for Organized Phase of Empyema

Patients who developed a thick fibrous rind on the visceral surface of the lung usually require
a standard posterior-lateral thoracotomy for effective decortication. The lung should be
ventilated during the decortication. The initial plane between the visceral pleural rind and
the lung is established with sharp dissection. The lung surface is then retracted with a sponge
stick and the plane is dissected bluntly (Fig. 21.3). Dense adhesions should be lysed with
cautery or a Metzenbaum scissor (Fig. 21.4). The lung should be completely mobilized from
the surface of the diaphragm. In some cases, the visceral pleural rind cannot be completely
removed due to dense adhesions or fibrosis. These areas can be managed with an excision of
the visceral pleura or by creating cross hatches on the visceral pleural rind with a scalpel
(Fig. 21.5). When there is residual trapped lung, a space may be present in the pleural cavity.
The residual pleural space can be filled with a rotational muscle flap or omentum for longterm management.

Figure 21.4 Sharp dissection is used for dense adhesions between the rind and the visceral pleura.

Figure 21.5 Cross hatchings are created with a scalpel when the pleural rind is too adherent to remove.

After the parietal rind has been dissected from the chest wall, the empyema cavity should
be opened and drained. The fibrinous debris should be debrided and the parietal pleural rind
should be excised. The pleural cavity is then irrigated with a copious amount of saline
solution. Usually, two large-bore chest tubes are placed for postoperative drainage. The chest
tubes are maintained on suction for 48 hours.

Patients are usually extubated in the operating room; however, some patients are maintained
on mechanical ventilation for 24 to 48 hours if they cannot be immediately extubated in the

operating room. The chest tubes are maintained on suction for 48 hours. The chest tubes are
removed when the drainage is less than 200 mL per 24 hours and the air leaks are resolved.
Patients who develop prolonged air leaks can be managed with a Heimlich valve and return
to outpatient clinic for chest tube removal. Postoperative x-rays are obtained daily to monitor
lung re-expansion and identify recurrent effusions.

The common postoperative complications after decortication included:
Prolonged air leak
Respiratory failure
Recurrent empyema
Subcutaneous emphysema
Phrenic nerve palsy
Diaphragm injury
Esophageal injury

In modern case series, VATS decortication has been proven to be effective in the management
of empyema. The complication rate ranges from 3% to 35% and the mortality rate ranges
from 0% to 6%. The rate of successful treatment ranges from 72% to 100%. The majority of
the VATS decortications were performed in the exudative or fibropurulent phase of empyema.
Patients with organized empyema usually require conversion to thoracotomy due to the dense
fibrosis and adherent visceral pleural rinds.

VATS decortication can be performed in patients with acute empyema in the exudative or
fibropurulent phase with effective outcomes. The morbidity and mortality is relatively low.
Patients who present in the organized phase of empyema typically have a thick, fibrous
pleural rind encasing the lung. These patients require a posterior-lateral thoracotomy to
achieve effective re-expansion of the lung.

Recommended References and Readings

Angelillo Mackinaly TA, Lyons GA, Chimondeguy DJ, et al. VATS debridement versus
thoracotomy in treatment of loculated postpneumonia empyema. Ann Thorac Surg.
Cassina PC, Hauser M, Hillejan L, et al. Video-assisted thoracoscopy in the treatment of

pleural empyema: Stage-based management and outcome. J Thorac Cardiovasc Surg.

Chan DT, Sihoe AD, Chan S, et al. Surgical treatment for empyema thoracis: Is video-assisted
thoracic surgery better than thoracotomy? Ann Thorac Surg. 2007;84(1):225231.
Colice GL, Curtis A, Deslauriers J, et al. Medical and surgical treatment of parapneumonic
effusions: An evidence-based guideline. Chest. 2000;118:11581171.
Landreneau RJ, Keenan RJ, Hazelrigg SR, et al. Thoracoscopy for empyema and hemothorax.
Chest. 1996;109(1):1824.
Luh SP, Chou MC, Wang LS, et al. Video-assisted thoracoscopic surgery in the treatment of
complicated parapneumonic effusions or empyemas: Outcome of 234 patients. Chest.
Solaini L, Prusciano F, Bagioni P. Video-assisted thoracic surgery in the treatment of pleural
empyema. Surg Endosc. 2007;21(2):280284.
Wurnig PN, Wittmer V, Pridun NS, et al. Video-assisted thoracic surgery for pleural empyema.
Ann Thor Surg. 2006;81(1):309313.

22 Pleurodesis, Indwelling Pleural Catheters

Jordan Kazakov and Moishe Liberman

The pleural cavity is a slit-like space surrounded by the parietal and visceral pleural surfaces,
which exist in all mammals, except the adult elephant. Normally, the human pleural space
contains a small amount (0.26 mL/kg) of fluid, which maintains a distance of 10 to 12 m
between the chest wall/diaphragm and the lung and allows for easy movement of the lung
and mechanical coupling during the respiratory cycle. The pleural fluid volume is the result
of complex interplay between hydrostaticosmotic pressure, vascular permeability, and
pleuro-lymphatic drainage. Fluid volume may increase significantly in pathologic conditions.
Pleurodesis (pleur(o)pleura, rib, side; desisfixation) is a procedure that aims to fuse the
pleural space. This is achieved with mechanical (abrasion, tunneled indwelling catheter) or
chemical (injection of sclerosing agent) injury of the pleura, which leads to fibrous tissue
formation and symphysis of the parietal and visceral pleural layers. The injury causes
mesothelial denudation, induction of inflammation, coagulation cascade activation, and
IL-8, TNF-, NO, MCP-1, adhesion molecules, and transforming growth factor-beta (TGF-),
among other factors, play important roles in the inflammatory process and fibrous tissue
formation. TGF- has a strong profibrotic effect and the direct administration of human
recombinant TGF- into rabbit and sheep pleural space induces pleurodesis faster than talc
slurry with lower pleural markers of inflammation than pleurodesis with talc or doxycycline.
The cellular component of the inflammation consists mainly of mesothelial cells, which can
undergo epithelialmesenchymal transformation becoming fibroblast-like cells, and
myofibroblasts, which migrate into the pleural space after injury and deposit proteins. Other
important participants in the generation and proliferation of the inflammatory response are
the macrophages and neutrophils. The importance of inflammation for the success of
pleurodesis is emphasized by the finding that corticosteroids decrease the effectiveness of talc
pleurodesis. It appears that mechanisms other than inflammation may also play role. This has
been observed in the experimental work with TGF-, where the coadministration of
corticosteroids did not inhibit pleurodesis.
Pleural inflammation is likely responsible for the symptoms associated with pleurodesis,
namely pain (severe in more than 50% of patients who receive intrapleural tetracycline) and
fever (up to 62% of patients who receive intrapleural talc).

Malignant Pleural Effusion
Many malignancies have been associated with pleural effusion, the most common being lung
and breast cancer. In a prospective study by Villena et al., neoplasm was the most common
cause (36%) of pleural effusion in 1,000 consecutive patients who underwent diagnostic
thoracentesis. The most common place of origin of the tumor was the lung, followed by

pleural mesothelioma. Rodriguez-Panadero et al. found pleural metastases in 29% of 191

patients with one or more malignant tumor elsewhere in the body; pleural effusion was
present in 55% of the patients with pleural involvement. A prospective study of 278
consecutive patients with malignant pleural effusion showed a median survival of 211 days.
Three factors predicted worse survivalleucocytosis, hypoxemia, and hypoalbuminemia.
Patients with pleural effusion from breast carcinoma have better survival.
Malignancy can cause pleural effusion by one or a combination of the following
mechanisms: Direct involvement of the pleura (breast, lung), seeding of the tumor to the
pleural space via lymphatic and hematogenous routes, involvement of the mediastinal lymph
nodes and lymphatic vessel embolization, involvement of the superior vena cava or the
pericardium, and obstruction of the ipsilateral mainstem bronchus.
Pleural effusion associated with malignancy may be transudate or exudate. Low glucose
(less than 60 mg/dL [3.33 mmol/L]) and low pH (less than 7.3) are associated with increased
tumor burden, higher yield of pleural cytology, poorer response to pleurodesis, and shorter
survival. The type and the mechanism of the pleural effusion are important for the
management of the pleural effusion and the outcome of the procedure. Pleurodesis is less
likely to be successful in the presence of bronchial obstruction or extensive tumor infiltration
of the ipsilateral lung or pleura in which cases reexpansion of the lung after effusion drainage
is unlikely. Other important factors to consider before making a decision regarding the best
therapeutic option for pleural effusion are presence of treatment options for the malignancy,
presence of symptoms and response to therapeutic thoracentesis, speed of reaccumulation of
the effusion, size of the effusion, expected survival, the performance status, the social milieu
of the patient, personal preference of the patient, clinician experience, and local availability.
Based on these factors there are different clinical scenarios. If the effusion is small and the
diagnosis points to a tumor sensitive to chemotherapy (breast, ovary, small-cell lung cancer,
lymphoma, etc.) the best choice would be to administer systemic chemotherapy. Mediastinal
radiation may be helpful in lymphoma and lymphomatous chylothorax. Further therapy may
not be necessary if the effusion disappears or remains stable and well tolerated.
When there is no response to systemic therapy, the effusion is progressing or recurring,
when the initial effusion is large and there is amelioration of the clinical signs and
reexpansion of the lung after therapeutic thoracentesis, the patient should be considered for
pleurodesis or indwelling pleural catheter (IPC). Exception of this rule is slowly (more than 1
month) recurring and short (less than 3 months) expected survival where the effusion can be
managed with repeat thoracentesis. Diagnostic and possibly therapeutic bronchoscopy is
mandatory before an attempt at pleurodesis when malignant airway obstruction is suspected.
If pleurodesis or IPC are considered they should be carried out as early as possible before the
development of trapped lung.
Benign Pleural EffusionCongestive Heart Failure, Hepatic Hydrothorax, and
Cardiac disease is a common cause for recurrent pleural effusion. Specific etiologies include
congestive heart failure, and acute and chronic pericarditis. The effusion in congestive heart
failure is more often bilateral and of transudative type (diuresis may change the appearance
of the fluid to exudative), whereas the effusion related to pericardial disease is more often

left-sided and more likely to be an exudate.

Increased left atrial pressure and pulmonary capillary wedge pressure are essential for the
development of pleural effusion associated with congestive heart failure. The mechanisms
responsible for pleural effusion associated with pericarditis include simultaneous involvement
of the pleura from the same process causing the pericarditis, contiguous inflammation, and
involvement of the mediastinal lymphatics.
The treatment for pleural effusion due to cardiac disease is the treatment of the underlying
cardiac problem itself combined with diuretic therapy in the case of congestive heart failure
or anti-inflammatory agents in the case of pericarditis. In a case of a refractory symptomatic
effusion, pleurodesis with talc or doxycycline may be considered. Unilateral pleurodesis may
worsen the effusion on the opposite side. Placement of indwelling pleural catheter or
pleuroperitoneal shunt can be considered as alternatives to pleurodesis.
Pleural effusion due to hepatic cirrhosis with portal hypertension in the absence of primary
pulmonary, pleural, or cardiac disease is called hepatic hydrothorax. The incidence of hepatic
hydrothorax is less than 5% of all cirrhotic patients. It usually appears in the presence of
ascites, which is believed to cross the diaphragm via diaphragmatic defects. Huang et al.
classified the defects to four types: type I, no obvious defect; type II, blebs lying on the
diaphragm; type III, broken defects (fenestrations); and type IV, multiple gaps in the
diaphragm. In as many as 20% of the patients with hepatic hydrothorax ascites cannot be
identified even with ultrasound, hence the presence of ascites is not required for the
diagnosis. The effusion is transudative in nature. In most of the cases, the hepatic
hydrothorax is right-sided, followed by left-sided, and bilateral.
Treatment of hepatic hydrothorax is similar to treatment of ascites. Sodium restriction and
diuretics may be effective. Patients who are compliant with the low sodium diet and have
recurrent effusion are considered to have refractory hydrothorax. Treatment options for this
group include repeated thoracentesis, peritoneovenous shunt, pleurodesis, video-assisted
thoracoscopic surgery (VATS) repair of diaphragmatic defects, transjugular intrahepatic
portosystemic shunt, and liver transplantation. Chest tube placement as a sole treatment may
cause massive fluid shifts with electrolyte and protein depletion, bleeding, renal failure, and
death and is not recommended. Huang et al. described 10 patients who underwent
thoracoscopic pleura or mesh onlay repair of diaphragmatic defects with no postoperative
recurrence of the effusion and improved pulmonary function. Pleurodesis in hepatic
hydrothorax is complicated by the rapid passage of fluid between the abdomen and the chest,
which does not allow for close contact between the parietal and visceral layers of the pleura.
Nevertheless, successful pleurodesis with tetracycline and thoracoscopic talc pleurodesis have
been described. Milanez de Campos et al. described 18 patients who underwent 21 VATS talc
pleurodesis procedures with immediate success in 48% of the procedures. The success rate of
the procedure increased to 60% when it was combined with suture of the diaphragmatic
defect. High morbidity (57.1%) and mortality (38.9%) in the 3-month follow-up period were
described. Ferrante et al. attempted VATS talc pleurodesis in 15 patients with successful
control of hepatic hydrothorax in 53% after a single procedure and in 73% after two
In conclusion, VATS talc pleurodesis for hepatic hydrothorax is effective in 40% to 75% but
may result in significant morbidity and mortality. Better results are seen in patients who

undergo closure of the diaphragmatic defect than in patients without demonstrable defect.
Some reports suggest CPAP may be helpful with chemical pleurodesis or alone by decreasing
the pressure gradient between the chest and the abdomen and thereby decreasing the transfer
of ascites.
Chylothorax is the presence of chyle in the pleural space due to leakage from the thoracic
duct or its tributaries. The diagnosis is supported by triglyceride concentration greater than
110 mg/dL; an intermediate level between 50 and 110 mg/dL should be followed by
lipoprotein electrophoresis of the pleural fluidchylothorax contains chylomicrons; levels
less than 50 mg/dL excludes the diagnosis of chylothorax. Pseudochylothorax is a chyliform
effusion with high concentration of cholesterol that occurs in the setting of chronic pleural
The thoracic duct ascends from the cisterna chyli at the level of first or second lumbar
vertebra in a rightward position. It enters the thoracic cavity from the abdomen through the
aortic hiatus and then ascends between the thoracic aorta and the azygos vein until it reaches
the fifth thoracic vertebra where it crosses the midline and continues in the left posterior
mediastinum to reach the left jugular or subclavian vein. Occasionally, there are two thoracic
ducts in the mediastinum or a single thoracic duct empties in the right-sided veins. The level
of the injury to the thoracic duct determines the side of the chylothorax.
The etiology of the chylothorax could be traumatic (surgical or nonsurgical) or
nontraumatic. The nontraumatic chylothorax may be further separated into malignant
(lymphomatous and nonlymphomatous) and nonmalignant. Exudative effusion is the most
common finding but transudative chylothorax has been reported.
Computed tomography of the thorax and abdomen and pleural fluid analysis are the initial
tests for evaluation of patients with chylothorax. Lymphangiography or lymphoscintigraphy
may be utilized in patients with uncertain diagnosis, recurrent chylothorax after thoracic duct
ligation, and suspected anomalous thoracic duct anatomy.
Treatment of the underlying condition is attempted if possible. Dietary measures include
modified enteral nutrition (high protein-low fat diet) with supplementation of medium chain
triglycerides and fasting with total parenteral nutrition. Intermittent drainage with
thoracentesis can be employed for relief of dyspnea. Chest tube placement is used in
traumatic (surgical and nonsurgical) chylothorax or with rapidly accumulating effusion. Tube
drainage should be limited to 14 days to minimize the risk of immunosuppression due to loss
of lymphocytes and immunoglobulins. Surgical treatment should be considered for patients
with chyle loss exceeding 1 to 1.5 L/day for more than 5 days in an adult or more than 100
mL/day in a child. The access side depends on the side of the effusion, the course of the
thoracic duct, the side of the initial surgery, and the presence of gastric conduit. Laparoscopic
approach may be used for subdiaphragmatic leak. The thoracic duct ligation can be combined
with mechanical or chemical (talc) pleurodesis. Talc pleurodesis without duct ligation may
also be performed with varying results. Maldonado et al. reported experience with 77 adult
patients. Fifty-seven patients (77%) had initial nonsurgical treatment. The rate of resolution
after the initial treatment was 27% for patients with nontraumatic chylothorax and 50% for
those with traumatic chylothorax. The rate of recurrence after additional therapeutic
maneuvers was 50% for the first group and 13% for the second. In another study Paul et al.
reported experience with 29 patients who underwent surgical procedure for a high output

(more than 1 L/day) or recurrent chylothorax. Twenty-two patients underwent thoracic duct
ligation and six underwent pleurodesis. The success rate after initial thoracic duct ligation
was 95% and after pleurodesis was 83%. Mares et al. treated 24 thoraces in 19 consecutive
patients with recurrent chylothorax as a complication of lymphoma. They utilized medical
thoracoscopy for talc insufflation pleurodesis with 100% success rate.
PneumothoraxRecurrent, Persistent Air Leak
Pneumothorax occurring without an inciting event is defined as spontaneous. It can be
further divided to primaryoccurring in patients without previous lung disease, and
secondaryoccurring in patients with known lung disease.
The primary spontaneous pneumothorax (PSP) is more common in tall, thin males and
varies geographically. Typically, the patients are young or middle aged (20 to 40 years old)
and at rest at the time of the occurrence of the pneumothorax. Predisposing factors for PSP
include family history, Marfan syndrome, BirtHoggDub syndrome, homocystinuria,
smoking, and thoracic endometriosis. The recurrence rate is highest during the first year and
varies between 25% and more than 50%. Risk factors for recurrence are continuing smoking,
female sex, height, and low body weight.
Treatment options for PSP include observation, pleural aspiration, chest tube insertion,
VATS, pleurodesis, and thoracotomy. Observation with supplemental oxygen is indicated for
small (less than 3 cm between the lung and the chest wall on a chest radiograph)
uncomplicated pneumothorax. The patient may be discharged home after 6 hours if follow-up
x-ray shows no progression and the patient has quick access to emergency medical services.
Pleural aspiration with an 8- to 9-French (Fr) catheter can be performed manually in
clinically stable patients with large pneumothorax. Chest tube insertion is indicated in
clinically stable patients with large pneumothorax or persistent symptoms like dyspnea or
pain. In clinically unstable patients, a chest tube should be inserted without delay, and if not
immediately available, a 14-gauge intravenous catheter can be used to decompress the
pleural space until more definite treatment is possible. Small- and large-bore tubes are
comparable in effectiveness in the treatment of pneumothorax but large-bore tube
thoracostomy is preferable in mechanically ventilated patients, patients with very large leak,
and hemothorax. Patients with good lung re-expansion and persistent air leak (more than 3
days) after tube thoracostomy can have their tube attached to a Heimlich valve and
discharged home. Thoracoscopy is the preferred treatment modality for PSP with concurrent
hemothorax, persistent air leak, failure of the lung to reexpand, and recurrent PSP. Chemical
pleurodesis is employed if the patient is unwilling or unable to undergo surgical procedure or
VATS is not available. Tetracycline, doxycycline, and talc have been used successfully for
pleurodesis after spontaneous pneumothorax and can be performed via the tube thoracostomy
or during VATS. Light et al. compared tetracycline pleurodesis with no treatment and found
significant decrease (41% to 25%) in the recurrence rate of spontaneous pneumothorax in the
pleurodesis group. Olsen et al. observed 16% recurrence after tetracycline pleurodesis in 390
patients who underwent thoracoscopy. Gyrik et al. performed talc pleurodesis via
thoracoscopy in 112 patients with persistent air leak or recurrence after PSP. Fifty-nine
patients were followed for median 118 months with success of the primary procedure in 95%
and recurrence rate of 5%.

Talc pleurodesis may cause deterioration of the respiratory function, which may not be
tolerated in patients with severe lung disease and hypoxic respiratory failure. Pleurodesis is
also contraindicated when close contact between the parietal and visceral pleura cannot be
achieved (lung entrapment and insufficient drainage). Treatment with steroids will decrease
the effectiveness of the pleurodesis and they should be stopped, if possible, 24 to 48 before
the procedure. Contraindications to indwelling tunneled pleural catheter include infection of
the skin at the insertion site, infected pleural effusion or empyema, inability of the patient to
tolerate the procedure, and inability to manage the catheter. Contraindications for
thoracoscopy include anatomic limitations and inability of the patient to tolerate surgical

Choice of Agent and Modality

Multiple agents have been used for chemical pleurodesistalc, doxycycline, minocycline,
erythromycin, bleomycin, florouracil, mitomycin C, cisplatin, cytarabine, doxorubicin,
etoposide, iodopovidone, silver nitrate, Corynebacterium parvum with parenteral
methylprednisolone acetate, and Streptococcus pyogenes A3 (OK-432).
Talc (hydrated magnesium silicate) is the most commonly used and most effective agent.
Talc can be delivered as slurry via a chest tube or as insufflation during thoracoscopy. Talc
insufflation was shown to be more effective than slurry in a prospective nonrandomized
trial by Stefani et al. A prospective randomized trial by Dresler et al. showed similar
efficacy overall but higher efficacy of insufflation in patients with either a lung or breast
primary. The choice of a modality should be made based on the condition of the patient
and additional diagnostic or therapeutic goals. The success rate of talc pleurodesis varies
between 60% and 90%.
Doxycycline is another commonly used agent. The success rate of doxycycline pleurodesis is
lower than the success rate of talc pleurodesis with recurrence rate of 13% to 35%.
IPCs and VATS can be used for management of pleural effusion. Both modalities may achieve
pleurodesis by mechanical irritation of the pleural layers with inflammation and connective
tissue formation. These modalities may also be used for application of pleural sclerosant such
as talc.
IPCs should be considered in patients with recurrent pleural effusion. They offer the
convenience of outpatient procedure, ease of care, fast symptom relief, and improved
quality of life. IPCs are the preferred modality for patients with lung entrapment or
nontreatable endobronchial obstruction. Van Meter et al. reported a rate of spontaneous
pleurodesis of 45.6% with indwelling catheters. In a study by Tremblay et al. spontaneous
pleurodesis was achieved in 70% of the cases with mean time to pleurodesis of 90 days. For
patients who do not achieve spontaneous pleurodesis, the catheter can be used to

administer pleural sclerosing agent. Data from an unblinded randomized controlled trial
comparing IPCs with talc pleurodesis showed no difference in dyspnea scores until 6
months, chest pain, and quality-of-life scores. Although, there were more nonserious
adverse events such as pleural, skin infection, and catheter blockage in the IPCs group,
there was no significant difference in the serious adverse effects between both groups. The
IPC group had shorter initial hospital stay, and decreased need for additional pleural
procedures. A multi-institutional prospective randomized study compared IPCs with
doxycycline pleurodesis in the management of malignant pleural effusions. The patients in
the IPC group had shorter hospital stay, less late recurrence of the effusion, and comparable
symptomatic improvement in dyspnea and quality of life.
VATS employs minimally invasive surgical procedures for diagnosis and treatment of
thoracic diseases including pleural effusions. VATS (thoracoscopy) with pleurodesis can be
performed as a primary diagnostic and therapeutic procedure or after an initial negative
thoracentesis or failed pleurodesis by other method. The efficacy of VATS talc pleurodesis
approaches 90%. A retrospective review by Hunt et al. comparing tunneled pleural
catheters (TPCs) to VATS talc pleurodesis for treatment of malignant pleural effusion
showed significantly fewer reinterventions for recurrent ipsilateral pleural effusions in the
TPC group, shorter length of stay, and postprocedure length of stay; no difference was
found in the complication rate or in-hospital mortality.

Pleurodesis via Chest Tube
Talc slurry50-mL sodium chloride 0.9% is injected in the bottle containing 5 g of sterile
talc. After assuring good mixing, the content of the bottle is aspirated back in one syringe
or divided in two syringes and further diluted with sodium chloride. The slurry should be
injected within 12 hours of mixing. After clamping the chest tube, the slurry is injected in
the pleural cavity and the catheter is kept clamped for 1 hour and the patient is rotated.
Suction is then reapplied (20 cm H2O). The chest tube is removed when the pleural fluid
drainage is less than 150 mL per 24 hours.
Doxycycline500 mg in 50-mL sodium chloride 0.9% is injected in the pleural cavity via
the chest tube. The chest tube is clamped for 4 hours and the patient is rotated. Suction is
than reapplied. The chest tube is removed after 24 hours if the drainage volume is less than
100 mL. If the drainage remains above 100 mL for more than 4 days, doxycycline is
readministered. Continued high chest tube output for more than 4 days after the second
doxycycline administration is considered as a treatment failure and other modalities for
pleurodesis should be sought. Local anesthetic such as lidocaine (25 mL, 1% solution) or
mepivacaine (20 mL, 2% solution) could be added to the doxycycline solution for local
The rotation of the patient does not increase the likelihood of successful pleurodesis. There is

no evidence that waiting for the drainage output to decrease, is better than removing the tube
after 24 hours regardless of the amount of fluid drainage.
Indwelling Pleural Catheter
The patient is positioned in lateral decubitus position or in semirecumbent position.
Ultrasound should be used to locate the most dependent area of the effusion. The chest is
prepped and draped in the usual sterile fashion. After the appropriate intercostal space is
identified local anesthetic is applied at the insertion site, along the tunnel track, and on the
exit site. The insertion site is usually located on the anterior axillary line and the exit site is
5 to 8 cm anterior to it. The guidewire introducer needle is then inserted in the appropriate
interspace just above the lower rib. The guidewire is inserted through the guidewire
introducer into the pleural cavity. A 1-cm incision is performed over the guidewire
insertion site and a second incision, 5 to 8 cm inferior and anterior to the first one. Next,
the catheter is inserted with a tunneler in the direction from the exit site to the insertion
site and the cuff advanced approximately 1 cm beyond the anterior incision. A 16F peelaway introducer sheath is advanced over the guidewire into the pleural space. The
guidewire and the dilator are then removed and the proximal fenestrated end of the
catheter is inserted through the peel-away sheath until all the fenestrations are inside the
pleural space. The sheath is peeled away while ensuring the catheter remains in place and
lays flat without any kinks. The insertion and exit sites are sutured and the catheter is
secured to the skin. The stitch is usually removed after 2 weeks. Once the catheter is in
place it is connected to the drainage system and 1 to 1.5 L fluid removed. The patient
and/or family members should be taught about catheter care, drainage, and signs of
infection. Visiting nurse arrangement should be made if the patient and the family
members are not able to manage the catheter independently. The initial instructions are for
catheter drainage every 1 to 2 days, not more than 1 L/day until less than 50 mL is
removed at three consecutive sessions at which point removal of the catheter should be
Video-assisted Thoracoscopic Surgery (VATS)
The patient is positioned in lateral decubitus position with the costal margin of the patient
placed at the break of the operating table. Appropriate padding at the pressure points is
required, as well as head and operative side arm support. The chest is prepped and draped
in the usual sterile fashion. A single port is sufficient in most cases of diagnostic
thoracoscopy and pleurodesis. A 10- to 15-mm incision is made at the anterior axillary line
and the soft tissues are dissected bluntly or using electrocautery. The choice of camera and
instruments depends on the preference of the surgeon and the expected procedure.
Pleurodesis can be achieved with insufflation of 3 to 5 g of talc powder or pleural abrasion.
A chest tube is placed via the same incision and the wound is closed primarily. The chest
tube is placed on negative pressure postoperatively and is removed after the output
decreases below 100 to 150 mL for 24 hours.
Inflammation/infectionsystemic inflammatory reaction with fever, increased white blood

cell count, and C-reactive protein is common. Empyema and local site infection are
uncommon complications.
Painpain is a common complication of pleurodesis. Talc pleurodesis in patients with
spontaneous pneumothorax is particularly painful. Local anesthetics such as lidocaine 1% and
mepivacaine 2% may be administered in the pleural space. Oral and intravenous opiates may
be necessary to control pain.
Respiratory failuredyspnea is a common symptom after pleurodesis. Respiratory failure is
more common with talc pleurodesis, preparations with higher proportion of smaller particles
(<5 to 10 microns in diameter), higher total talc doses, bilateral pleurodesis, and presence of
factors that increase systemic absorption of talc particles (inflammation, pleural defects) are
associated with more severe local and systemic inflammatory reaction. Respiratory failure
and ARDS are rare if less than 5-g size-calibrated talc is used. The type of talc preparation
(slurry or insufflation) has no importance for the development of respiratory failure.
IPC complications can be related to the techniquepneumothorax, lung injury, bleeding,
and infection, or can be delayed; infection at the insertion site, empyema, catheter
obstruction, accidental dislodgement, pleural fluid leakage around the catheter, catheter
fracture with retention of fragments upon catheter removal, metastases along the catheter
tract, and symptomatic loculations. In a systematic review by Van Meter et al. including 19
studies and 1,370 patients, complications were seen in 12.5% of the patients.

There are different modalities for achieving pleurodesis. The choice of procedure should take
into account multiple factors including the primary diagnosis, the status of the patient,
comorbidities, pleural anatomy, presence of lung entrapment, additional diagnostic and
therapeutic goals, and patient preference.

Recommended References and Readings

Davies HE, Davies RJ, Davies CW; BTS Pleural Disease Guideline Group. Management of
Pleural Infection in adults: British Thoracic Society Pleural Disease Guideline 2010. Thorax.
2010; 65(suppl 2):ii41ii53.
Davies HE, Mishra EK, Kahan BC, et al. Effect of an indwelling pleural catheter vs chest tube
and talc pleurodesis for relieving dyspnea in patients with malignant pleural effusion: The
TIME2 randomized controlled trial. JAMA. 2012;307(22):23832389.
Fysh ET, Tremblay A, Feller-Kopman D, et al. Clinical outcomes of indwelling pleural
catheter-related pleural infections: An international multicenter study. Chest.
Havelock T, Teoh R, Laws D, et al; BTS Pleural Disease Guideline Group. Pleural procedures
and thoracic ultrasound: British Thoracic Society pleural disease guideline 2010. Thorax.
2010; 65(suppl 2):ii61ii76.
Hooper C, Lee YC, Maskell N; BTS Pleural Guideline Group. Investigation of a unilateral
pleural effusion in adults: British Thoracic Society Pleural Disease Guideline 2010. Thorax.
2010;65(suppl 2):ii4ii17.

Light R. Pleural Diseases. 6th ed. Philadelphia, PA: Lippincott Williams & Willkins; 2013.
MacDuff A, Arnold A, Harvey J; BTS Pleural Disease Guideline Group. Management of
spontaneous pneumothorax: British Thoracic Society Pleural Disease Guideline 2010.
Thorax. 2010; 65(suppl 2):ii18ii31.
Parsaei N, Khodaverdian R, Mckelvey AA, et al. Use of long-term indwelling tunneled pleural
catheter for the management of benign pleural effusion. Chest. 2006;130(4):S271.
Paul S, Altorki NK, Port JL, et al. Surgical management of chylothorax. Thorac Cardiovasc
Surg. 2009;57(4):226228.
Pien GW, Gant MJ, Washam CL, et al. Use of an implantable pleural catheter for trapped lung
syndrome in patients with malignant pleural effusion. Chest. 2001;119(6):16411646.
Roberts ME, Neville E, Berrisford RG, et al; BTS Pleural Disease Guideline Group.
Management of a malignant pleural effusion: British Thoracic Society Pleural Disease
Guideline 2010. Thorax. 2010;65(suppl 2):ii32ii40.
Shaw P, Agarwal R. Pleurodesis for malignant pleural effusions. Cochrane Database Syst Rev.
Tan C, Sedrakyan A, Browne J, et al. The evidence on the effectiveness of management for
malignant pleural effusion: A systematic review. Eur J Cardiothorac Surg. 2006;29(5):829

23 Eloesser Flap and Clagett Procedures

Shair Ahmed and Allan Pickens


Originally described by Hippocrates over 2,000 years ago, the clinical signs and symptoms of
an empyema were recorded, including the implication for abscess drainage, in order for the
patient to improve. In the early 1900s, Samuel Robinson from the Mayo Clinic reviewed
techniques of thoracoplasty for empyema cavity obliteration known during the early 1900s;
however, he advocated for open pleural drainage with rib resection and subsequent muscle
interposition as the treatment for chronic nontuberculous empyema. Following this, two
pinnacle papers served as the foundation to the current management of chronic empyema.
First in 1935, Eloesser introduced a U-shaped flap for the treatment of tuberculous
empyema; subsequently, Clagett and Geraci from Mayo Clinic reported on their experience
with a two-stage procedure for the treatment of postpneumonectomy empyema in 1963.
Modifications of both procedures have led to the current treatment termed the open thoracic
window (OTW) for chronic empyemas and postpneumonectomy empyema.
Thoracic empyema is defined as an inflammatory process between the visceral and parietal
pleura. Empyema is diagnosed by one or more of the following methods: (1) the visualization
of frank pus by aspiration, tube thoracostomy, or at time of surgery; (2) biochemical evidence
of inflammation defined as white blood cell count greater than 500/mL, protein level greater
than 2.5 g, glucose level less than 40 mg/dL, lactate dehydrogenase level greater than 1,000
IU/L, or pH less than 7.1; or (3) positive culture from fluid-aspirated pleural fluid. The most
common etiology of an empyema is parapneumonic infection, while less than 30% originates
from thoracic operations. Less than 5% of cases of empyema result from thoracic trauma.
Table 23.1 below lists all the modalities of treatment that exist for dealing with empyema, the
main focus of this chapter will describe the technical aspects of the Eloesser flap and Clagett

The indications for an OTW (Eloesser flap or Clagett window) are as follows:
Chronic empyema
Patients with significant comorbidity and prohibitive surgical risk who are not able to
tolerate decortication.

TABLE 23.1 Treatment Modalities for Thoracic Empyema

Patients waiting for a more radical procedure (allows for nutritional buffering)
No response to conventional therapy
Patients who are unresponsive to treatment modalities, which include tube thoracostomy
and decortication.
Patient too debilitated for a major thoracic procedure
Expectation of long-term drainage
Discomfort from tube drainage placed posteriorly
Patients who are noncompliant
Postpneumonectomy empyema (with or without bronchopleural fistula)

Original Description of Eloesser Flap
The original procedure was described using local anesthesia. A U-shaped flap of skin and
subcutaneous tissue is initially marked before making incision (Fig. 23.1). This U-shaped flap
is half way between the posterior axillary line and the line at the inferior most portion of the
scapula. The base of the flap is 2-in wide and is one rib space above the lower extent of the
empyema cavity. The length of the flap is equivalent to the length of two rib spaces to ensure
the flap reaches the pleural space. The rib and associated intercostal muscle directly beneath
the flap is resected to the length of the flap itself. The tip of the flap is placed into the chest
and the flap is sutured to the pleura at the apex and laterally using absorbable suture (Fig.
23.2). The wound is subsequently packed. As the lung parenchyma expands, the cavity
collapses. The flap acts as a one way valve as an increase in intrapulmonary pressure creates
negative pressure within the empyema cavity allowing the lung to re-expand and obliterate
the space (Fig. 23.3).
Modified Eloesser Flap (MEP)
This technique was introduced into the literature in 1971 by Symbas et al. Essentially the
principles are the same as the original technique described by Eloesser in 1935. Again, the
procedure can be performed with local or general anesthesia. The location of the MEP is
dependent on the location of the empyema cavity. In contrast to the original technique, an

inverted U flap is incised over the empyema cavity. The flap includes skin and the
subcutaneous tissue. The base of the flap is directly over the lower most extent of the
empyema (in contrast to the original EF where the base of the flap is two rib spaces over the
lower extent of the empyema cavity). The length of the flap is approximately two ribs
including intercostal spaces. A segment of the underlying rib is resected, or multiple segments
of one or more ribs may be resected depending on the size of the empyema and the body
habitus of the patient. The flap is then sutured to the base of the cavity using large absorbable
suture (Fig. 23.4AF).

Figure 23.1 Flap of skin outlined.

Figure 23.2 Cross section of chest wall showing skin flap turned into chest and attached to pleura.

Figure 23.3 Skin flap turned into chest cavity; edges of defect approximated by sutures.

Figure 23.4 AF: Creation of MEP.

Original Description of Clagett Procedure

The Clagett procedure is a two-stage procedure. If the patient has a previous thoracotomy, the
anterior most portion of the thoracotomy is opened and the underlying rib is exposed.
Approximately 7 to 9 cm of rib is exposed and resected including the associated intercostal
muscle and neurovascular bundle. The pleura is then opened and the empyema cavity is
drained and thoroughly irrigated. The superficial fascia is sutured to the periosteum of the
resected rib. No drainage tubes are required. The cavity is irrigated daily and the quality of
infected drainage should improve to a serous composition.
The original time recommended between phase one and phase two was 6 to 8 weeks. This
time span allows the empyema cavity to reduce due to the ipsilateral shift of the mediastinum
and the elevation of the diaphragm. At this point, the cavity should have a fibrotic lining free
of any purulence. The edges of the wound should be debrided sufficiently and the underlying
muscle and fascia should be mobilized. The cavity is irrigated with an antibiotic solution.
Following thorough irrigation, antibiotic solution should be placed in the cavity to fill the
entire space. Debridement antibiotic solution (DAB, 500-mg neomycin, 100-mg polymixin B

sulfate, and 80-mg gentamicin per liter of saline) has been described for this purpose. Care
should be taken to not overfill the pleural space with antibiotic solution. The muscle and
fascia are closed over the cavity in multiple layers with no drainage tube.
Modifications to Both the Eloesser Flap and Clagett Procedure
Over time, there have been several modifications to both procedures. Consequently, the
operation is now referred to as an OTW. An Eloesser flap usually implies a one-stage
procedure and is performed in patients who have significant comorbidity that precludes
multiple procedures or general anesthesia. Multiple approaches to the incision used over the
empyema cavity have been described including the original U shape, the inverted U shape, an
H shape, and triradiate. The surgical principle is to create musculocutaneous flaps in a
window that is large enough to drain the cavity and prevent spontaneous closure of the
cavity. When the window is marsupialized and anchored to the pleura, the chance of
spontaneous closure is reduced by assuring that epithelial skin is sutured to the parietal
pleura. The large epithelialized fistula into the chest allows free drainage of the empyema.
Dressing changes are frequent at the creation of the window; however, the frequency
gradually decreases to once daily. Over time, the cavity decreases in size and reepithelializes
with minor-to-moderate chest wall deformity. If the cavity is too large, a second procedure is
required to close the defect. Contraindications to closure include persistent infection,
communicating bronchopleural fistula, or disseminated carcinoma.
Two other important concepts exist in management of chronic empyemas, especially ones
due to a bronchopleural fistula. First, the bronchopleural fistula must be closed. BPFs are
controlled by debridement and reclosure of the bronchial stump, reresection of the stump
with carinal closure, or muscle flap transfer. The second concept involves those circumstances
where the pleural cavity remains too large and requires obliteration. Muscle flap transfer for
obliteration of residual plueral cavity has been well described in the literature and muscle
flaps used include latissimus dorsi, serratus anterior, pectoralis major, omentum, and rectus
abdominus. Figure 23.5 demonstrates the commonly used muscle flaps for thoracomyoplasty.
Key principles in muscle flap closure include tailoring antibiotics specific to the cultures
from the empyema, reopening the original incision with debridement of the empyema cavity
to ensure a healthy granulation tissue base, addressing a BPF if present, using indicated
muscle flaps to fill the pleural space and to ensure the entire pleural cavity is filled. Entry
sites for latissimus dorsi flaps include the second or third rib (with segment of rib resected) to
cover the superior mediastinum, or the fifth/sixth rib for coverage of the middle to inferior
mediastinum. Serratus anterior and pectoralis minor usually require removal of a segment of
the second or third rib in the midaxillary line and provide coverage for the mediastinum.
Rectus abdominus and omental flaps are both transposed through the diaphragm. In the case
of rectus abdominus, the flap is transposed specifically through the anterior portion of the
diaphragm. Omentum is particularly useful in the buttressing and closure of a bronchial

Figure 23.5 Commonly used muscle flaps for thoracomyoplasty.

Once an OTW has been created, management involves daily dressing changes to sterilize the
cavity over time. A recent study from Cleveland Clinic demonstrated a median time to closure
of 454 days, (range: 90 days to 3 years). Zaheer et al. in 2006 reviewed their 16-year
experience with the Clagett procedure for postpneumonectomy empyema in which 89.5% of
patients had successful closure of the Clagett procedure. A literature review in 2002 reviewed
all reported results of the Clagett procedure from 1972 to 1990 with nearly 79% success; the
majority of failures resulting from a recurrent or persistent BPF. An institutional review
described factors that affected closure of an OTW. An immediate decision for an OTW had
significantly less closure time of 3 months compared with delayed timing and a median time
to closure of 11 months. Early empyemas were associated with longer closure times as
opposed to empyemas that developed late. With the more frequent use of vacuum-assisted
closure (VAC) device for chronic wounds, an application to OWT has been reported. The
largest study known from Palmen et al. in 2009 compared VAC to the contemporary
management of OWT. Patients excluded from VAC therapy included patients with esophageal

fistula, postpneumonectomy fistulas, and large bronchopleural fistulas. The use of VAC
devices allowed for re-expansion of the pulmonary parenchyma and establishment of
granulation tissue. All wounds were subsequently closed using pedicled latissimus dorsi or
rectus abdominus flaps. There were no associated VAC complications reported in this study.

OTW includes the Eloesser flap and the Clagett procedure with subsequent modifications that
have been introduced in the literature. This largely remains the treatment for chronic
empyema and postpneumonectomy empyema. Key concepts include early recognition and
treatment. The underlying etiology of the empyema should be identified. While this remains a
long-term chronic surgical issue with relative morbidity to patients, this is an entity that can
be managed with successful outcomes as demonstrated in the literature since the 1970s.

Recommended References and Readings

Adams F. The Genuine works of Hippocrates. New York, NY: W. Wood and Company;
Clagett OT, Geraci JE. A procedure for the management of postpneumonectomy empyema. J
Thorac Cardiovasc Surg. 1963; 45:141145.
Deslauriers J, Jacques LF, Gregoire J. Role of Eloesser flap and thoracoplasty in the third
millennium. Chest Surg Clin N Am. 2002; 12:605623.
Eloesser L. An operation for tuberculous empyema. Surg Gynecol Obstet. 1935;60:10961097.
Harris SU, Nahai F. Intrathoracic muscle transposition. Surgical anatomy and techniques of
harvest. Chest Surg Clin N Am. 1996; 6:501518.
Massera F, Robustellini M, Pona CD, et al. Predictors of successful closure of open window
thoracostomy for postpneumonectomy empyema. Ann Thorac Surg. 2006;82:288292.
Miller JI Jr. The history of surgery of empyema, thoracoplasty, Eloesser flap, and muscle flap
transposition. Chest Surg Clin N Am. 2000;10:4553.
Molnar TF. Current surgical treatment of thoracic empyema in adults. Eur J Cardiothoracic
Surg. 2007;32(3):422430.
Palmen M, van Breugel HN, Geskes GG, et al. Open window thoracostomy treatment of
empyema is accelerated by vacuum-assisted closure. Ann Thorac Surg. 2009;88(4):1131
Puskas JD, Mathisen DJ, Grillo HC, et al. Treatment strategies for bronchopleural fistula. J
Thorac Cardiovasc Surg. 1995;109(5):989996.
Reyes KG, Mason DP, Murthy SC, Su JW, Rice TW. Open window thoracostomy: Modern
update of an ancient operation. Thorac Cardiovasc Surg. 2010;58:220224.
Robsinon S. The treatment of chronic non-tuberculous empyema. Surg Gynecol Obstet.
Shamji FM, Ginsberg RJ, Cooper JD, et al. Open window thoracostomy in the management of
postpneumonectomy empyema with or without bronchopleural fistula. J Thorac Cardiovasc
Surg. 1983;86:818822.
Symbas PN, Nugent JT, Abbott OA, Logan WD, Hatcher CR Jr. Non tuberculous pleural

empyema in adults. Ann Thorac Surg. 1971; 12:6978.

Thourani VH, Lancaster RT, Mansour KA, Miller JI. Twenty-six years of experience with the
modified Eloesser flap. Ann Thorac Surg. 2003;76:401406.
Zaheer S, Allen MS, Cassivi SD, et al. Postpenumonectomy empyema: Results after the Clagett
procedure. Ann Thorac Surg. 2006;82:279287.

24 Thoracic Duct Ligation

Stephen R. Broderick and Traves D. Crabtree

The thoracic duct is the main conduit for the transit of lymphatic drainage through the chest.
The normal thoracic duct is a thin-walled, valved, 2 to 5 mm structure. It originates at the
cisterna chyli and enters the chest through the aortic hiatus. The duct travels cephalad
between the azygous vein and the aorta (Fig. 24.1) until approximately the fifth thoracic
vertebra where it crosses over to the left side of the vertebral column, behind the aortic arch
and terminates at the junction of the left internal jugular and subclavian veins. The anatomy
of the thoracic duct is quite variable. The most frequent anatomic variation is a duplication of
the lower thoracic duct due to persistence of the left embryonic trunk in approximately 40%
of individuals.
Ligation of the thoracic duct is indicated in any patient with a thoracic duct leak that has
failed conservative measures, which include a trial of low-fat diet, total parenteral nutrition,
and octreotide. The manifestation of a thoracic duct leak is variable, but patients most
commonly present with chylothorax. Alternative presentations include chylopericardium and
rarely chyloptysis. Most clinically significant chylothoraces are the result of traumatic or
iatrogenic injury of the thoracic duct such as may occur during esophagectomy.
Chylothoraces associated with pulmonary resection generally result from injury to a branch
duct during nodal dissection and resolve with conservative management. Mediastinal
lymphoma is the most common cause of spontaneous chylothorax and may require duct
High-volume chylothorax following esophagectomy mandates reoperation for ligation of
the thoracic duct. While a critical volume of chest tube effluent has not been defined,
persistent drainage post esophagectomy can lead to volume depletion, leukopenia, and
nutritional compromise. Prior to initiation of enteral nutrition, effluent will be serous. Debate
remains regarding what constitutes high-output versus low-output chyle leak. However, daily
drainage over 800 mL has historically prompted consideration of duct ligation. The literature
supports early intervention in postesophagectomy chylothorax.
Prophylactic ligation of the thoracic duct during esophagectomy remains controversial. A
single randomized controlled study supports mass ligation during transthoracic
esophagectomy. Results from retrospective reports are mixed. The authors support
prophylactic thoracic duct ligation during transthoracic esophagectomy as reoperation for
duct ligation requires mobilization of the gastric conduit, which may result in tension on the
esophagogastric anastomosis.

Figure 24.1 The thoracic duct usually lies in the posterior mediastinum, between the azygous vein, aorta, and esophagus.

Lymphangiography is a difficult study to perform and its application is limited by local
expertise. However, if available, this study can be a useful adjunct to preoperative
planning. Lymphangiography can clarify the anatomy of the thoracic duct and potentially
identify duplicate or aberrant anatomy. The study may also identify the leak (Fig. 24.2). If
the expertise is available, an attempt at embolization of the thoracic duct is reasonable.
Lymphangiography is most useful in complicated chyle leaks where the etiology or source
of the leak is unclear or in situations where mass ligation fails to control the leak.
Enteral administration of cream may aid in visualization of the chyle leak. Cream should be
given 30 to 60 minutes before operation to enhance the flow of chyle during inspection of
the chest. This can be administered through a nasogastric or orogastric tube after induction
of anesthesia.
The surgeon should ensure adequate volume resuscitation preoperatively.
An epidural catheter should be placed if the initial catheter has been removed.

Figure 24.2 Lymphangiography can demonstrate the anatomy of the thoracic duct as well as the location of a thoracic duct
injury. This lymphangiogram demonstrates the main thoracic duct in its normal anatomical location and a chyle leak into the
right pleural space.

The drainage tube for the gastric conduit (retrograde gastrostomy or nasogastric tube)
should remain to intermittent suction to drain the conduit and reduce the risk of aspiration
with induction of anesthesia.
A double-lumen endotracheal tube is mandatory for visualization.
Preoperative planning is similar for open or thoracoscopic visualization of the thoracic duct.

The technique of thoracic duct ligation is discussed for two scenarios: Ligation following
transthoracic esophagectomy and VATS thoracic duct ligation for spontaneous chylothorax.
The approaches and technical steps discussed apply to most indications for duct ligation.

Thoracic Duct Ligation Following Transthoracic

The patient is positioned in the left lateral decubitus position, rotated slightly forward. This
positioning is identical to that used for Ivor Lewis esophagectomy. If the esophagectomy was
performed in a minimally invasive fashion, the patient should be positioned as for that
If the patient underwent a recent thoracotomy then the thoracotomy is reopened and any
residual effusion drained from the hemithorax. If no previous thoracotomy has been
performed then the incision can be made slightly lower through the seventh or eighth
intercostal space. For exposure of the thoracic duct, a complete muscle sparing posterior

thoracotomy can be made with elevation and preservation of the latissimus muscle. The
conduit is mobilized from the chest wall and posterior mediastinum and the pedicle
identified. This is facilitated by early reoperation but can be more tedious if reoperation is
delayed. Throughout the procedure care must be taken by the assistant retracting the conduit
to avoid tension on the anastomosis and to prevent trauma to the right gastroepiploic artery.
Once the conduit is mobilized the mediastinum is inspected for leaks. If identified, a leak
should be closed by suture ligation or clipping. So me authors recommend the use of
pledgeted sutures. This has not been our practice, but is certainly reasonable. Regardless of
whether a leak is visualized or not we perform a mass ligation of the thoracic duct as inferior
as possible.
A figure-of-eight heavy polypropylene suture is placed in the dome of the diaphragm and
brought through a chest tube incision to retract the diaphragm. The visceral pleura overlying
the vertebral body adjacent to the aortic hiatus is incised with electrocautery. A large rightangle dissector is then used to elevate all of the soft tissue between the vertebral column and
the medial aspect of the aorta. This tissue is then doubly ligated with heavy silk sutures (Fig.
24.3). Mass ligation of the duct as low as possible is important to control leaks that are not
identified visually at the time of surgery. After ligation, some surgeons advocate mechanical
pleurodesis as an adjunct. This is followed by placement of chest tubes to widely drain the
hemithorax. The chest is closed in the standard fashion.
For patients in whom minimally invasive esophagectomy was performed, the same
approach to ligation of the thoracic duct can be performed through the minimally invasive
esophagectomy (MIE) incisions. We routinely perform prophylactic ligation of the thoracic
duct during transthoracic esophagectomy using the technique described.

Figure 24.3 Mass ligation of the thoracic duct performed during transthoracic (Ivor Lewis) esophagectomy. All of the soft
tissue between the vertebral body and aorta is elevated and mass ligated with a heavy silk suture.

Postoperatively, the patient can usually be returned to the surgical ward or step-down unit.
Chest tube drainage is monitored closely. Enteral nutrition is generally resumed 24 to 48
hours after reoperation if there is no other contraindication. Chest tubes are removed when
the output is minimal and an esophagram has demonstrated the absence of anastomotic leak.
Postoperatively, the patient is given a clear liquid diet for 24 hours. After 24 to 48 hours
the patient may be advanced to a regular diet. The quality of the chest tube output is
monitored and the absence of chylous drainage suggests successful ligation of the duct.
Removal of the chest tube is at the discretion of the surgeon, usually when drainage is less
than 200 cc per day.
Vats Thoracic Duct Ligation
The patient is positioned in the left lateral decubitus position, rotated slightly forward, and
flexed at the hip.
The camera port for VATS thoracic duct ligation is placed in the seventh or eighth intercostal
space in the posterior axillary line. A retraction port is placed in the seventh or eighth space
in the midscapular line. Finally, a working incision is created in the fifth intercostal space
The diaphragm is gently depressed with a sponge stick while the lower lobe is retracted
cephalad, exposing the inferior pulmonary ligament. The ligament is divided to the level of
the inferior pulmonary vein with a combination of electrocautery and blunt dissection. The
lung is then retracted anteriorly, exposing the posterior mediastinum. A heavy prolene suture
is placed in the dome of the diaphragm in a figure-of-eight fashion and brought out through a
stab incision low in the hemithorax to allow for continued retraction of the diaphragm. The
mediastinal pleura is opened longitudinally, lateral to the azygous vein (Fig. 24.4). The
azygous vein is dissected free from surrounding structures and retracted laterally; branches of
the vein may be clipped and divided as necessary. Next the mediastinal pleura overlying the
esophagus is opened and the esophagus retracted medially. Blunt dissection between the
azygous vein and the esophagus will reveal the thoracic duct overlying the aorta (Fig. 24.5).
Application of several 10-mm clips is sufficient for ligation (Fig. 24.6). Several centimeters of
the duct should be identified to allow sufficient room for ligation. A small incision can be
made in the wall of the duct with an endoscopic scissor; the presence of chylous fluid
confirms the identity of the structure being ligated. Alternatively, a small portion of the wall
of the duct can be removed for pathologic confirmation. If the duct is not able to be identified
directly, which is most the case, mass ligation is performed by encircling all of the soft tissue
between the azygous vein and the esophagus with a large right angle and doubly ligating it
with heavy silk ligatures.

Figure 24.4 A retraction stitch placed in the dome of the diaphragm aids in exposure of the posterior mediastinal during
thoracoscopic thoracic duct ligation. The mediastinal pleura is incised with electrocautery lateral to the azygous vein.

Figure 24.5 Dissection between the azygous vein and esophagus reveals the thoracic duct overlying the aorta during
thoracoscopic duct ligation.

Figure 24.6 Ten-millimeter endoscopic clips are used to ligate the thoracic duct.

Before closing, the thoracic duct is inspected for leakage of chylous material and
hemostasis is ensured. A mechanical pleurodesis is performed and a single chest tube is
placed in a posterior location. In the absence of an epidural catheter an intercostal nerve
block is performed with 0.5% bupivacaine. The lung is reinflated and the incisions closed in
the standard fashion.

The results of transthoracic ligation of the thoracic duct are excellent. For postesophagectomy
chylothorax, reoperation with ligation of the thoracic duct results in cessation of the chyle
leak in over 90% of patients as reported by two large-volume centers.

Thoracic duct ligation is an effective means of managing the various manifestations of
chylous fistula. Following esophagectomy we recommend early intervention through mass
ligation of the thoracic duct. Chyle leak in this setting is usually the result of traumatic injury
to the main thoracic duct and nonoperative management is unlikely to be effective. For other
indications, VATS thoracic duct ligation is effective and can be accomplished with minimal

Recommended References and Readings











Inc. posted 6
October, 2009.
Cerfolio RJ, Allen MS. Postoperative chylothorax. J Thorac Cardiovasc Surg. 1996;112:1361
Hayden JD, Sue-Ling HM, Sarela AI, et al. Minimally invasive management of chylous fistula
after esophagectomy. Dis Esophagus. 2007;20(3):251255.
Lai FC, Chen L, Tu YR, et al. Prevention of chylothorax complicating extensive esophageal
resection by mass ligation of thoracic duct: A random control study. Ann Thorac Surg.
Schuchert MJ, Luketich JD, Fernando HC. Complications of minimally invasive
esophagectomy. Semin Thorac Cardiovasc Surg. 2004;16:133141.
Shah RD, Luketich JD, Schuchert MJ, et al. Postesophagectomy chylothorax: Incidence, risk
factors, and outcomes. Ann Thorac Surg. 2012;93(3):897903.
Sieczka EM, Harvey JC. Early thoracic duct ligation for postoperative chylothorax. J Surg
Oncol. 1996;61:5660.
Sukumar M, Schipper P, Komanapalli C. Thoracoscopic ligation of the thoracic duct. CTSNet
posted 6 October, 2009.
Wurnig PN, Hollaus PH, Ohtsuka T, et al. Thoracoscopic direct clipping of the thoracic duct
for chylopericardium and chylothorax. Ann Thorac Surg. 2000;70:16621665.

25 Thoracic Sympathectomy

James S. Allan and Maria Lucia L. Madariaga


Hyperhidrosis is defined as the secretion of perspiration in amounts greater than

physiologically necessary for thermoregulation. When generalized, hyperhidrosis often
indicates the presence of a systemic disease, such as a febrile illness, an endocrinopathy, or a
paraneoplastic syndrome. However, in many patients, hyperhidrosis is confined to focal
regions and is a constitutive characteristic of the patient, as opposed to a manifestation of
disease. This subset of hyperhidrosis is termed primary focal hyperhidrosis, and may, in
some cases, benefit from a thoracic sympathectomy.
Primary focal hyperhidrosis affects about 1% to 3% of the general population and often
leads to severe functional and psychosocial impairment. Its presence is often observed in
early childhood and typically becomes worse as a patient enters adulthood. While not well
studied, it seems that such hyperhidrosis begins to abate in the fourth and fifth decades of
life. Primary focal hyperhidrosis may affect the axillae (51%), hands (25%), feet (29%), and
craniofacial region (20%). Although constitutive in nature, many patients report that their
hyperhidrosis is exacerbated by heat or anxiety.
In 2004, the Multi-specialty Working Group on the Recognition, Diagnosis, and Treatment of
Primary Focal Hyperhidrosis delineated diagnostic criteria for this disorder:
1. focal, visible, excessive sweating for at least 6 months; and at least two of the following:
2. bilateral and symmetric,
3. impairs daily activities,
4. at least one episode per week,
5. onset before age 25,
6. family history of idiopathic hyperhidrosis (a positive family history occurs in 25% to 50%
of all cases),
7. focal sweating stops during sleep.
After systemic illness is ruled out as the cause of hyperhidrosis (which can usually be done
on the basis of the medical history alone), no further diagnostic testing is needed.
Quantification of sweat production can be performed by galvimetric testing, the Minor starchiodine test, or the ninhydrin test; however, these data are more useful in the research setting.
Once the diagnosis of primary focal hyperhidrosis is made, the choice of therapy will be
based primarily upon the location and the severity of the condition. In general, thoracic
sympathectomy (T2-T3) is most efficacious and satisfactory in patients with severe palmar
hyperhidrosis that is functionally impairing and refractory to medical therapy (>95%
efficacy). It is partially effective in managing hyperhidrosis of the axillae (70% partial
The effect of thoracic sympathectomy on pedal hyperhidrosis is much more variable, and
we do not recommend it to patients who present with pedal hyperhidrosis as their principal

The reliable surgical treatment of craniofacial hyperhidrosis requires a high

sympathectomy, usually requiring ablation of T1 and possibly the lower portion of the stellate
ganglion. Because this operation carries a high risk of inducing the Horner syndrome, we do
not feel that the benefits of high sympathectomies outweigh the risk.

Assessment of hyperhidrosis severity is important for effective management. The
Hyperhidrosis Disease Severity Scale (HDSS, Table 25.1) categorizes disease into mild
(sweat that is not noticeable and does not interfere with daily activities), moderate (sweat
is tolerable and sometimes interferes with daily activities), and severe (sweat is intolerable
and interferes with daily activities). Patients who fall into the severe category often fail
medical management.
While patients with severe palmar hyperhidrosis are likely to fail medical management, we
feel that all patients should undergo a trail of medical therapy tailored to their specific
symptoms. First-line treatment generally consists of topical therapy using antiperspirants
and/or anticholinergic preparations. The most common, effective topical antiperspirants
contain aluminum salts. We usually recommend that a 20% prescription strength aluminum
salt antiperspirant be applied daily at bedtime to the affected areas. For many patients, a
residual benefit lasts throughout the next day. Typical side effects include irritation or
maceration of the skin, which is usually dose dependent. We also frequently recommend a
compounded preparation of topical glycopyrrolate (2% to 4% w/w), as a cream, lotion, or
alcoholic spray. This is typically applied up to three times per day and can be used in
conjunction with an antiperspirant. Occasional systemic anticholinergic side effects are seen
when large areas are treated aggressively.
As a next line of medical therapy, we typically prescribe an oral anticholinergic agent, such
as oxybutynin, which is available in a long-acting formulation suitable for daily use. This
class of medication is recommended with all of the caveats and precautions associated with
any systemic anticholinergic therapy. Particular care is needed to educate patients about its
potential effect of over-inhibiting perspiration, putting the patient at risk for heat stroke. It is
best used in combination with topical therapies to maximize effect and minimize the dosedependent side effects associated with any one particular drug.

TABLE 25.1 Hyperhidrosis Disease Severity Scale (HDSS)

For small areas of focal problematic hyperhidrosis, treatment with botulinum toxin
injections is also an option. The drawback to this treatment modality is the need for repeated,
often expensive, treatments. It is not practical for use on large areas.

Finally, for axillary hyperhidrosis only, the proprietary miraDry system is also of potential
benefit. This treatment modality relies on the use of externally applied microwave energy to
ablate the eccrine glands in the axillae. It is not currently approved for use outside the
We have found other treatments such as clonidine, beta-blockers, calcium channel blockers,
benzodiazepines, and iontophoresis to be largely ineffective for most patients.
For patients who fail medical therapy, and who are principally bothered by palmar
hyperhidrosis, we will offer a video-assisted thoracoscopic surgery (VATS) sympathectomy,
ablating the T2-T3 ganglia. We will also offer this operation to patients with refractory
axillary hyperhidrosis, with the understanding that the efficacy of this procedure is somewhat
less in this subset of patients. It is imperative that all patients understand that some
unpredictable degree of compensatory hyperhidrosis (usually below the T4 dermatomal level)
is an expected result of this operation. It is incumbent upon the patient to make the final
decision to accept this trade-off. In our experience, a small percentage of patients (<5%)
regret having surgery due to excess compensatory hyperhidrosis, despite our best efforts to
select and inform patients properly.

There is much controversy over the appropriate level(s) and length of sympathectomy. As
stated above, sympathectomies higher than the T2 level are often needed for reliable relief of
craniofacial hyperhidrosis, and such sympathectomies carry a very high risk of inducing
Horner syndrome. Palmer hyperhidrosis appears to be well controlled with ablations
involving T2 and/or T3. Control of axillary hyperhidrosis typically requires a T3-T4
sympathectomy. There is also some evidence to suggest that shorter sympathectomies
minimize compensatory hyperhidrosis, usually with some detriment to the primary efficacy of
the operation.
In 2011, the International Society on Sympathetic Surgery (ISSS) and The Society of
Thoracic Surgeons (STS) General Thoracic Task Force on Hyperhidrosis provided a consensus
statement about the surgical treatment of hyperhidrosis. Among their recommendations was
the use of a rib-oriented nomenclature, with R referring to rib, followed by the rib number
and location of nerve division. In practice, the rib level is easier for the surgeon to identify
than the sympathetic chain or ganglia, which does not, in reality, have the obvious stylized
appearance presented in most anatomy texts.
Using this convention, our practice has focused on reliably treating patients whose primary
complaint is palmar hyperhidrosis by means of a sympathectomy beginning on the middle of
the second rib, and extending down to the top of the fourth rib, which corresponds roughly to
a T2-T3 sympathectomy, allowing for individual anatomic variation. We have found that this
approach produces nearly 100% complete and permanent control of palmar sweating, with no
occurrences of Horner syndrome, and little (<5%) dissatisfaction due to excessive
compensatory hyperhidrosis.


Historically, upper thoracic sympathectomy was performed in an open fashion through

posterior, supraclavicular, anterior thoracic, or transaxillary approaches. However, adequate
exposure is often difficult via open approaches, and such cases were often accompanied by
debilitating muscular pain/dysfunction, scarring, and increased risk of Horner syndrome
particularly with the supraclavicular approach.
The advent of videothoracoscopy greatly facilitated the performance of a thoracic
sympathectomy, by providing superior visualization and smaller incisions. Today, a bilateral
VATS sympathectomy is typically a well-tolerated outpatient procedure that can be
accomplished in under an hour.

Figure 25.1 Left axillary exposure with markings for both 5-mm port sites.

After intubation with a left-sided double-lumen endotracheal tube, the patient is initially
placed onto his/her left side in anticipation of a right-sided procedure. The right arm is
abducted and supported to expose the right axilla (Fig. 25.1). The table is placed in steep
reverse Trendelenburg and rotated away from the operative side. This allows the isolated
lung to lie inferiorly and anteriorly, facilitating exposure to the sympathetic ganglion chain
running vertically across the heads of each rib. It is most convenient for both the operating
surgeon and assistant to stand at the left side of the table for the right-sided procedure. At the
conclusion of the right-sided procedure, it is our preference to reposition the patient onto the
opposite side, reprepping and draping, for the left-sided sympathectomy.
Other surgeons have had success positioning the patient supine with arms extended over
the head, facilitating exposure by rolling the table hard to one side and then the other.
Although our positioning routine is a bit more time-consuming, we feel that the exposure is
superior and have never needed to insufflate the chest with CO2. There is also less chance of
inducing an ulnar neuropathy, which can be problematic when arms are positioned overhead.
After prepping and draping, two ports are placed to accommodate 5-mm instruments in the
inferior axilla. One is placed over a convenient rib just posteriorly to the pectoral muscle. The
other is placed just anterior to the latissimus dorsi muscle (Fig. 25.1). A 5-mm 0-degree
straight thoracoscope is inserted through the anterior port, and a long, protected tip cautery

is inserted through the posterior port. The thoracoscopic view and a corresponding anatomic
diagram are presented for both the right and left sides (Figs. 25.2AC and 25.3AC).
Using the cautery, the sympathetic ganglion chain is ablated from the middle of the second
rib down to the top of the fourth rib (Fig. 25.4). Care should be taken not to linger with the
cautery when ablating the chain over the second rib, to avoid any risk of transmitting cautery
energy cephalad toward the region of the stellate ganglion. It is usual for some of the
ganglion chain to be obscured by crossing veins. Because unipolar cautery has a zone of effect
that extends radially from the instrument tip, we have not found it necessary to dissect out or
otherwise manipulate these crossing veins. They can simply be skipped over, resuming the
ablation immediately below the vein.

Figure 25.2 A: Thoracoscopic view of right superior-posterior mediastinum. The sympathetic chain runs over the anterior
surface of the posterior rib heads. The first rib is not visualized but can be palpated. B: Schematic diagram of right superiorposterior mediastinum. The first rib is outlined. Each sympathetic ganglion and its rami communicantes are seen just below
the respective rib level. C: Thoracoscopic view of right thoracic sympathectomy in progress. a, artery; n, nerve; R1, first rib;
R2, second rib; R3, third rib; SVC, superior vena cava; symp, sympathetic.

In addition to the direct ablation of the sympathetic chain, it is important to extend a

lateral cautery line along the body of the second rib for about 5 cm to divide any accessory
sympathetic fibers that might not run with the main body of the sympathetic chain. These
accessory sympathetic fibers, which are not always visualized, carry the eponym accessory
nerves of Kuntz after the neuroanatomist who described them in 1917. The location of the

lateral cautery line is shown in Figure 25.4 and can be continuous with the main
sympathectomy ablation on the second rib.
After the sympathectomy is complete, the posterior port site is closed, and a temporary
pleural drain is placed through the anterior port site. With the drain on suction, the right lung
is reinflated, and the patient is repositioned for the left-sided sympathectomy. An identical
procedure is performed on the left. The patient is then repositioned supine. Once both lungs
are reinflated, and no air is observed to be leaking through either of the pleural drains, the
drains are removed, and the anterior port sites are now closed. The patient is recovered from
It should be noted that some surgeons dissect out the sympathetic chain, as a surgical
specimen. We have found this not to be necessary and feel that it puts the patient at greater
risk of bleeding and conversion to open surgery. Other surgeons prefer to clip (crush) the
sympathetic chain at one or more levels. This is often done in hope of the potential benefit of
reversibility, should intolerable postoperative compensatory hyperhidrosis occur. However, in
practice, clip removal at a second operation is usually not effective in reversing the operation;
and when it is effective, the original condition typically returns. We prefer to inform and
select patients carefully, so that even if significant hyperhidrosis occurs, the trade-off will be
acceptable to the patient.

Figure 25.3 A: Thoracoscopic view of left superior-posterior mediastinum. The sympathetic chain runs over the anterior
surface of the posterior rib heads. The first rib is not visualized but can be palpated. B: Schematic diagram of left superiorposterior mediastinum. The first rib is outlined. Each sympathetic ganglion and its rami communicantes are seen just below
the respective rib level. C: Thoracoscopic view of left thoracic sympathectomy in progress. a, artery; R1, first rib; R2, second
rib; R3, third rib.

Figure 25.4 Pink-shaded area from middle of rib 2 to top of rib 4 shows region of sympathetic chain to cautery ablate.
Dashed line depicts cautery line on the second rib to divide accessory sympathetic fibers.

Once a postoperative chest radiograph and the patients clinical condition are satisfactory, the
patient can be discharged home with oral pain medication. Patients should be instructed to
expect some pain at the incision sites, as well some pleuritic pain in the chest and back.
Patients are seen in the office 1 to 2 weeks after surgery for a postoperative evaluation with a
chest radiograph.

Intraoperative complications include all of those typical for any VATS procedure, including
bleeding, unintended injury to an adjacent structure, and the need to convert to open surgery
to remediate a problem.
Postoperative complications include pneumothorax (requiring a drain in 0.3% to 6% of
cases), subcutaneous emphysema (30%), pleural effusion, hemothorax (<1%), chylothorax
(rare), brachial plexus injury (rare), wound infection, and Horner syndrome (0% to 5%,
usually caused by damage to T1 when the second rib is improperly localized or one is
operating for craniofacial hyperhidrosis). In addition, some patients may experience gustatory
sweating, defined as facial sweating when eating certain foods (usually spicy or acidic). The
rates reported in the literature range from 0% to 38%.
Although not truly a complication, some degree of compensatory hyperhidrosis is an
undesired result of most thoracic sympathectomies. It usually involves the trunk, groin,
and/or lower extremities. It is to a great extent idiosyncratic although there is some evidence

that higher and longer sympathectomies produce more compensatory symptoms. The rates of
severe compensatory hyperhidrosis are quite variable in the literature, due to the different
sympathectomy techniques that are in common use, and because degree of severity is
inherently a subjective complaint. Patients with excessive compensatory hyperhidrosis can be
treated with the medical modalities discussed above.

The patients overall satisfaction following surgery is the most important determinant of
surgical success. Questionnaires can be given to patients to determine the symptom baseline
and whether surgery was effective. For example, using the HDSS, a one-point improvement in
HDSS score is associated with 50% reduction in sweat production; a two-point improvement
in HDSS score is associated with 80% reduction in sweat production. Ultimately, satisfaction
is mainly determined by the success of primary symptom control.
For facial blushing and facial hyperhidrosis, patient satisfaction rates were 85% to 94%,
failure rates were 6% to 15%, and the incidence of compensatory hyperhidrosis rates was
67% to 95%.
For palmar hyperhidrosis, among the largest series (78 to 1,360 patients), patient
satisfaction rates were 92% to 97%, failure rates were 1% to 25%, and the incidence of
compensatory hyperhidrosis rates was 67% to 92%. Two other large series of patients where
T4 and T5 block was performed showed that patient satisfaction rates were 99%, failure rates
were 0% to 8%, and the incidence of compensatory hyperhidrosis rates was 0% to 17%.
For axillary hyperhidrosis, patient satisfaction rates were 60% to 90%, failure rates were
0.9% to 21%, and the incidence of compensatory hyperhidrosis rates was 17% to 82%.
For plantar hyperhidrosis, about 50% of patients see improvement in symptoms initially;
this decreases to 25% over time.

Severe focal hyperhidrosis affects a small percentage of the population but can be
functionally impairing and psychosocially undesirable. For patients who present with focal
hyperhidrosis, a trail of medical therapy is appropriate, recognizing that patients with severe
symptoms are likely to be refractory to medical treatment. For patients with palmar
hyperhidrosis (and to a lesser extent, axillary hyperhidrosis), a T2-T3 sympathectomy, as
described above, provides near universal control of symptoms, with a low rate of severe
compensatory hyperhidrosis. We are reluctant to operate on patients whose primary
complaint is craniofacial hyperhidrosis, due to the need for a higher sympathectomy and the
attendant risks with that procedure. We are also reluctant to perform thoracic sympathectomy
for isolated pedal hyperhidrosis, as its efficacy is poor and unreliable.
The operative procedure that we have presented above is one that is designed to maximize
surgical exposure, minimize surgical manipulation, and reduce the likelihood of surgical
complications. For patients with severe medically refractory palmar hyperhidrosis, we have
recorded an overall satisfaction rate exceeding 90% on a large number of cases without any

serious complications. Further investigation and experience is still needed to determine the
optimal sympathectomy level for specific patient populations.

Recommended References and Readings

Baumgartner FJ. Surgical approaches and techniques in the management of severe

hyperhidrosis. Thorac Surg Clin. 2008;18(2):167181.
Cerfolio RJ, De Campos JR, Bryant AS, et al. The Society of Thoracic Surgeons expert
consensus for the surgical treatment of hyperhidrosis. Ann Thorac Surg. 2011;91:1642
Gossot D, Toledo L, Fritsch S, et al. Thoracoscopic sympathectomy for upper limb
hyperhidrosis: Looking for the right operation. Ann Thorac Surg. 1997;64:975978.
Hsia JY, Chen CY, Hsu CP, et al. Outpatient thoracoscopic limited sympathectomy for
hyperhidrosis palmaris. Ann Thorac Surg. 1999;67:258259.
Krasna MJ. Thoracoscopic sympathectomy: A standardized approach to therapy for
hyperhidrosis. Ann Thorac Surg. 2008;85:S764S767.
Kwong KF, Hobbs JL, Cooper LB, et al. Stratified analysis of clinical outcomes in
thoracoscopic sympathicotomy for hyperhidrosis. Ann Thorac Surg. 2008;85:390393;
discussion 393394.
Li X, Tu YR, Lin M, et al. Endoscopic thoracic sympathectomy for palmar hyperhidrosis: A
randomized control trial comparing T3 and T2-4 ablation. Ann Thorac Surg. 2008;85:1747
Ram R, Lowe NJ, Yamauchi PS. Current and emerging therapeutic modalities for
hyperhidrosis, part 1: Conservative and noninvasive treatments. Cutis. 2007;79:211217.
Sciuchetti JF, Corti F, Ballabio D, et al. Results, side effects and complications after
thoracoscopic sympathetic block by clamping. The monza clinical experience. Clin Auton
Res. 2008;18(2):8083.
Tan V, Nam H. Results of thoracoscopic sympathectomy for 96 cases of palmar hyperhidrosis.
Ann Thorac Cardiovasc Surg. 1998; 4:244246.
Walling HW, Swick BL. Treatment options for hyperhidrosis. Am J Clin Dermatol.
Weksler B, Luketich JD, Shende MR. Endoscopic thoracic sympathectomy: At what level
should you perform surgery? Thorac Surg Clin. 2008;18(2):183191.
Wolosker N, Yazbek G, Ishy A, et al. Is sympathectomy at T4 level better than at T3 level for
treating palmar hyperhidrosis? J Laparoendosc Adv Surg Tech A. 2008;18:102106.

Part VII
Mediastinal Tumors: Thymus

26 Robotic Resection: Thymus

Mahmoud Ismail, Marc Swierzy, and Jens C. Rckert

Thymectomy is one of the rare indications in thoracic surgery. Thymectomy is most
commonly considered to be a part of the complex treatment of myasthenia gravis (MG) and
thymoma. Ectopic thymic tissue can be located at various locations throughout the anterior
mediastinum; therefore, the radicality of thymectomy is crucial for tumor resection and
complete remission of MG. Robotic thymectomy is the latest advancement in the surgery of
the thymus gland. This is primarily due to the fact that it allows for a complete radical
thymectomy, which improves the complete remission rate for MG when compared to the
conventional thoracoscopic technique. The oncologic outcome in terms of overall survival
and thymoma-related survival is promising, but a longer follow-up is needed to consider
robotic thymectomy as a standard approach.
The first robotic thymectomy was published in 2001 though it was only a partial
thymectomy for thymoma in this particular case. In 2003, a complete robotic thymectomy
was described and after that many thoracic centers have started or switched to the robotic
approach. Since that time, there were more than 3,500 robotic thymectomies registered by
Intuitive Surgical.
MG is an antibody-mediated autoimmune disease of the neuromuscular junction. In the
majority of patients (80% to 85%), autoantibodies to the muscle nicotinic acetylcholine
receptor (AChR) are present. These antibodies lead to failure of neuromuscular transmission
with muscle weakness. The minority of MG patients are seronegative for AChR antibodies. A
second category of MG is due to autoantibodies against the muscle-specific kinase (MuSK)
protein. These are present in 3% to 5% of MG patients. Thymectomy is considered for
patients with seropositive AChR and negative for MuSK.
Other factor with relevance for the indication of thymectomy for MG is the clinical
classification according to the Myasthenia Gravis Foundation of America (MGFA). According
to the severity of the MG we distinguish two relevant groups, only ocular form (MGFA I) or
generalized form (MGFA II). According to the meta-analyses from Gronseth and Barohn,
patients with moderate till severe form of generalized MG (MGFA IIb) benefit from the
thymectomy but not the ocular form. However, there is a controversy because 50% of MG
patients initially have only an ocular form which in 50% to 70% of the cases change to
generalized form in the first 2 to 3 years. In this case, a thymectomy is not possible in the first
2 years of the diagnoses of MG where benefit from thymectomy could be reached. Therefore,
and according to retrospective studies, thymectomy is also indicated for patients with ocular
Thymectomy is performed in all age categories according to many studies. Though many
text books restrict the indication to mainly patients between 8 and 60 years there is no

evidence on that. Our series contains successfully selected cases of patients down to the age of
4 years or beyond 60 years up to the age of 85 years.
Surgery is the mainstay of treatment for thymoma. When the tumor is at an early stage
(Masaoka/Koga I through IIB), surgery is the first choice of treatment. If the tumor is
apparently invasive and large (Masaoka/Koga II through III), preoperative (neoadjuvant)
chemotherapy and/or radiotherapy may be used to decrease the size and improve
resectability, before surgery is attempted.
Generally, thymectomy for MG without thymoma is relatively indicated when three of the
following five factors are present: Generalized form of MG, seropositive AChR, suspicious
thymic hyperplasia, initial diagnosis less than 2 years, and patient age between 8 and 60.
There is still doubt on the indication for thymectomy for patients with seronegative AChR
antibodies, ocular MG, and MuSK positive antibodies. However, with the exception of MUSKantibody-positive patients, there is some data that show benefit from thymectomy for these
Due to unstable MG or patients in myasthenic crisis thymectomy always requires
preparation with stabilization of MG by plasma exchange strategies or intravenous
immunoglobulin treatment.
The principal contraindication to the performance of a thymectomy is advanced stage
thymoma (Masaoka III through IVB). However, for Masaoka stage III, resectability should be
judged upon the invaded organs.

All patients with MG should be evaluated by a neurologist, ideally in a center specialized for
MG. All tests to diagnose MG should be reviewed. The antibody status for AChR and MuSK
should be evaluated. All patients should undergo a contrast-enhanced CT scan of the thoracic
cavity. Pulmonary function tests and arterial blood gas analyses are necessary. Beside these
tests all patients have to be checked for operability due to other diseases. Optimally patients
with a thymoma are discussed in a tumor board in large centers.

The Left-Sided Robotic Thymectomy
The left-sided minimally invasive thoracoscopic surgery employing the da Vinci telemetric
robotic system is used. Surgery is performed under general anesthesia with one-lung
ventilation. The patient is placed in a supine position on a vacuum mattress with the
operating table slightly tilted to the right patients side. The left arm is positioned below the
table level with flexion at the elbow. The initial position of the surgeon and his assistant is on

the left side of the patient. The operation field is always prepared and draped for a conversion
to median sternotomy or additional cervical approach or right-sided, thoracoscopy,
respectively. The 12-mm trocar for the binocular camera is placed in the fourth intercostal
space at the left anterior axillary line. A thoracoscopic 10-mm camera with a 30-degree optic
is introduced to evaluate the operation field and help positioning the other two 8-mm trocars.
The cranial trocar is introduced in the third intercostal space whereas the caudal trocar is
located in the fifth intercostal space, both between the anterior axillary line and the
midclavicular line. Thus, all three trocars are placed exactly along the submammary fold. The
special da Vinci trocars are connected with the three robotic arms of the table cart. A
harmonic scalpel is placed in the upper trocar whereas a bipolar forceps in the lower one.

Figure 26.1 Operation field after mobilization of the thymic gland along the left phrenic nerve.

Step 1 (Fig. 26.1): The left phrenic nerve is the point of reference for the dissection of the
thymic gland. The dissection starts caudally in the middle of the pericardium along the left
phrenic nerve. This area is very often completely free of fatty tissue, and the left phrenic
nerve can be well recognized. In some cases, the thymic gland extends below or over the
phrenic nerve. In these cases it is necessary to isolate the phrenic bundle and mobilize the
tissue in the aortopulmonary window completely.
Step 2 (Fig. 26.2): Further dissection is performed cranially along the phrenic nerve till
identifying and opening the cervical pleura at the entrance of the left innominate vein. The
incision of the cervical pleural fold is extended till the median retrosternal line. The
dissection is continued to the right side until the subxiphoid pleural fold is reached. With
blunt gentle dissection the right lung is made visible and is covered only by the right pleura
parietalis. Whenever possible the right pleural cavity should stay closed at that stage of the
operation. This allows for extension of the operation field by insufflation of CO2.

Figure 26.2 Incision of the pleural fold to localize the innominate vein as a guiding structure for the robotic thymectomy.

Figure 26.3 Opening of the cervical compartment of the anterior mediastinum. With the exception of anatomical deviations
the upper poles of the thymic gland are mobilized behind the sternum and in front of the innominate vein. Exceptionally, the
hook is used in this case. The use of harmonic scalpel is recommended.

Step 3 (Fig. 26.3): The upper poles, mobilized after careful dissection of their capsule, are
gently grasped and then pulled down. At the cranial end, the thyrothymic ligament becomes
clearly visible. Under tension of the completely exposed upper thymic pole, this ligament is
severed by ultrasonic dissection or between clip ligatures.
Step 4 (Fig. 26.4): In the majority of cases there are two to four thymic veins. These veins
have to be dissected without tension and injury to the innominate vein. The veins are divided
between clip ligatures while severing seems also to be possible by using the ultrasonic scalpel.
Atypical locations of thymic veins have to be noticed, but they are rare.
Step 5 (Fig. 26.5): The whole median retrosternal tissue portion is mobilized. Often, the
right main thymic lobe may be demarcated from the surrounding fatty tissue. The aortocaval
groove is dissected free and the right lung, only covered by the mediastinal pleura, is
Step 6 (Fig. 26.6): Preparation of the right thymic lobe follows under CO2 insufflation. In
most cases, the right phrenic nerve can be identified. After opening the mediastinal pleura of
the right lung, the right phrenic nerve can be well recognized.

Figure 26.4 The thymic veins are dissected by the harmonic scalpel, for large vessels a clip may be necessary.

Figure 26.5 Dissection of the thymic tissue portion inside the aorto-caval groove, where sometimes a prominent right main
thymic lobe may be found.

The en bloc resected specimen of the thymus with all surrounding fatty tissue is placed in
an endobag and then removed through the middle trocar incisions. The operation field with
the venous confluence, the supra-aortal arteries, and parts of the anterior tracheal wall is
examined for the presence of residual tissue and hemostasis. A chest tube is placed in the left
pleural cavity. Reinflation of both lungs is followed by closure of the trocar incisions.
Technical Note
Thoracoscopic operation technique has been reported in bilateral or unilateral modifications.
Actually the preferred side of unilateral thoracoscopic thymectomy is most frequently
discussed. Both left- and right-sided unilateral robotic thymectomy are feasible. Radical
thoracoscopic thymectomy seems to be better accomplished by the left-sided technique. In
the learning curve and with less experience many surgeons prefer the right-sided technique.
Surgical school, habits, and traditions influence the choice of the procedure. Optimal longterm results require the ability to perform either left- or right-sided technique. Robotic
assistance is the adequate technical refinement for thymectomy.

Figure 26.6 For demonstration of the right phrenic nerve the wristed tips of the instruments, CO2-insufflation, and 3dimensional view is required.

After the operation, the patient is extubated immediately and put on patient-controlled
analgesia. Peridural analgesia is not required. A chest drain is only necessary for a short
postoperative period and may be removed after normal x-ray and with adequate clinical
findings. The hospital stay usually is about 2 to 3 days but may be reduced to 1 day in
selected cases.

The robotic thymectomy has been proven to be feasible and safe. The perioperative morbidity
rate in our series is less than 2%. The general risks of robotic thymectomy include incomplete
removal of the thymic gland, nerve injuries (phrenic nerves, laryngeal recurrent nerves, and
intercostal nerves), and bleeding (innominate vein and tributaries, aortic arch, mammarian
vessels). For complete thymic resection, every single step of the technique needs to be
controlled. If it cannot be completed satisfactorily, an extension of the technique is required.
This does not necessarily mean a conversion as the first step, but the effective use of extra
incisions or trocars. A rapid conversion to sternotomy, however, should be possible at any
time during robotic thymectomy.

The cosmetic results are very acceptable and highly appreciated by the patients. Moreover,
there is no interference with immunosuppression. After robotic thymectomy, a sternotomy
could be easier if necessary in later life. The impairment of the patient by this operation is
minimal. According to our experience the development of chronic pain at the trocar sites is a

very rare condition. Until 2002 we have performed 80 thoracoscopic thymectomies without
robotic assistance. Between 2003 and 03/2013 we performed 335 robotic thymectomies
(Tables 26.1 and 26.2). There are approximately 3,500 robotic thymectomies registered
worldwide between 2001 and 2012. The real number of these operations might be even
larger and is growing rapidly. A literature summary of all published robotic thymectomy
series including more than 20 cases is presented in Table 26.3. A special advantage of robotic
assistance is its practicability even for demanding indications such as small children, obese
patients, and older patients with large amounts of tissue inside the mediastinal area. The
main outcome parameter after thymectomy for MG is the cumulative complete stable
remission rate of myasthenia symptoms. This is prospectively estimated according to the
recommendations of the MGFA. After robotic thymectomy, the cumulative complete stable
remission rate was 58%. This is comparable to the results published by the group around
Jaretzki et al.

TABLE 26.1 Patient Characteristics and Degree of Severity of Myasthenia

Gravis according to MGFAClassification

TABLE 26.2 Results of Robotic Thymectomy, Thymoma-classification, and

Preoperative Morbidity

TABLE 26.3 Literature Summary of Robotic Thymectomy Series Including

More Than 20 Cases

Thymectomy is a rare operation in thoracic surgery. The main indication is MG and
thymoma. The indication for thymectomy should be discussed in a certified interdisciplinary
center for MG and in tumor board for thymoma. The robotic approach seems to have greater
potential for new technical developments than other nonrobotic minimally invasive
procedures. Due to the promising results of the robotic thymectomy, many thoracic surgeons

and neurologists are more convinced of this procedure.

Recommended References and Readings

Masaoka A, Maeda M, Monden Y, et al. [Distribution of the thymic tissue in the anterior
mediastinumstudies on the methods of thymectomy]. Nihon Kyobu Geka Gakkai Zasshi.
Jaretzki A 3rd, Penn AS, Younger DS, et al. Maximal thymectomy for myasthenia gravis.
Results. J Thorac Cardiovasc Surg. 1988; 95(5):747757.
Marulli G, Schiavon M, Perissinotto E, et al. Surgical and neurologic outcomes after robotic
thymectomy in 100 consecutive patients with myasthenia gravis. J Thorac Cardiovasc Surg.
2013;145(3):730735; discussion 56.
Ruckert JC, Swierzy M, Ismail M. Comparison of robotic and nonrobotic thoracoscopic
thymectomy: A cohort study. J Thorac Cardiovasc Surg. 2011;141(3):673677.
Yoshino I, Hashizume M, Shimada M, et al. Thoracoscopic thymomectomy with the da Vinci
computer-enhanced surgical system. J Thorac Cardiovasc Surg. 2001;122(4):783785.
Ashton RC Jr, McGinnis KM, Connery CP, et al. Totally endoscopic robotic thymectomy for
myasthenia gravis. Ann Thorac Surg. 2003;75(2):569571.
Bodner J, Wykypiel H, Wetscher G, et al. First experiences with the da Vinci operating robot
in thoracic surgery. Eur J Cardiothorac Surg. 2004;25(5):844851.
Ismail M, Swierzy M, Ruckert JC. State of the art of robotic thymectomy. World J Surg.
Drachman DB. Myasthenia gravis. N Engl J Med. 1994;330(25):17971810.
Silvestri NJ, Wolfe GI. Myasthenia gravis. Semin Neurol. 2012;32(3):215226.
Gronseth GS, Barohn RJ. Practice parameter: Thymectomy for autoimmune myasthenia gravis
(an evidence-based review): Report of the Quality Standards Subcommittee of the American
Academy of Neurology. Neurology. 2000;55(1):715.
Grob D, Brunner N, Namba T, et al. Lifetime course of myasthenia gravis. Muscle Nerve.
Mineo TC, Ambrogi V. Outcomes after thymectomy in class I myasthenia gravis. J Thorac
Cardiovasc Surg. 2013;145(5):13191324.
Hohlfeld R, Goebels N, Engel AG. Cellular mechanisms in inflammatory myopathies. Baillieres
Clin Neurol. 1993;2(3):617635.
Toker A, Sonett J, Zielinski M, et al. Standard terms, definitions, and policies for minimally
invasive resection of thymoma. J Thorac Oncol. 2011;6(7 suppl 3):S1739S1742.
Eng TY, Thomas CR Jr. Radiation therapy in the management of thymic tumors. Semin Thorac
Cardiovasc Surg. 2005;17(1):3240.
Yuan HK, Huang BS, Kung SY, et al. The effectiveness of thymectomy on seronegative
generalized myasthenia gravis: Comparing with seropositive cases. Acta Neurol Scand.
Ruckert JC, Ismail M, Swierzy M, et al. Thoracoscopic thymectomy with the da Vinci robotic
system for myasthenia gravis. Ann N Y Acad Sci. 2008;1132:329335.
Cea G, Benatar M, Verdugo RJ, et al. Thymectomy for non-thymomatous myasthenia gravis.
Cochrane Database Syst Rev. 2013;10:CD008111.
Keijzers M, Dingemans AM, Blaauwgeers H, et al. 8 years experience with robotic

thymectomy for thymomas. Surg Endosc. 2013. [Epub ahead of print].

Freeman RK, Ascioti AJ, Van Woerkom JM, et al. Long-term follow-up after robotic
thymectomy for nonthymomatous myasthenia gravis. Ann Thorac Surg. 2011;92(3):1018
1022; discussion 2223.
Melfi F, Fanucchi O, Davini F, et al. Ten-year experience of mediastinal robotic surgery in a
single referral centre. Eur J Cardiothorac Surg. 2012;41(4):847851.
Augustin F, Schmid T, Sieb M, et al. Video-assisted thoracoscopic surgery versus roboticassisted thoracoscopic surgery thymectomy. Ann Thorac Surg. 2008;85(2):S768S771.
Cerfolio RJ, Bryant AS, Minnich DJ. Starting a robotic program in general thoracic surgery:
Why, how, and lessons learned. Ann Thorac Surg. 2011;91(6):17291736; discussion 3637.
Castle SL, Kernstine KH. Robotic-assisted thymectomy. Semin Thorac Cardiovasc Surg.
Goldstein SD, Yang SC. Assessment of robotic thymectomy using the Myasthenia Gravis
Foundation of America Guidelines. Ann Thorac Surg. 2010;89(4):10801085; discussion 5
Tomulescu V, Stanciulea O, Balescu I, et al. First year experience of robotic-assisted
laparoscopic surgery with 153 cases in a general surgery department: Indications,
technique and results. Chirurgia (Bucur). 2009;104(2):141150.
Seong YW, Kang CH, Choi JW, et al. Early clinical outcomes of robot-assisted surgery for
anterior mediastinal mass: Its superiority over a conventional sternotomy approach
evaluated by propensity score matching. Eur J Cardiothorac Surg. 2013;45(3):e68e73.
Schneiter D, Tomaszek S, Kestenholz P, et al. Minimally invasive resection of thymomas with
the da Vinci(R) Surgical System. Eur J Cardiothorac Surg. 2013;43(2):288292.

27 Transcervical Thymectomy
Henning A. Gaissert

The transcervical approach to thymectomy (TCT) is almost exclusively reserved for
nonthymomatous myasthenia gravis (MG). TCT is an attractive surgical option because it is
the least invasive approach for an operation to treat generalized weakness with the lowest
reported rate of postoperative myasthenic crisis, the single most concerning disease-specific
morbidity. Detractors of TCT argue that this less invasive technique limits the complete
resection of thymic tissue. There are no prospective randomized comparisons between
thymectomy and medical therapy, and none between the various approaches to the
The practice guideline of the American Academy of Neurology regards thymectomy as an
option to increase the probability of remission or improvement of MG. Complete remission
and clinical improvement of symptom severity have been reported in multiple observational
studies: These provide the basis for selective resection of the gland. Thymectomy for purely
ocular MG is not supported by some neurologists; however, about one half of these patients
later progress to generalized MG; early thymectomy may reduce this proportion.
By inference, thymectomy is also an option in other immunologic disease associated with
thymic hyperplasia, aplastic anemia for example.
TCT has been reported for the resection of selected, small thymomas, an indication not
favored by the author.
TCT may be selected for resection of an intrathymic parathyroid. The resection of
parathyroid adenoma, known or suspected to be located within the mediastinal thymus, has
been recommended at the time of neck exploration, particularly when less than four glands
are found.

Antecedent sternotomy leaves planes obliterated on which the execution of this operation
depends. Prior tracheostomy or neck exploration create obstacles, but do not preclude TCT.
Thymoma, however small or favorable in location, is not an appropriate target for the
cervical approach, no matter whether associated with MG.
Emergent thymectomy for severe MG with respiratory impairment is inadvisable due to the
high risk of postoperative respiratory failure.
Antecedent cervical vertebral operations may lead to severe restriction in the range of neck
extension and obstruct the surgeons view. A different approach should be selected in these

The diagnosis of MG is considered in patients with muscle weakness and easy fatigability and
must be secured by at least one or all three of the following tests: Presence of acetylcholine
receptor antibodies in peripheral blood, a positive edrophonium chloride (Tensilon) test, or
characteristic electromyographic findings in extremity muscles.
The operation has no role in the management of acute, severe MG since postoperative
results as measured in remission or improvement evolve one or more years after thymectomy.
Symptoms of MG should be controlled before thymectomy with cholinesterase inhibitors,
with or without addition of immunosuppressive agents. In preparation for thymectomy,
neurologist and surgeon should mutually consider the prevention of postoperative myasthenic
crisis. The incidence of myasthenic crisis after TCT is reported as 0.7% to 1%, the lowest of
all operative approaches. Intravenous immunoglobulins (IVIG) or plasmapheresis should,
therefore, be administered before the operation only to selected patients at increased risk of
respiratory failure.
To evaluate respiratory muscle function, forced vital capacity (FVC) is useful as a simple
test suitable for bedside comparison early after operation. An FVC of less than 15 to 20
mL/kg, a value extrapolated from other conditions, predicts postoperative respiratory failure.
The most sensitive test of clinical respiratory fatigability, however, is the maximal breathing
capacity (MBC) measured as the product of frequency and volume of breaths during 1
minute. An impaired MBC may initiate the preoperative administration of IVIG or
plasmapheresis, although the precise indication for either treatment in TCT has not been
In every patient undergoing thymectomy for MG, the absence of thymoma should be
confirmed either with chemical shift magnetic resonance imaging or computed tomography.
In the surgeons office, neck mobility and maximal extension are tested to ensure exposure of
the mediastinum during operation. The anesthetic team must be aware of the underlying
diagnosis to plan the respiratory management of MG and avoid depolarizing muscle relaxants.
Following IVIG administration and immediately before operation, a complete blood count is
repeated to exclude hemolytic anemia.

The description follows the technique of Cooper et al.
Correct positioning of the patient on the operative table is critical to surgical exposure and
thus to the success of the operation. The patient is placed supine and the crest of the head is
flush with the top of the table. The arms are padded and tucked at the patients side. An
inflatable bag is placed underneath the shoulders. Once anesthetized, the patient is intubated
with a single-lumen endotracheal tube. The operating table is turned 90 degrees
counterclockwise and the shoulder bag is inflated to achieve maximum neck flexion while the
head remains supported on a head rest. Neck, chest, and upper abdomen are included in the

sterile field.

Figure 27.1 The cervical incision as placed within the contours of the sternocleidomastoid muscles exposes thymus following
separation of the strap muscles.

A short cervical collar incision and subplatysmal flaps extending to manubrium and cricoid
expose the strap muscles; these are divided in midline. Self-retaining Gelpi retractors are
inserted (Fig. 27.1). The surgeon inserts an index finger between sternum and thoracic
thymus to enlarge this plane and gently separate thymus and underlying innominate vein
from the bone. In the neck, the left cervical thymus is commonly observed to be longer while
the right cervical thymus is often short and blunt. Both sides are bluntly mobilized using
peanut gauze at the tip of a short clamp. The superior pole vessels are isolated, ligated with
silk ties, and divided. The cervical thymus is lifted from its bed down to the thoracic inlet.
Intraoperative Positioning
To expose the mediastinum to the surgeon (and, unfortunately, only the surgeon), Gelpi
retractors are removed. A right-angle blade, part of the Cooper thymectomy retractor (Pilling
Company, Ft. Washington, PA, Fig. 27.2), is inserted behind the manubrium and suspended
on a cross bar. The cross bar and its supporting poles are placed by the surgeon precisely
above the manubrium. The manubrial blade is lifted and secured on the bar, with the
patients head still supported on a rest; the head should not be floating (Fig. 27.3). The rubber
bag lifting the shoulders is now deflated to open the thoracic inlet. Two Parker retractors,
available from various sources, are inserted to retract the skin and kept in place by a loop
fashioned of two 1-in Latex Penrose drains; non-Latex drains do not possess sufficient
extensibility. The other end is hooked on the side rail of the operating table.

Figure 27.2 The components of the Cooper thymectomy retractor (Pilling Company, Ft. Washington, PA): Manubrial
retractor on crossbar with hinges detached from both lateral posts, Parker retractors, and clamps to anchor the posts.

Figure 27.3 The inserted manubrial retractor lifts the sternum to open the thoracic inlet. Note support of the head in neck
extension. The Parker blades are inserted and retracted by a latex loop.

The surgeon, seated with a headlight above the patients head, establishes by dissection
whether both poles of the thymus are located anterior to the innominate vein; venous
branches are also identified. Sometimes, the left thymus passes underneath the vein; this
variant requires recognition and dissection at this time.
The accurate division of thymic veins and the complete removal of the gland are the central
technical issues. With gentle traction on the ligatures, the cervical thymus is pulled forward
and handed to the first assistant. The venous branches entering the top and anterior faces of
the vein are sequentially identified and encircled with thin silk ties (Fig. 27.4). While clips
seem desirable, they are easily dislodged during the subsequent dissection in front of the vein;
all branches are, therefore, individually ligated. A tonsil sponge is used to expose these
branches. Those entering the lower surface of the innominate vein are ligated last.

Figure 27.4 Surgeons view of the mediastinal dissection during separation of the thymus from the innominate vein. Note
retraction of the superior thymic pole ties by the assistant and depression of the innominate vein with a tonsil sponge.

Returning the thymus to its bed covering the vein, the mediastinum is entered with two
tonsil sponges, one to fix the gland with gentle downward pressure, the other to separate both
pleurae and the pericardium from the gland. A systematic approach begins to separate the
thymus from pleura and pericardium (Fig. 27.5) on one side, establishes the lower extent of
the gland and ends on the other pleura. Pericardial fat is excluded, while the fatty tissues of
the aortopulmonary window close to the left phrenic nerve are cautiously included. The gland
is then folded off the pericardium with judicious use of electrocautery.
The gland is delivered into the wound and marked with respect to side so pathologic
findings may be correlated. The mediastinum is checked for bleeding and any violation of the
pleural space. The neck incision is closed in layers. The lungs are inflated just before the
platysma is closed.

Figure 27.5 Below the innominate vein, the thymic gland is separated from pleura and pericardium with blunt dissection.

Following recovery from anesthesia, patients are usually discharged on the day of operation
unless postanesthetic symptoms require overnight observation. A chest radiograph is

Total rates of complications are below 10%. Myasthenic crisis, postoperative respiratory
failure due to muscle weakness, is the most severe occurring in one series once in 100
consecutive patients and in another series once in 151 patients; both patients responded to
treatment. The incidence of myasthenic crisis is thus either the lowest or among the lowest
among the reported approaches.
Uncontrolled intraoperative bleeding is not reported in clinical series. The management of
bleeding from thymic branches or the innominate vein consists of compression of the
bleeding vessel and passage of ties around the branch. Bleeding from the innominate vein
itself, not previously encountered by the author, may be controlled either with Swedish
DeBakey clamps on either side of the injury or after passage of vascular tapes around the
vein; sternotomy or transfusion should remain an exception.
Pneumothorax is occasionally observed and may require aspiration when symptomatic.

The outcome measures after thymectomy for MG are (1) complete remission referenced to
follow-up period; (2) improvement in the Osserman classification, a severity measure of MG
consisting of five grades originally proposed as a pretreatment assessment (Table 27.1).

Calhoun et al. reported operative results in 78 patients who underwent TCT more than 12
months before assessment; the mean Osserman grade improved from a preoperative 2.73 to
0.94 after a mean of 5-year follow-up. The need for pyridostigmine declined from 90% to
54%, whereas the proportion of patients receiving prednisone decreased from 33% to 27%
and the mean dose from 27 to 16 mg per patient. While more than half of all patients had
thymic hyperplasia, 80% of preoperative prednisone use was observed in patients with
involuted glands.
Khicha et al. observed 151 patients after extended TCT over a mean interval of 53 months.
The KaplanMeier estimates of complete stable remission were 33% at 3 and 35% at 6 years.
When they included asymptomatic patients on low-dose, single immunosuppressive therapy
in their definition of complete remission, the rates were 43% at 3 and 45% at 6 years. These
results were preserved in the patients with longer follow-up.
DeFilippi et al. reported TCT in 53 selected patients with MG with a mean follow-up of 4.3
years. Freedom from symptoms was observed in 81% and 43% (9 of 21) were in complete
remission 5 or more years after operation. Thymectomy within the first year after onset of
symptoms was associated with a higher rate of improvement or remission.

TABLE 27.1 Modified Osserman Classification[s3]

In summary, TCT is a minimal invasive technique of thymectomy that is followed by a
consistent response to treatment with improvement of symptoms in a large majority of
patients and complete remission in 30% to 40% of patients. Comparisons with medical and
alternative surgical therapy are pending. The technique requires most attention during the
ligation of thymic branches of the innominate vein and in the clear separation of the tissues
that are, and are not, part of the specimen. Maximal mediastinal dissection should not be
attempted via a cervical incision.

Recommended References and Readings

1. Gronseth GS, Barohn RJ. Practice parameter: Thymectomy for autoimmune myasthenia
gravis (an evidence-based review): Report of the Quality Standards Subcommittee of the
American Academy of Neurology. Neurology. 2000;55(1):715.
2. Monsul NT, Patwa HS, Knorr AM, et al. The effect of prednisone on the progression from
ocular to generalized myasthenia gravis. J Neurol Sci. 2004;217(2):131133.
3. Deeb ME, Brinster CJ, Kucharzuk J, et al. Expanded indications for transcervical
thymectomy in the management of anterior mediastinal masses. Ann Thorac Surg.

4. Powell AC, Alexander HR, Chang R, et al. Reoperation for parathyroid adenoma: A
contemporary experience. Surgery. 2009; 146(6):11441155.
5. Khicha SG, Kaiser LR, Shrager JB. Extended transcervical thymectomy in the treatment of
myasthenia gravis. Ann N Y Acad Sci. 2008;1132:336343.
6. Calhoun RF, Ritter JH, Guthrie TJ, et al. Results of transcervical thymectomy for
myasthenia gravis in 100 consecutive patients. Ann Surg. 1999;230:555561.
7. Inaoka T, Takahashi K, Mineta M, et al. Thymic hyperplasia and thymus gland tumors:
Differentiation with chemical shift MR imaging. Radiology. 2007;243:869876.
8. Tsukada H, Sunkara R, Dorcas DC, et al. Intravenous immunoglobulin-induced hemolytic
anemia following thoracoscopic thymectomy for myasthenia gravis: Case report. Ann
Thorac Surg. in press.
9. Cooper JD, Al-Jilaihawa AN, Pearson FG, et al. An improved technique to facilitate
transcervical thymectomy for myasthenia gravis. Ann Thorac Surg. 1988;45:242247.
10. DeFilippi VJ, Richman DP, Ferguson MK. Transcervical thymectomy for myasthenia
gravis. Ann Thorac Surg. 1994;57:194197.

28 Transsternal Thymectomy for Invasive Thymoma and

Thymic Carcinoma
John C. Kucharczuk

Controversy surrounds the selection of the surgical approach to thymectomy. Clearly, the
emergence and refinement of minimally invasive procedures has challenged the routine
application of transsternal thymectomy. Patients with nonthymomatous myasthenia gravis
likely benefit from a minimally invasive approach as long as the resection is complete.
Similarly, patients with small, well-encapsulated thymomas are likely good candidates for
minimally invasive approaches. In our current practice patients with large (>5 cm), wellencapsulated thymomas, patients with clearly invasive lesions who are pretreated with
chemotherapy, and all patients with thymic carcinoma undergo a transsternal thymectomy.
Figure 28.1 shows the pre- and post-treatment images of a patient who is offered a
transsternal resection. This approach allows for easy resection of concomitant involved
structures such as lung, chest wall as well as major vascular structures requiring resection and
possible reconstruction. Table 28.1 summarizes our current approach to thymectomy based
on the clinical situation.
There are no major contraindications to transsternal thymectomy. In patients with prior
cardiac surgery it is important to know the route of any coronary grafts and their proximity
to the inner table of the sternum and the thymoma. These patients should be approached in
the same way one would approach a redo sternotomy for cardiac surgery. The graft location
should be mapped out preoperatively with either coronary catheterization or CT angiogram. I
prefer CT angiogram. The sternum must be opened carefully to avoid damage to any
underlying patent grafts. Cardiopulmonary bypass should be available and a plan must be in
place should replacement of coronary graft be required either due to injury opening the
sternum or due to tumor involvement.
Patients with pectus excavatum can present a challenge. In my experience I have performed
transsternal thymectomy with no attempt to repair the pectus resulting in satisfactory
outcomes. The lack of working domain makes minimally invasive approaches difficult in
these cases although some have reported sternal lift type procedures, which may be
applicable and may allow for adequate working domain.

Figure 28.1 CT scan of the chest showing a patient with a thymic carcinoma. A: Shows the initial presenting scan and (B)
shows the postchemotherapy scan. The patient subsequently underwent complete resection including partial resection of the
sternum and right anterior chest wall. He was reconstructed with a combination of mesh and methylmethacrylate, which was
covered with a pedicled muscle flap.

All patients should have a CT scan with intravenous contrast. With large, poorly encapsulated
lesions suggestive of invasive thymoma or thymic carcinoma the patient undergoes a
preoperative biopsy either by CT-guided needle biopsy or by anterior mediastinotomy
(Chamberlain procedure) followed by preoperative chemotherapy. Following chemotherapy
treatment patients undergo repeat enhanced CT scan prior to definitive resection for planning
purposes. In these situations attention is focused on the possible need for vascular
If not already performed we also obtain acetylcholinesterase antibodies in all patients
undergoing thymectomy. These tests can be helpful in uncovering patients with impeding
myasthenia gravis despite noticeable symptoms. As part of the preoperative discussion we
always inform patients that a percentage of patients with thymoma and no symptoms of
myasthenia gravis may develop the disease later in life.

TABLE 28.1 Current Surgical Approach to Thymoma Based on Clinical


Clinically, many large thymomas are phrenotropic. Although most, none myasthenic
patients can tolerate a neuropraxia or paralysis of a single phrenic nerve, this can have
catastrophic effects in the myasthenic patient. The possibility of phrenic nerve injury should
be discussed with all patients undergoing thymectomy by any approach.
Patients undergo preoperative pulmonary function testing. In myasthenia patients these
serve as a base line; following the force vital capacity postoperatively to ensure adequate
muscle strength for unassisted respiration.
As mentioned above, patients with prior coronary artery bypass surgery undergo graft
mapping to determine the location and patency of each graft. Completely occluded grafts,
which are involved with an invasive thymoma or thymic carcinoma, can be sacrificed. Patient
grafts coursing through or inseparable from the thymoma must be bypassed.

The patient is brought to the operating room receives routine prophylactic antibiotics and
preinduction subcutaneous heparin for DVT prophylaxis. For myasthenic patients the
anesthesia team, surgical team, and nursing team review the list of contraindicated drugs in
the preoperative meeting to assure they are not administered during or after the case. General
anesthesia is administered and the patient is intubated with a left-sided double-lumen
endotracheal tube. The tube is positioned for isolated lung ventilation with the help of a
pediatric bronchoscope to allow for lung isolation if required during the resection.
The patient is placed in a supine position with the arms tucked at the sides. A roll is placed
length wise under the shoulder blades to extent the neck and drop the shoulders. For
particularly large difficult lesions and for those patients with prior sternotomy the groins are
prepped into the field and additional arterial or venous access should be acquired. When the
lesion appears to involve the superior vena cava, caval atrial junction, or the innominate vein
I always place intravenous access above and below the diaphragm, so that intravenous
medication can be administered during times of intermittent caval clamping. For complex
caval reconstruction, which requires more than a side-biting caval clamp with partial
occlusion or a short complete clamping cavalatrial bypass, should be considered to avoid
cerebral congestion due to venous outflow occlusion.
For lesions abutting the innominate artery, I usually place a right radial arterial line and a
femoral arterial line to allow for monitoring of arterial blood pressure during innominate
arterial reconstruction. The right radial arterial wave can also help document reestablishment
of flow through and adequate reconstruction.
The chest is depilated with an electric clipper. The skin is prepared with 3M DuraPrep
Surgical solution (iodine povacrylex and isopropyl alcohol) patient preoperative skin
preparation. The drapes are applied. A midline sternal skin incision is made from the Angle of
Louis to just above the tip of the xiphoid. Electrocautery is used to achieve hemostasis and

the midline of the sternum is scored. An army-navy retractor is used to retract the skin and
soft tissue in a cephalad direction above the sternal notch. The sternal notch is developed
with electrocautery and finger dissection to develop a pathway above the suprasternal
ligament. The midline of the sternum is found by palpation and the periosteum of the sternal
midline is scored with cautery. Ventilation is temporarily suspended and the sternum is
opened in the midline with a sternal saw. Upward lifting on the sternal saw minimizes the
risk of injury to the pleura and underlying mediastinal structures. Once the sternum is open,
electrocautery is used to achieve hemostasis along the inner and outer bony tables of the
sternum. I avoid the application of bone wax or any other foreign material to achieve
Sternotomy for resection of a mediastinal mass after prior cardiac surgery presents requires
special attention. First and foremost is to be sure that the target lesion is a thymoma and not
a pseudoaneurysm from prior surgery; with modern imaging and preoperative biopsy
techniques this confusion should not occur. The techniques for redo sternotomy are well
described in the cardiac surgery literature. The major tenants of redo sternotomy are the
avoidance of injury to mediastinal structure directly underneath the sternum and the
complete resection of the thymic mass. Cardiac bypass is immediately available for these
cases and in particularly difficult cases the arterial and venous groin cannula are placed prior
to any attempt at opening the sternum. The previous sternal wires are left in place as a depth
guide and an oscillating saw is used. The final inner table of the sternum is opened below
with a heavy scissors. In these complex cases it is probably best to have a joint surgical team
including an experienced thymic surgeon and a cardiac surgeon skilled at redo operations.
Once the sternum is open and the retractors are placed attention is turned toward
resection. I start my dissection as inferiorly as possible; usually at the right inferior pole,
sweeping up all the mediastinal contents with the dissection just superficial to the plane of
the pericardium. Laterally, the dissection extends out to the pleural envelope. I avoid
dissection around the main lesion and division involved structures until the final step in the
procedure. Next I identify the innominate vein. If the vein is involved and requires resection,
this is left for later in the procedure and we continue on to dissect out the cervical poles of
the thymus. The cervical poles are followed up to their distal extent in the neck and tagged
with silk sutures for retraction both for later pathologic orientation and for intraoperative
Finally, I turn my attention to the main lesion and the surrounding structure. If the lesion is
adherent to the pericardium, no attempt is made at separation. A wide en bloc resection of
the pericardium is performed. The pericardium is not reconstructed. In cases involving the
innominate vein, the vein is generally divided with vascular staplers proximal and distal to
the lesion with vascular staplers. No attempt at repair is made, accepting some postoperative
upper extremity swelling, which responds to elevation and usually resolves as collateral
venous pathways open. Innominate arterial involvement with resection is best reconstructed.
A prosthetic ringed graft is used.
Superior vena cava involvement requires special mention. Although clamping of a partially
occluded SVC is usually well tolerated, prolong complete clamping may cause intracranial
edema and bleeding due to increased cerebral venous pressure. The increase in pressure is
evident by the cyanotic facies patients develop under the drapes. Rapid clamping can also

cause cardiovascular collapse due to acute decreased venous return to the right heart.
Working closely with the anesthesia team, fluid administration and vasoconstrictive agents
are used to increase the mean arterial blood pressure and normalized the brain arterial
venous pressure gradient. The surgical team should also have a low threshold for
intraoperative shunting or venoveno bypass during particularly complex or lengthy
reconstruction. Figure 28.2 shows the CT scan of a patient with an invasive thymoma
following preoperative chemotherapy who required atrialcaval reconstruction at the time of

Figure 28.2 Post chemotherapy, presurgical CT scan showing invasion into the superior vena cava, which extended down to
the level of the right atrium.

Figure 28.3 Post chemotherapy, presurgical CT scan showing an invasive thymoma with phrenic nerve involvement. A: The
scout films show elevation of the left diaphragm consistent with phrenic nerve paralysis, (B) the axial image shows the
primary lesion, which was completely removed via a transsternal approach including resection of the left phrenic nerve.

It is not uncommon for large invasive lesions to grow through the pleural envelope and into
the adjacent lung. In most cases en bloc wedge resection with a generous gross margin is all
that is required. Infrequently, a formal anatomic lung resection is required, which,
nevertheless, can easily be performed from via the anterior approach through a sternotomy.
The phrenic nerves are at risk especially with large thymomas, which seem to have a
predilection to abut, invade, and grow around the phrenic nerve. The most common place to
injure the phrenic nerve is at the cephalad extent where it is in close proximity to the origin

of the internal mammary arteries. To avoid injury I do not use electrocautery in these
locations. When the thymic mass extends into the pleura at these locations I widely open the
pleural space, locate the phrenic nerve lower in the chest, and follow it back up to the area of
concern to avoid injury. The second most common location to injure the phrenic is lower
down in the chest when the mass extends laterally over the pericardium. Often an
intraoperative decision must be made as to whether or not to sacrifice the phrenic nerve or
peel the lesion off the phrenic hoping that function will return. The decision is easier when
the phrenic nerve is invaded by tumor, it is inseparable surgically and the diaphragm is
paralyzed preoperatively as shown in Figure 28.3. I generally will sacrifice one phrenic nerve
in a nonmyasthenic patient if I am confident that the resection will be complete. In patients
with myasthenia I will not resect the phrenic nerve accepting a slightly higher risk of local
recurrence. Instead I sharply dissect of the lesion sparing the nerve along its entire course.
When the phrenic nerve is sacrificed, I do not perform diaphragmatic plication at the time of
the sternotomy and I have not had any instance of patients requiring later plication.
Consideration of nerve grafting is possible, but I have not had any experience with the
application of these techniques.
Once the specimen is resected it is oriented for the pathology. The orientation is
particularly important for postoperative radiation treatment should pathologic areas of
invasion and/or positive surgical margins be confirmed microscopically. A photograph is
generally taken as shown in Figure 28.4 utilizing either a hand-drawn background or a
standardized mediastinal board for use in postresection treatment planning.
I open both pleural spaces and examine for unsuspected pleural drop metastasis. A single
soft Blake drain is placed across the mediastinum crossing both pleural spaces. The sternum is
closed with sternal wires and the remaining incision is closed in layers. The patient is
extubated in the operating room and transported to our thoracic surgical unit for
postoperative care.

Figure 28.4 Images show resected invasive thymomas following pretreatment with chemotherapy. The specimens are
photograph for orientation and the pictures are placed in the patients electronic medical record should postoperative
radiation planning be needed. A: Demonstrates a specimen, which included resected lung as well as the midportion of the
innominate vein. It is oriented on a hand-drawn picture to document the associate with nearby structures. B: Demonstrates a
specimen oriented on a standard medisatinal board.

The mediastinal tube is placed to a Pleuravac drainage system. The tube is maintained on
suction for 24 hours and then converted to water seal. Once the drainage tapers off the tube
is removed, usually at 48 to 72 hours. Patients are generally discharged 24 hours following
tube removal to allow for titration of pain medications. They are restricted from heavy lifting
and twisting exercises and athletics for 6 weeks.

Complications are best divided into acute and long term. The most common acute
complication is bleeding requiring reexploration. Fortunately this is rare especially in the
absence of vascular reconstruction. Respiratory complications occur but can be avoided by
very aggressive pulmonary physiotherapy and early ambulation, which is instituted on the
morning following surgery. Special attention is required in the myasthenia patient who
should be restarted on all preoperative medications especially mestinon and
immunosuppression. Dose timing of these drugs can be critically important in the brittle
myasthenic and a well-informed nursing staff is essential. A number of commonly
administered drugs can initiate a myasthenic crisis. A current list of contraindicated

medications in myasthenia is kept updated by the pharmacist on the thoracic surgical unit
and reviewed with all house staff and nurses caring for these patients.

The results following transsternal resection of a large thymoma are driven by on the stage of
disease and the completeness of resection. In early-stage disease with smaller lesions
minimally invasive techniques probably provide similar outcomes to transsternal resection. In
more advanced-stage disease with larger lesions, local invasion, and/or preoperative
treatment the transsternal approach provides outstanding exposure with the opportunity to
carry out a complete resection.

Thymectomy for nonthymomatous myasthenia is probably best approached through
minimally invasive techniques (VATS, robotic, transcervical).
Thymectomy for small thymomas with or without myasthenia can be approached
successfully with either minimally invasive techniques or a transsternal approach (full or
partial sternotomy) with good results.
Patients with large thymomas (>6 cm), thymomas invading adjacent structures, and those
pretreated with chemotherapy are probably best served by transsternal thymectomy.

Recommended References and Readings

Detterbeck FC, Moran C, Huang J, et al. Which way is up? Policies and procedures for
surgeons and pathologists regarding resection specimens of thymic malignancy. J Thorac
Oncol. 2011;6(7 suppl 3):S1730S1738.
Hamdi S, Mercier O, Fadel E, et al. Is sacrificing the phrenic nerve during thymoma resection
worthwhile? Eur J Cardiothorac Surg. 2014;45(5):e151e155. doi: 10.1093/ejcts/ezu025.
Epub 2014 Feb 23.
Huang J, Detterbeck F, Wang Z, et al. Standard outcome measures for thymic malignancies. J
Thorac Oncol. 2010;5(12):20172023.
Manoly I, Whistance RN, Sreekumar R, et al. Early and mid-term outcomes of trans-sternal
and video-assisted thoracoscopic surgery for thymoma. Eur J Cardiothorac Surg.
Ruffini E, Detterbeck F, Van Raemdonck D, et al. Thymic carcinoma: A cohort study of
patients from the European society of thoracic surgeons database. J Thorac Oncol.

Mediastinal Tumors: Neurogenic

29 Posterior Neurogenic Tumors VATS/Open

Frank C. Detterbeck and Andrew T. Arndt


This chapter addresses the clinical approach to and management of posterior mediastinal
tumors in adults. The majority of these are neurogenic tumors, and conversely most
neurogenic tumors are in the posterior mediastinum. Various benign systemic conditions can
also cause posterior mediastinal abnormalities, such as tuberculous vertebral infections and
hematopoietic disorders (e.g., sickle cell anemia, thalassemia). These conditions are generally
obvious from the clinical presentationthe posterior mediastinal/vertebral lesions are
usually noted secondarily when the diagnosis of an infection or hematopoietic disorder is
already clear. Therefore, the features and management of these conditions are not addressed
here; interested readers are referred to internal medicine textbooks or other specialty books.
This chapter provides a structure for how to approach the assessment and management of a
patient with a posterior neurogenic lesion presenting for evaluation. The approach starts with
making a clinical diagnosis and assessing the likelihood that this is correct. These factors
guide the need for further investigations and eventually management of the condition.
We have taken a clinically oriented approach, using readily available information (e.g.,
age, gender, symptoms), leading to a presumptive diagnosis and eventually to a final
diagnosis and management strategy. This is opposite to most publications, which start with a
known specific diagnosis and use this to estimate the age, gender, etc. of a cohort of such
The most fundamental issue is whether a posterior mediastinal mass is benign or
malignant. A more detailed question is which additional tests (imaging, biopsy) are needed to
efficiently and sufficiently confirm the initial diagnosis. This includes deciding how certain
and detailed one must be in to develop an appropriate management plan.
Details of a management plan may require investigation of particular aspects of the
condition (e.g., Is there extension through a neural foramen?). While some imaging tests can
help solidify a diagnosis as well as identify features that impact details of management, it is
better to maintain a structured approach to patient evaluationnamely, to separate thinking
through what the likely clinical diagnosis is, what (if anything) is needed to sufficiently
confirm this, and what details need to be defined to carry out the management plan. Because
posterior mediastinal masses are uncommon, most physicians have not evolved to an
internalized routine in how they approach patients. Therefore, a structure for how to think
through the approach to patients is needed. This prevents getting sidetracked by details and
questions that are not germane to a particular patient at a particular point in the evaluation

Definition of Posterior Mediastinum

Dividing the mediastinum into compartments has proven useful in the evaluation of
mediastinal masses, but these have been defined in many ways. The International Thymic
Malignancy Interest Group (ITMIG) has recently developed a modern, computed tomography
(CT)-based international standard.1 This schema defines the paravertebral (posterior)
compartment as bounded by the thoracic inlet, the diaphragm, the chest wall posteriorly, the
tip of the transverse processes laterally, and anteriorly a line 1 cm behind the anterior border
of the vertebral bodies. The contents of the posterior mediastinum include sympathetic
nerves, intercostal nerves and ganglia, azygos and hemiazygos veins, and posterior intercostal
arteries and veins. Tumors may arise from any of these structures, but the most common
primary tumors of the posterior mediastinum are neurogenic tumors, arising from the
sympathetic chain, paraganglionic cells, intercostal nerves, or nerve sheath cells.
Posterior neurogenic tumors are often classified by tissue of origin and as benign or
malignant, thus defining four groups (Table 29.1). In adults, most posterior neurogenic
tumors are of nerve sheath origin (Fig. 29.1); however, the cell of origin has no clinical
importance. The key feature is that the vast majority are benign. In children, most posterior
neurogenic tumors are malignant, especially in younger age groups (Fig. 29.2). Because
general thoracic surgeons deal largely with adults, this chapter does not address the distinct
group of tumors encountered in children.
Natural History
An understanding of the natural history (i.e., course without treatment) of posterior
neurogenic tumors is important in defining a management algorithm. There is limited direct
data because these tumors are rare and immediate resection has been the traditional
approach. Recurrence and survival data from case series of treated patients with adequate
long-term follow-up can also provide some insight.
Malignant Lesions
Malignant posterior neurogenic tumors in adults carry a very poor prognosis if left untreated.
The more common malignant neurogenic tumors, such as malignant schwannomas, are
typically quite aggressive. The natural history of untreated patients has not been reported.
The survival after treatment attempts is generally short with patients developing a recurrence
and/or dying in 2 to 18 months.24 Only 14 cases of adult mediastinal neuroblastoma have
been reported, with only three of these occurring in the posterior mediastinum.5 The time to
recurrence is generally only a few months.6 Inference drawn from this limited data is that
untreated lesions portend a progressive course with early mortality, likely within 1 year.

TABLE 29.1 Classification of Posterior Neurogenic Tumors

Figure 29.1 Proportion of posterior mediastinal tumor types by decades of age in adults. Legend: N/GNblastoma,
neuroblastoma/ganglioneuroblastoma; PNET, primitive neuroectodermal tumor. Reproduced with permission from
Detterbeck: Mediastinal Tumors.32

Benign Lesions
Limited data corroborates the conventional wisdom that benign neurogenic posterior
mediastinal lesions are very indolent. Benign tumors have a very low recurrence rateeven if
incompletely resected; for example, one recurrence occurring 4 years after an incomplete
resection was reported out of 87 resected benign posterior neurogenic tumors.2 Four other
incompletely resected benign lesions in this series did not recur during 10 years of follow-up.2
Experts in these tumors have remarked that resection of benign lesions has no influence on
patient survival although they recommend resection of benign lesions.2,7
There is limited data on observation of posterior neurogenic tumors in patients deemed to
be too high risk for resection. No progression was noted over 5 years of observation in a
patient with chronic rejection of a transplanted kidney with foraminal extension of a
posterior neurogenic tumor.8 In another series of neurogenic tumors (in various locations, not
only thoracic), six tumors that were considered benign based on positron emission
tomography (PET) activity were observed and were all found to be unchanged at a median
follow-up of 17 months.3

Figure 29.2 Proportion of posterior mediastinal tumor types by age in children and adolescents. Legend: N/GNblastoma,
neuroblastoma/ganglioneuroblastoma; PNET, primitive neuroectodermal tumor. Reproduced with permission from
Detterbeck: Mediastinal Tumors.32

In conclusion, anecdotal data suggests that growth occurs in only a minority of benign
neurogenic tumors during several years of observation.
Specific Clinical Questions
The traditional recommendation has been to resect all posterior mediastinal neurogenic
tumorseven if benignbecause of concern about malignant degeneration or complications
due to growth. However, to appropriately apply these arguments it is necessary to define how
high the risk of these events actually is.
What Is the Risk of Malignant Degeneration?
Papers justifying resection of benign neurogenic tumors because of a risk of malignant
degeneration invariably provide no data or references. An extensive literature search revealed
no well-documented benign neurogenic tumor that became malignant in adults without
neurofibromatosis. Several case reports of malignant degeneration of neurogenic tumors
involve either children, tumors of other areas of the body, or tumors not arising
spontaneouslyfor example, after prior irradiation of a neuroblastoma or in an
immunocompromised patient.911 One case report12 of a thoracic neurogenic tumor in an
adult speculated about malignant degeneration because it involved a composite tumor with
features of ganglioneuroma as well as neuroblastoma; however, this could also be a
manifestation of the heterogeneity of tumors or spontaneous maturation from neuroblastoma
to ganglioneuroma, as has been described.13
Another case14 involved a malignant neuroblastoma that developed at the site of a
previously resected benign retroperitoneal ganglioneuroma 11 years earlier. Local control was
achieved with partial reresection and radiation, but eight years later a metastasis at a
separate site was found. It was argued that this might represent malignant transformation
because it would be unlikely to have had two distinct tumors, and the typically rapid growth
of neuroblastoma makes it unlikely, this was a present but missed component in the original
tumor. However, this case is very atypical because the indolent behavior (metastasis after 8
years) and the age at diagnosis (age 32) are highly unusual for a neuroblastoma.
Therefore, malignant degeneration of a benign neurogenic tumor is not clearly documented

in the literature in patients without neurofibromatosis, and such speculation rests on

anecdotal cases of composite tumors and one potential case report in which the malignant
tumor exhibited unusual (indolent) behavior. The argument for resection of benign
neurogenic tumors because of potential malignant degeneration must be viewed as not being
clearly substantiated.
What Is the Risk of Development of Symptoms/Clinical Problems?
An extensive literature search revealed no series of prolonged observation of benign
neurogenic tumors that allow estimation of a rate of growth and subsequent development of
complications. The lack of case reports of patients eventually resected after initial observation
suggests that the rate of growth and development of symptoms is rare. Thus, the potential for
clinically significant growth is not well defined but appears likely to be rather low.
A rational argument can be made to resect asymptomatic lesions that involve the spinal
canal, given the potentially major consequences if one waits for symptoms to develop.
Whether careful surveillance with regular imaging is a safe alternative is not documented in
the literature.
What Is the Risk of Malignant Neurogenic Tumor in Patients With Neurofibromatosis?
Patients with familial neurofibromatosis who have intrathoracic tumors present a unique
clinical challenge. The lifetime incidence of a malignant peripheral nerve sheath tumor is 2%
to 5% in this population, as compared to 0.001% in the general population.15 Nordback et al.
suggest a 10% risk of malignancy in intrathoracic neurogenic tumors in patients with
neurofibromatosis16; they additionally surmise that surgical trauma may induce malignant
transformation based on cases of early appearance of malignant tumors at the site of
previously completely resected benign tumors.16 Finally, malignant neurogenic tumors in
these patients are said to have higher rates of local recurrence, distant metastases and worse
overall survival.17

Making a Clinical Diagnosis

The first step in approaching patients is to establish a presumptive clinical diagnosis and an
assessment of how confident one can be of this. The primary clinical issue is knowing when to
suspect malignancy. Specific characterization of benign lesions has no clinical relevance.
Potential factors to help identify malignancy are reviewed in the next sections.
Demographic Features
Demographic features are of little benefit in defining the nature of a posterior mediastinal
mass in adults. Posterior neurogenic tumors occur with similar frequency in all ages from
infancy to the eighth decade of life.8 While the probability of malignancy is high in children
(40% overall, 100% if under age 2 years; Fig. 29.2),8 it is 1% to 6% in adults and is
relatively constant across all adult ages (Fig. 29.1).7,17
Posterior neurogenic tumors occur equally in men and women; this is true of malignant
tumors as well.8 Small differences exist in the incidence of specific benign tumors, but this
has no clinical impact (e.g., ganglioneuromas are slightly more common in men and nerve
sheath tumors slightly more common in women).2

Medical History
In patients with a posterior mediastinal mass one should specifically ask about a history of
neurofibromatosis and look for superficial signs such as caf au lait spots or subcutaneous
neurofibromas. While neurofibromatosis is associated with 14% of posterior neurogenic
tumors overall, it is present in roughly one-half of all cases with malignant tumors.2 In
addition, neurofibromas in the setting of neurofibromatosis classically carry a risk of
malignant transformation (to be discussed in further detail). However, these rates still imply
that in patients with neurofibromatosis the vast majority (85%) of posterior mediastinal
tumors will be benign.
Posterior mediastinal masses in adults are often detected incidentally on imaging for other
reasons. Only 12% to 37% of patients present with symptoms,2,4,8,18 typically related either
to neurologic compromise of the spinal cord or local intrathoracic mass effect (chest pain,
Horner syndrome, cough, dyspnea, or dysphagia).
Symptoms Suggestive of Malignancy
The presence of symptoms in general is not a significant predictor of malignancy in adults,
nor does the absence of symptoms guarantee benignity. (In children, absence of symptoms is
a statistically significant predictor of benignity). However, pain or dyspnea specifically was
found to be highly indicative of a malignant tumor in adults.2
Symptoms Suggestive of Spinal Involvement
The presence of neurologic symptoms correlates with the likelihood of intraspinal tumor
involvement (so-called dumbbell tumors connected by a thin isthmus extending through a
neural foramen). However, about 40% of patients with intraspinal tumors have no neurologic

Figure 29.3 Benign and malignant neurogenic tumors. A: Benign neurogenic tumor with bony erosion, widening of the
foramen, and extension into the spinal canal. None of these signs are associated with malignancy. B: Ganglioneuroblastoma
in an adult. The large size is associated with a likelihood of malignancy.


A study of CT imaging of posterior neurogenic tumors in 68 adults identified four imaging
features that were associated with malignancy: (a) Size >10 cm (malignancy in almost all
patients), (b) bone destruction (four out of four patients), (c) pleural effusion (two out of two
patients), and (d) mediastinal displacement (one out of two patients).2 However, while bone
destruction was strongly predictive of malignancy, some degree of bony abnormality was
noted in 32% (22/68); these findings include erosions, splaying of the ribs, foraminal
enlargement, or localized scoliosis and were not associated with malignancy (Fig. 29.3A,B).2
MRI is an accurate test to assess for a dumbbell tumor.21 Because CT may miss an intraspinal
component,20 MRI is indicated whenever the tumor is contiguous with a neural foramen,
there is a widened intervertebral foramen or erosion of a vertebral body or pedicle (Fig.
29.4A,B).21 MRI is more sensitive than traditional myelography.20 In addition, magnetic
resonance angiography (MRA) can be useful in lower posterior mediastinal tumors to locate
the artery of Adamkiewicz instead of arteriography, which has a 2% complication rate.20
MRI features suggestive of malignancy include size >5 cm, prominent vascularity or
enhancement, infiltrative margins, marked heterogeneity with central necrosis, rapid growth
from a recent imaging study, and increased uptake of Ga-67 citrate.22 However, how well
these features predict malignancy is not defined, and MRI is not recommended to categorize
posterior mediastinal tumors as benign or malignant.
The role of PET and how to interpret results in posterior neurogenic tumors has not been
defined. A retrospective analysis of PET in adult patients found a statistically significantly
higher standard uptake value (SUV) in malignant versus benign tumors (median SUV of 2.9
[range 1.8 to 12.3] vs. 1.1 [range 0.5 to 1.8]). A retrospectively applied SUV cutoff of 1.8
yielded a sensitivity of 100% and a specificity of 83%.3 However, in another study of benign
tumors in a woman with neurofibromatosis type 1 the SUV ranged from 1.8 to 5.3.23 Further
validation is needed to define a specific cutpoint and the false-positive and false-negative
rates associated with it. Nevertheless, a strongly positive or negative PET may help confirm a
clinical diagnosis and define the extent of disease in some patients.

Figure 29.4 Schwannoma in a woman with neurofibromatosis. A: CT with IV contrast does not clearly show invasion
through the foramen. B: MRI (T1 postcontrast) image shows invasion through the foramen into the spinal canal.

Laboratory Studies
In children (especially under 5 years) the incidence of neuroblastoma or
ganglioneuroblastoma is quite high. Serum vanillylmandelic acid (VMA) or hydroxylvanillylmandelic acid (HVMA) was elevated in approximately 30% of malignant
neuroblastomas or ganglioneuroblastomas in children.2 The combination of a typical
presentation in young children with an elevated serum VMA or HVMA is essentially
diagnostic without a biopsy,2 and measurement of these markers in children suspected of
having such tumors is clearly justified.
Posterior mediastinal neurogenic tumors in adults are typically nonfunctional.24 No
posterior neurogenic tumor in adults showed an elevation of VMA or HVMA in one series.2
Routinely checking VMA or HVMA levels in an adult with a posterior mediastinal tumor is
not indicated, as these markers are potentially useful only when neuroblastoma or
ganglioneuroblastoma is present, which is extremely rare in adults. These tests are not useful
to predict malignancy. These laboratory studies may be useful if there are clinical
manifestations of a secretory tumor, but not indicated if such symptoms are absent.

Clinical Approach to Patients

Patients have typically had a chest CT before being referred to a specialist such as a thoracic
surgeon. The initial clinical evaluation and the CT almost always provide enough information
to develop a treatment plan, which hinges on whether the lesion is likely or unlikely to cause
health issues if left alone. Patients can be grouped into four categories: (a) Asymptomatic and
CT not concerning, (b) symptomatic but CT not concerning, (c) spine symptoms or spine
concern on CT, or (d) concern for malignancy (Fig. 29.5).
Asymptomatic Patients with Benign CT Findings
Most adult patients with a posterior mediastinal tumor are asymptomatic (75%) and have a

simple well-defined mass with no concerning features. The preceding discussion suggests that
in such patients (without neurofibromatosis), a diagnosis of a benign tumor can be made with
a high degree of certainty (99%).

Figure 29.5 Clinical approach to patients with a posterior mediastinal tumor.

Routine biopsy of posterior mediastinal lesions is rarely useful.25,26 A needle biopsy of

posterior mediastinal tumors in adults was concordant with the final pathology in only about
50% or less in several older studies (involving eight and 16 patients who had benign
lesions).25,26 Furthermore, the histologic type of benign tumor has no impact on clinical
management. Pneumothorax occurred in 18% (one patient required a chest tube) and one
patient developed a pericardial effusion with tamponade.25 There is also no justification in
adults to obtain routine serum markers for neuroblastoma or ganglioneuroblastoma. Unless
the CT or clinical presentation is unusual, further imaging or tests are not indicated.
In asymptomatic patients with a smooth, homogeneous mass without bony changes or
contiguity to the neural foramen, observation is a reasonable management policy. Although
the data is limited, whether growth, symptom development, or malignant degeneration
(outside of neurofibromatosis) actually occurs is questionable at best. On the other hand,
resection of such lesions is generally easy (usually by thoracoscopy). Therefore, while
arguments for resection are dogmatic and unfounded, the argument against resection is also
In situations in which the evidence for benefit and for harm is very weak, patient
preferences should play a significant role. Some may prefer resection to prolonged follow-up;
others may prefer the opposite. Patients should be informed that both observation and
resection are reasonable, without strong evidence of benefit or harm in either case. (Note:
This discussion applies to patients without major comorbidities.)
Concern of Spinal Cord Compression

It is crucial to identify patients who are at risk for spinal cord compression. Retrospectively,
approximately 40% of patients with confirmed intraspinal tumors had no neurologic
symptoms.19 Furthermore, CT fails to show the intraspinal involvement in a substantial
minority of patients.20 Therefore, an absence of symptoms is not sufficient and recognition of
radiographic features that elevate or diminish the suspicion is important. If a posterior
mediastinal tumor is not contiguous with the neural foramina by CT, clinical experience and
common sense suggest this is sufficiently reliable. CT findings of neuroforaminal enlargement
or erosion of a vertebral body, spinous process, or pedicle have been found to correlate with
the presence of a dumbbell tumor.20 MRI should be done in all patients with such findings or
with a tumor adjacent to the neural foramina.20
If there is symptomatic cord compression, the need for surgical intervention is obvious. In
asymptomatic patients with an intraspinal tumor, concern about cord compression creates
strong pressure to intervene although the incidence of cord compression with observation is
not well defined but appears anecdotally to be low. In patients without an intraspinal
component but with neural foraminal involvement, the same arguments apply. In this case it
may be easier to consider observation with subsequent intervention should intraspinal growth
develop, but this is countered by the argument that resection can often be accomplished
easily (by thoracoscopy) when there is only limited neural foraminal involvement. For all
practical purposes, however, resection is undertaken in all patients with symptoms, imaging
evidence of cord compression, or with a lesion that is asymptomatic but is close to the spinal
canal (unless there are major comorbidities).
Symptoms Due to Intrathoracic Mass Effect
If patients are symptomatic due to intrathoracic mass effect, there is strong pressure to
intervene. However, in these cases the size of the lesion and the structures involved typically
make this a difficult undertaking. In addition, the symptoms have generally been present for a
long time, making it difficult to determine when to intervenethat is, when symptoms are
only mild and the procedure might be easier, or when they are more severe, but intervention
is quite difficult.
Neurogenic tumors causing symptoms due to intrathoracic mass effect are usually benign
tumors. Nevertheless, usually malignancy must be conclusively ruled out. Furthermore, often
these tumors occur in patients with neurofibromatosis, which raises specific considerations
(discussed in the next section). A needle biopsy may be sufficient, but often a surgical biopsy
is needed (i.e., via video-assisted thoracoscopic surgery [VATS]). It is generally better to
obtain a biopsy first as a separate procedure rather than rely on a frozen section at the time of
resection. These tumors are rare and therefore often require careful review by the pathologist
before a conclusive diagnosis can be made. In addition, the difference in operative planning
for a benign or malignant lesion makes it difficult in most cases to adequately plan for either
situation. PET need not be obtained before biopsy but should be done if malignancy is
Intrathoracic Tumors in Patients with Neurofibromatosis
Patients with neurofibromatosis present a particular challenge. The effectiveness of
prophylactic resection of benign neurofibromas in preventing malignant schwannomas is

undefined. This population has a 2% to 5% lifetime risk of a malignant neurofibroma,15 and a

10% risk for intrathoracic tumor has been reported.16 However, it is unclear if this is due to
the transformation of a preexisting neurofibroma, spontaneous development of a malignant
tumor, or somehow induced by surgical intervention.16 Thus, whether surgical intervention is
beneficial, has no impact, or should be avoided is unclear. No data defining the incidence of
malignant tumors in various settings (resection, observation) is available.
It certainly seems appropriate to resect a lesion causing symptoms. The presence of
neurofibromatosis provides a reasonable argument to remove a single easily resectable lesion
even without symptoms. A suspicion of malignancy should be confirmed or ruled out (biopsy,
possibly PET imaging) and treated accordingly.
However, patients with neurofibromatosis often present with many lesions, making it
relatively difficult or morbid to resect all of them. Furthermore, these patients often present
because of a large lesion that is difficult to resect. In the absence of symptoms, intraspinal
involvement, or data that resection diminishes the development of malignant tumors, it seems
better to avoid surgery. The argument against surgery is strong in the face of difficult
resection whereas arguments of benefit are weak at best.
If a decision is made to observe, surveillance should be carried out to rule out growth over
time. How often this happens, the rate at which this happens, or even whether this happens is
not defined. Furthermore, there are no known patient or lesion characteristics that predict a
greater likelihood that a malignant tumor will develop. We suggest MRI is the best imaging
test because it avoids radiation, with surveillance at 6- to 12-month intervals. Evidence of
growth supports a decision to proceed with resection.
Concern of Malignancy
It is crucial to identify the small subset of patients who have a malignant posterior
mediastinal tumor. Certain specific symptoms tend to correlate with malignancy, such as pain
or dyspnea.2 Certain specific CT findings have also been found to correlate with malignancy:
Size >10 cm, bone destruction, pleural effusion, and mediastinal displacement.2 However,
other CT findingssuch as erosions, rib splaying, foraminal enlargement, or scoliosisare
common and not suggestive of malignancy.
A clinical or radiographic concern for malignancy necessitates further investigation to
confirm the diagnosis (biopsy) and define the extent of disease (PET, MRI). A tissue diagnosis
is almost always needed because preoperative chemotherapy is often considered. If a needle
biopsy is not diagnostic, a limited surgical biopsy (e.g., VATS) is indicated.

Simple Benign Neurogenic Tumors
Small benign tumors in the asymptomatic patient may be safely observed. If resection is
chosen, a VATS approach is recommended. VATS is safe, associated with shorter hospital
stays (2.6 vs. 4.5 days) and a more rapid return to work (4.3 vs. 7.7 weeks) compared with
thoracotomy.4,27 Operative times are reported as either being similar4 or slightly longer27

with VATS. There is no absolute size limit, and even large tumors may be thoracoscopically
mobilized and then removed through a subxiphoid incision without incurring the morbidity
of a thoracotomy.
The goal of surgery should be complete excision of the tumor. A margin of normal tissue is
not needed. The overlying pleura is incised, followed by primarily blunt dissection in the
plane of the capsule of the lesion. These tumors are generally easy to separate from the
surrounding tissues. If technical difficulties are anticipated leading to an incomplete
resection, it is questionable whether surgery should be undertaken for an asymptomatic
simple benign lesion without neural foraminal involvement or mass effect.
Recurrence after complete resection of a benign neurogenic tumor is extremely rare. Even
among incompletely resected lesions recurrences are quite low.2
Tumors with Intraspinal or Neural Foraminal Involvement
It is critical to fully assess the presence of and degree of intraspinal involvement whenever
there is any suspicion that this might be present. Lack of awareness of a spinal extension may
lead to undue traction on the spinal cord, leading to permanent damage. In addition, it could
lead to an incomplete resection, leaving an intraspinal component, which is the real concern
in the first place. Finally, hemorrhage at the vertebral foramen is particularly difficult to
control from a thoracic approach.19 Therefore, preoperative planning and collaboration of
surgeons with the appropriate skills is needed.
Older approaches to dumbbell tumors involved two stagesfirst a laminectomy through a
posterior approach followed later by a standard thoracotomy. Single-stage operations have
since been described, including a two-position procedure consisting of a posterior vertical
midline incision in the prone position followed by thoracotomy in the lateral decubitus
position,28 and a single-position (lateral decubitus) approach involving a posterior midline
vertical incision starting 5 cm above the foramen of interest and extending 5 cm caudally
before curving to meet a standard posterolateral thoracotomy. This approach may provide
superior visualization.19 Regardless of positioning, laminectomy and thoracic mobilization of
the tumor should take place during the same procedure. No specific intraoperative
complications have been reported with either single-stage approach.19,28
Other single-field, posterior-only techniques have been described for dumbbell tumors, with
laminectomy for access to the intraspinal component and rib resection for access to the
mediastinal component; both components may be performed from a vertical posterior midline
incision. The primary advantages of this approach are avoiding a thoracotomy, an
extrapleural dissection, and greater stability of the laminectomized spine.29
Several centers use a two-field thoracoscopic approach that combines a posterior
laminectomy with VATS mobilization of the intrathoracic component.30 No specific major
perioperative complications are common with this approach.
Perioperative and long-term results of resection of tumors with intraspinal involvement are
very good regardless of which technique is used. No deaths and no neurologic or other major
complications occurred in one series of 16 dumbbell tumors resected using a posterolateral
thoracotomy either alone or with a posterior midline extension. No recurrences were seen at
a mean follow-up of 7.5 years, including a patient with a malignant schwannoma treated with
adjuvant radiotherapy and a patient with lymphoma.20

Large Benign Neurogenic Tumors

Neurogenic tumors that are benign but cause symptoms due to size present a difficult
problem. While the presence of symptoms favors resection, one must weigh the symptoms
against the complexity and risks associated with resection of large tumors. Because the rate of
growth (if any) appears to be quite small, observation is reasonable if symptoms are mild. A
fear of malignant degeneration is so poorly substantiated that it should probably not play into
decision making. Whether to resect is a judgment call, based on weighing the risks and
morbidity of resection, the severity of symptoms, and the rate of growth (as assessed by the
progression of symptoms or serial imaging).
A resection should be complete, provided this does not pose excessive risk. These tumors
generally push against adjacent structures rather than invading them. However, the morbidity
posed by an extensive but complete resection in some cases makes it reasonable to undertake
an incomplete resection. There is very little data specifically on large tumors; however, after
an incomplete resection recurrence occurs in only a minority of patients and then typically
after several years.2,8
Patients with Neurofibromatosis
Patients with neurofibromatosis present a particular conundrum. Arguments both for and
against resection are usually stronger but not more clear. Malignant tumors can develop, but
it is unclear if this represents de novo development of a malignant tumor or transformation of
an existing lesion. Usually there are many tumors, so resection of all of them is not possible.
Larger tumors usually are the most concerning but are difficult to resect. There should be
greater hesitation to accept an incomplete resection given the possibility of development of a
malignant tumor.
The decision to resect is usually driven by the morbidity of resection. If it is easy, it should
probably be done, especially if the lesion is causing symptoms. If it is complex, it is probably
better to avoid surgery unless there is documented evidence of growth or a suspicion of
Malignant Tumors
Malignant posterior neurogenic tumors are treated primarily by surgery (i.e., complete
resection). Because these tumors invade surrounding tissues, this includes en bloc removal of
adjacent structures. Many centers advocate postoperative radiation for malignant tumors,8
although it is not clear that chemotherapy or radiation is effective.2,7 Survival after treatment
is generally short with patients developing a recurrence and/or dying in 2 to 18 months,24
although rare cases of long-term recurrence-free survival with adjuvant radiotherapy are
described.20 There is no evidence suggesting that the specific tumor type matters for the
treatment strategy or outcome.
Adult patients with neuroblastoma and ganglioneuroblastoma are exceedingly rare; as of
2011, there were 14 case reports of mediastinal neuroblastoma in adults, only three of which
occurred in the posterior mediastinum.5 A 36% 5-year survival rate with treatment has been
reported for adult neuroblastoma in any location although the survival appears shorter for
mediastinal lesions.6 The optimal therapy for these rare tumors is undefined, but a
multimodality approach seems to be warranted.

Infants with neuroblastoma are classified as low, intermediate, or high risk, according to
several factors: International Neuroblastoma Staging System (INSS) stage, age, International
Neuroblastoma Pathologic Classification (INPC), ploidy, and presence of MYCN oncogene
amplification.31 Treatment is generally resection for low-risk, chemotherapy followed by
surgery for intermediate-risk, and chemotherapy, surgery, radiation, stem cell transplantation,
and immunotherapy for high-risk tumors.31
Complications and their Management
In general, simple benign posterior mediastinal tumors can be resected with minimal
morbidity. The complications that arise are mostly general (e.g., wound infection, incisional
pain, atelectasis) and will not be discussed. However, resection of extensive tumors can be
associated with significant morbidity. This is quite varied and depends on the additional
structures involved (e.g., chest wall, aorta, esophagus, heart). More information can be found
in other chapters dealing specifically with surgery involving these structures. Finally,
complications associated with the spine component of some larger resections (e.g.,
stabilization) lie beyond the scope of this chapter in the purview of the spine surgeon.
A specific issue relevant to the thoracic surgeon is unrecognized tumor extension into the
spinal foramen or canal. The liberal use of MRI whenever the possibility of extension exists
(e.g., tumor abutting the foramen) should prevent this. If intraoperative unsuspected
extension is found, it is best to abort the procedure and enlist the help of a spine surgeon.
There is a danger of incomplete resection, retraction of the nerve root into the spinal canal,
and intracanalicular bleeding.
Proximal division of a nerve root (i.e., within the foramen) can result in leakage of
cerebrospinal fluid (CSF). It is best to proximally ligate or clip the nerve root to prevent a CSF
leak. Intraoperative recognition and involvement of a spine surgeon allows the hole to be
closed. Postoperative ongoing leak is heralded by postural headache. Although the leak may
resolve with several days of bed rest, a pseudomeningocele may form due to the negative
intrathoracic pressure. If the leak persists, reoperation with suture, sealant, or muscle
transposition is needed.
Dissection around a nerve root must be done with care. Excessive traction can cause spinal
cord damage. Unipolar electrocautery should be avoided to prevent cord injury. Prevention is
the keytreatment once it has occurred has little impact.

Posterior mediastinal neurogenic tumors are infrequent, and even busy centers encounter
only several per year. Therefore, it is difficult to develop a comfortable routine in how to
approach these patients. The traditional management has been to resect all posterior
mediastinal tumors once identified. However, this approach is largely based on dogma and
speculation; with an increase in incidentally detected lesions a more evidence-based approach
is needed. Most of these tumors (75%) do not cause symptoms and the vast majority
(95%) are benign. There is no clear evidence that observed tumors will grow, become
symptomatic, or develop malignant transformation (except in patients with

Patients can be grouped into five categories. The largest group is asymptomatic with a
simple, well-defined, benign lesion. If the tumor is contiguous with the neural foramen or
there are bony changes, an MRI should be performed to rule out an intraspinal component.
Either observation or resection is reasonable for this group, depending on patient preferences.
If undertaken, surgery should involve complete resection (enucleation), ideally by VATS.
With either approach, long-term outcomes are excellent.
A complete resection is suggested for patients with an intraspinal tumor, typically involving
both a thoracic and a spine surgeon. Although the incidence of growth or development of
symptoms in asymptomatic patients appears low, resection is reasonable. Surgical techniques
vary but have generally shifted to single-stage and less-invasive approaches; the intraspinal
component is usually mobilized first.
Patients with large, benign neurogenic tumors should probably be resected if there are
significant symptoms due to intrathoracic organ compression and observed if symptoms are
mild, growth appears to be limited, or resection involves major risk. A complete resection is
ideal but an incomplete resection is reasonable if it avoids major morbidity.
Patients with neurofibromatosis are challenging. They usually present with multiple
tumors, large lesions that are difficult to resect, and a risk (albeit low) of developing a
malignant tumor. Whether resection decreases or increases the risk of malignancy is unclear.
In general it appears that observation is reasonable unless there are major symptoms, growth,
or rarely only limited tumors that are simple to resect.
A careful evaluation and preoperative diagnosis is needed when a malignant posterior
mediastinal tumor is suspected. The primary treatment is complete en bloc resection, but
outcomes are poor, despite multimodality therapy.
A structured approach to evaluating patients with posterior mediastinal tumor, such as is
provided here, can help clinical management. The clinical presentation and CT usually allows
patients to be placed in one of five categories. This guides the need for further evaluation and
subsequent patient management.

Recommended References and Readings

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30 Dumbbell Neurogenic

Mathew Thomas and K. Robert Shen

Background and Indications for Surgery

Posterior mediastinal tumors are rare neoplasms. A small percentage of these tumors extend
into the neural foramen, causing spinal cord compression and neurologic symptoms. The term
dumbbell tumor refers to posterior mediastinal tumors that extend into the spinal canal
from the thoracic cavity by passing through the narrow spinal foramen (Figs. 30.1A,B). These
are mostly benign neurogenic tumors such as schwannomas and neurofibromas. Other tumors
that have been reported in individual case reports include meningiomas, lipomas,
paragangliomas, hemangiomas, and lymphomas.
Symptoms commonly arise from mechanical compression of the spinal cord by the
intraspinal component. The extension into the spinal canal may not be easily detected on
routine imaging, and because of the rare nature of these tumors, a high index of suspicion
must be maintained to identify neuroforaminal involvement. Intraspinal extension in
posterior mediastinal tumors may be suggested by bony erosion of the vertebral body or
The diagnosis or suspicion of a posterior mediastinal tumor is enough to warrant further
investigation for surgical resection. The long-term course of an untreated dumbbell tumor in
asymptomatic patients is unclear. Early resection is advised due to a theoretical increased risk
for serious neurologic complications including paraplegia, from continued tumor growth.

Few contraindications exist for surgical resection of neurogenic dumbbell tumors.
Patients with bleeding dyscrasias are at a higher risk for intraspinal bleeding and such
abnormalities must be corrected before surgery.
Those patients who have undergone endovascular or open thoracic aortic aneurysm repairs
may have altered spinal arterial anatomy due to occlusion of some