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EDITORS

Rao R. Ivatury
Division of Trauma, Critical Care and Emergency Surgery
Department of Surgery
Virginia Commonwealth University
VCU Reanimation Engineering Shock Center (VCURES)
Richmond, Virginia, U.S.A.
Email: rivatury@hsc.vcu.edu
Chapters 2, 9, 23
Michael L. Cheatham
Department of Surgical Education
Orlando Regional Medical Center
Orlando, Florida, U.S.A.
Email: michael.cheatham@orhs.org
Chapters 4, 6, 23
Manu L. N. G. Malbrain
Intensive Care Unit
ZiekenhuisNetwerk Antwerpen
Campus Stuivenberg
Antwerp, Belgium
Email: manu.malbrain@skynet.be
Chapters 3, 4, 5, 6, 23
Michael Sugrue
Department of Trauma
Liverpool Hospital
Liverpool, Sydney, Australia
Email: michael.sugrue@swsahs.nsw.gov.au
Chapters 8, 23

CONTRIBUTORS

Georg Auzinger Institute of Liver Studies Kings College Hospital London, U.K.
Chapter 10
Zsolt Balogh Department of Traumatology University of Szeged Szeged, Hungary Email: zsoltbalogh@yahoo.com
Chapters 13, 22
Lorenzo Berra Intensive Care Unit San Gerardo Hospital University of Milano-Bicocca Milan, Italy
Chapter 11
Gianni Biancofiore Post-Surgical and Transplant
Intensive Care Unit Azienda Ospedaliera Pisana Pisa, Italy Email: g.biancofiore@med.unipi.it
Chapter 10
Martin Björck Vascular Surgery Uppsala University Hospital Uppsala, Sweden Email: martin@bjorck.pp.se
Chapter 16
L. D. Britt Department of General Surgery Eastern Virginia Medical School Norfolk Viriginia, U.S.A.
Foreword
Giuseppe Citerio UO Neuroanestesia
e Neurorianimazione
Dipartimento di Medicina Perioperatoria
e Terapie Intensive H San Gerardo, Monza (Mi), Italy Email: g.citerio@hsgerardo.org
Chapter 11
Scott D’Amours Department of Trauma Liverpool Hospital Liverpool, Sydney, Australia Email: Scott.Damours@swsahs.nsw.gov.au
Chapter 8
Dries H. Deeren Department of Internal Medicine University Hospital Leuven Leuven, Belgium
Chapter 5
Lawrence N. Diebel Department of Surgery Wayne State University Detroit, Michigan, U.S.A. Email: ldiebel@med.wayne.edu
Chapter 9
Davis Elliot Departments of Surgery and Radiology Vancouver Hospital
and Health Sciences Centre Vancouver, British Columbia, Canada
Chapter 16
Luciano Gattinoni Department of Anesthesia
and Intensive Care University of Milan Istituto di Anestesia e Rianimazione,
Fondazione IRCCS Ospedale Maggiore Policlinico
Mangiagalli Regina Elena Milano, Italy Email: gattinon@policlinico.mi.it
Chapter 20
Claudia E. Goettler Department of Surgery Brody School of Medicine East Carolina University Greenville, North Carolina, U.S.A. Email: cgoettle@pcmh.com
Chapter 22
Ali Hallal Department of Trauma Liverpool Hospital Liverpool, Sydney, Australia Email: ali.hallal@swsahs.nsw.gov.au
Chapter 8
Giselle G. Hamad Department of Surgery University of Pittsburgh Medical Center Pittsburgh, Pennsylvania, U.S.A. Email: hamadg@upmc.edu
Chapter 15
Michael E. Ivy Department of Surgery Hartford Hospital Hartford, Connecticut, U.S.A.
and
Department of Surgery University of Connecticut
School of Medicine Farmington, Connecticut, U.S.A. Email: mivy@harthosp.org
Chapter 14
Andrew Kirkpatrick Departments of Surgery, Critical Care
Medicine and Radiology
Vancouver Hospital
and Health Sciences Centre Vancouver, British Columbia, Canada Email: andrew.kirkpatrick@
calgaryhealthregion.ca
Chapter 16
Karel A. Kolkman Department of Surgery Rijnstate Hospital Arnhem Arnhem, The Netherlands Email: KKolkman@rijnstate.nl
Chapter 21
M. Ann Kuhn Department of Surgery Section of Pediatric Surgery The University of Oklahoma
College of Medicine Oklahoma City, Oklahoma, U.S.A. Email: Ann-Kuhn@ouhsc.edu
Chapter 17
Ari Leppäniemi Department of Surgery Meilahti Hospital University of Helsinki Helsinki, Finland Email: ari.leppaniemi@hus.fi
Chapters 2, 16
Felicity Jones Department of Trauma Liverpool Hospital Liverpool, Sydney, Australia
Chapter 3
Mark J. Kaplan Division of Trauma
and Surgical Critical Care Albert Einstein Medical Center Philadelphia, Pennsylvania, U.S.A. Email: kaplanm@einstein.edu
Chapter 22
John C. Mayberry Department of Surgery Oregon Health and Science University Portland, Oregon, U.S.A. Email: mayberrj@ohsu.edu
Chapter 18
Ingrid R. A. M. Mertens zur Borg Department of Anesthesiology Erasmus Medical Center Rotterdam, The Netherlands Email: i.mertenszurborg@erasmusmc.nl
Chapters 7, 21
Ernest E. Moore Department of Surgery Denver Health Medical Center Denver, Colorado, U.S.A. Email: Ernest.Moore@dhha.org
Chapter 12
Frederick A. Moore Department of Surgery University of Texas Medical School
at Houston
University of Texas Health Science
Center Houston, Texas, U.S.A. Email: Frederick.A.Moore@uth.tmc.edu
Chapters 13, 22
David J. J. Muckart Department of Surgery Nelson R. Mandela School of Medicine University of KwaZulu/Natal Durban, Republic of South Africa Email: MuckartD@ukzn.ac.za
Chapter 2
Savvas Nicolaou Trauma Program Foothills Medical Centre Calgary, Alberta, Canada
and
Department of Radiology Vancouver Hospital
and Health Sciences Centre Vancouver, British Columbia, Canada
Chapter 16
Claudia I. Olvera Department of Critical Care Medicine The American British Cowdray
Medical Centre Mexico City, Mexico Email: Claudia_olvera@hotmail.com
Chapters 7, 19
Michael J. A. Parr Intensive Care Units Liverpool and Campbelltown Hospitals University of New South Wales Sydney, Australia Email: Michael.Parr@swsahs.nsw.gov.au
Chapter 19
Andrew B. Peitzman Department of Surgery University of Pittsburgh Medical Center Pittsburgh, Pennsylvania, U.S.A. Email: peitzmanab@upmc.edu
Chapter 15
Christopher D. Raeburn Department of Surgery University of Colorado
Health Sciences Center Denver, Colorado, U.S.A. Email: christopher.raeburn@uchsc.edu
Chapter 12
Michael F. Rotondo Department of Surgery Brody School of Medicine East Carolina University Greenville, North Carolina, U.S.A. Email: MFRotond@PCMH.com
Chapter 22
Anastazia Salazar Departments of Surgery
and Transplantation Vancouver Hospital
and Health Sciences Centre Vancouver, British Columbia, Canada
Chapter 16
Moshe Schein Surgical Specialists of Keokuk Keokuk Area Hospital Keokuk, Iowa, U.S.A. Email: mschein1@mindspring.com
Chapter 1
C. William Schwab Department of Surgery University of Pennsylvania Philadelphia, Pennsylvania, U.S.A.
Chapter 22
Serge J. C. Verbrugge Department of Anesthesiology Erasmus Medical Centre Rotterdam, The Netherlands
Chapters 7, 21
R. Stephen Smith Department of Surgery University of Kansas School
of Medicine - Wichita Wichita, Kansas, U.S.A. Email: rsmith3@kumc.edu
Chapter 2
David W. Tuggle Department of Surgery Section of Pediatric Surgery The University of Oklahoma
College of Medicine Oklahoma City, Oklahoma, U.S.A. Email: David-Tuggle@ouhsc.edu
Chapter 17
Franco Valenza Universita degli Studi di Milano Istituto di Anestesia e Rianimazione Ospedale Maggiore di Milano Milano, Italy Email: Franco.valenza@unimi.it
Chapter 20
Jean-Louis Vincent Professor, Intensive Care University Hospital Erasme Brussels, Belgium
Foreword
Julia Wendon Institute of Liver Studies Kings College Hospital London, U.K. Email: julia.wendon@kcl.ac.uk
Chapter 10

FOREWORD

Abdominal compartment syndrome is a condition that, until relatively recently, has been poorly appreciated, despite the important potential implica­tions for all organ systems. Recent interest has helped clarify the local and systemic effects of increased intra-abdominal pressure and heightened aware­ness of the importance of early recognition and treatment. This book, written by international experts in the field follows the first World Congress on Abdominal Compartment Syndrome held in Noosa, Australia in December 2004, and provides an excellent update on this very topical subject. Compre­hensively constructed, the book covers all key aspects of the syndrome from definitions and diagnosis to monitoring and management, and is supported throughout by appropriate and ample illustrations. Many of the detrimental consequences of abdominal compartment syndrome are reversible with appro­priate and timely intervention, and although many questions remain unanswered regarding this relatively newly recognized condition, this book provides a wel­come and detailed source of current information and opinion on abdominal compartment syndrome, which will be helpful to all health care practitioners, and ultimately to our patients.
Jean-Louis Vincent, M.D., Ph.D., F.C.C.M.
Professor, Intensive Care
University Hospital Erasme
Brussels, Belgium
Abdominal compartment syndrome is now a well-known entity. It is defined as intra-abdominal hypertension with associated renal, pulmonary, or hemodynamic compromise. However, our profession was late in recognizing abdominal compartment syndrome and the devastating complications. Although Henricus first implicated abdominal compartment syndrome as a cause of death in 1890, Kron et al highlighted this syndrome in 1984. They reported a series of 11 patients with elevated intra-abdominal pressure and oliguria following aneurysm surgery. Unfortunately, only recently has there been a widespread awareness of this syndrome. Trauma patients represent a heterogenous group who are at risk for the development of both primary and secondary abdominal compartment syndrome with the latter occurring when there is no primary intra-abdominal injury. Early identification of patients who are prone to devel­oping this syndrome is essential.
After a highly successful first World Congress on abdominal compart­ment syndrome, Dr. Rao Ivatury and the other international experts have produced the most definitive publication on this topic. This well-written book covers every aspect of the abdominal compartment syndrome, including diagnosis, complications, management, and prevention. To date, there is noth­ing comparable. This is a landmark contribution to the literature.
L. D. Britt, M.D., M.P.H., F.A.C.S.
Chairman, Brickhouse Professor of Surgery
Department of General Surgery
Eastern Virginia Medical School
Norfolk Viriginia, U.S.A.

PREFACE

First suggested in 1863 by Marey, abdominal compartment syndrome (ACS) is a constellation of the physiologic sequelae of increased intra-ab­dominal pressure (IAP), termed intra-abdominal hypertension (IAH). Re­cent observations suggest an increasing frequency of this complication in all types of patients, neonates to the elderly and in diverse clinical conditions, surgical to non-surgical. Even chronic elevations of IAP seem to effect the various organ systems in the body. Despite its obvious clinical implications, not enough attention is paid to IAP and IAH. ACS still is not uniformly appreciated or diagnosed. Only a few medical and surgical intensivists be­lieve in the concept of IAH and actively attempt its prevention and treat­ment. The result, as is strongly substantiated by retrospective and prospec­tive data, is a successful reduction in organ failures and mortality.
The literature on IAH and ACS has exponentially increased in the last decade. Several unanswered questions, however, cloud our understanding of the pathophysioology of elevated IAP. To name a few, what is the ideal method of measuring IAP? What level of IAP requires abdominal decompression? Is it a level at which the classic manifestations of ACS become evident? Or is it a level at which subtle changes in physiology precede the development of ACS? Is it the IAP that is important or is abdominal perfusion pressure (APP) the critical determinant? Are IAH and ACS synonymous?
This book is an overview of the current knowledge on IAH and ACS. The authors have been chosen for their original work in the field. They write with conviction from personal experience. We have preserved to the fullest extent possible their own concepts in their own writing style. As a conse­quence, some repetition of basic concepts is unavoidable and may be ex­cused. We sincerely hope that this work will stimulate interest and attract clinicians and scientists to the fascinating field of IAH and its sequelae.
Finally, our heartfelt appreciation to the authors for their labor of love in contributing to this work, despite their over-filled calenders. We sincerely thank Cynthia Conomos and Sara Lord at Landes Bioscience for their ex­pertise and commitment to the publication of this book. We are profoundly thankful to Ms. Charmaine Miranda for her labor of love in bringing to life the WSACS.
Rao R. Ivatury
Michael L. Cheatham
Manu L. N. G. Malbrain
Michael Sugrue
CHAPTER 1
Abdominal Compartment Syndrome:
Historical Background
Moshe Schein*
Abstract
he brief history of IAH and ACS are typical of any medical innovation: described, forgotten, rediscovered, and faced with skepticism and ridicule. Eventually, after being scientifically proven and reproven and supported by “clinical leaders” and widely pub-
T
lished in reputable journals—it is accepted as “truth”. This chapter summarizes phases in the history of IAH and ACS from the mid 19th century until today.
At a first glance, a comprehensive history of the abdominal compartment syndrome (ACS)
is an impossible task. It is like writing the history of vomiting or urinating or any other basic human (and mammalian) physiological activity. For as long as humans existed, abdomens ballooned with gas, fluid, blood, pus—resulting in all the physiological changes that we today call intra-abdominal hypertension (IAH) and ACS.
Obviously, IAH and ACS always existed but were not understood as such. For example: in
his book Surgical Errors and Safeguards” recognize acute dilation of the stomach at once. Practically all unrecognized cases die.” He mentioned that (according to Hamilton Bailey) “the condition can be diagnosed even before the patient vomits…if the pulse is rising…and if the urine is scanty in amount.” Clearly, what was described was yet another example of the ACS—the syndrome which remained, until very recently, elusive and almost unknown.
Even we—so called modern surgeons—until a decade ago observed patients with full-blown
ACS, failing to understand what we see. We saw massively distended patients dying after op­erations for ruptured abdominal aneurysm and blamed their death on myocardial infarction or respiratory failure; we watched patients with massive abdomens in the early days of severe acute pancreatitis—blaming their cardiorespiratory demise on pancreatic toxins; we rushed to resuture dehisced abdomens—pushing everything back, and tightly closing with “retention sutures”— wondering why these patients spend weeks on the ventilator and then die.
1
Max Thorek wrote: “It is of paramount importance to
What Is History?
At what point in time should we start looking at the history of the abdominal compartment
syndrome and where should we stop? Various dictionaries define history as “A branch of knowl­edge that records and explains past events”, or “the aggregate of past events”. History is also defined as “the discipline that records and interprets past events involving human beings”, or “the continuum of events occurring in succession leading from the past to the present and even into the future.”
*Moshe Schein—Surgical Specialists of Keokuk, Keokuk Area Hospital, Keokuk, Iowa
52632, U.S.A. Email: mschein1@mindspring.com
Abdominal Compartment Syndrome, edited by Rao R. Ivatury, Michael L. Cheatham, Manu L. N. G. Malbrain and Michael Sugrue. ©2006 Landes Bioscience.
2
Abdominal Compartment Syndrome
Since the present, the future—and even the recent past—of all aspects of ACS are covered
in great details elsewhere in this book I will start this historical overview at mid 19th century— at the time when people started measuring intra-abdomianl pressure (IAP) and study its physi­ological consequences. I still do not know how late into the 20th should I carry this narrative on.
Early Rays of Light
Haven Emerson’s (1874-1957) comprehensive treatise “intra-abdominal pressures”2 (1911)
spares us the arduous task of finding yet older and hard to retrieve manuscripts. Emerson’s manuscript was typical of its day when people had more to write about the history of things than about what is actually new. His started his manuscript with 10 pages of “historical sketch” covering the second half of the 19th century. His opening testament may be true even today:
“ The standard text-books of obstetrics, gynecology and surgery treat of the matter so rarely,
and when it is mentioned, so inaccurately, that no information is to be had from them…Most of the text-books of physiology fail to mention intra-abdominal pressure at all.”
Emerson provided a detailed historical review of which I will mention only selected key points:
• It is difficult to define with certainty who was the first to write about the physiology of IAP. Contemporary reviews bestow such honor on Marey of Paris who in his paper “Physiologie médicale de la circulation du sang” (1863) wrote that the “effects that respiration produces on the thorax are the inverse pf those present in the abdomen.” However, according to Emerson,
• Braune of Germany (1865) appears to be the first to measure IAP through the rectum.
• Another pioneer mentioned by Coombs3 and contemporary reviews is Paul Bert who in
1870 published a volume on “Physiologie comparée de la respiration.” Based on experi­ments in anesthetized animals, measuring thoracic and abdominal pressures through tubes inserted in the trachea and rectum, respectively, Bert described elevation of IAP on inspira­tion and the descent of the diaphragm.
• Schroeder of Germany (1886) noted the slightly increased IAP in pregnancy, hypothesizing that there must be some adaptation of abdominal wall tension to the increasing size of the uterus.
• Schatz of Germany (1872) used balloon tube connected to a mercury manometer to mea­sure pressures within the gravid uterus. According to him IAP is positive and during preg­nancy IAP rises slightly, though not in proportion to the increase in the size of the uterus, until the last month, when usually the abdominal muscles are stretched beyond their ability to respond, and there is then a fall of pressure below normal. He also noted that the pressure in the inferior vena cava must be at least as high as IAP to avoid obliteration of its lumen, and that a moderately positive IAP—increased in the erect position—assists the return of blood flow, and the flow of chyle from the abdominal viscera.
• Wendt of Germany (1873) measured IAP through the rectum, noting that the higher the abdominal pressure the less the secretion of urine.
• Oderbrecht of Germany (1875) measured pressures within the urinary bladder, concluding that IAP is normally positive.
• Wegner of Germany (1877) noted that the normal positive IAP aids absorption of fluids from the peritoneal surface.
• Quinke of Germany (1878) noted in patients with ascites the obstructive effects of high IAP on venous return from abdominal viscera.
• Mosso and Pellacani of Italy (1882) measured positive IAP through the urinary bladder.
• Senator of France (1883) noted that IAP is much diminished by weakness of the abdominal
walls.
• Heinricius of Germany (1890) found that IAP’s between 27 to 46 cm. water were fatal to animals owing to prevention of respiration, decreasing cardiac diastolic distention and a low blood pressure. He also contended that rapid abdominal distention at low pressure is of much harm while gradually established high pressure may be well tolerated.
2
Marey “describes no tests and gives no records or figures.”
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• During the late 19th century, and the early years of the 20th, many other authors con-
firmed, or refuted, the above observations in multiple experimental and clinical observa­tions. The latter included a few fallacies which led to confusion: that the “normal” IAP is subatmospheric, that IAP varies in the different regions of the abdomen and that trans-visceral measurements are not accurate.
2
Emerson himself (1911)2 conducted numerous experiments in dogs—showing what was to be rediscovered again and again: that contraction of the diaphragm is the chief factor in the rise of IAP during inspiration; that anesthesia and muscle paralysis—with loss of muscle tone— decreases the IAP; that elevated IAP increases peripheral vascular resistance; that excessive IAP can cause death from cardiac failure even before terminal asphyxia develops (“Pressure as high as 45 cm. Aq. Will kill a small animal”)... Emerson understood that elevated IAP decreases blood pressure because of diminished venous return to the heart as well as depressed cardiac contractility. He then provided amazingly relevant clinical correlation, which subsequently has been totally ignored by many generations of surgeons:
“(in) excessive IAP, the difficulty in breathing is even more marked, and this often plays an important role in the circulatory emergencies in infectious disease where meteorism, abdomi­nal distention and interference with the descent of the diaphragm may determine cardiac fail­ure.”
Emerson understood that the cardiovascular collapse associated with “distention of the ab­domen with gas or fluid, as in typhoid fever, ascites, or peritonitis” are caused by “overloading the resistance in the splanchnic area” and that “relief of the laboring heart is constantly seen after removal of ascitic fluid.”
Thus we see that almost 100 years ago, before the world was engulfed by the chaos of WW-I, ample evidence existed concerning the adverse physiological effects of high IAP on cardiac, respiratory and renal function. There were also those who understood the clinical implications of such knowledge: that high IAP due to ascites, ileus and peritonitis results in morbidity and mortality. Such early rays of light however failed to penetarte the opaque minds of contemporary clinicians and researchers, and the significance of IAP has almost dissapeared druing the ensuing Dark Age.
3Abdominal Compartment Syndrome: Historical Background
The Dark Age
This long era of gloom lasted for over 50 years with only scattered but totally ignored attempts to shed old or new light on IAP.
• Thorington and Schmidt (1923) studied urinary output and blood pressure changes in experimental ascites.
• Overholt (1931) seemed to be the first to introduce the issue in an American surgical jour-
5—
nal
showing and postulating what essentially has been already known.
• Bellis and Wangensteen (1939) demonstrated changes in venous flow in the abdomen and extremities associated with abdominal distention
• Bradely and Bradely (1947) showed decreased glomerular filtration rate and renal plasma flow with increased IAP.
• Gross (1948) introduced the so-called “staged abdominal repair” in the management of omphalocele, thus acknowledging the importance of avoiding abdominal closure under excessive tension.
• Olerud (1953) studied the effects of increased IAP on portal circulation.
But it was M.G Baggot, an anesthesist from Dublin (currently retired in Granite City, Illinois) who really saw the light. back into the abdominal cavity of limited size might kill the patient. He had conceived that the factor leading to the high mortality rate associated with abdominal wound dehiscence is not the dehiscence itself but the emergency procedure to correct it—that produces high IAP. He termed such abdominal dehiscence “abdominal blow-out” and concluded that the ensuing death is due to respiratory dysfunction. Baggot coined also the term “acute tension pneumo­peritoneum” believing that excessive free air trapped in the abdomen during its closure
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Already in 1951 he suggested that forcing distended bowel
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