Following are links to a few of my articles, monographs, or chapters from books.

(more to come)

Moshe Schein, M.D., FACS
Send me email
You requested the medical article below. Choose another one from the list on the right.

The History of Abdominal Compartment Syndrome

[This is a chapter from the book “Abdominal Compartment Syndrome”, edited by Rao Ivaturi.  Landes Bioscience, 2006

Moshe Schein

Abstract

The brief history of IAHT and ACS are typical of any medical innovation: described, forgotten, re-discovered, and faced with skepticisms and ridicule.  Eventually, after being scientifically proven and re-proven and supported by “clinical leaders” and widely published in reputable journals—it is accepted as “truth”.  This chapter summarizes phases in the history of IAHT 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 (IAHT) and ACS. 

Obviously, IAHT and ACS always existed but were not understood as such.  For example: in his book Surgical Errors and Safeguards” 1 Max Thorek wrote: “It is of paramount importance to 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 re-suture dehisced abdomens – pushing everything back, and tightly closing with “retention sutures” –wondering why these patients spend weeks on the ventilator and then die. 

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 nvolving human beings”, or “the continuum of events occurring in succession leading from the past to the present and even into the future.”

Since the present, the future-- and even the recent past-- of all aspects of ACS are covered in great details elsewhewre 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 2 , Marey “describes no tests and gives no records or figures.” 
  • Braune of Germany (1865) appears to be the first to measure IAP through the rectum. 2
  • Another pioneer mentioned by Coombs 3 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. 2 
  • 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. 2
  • 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. 2
  • Wendt of Germany (1873) measured IAP through the rectum, noting that the higher the abdominal pressure the less the secretion of urine. 2
  • Oderbrecht of Germany (1875) measured pressures within the urinary bladder, concluding that IAP is normally positive. 2
  • Wegner of Germany (1877) noted that the normal positive IAP aids absorption of fluids from the peritoneal surface. 2
  • Quinke of Germany (1878) noted in patients with ascites the obstructive effects of high IAP on venous return from abdominal viscera. 2
  • Mosso and Pellacani of Italy (1882) measured positive IAP through the urinary bladder. 2
  • Senator of France (1883) noted that IAP is much diminished by weakness of the abdominal walls. 2
  • 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 
  • During the late 19th century, and the early years of the 20th, many other authors confirmed, 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 re-discovered 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 diminish 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. 

The Dark Age

This long era of gloom lasted for over 50 years with only scattered but totally ignored attempts to shade old or new light on IAP. 

  • Thorington and Schmidt (1923) studied urinary output and blood pressure changes in experimental ascites. 4
  • Overholt (1931) seemed to be the first to introduce the issue in an American surgical journal. 5 –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 6

§         Bradely and Bradely (1947) showed decreased glomerular filtration rate and renal plasma flow with increased IAP. 7

§         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. 8

§         Olerud (1953) studied the effects of increased AIP on portal circulation. 9

But it was M.G Baggot, an anesthesist from Dublin (currently retired in Granite City, Illinois) who really saw the light. 10  Already in 1951 he suggested that forcing distended bowel 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 increases IAP.  Significantly, he recommended avoiding abdominal closure under tension, leaving instead such abdomens open, using a technique described during WW-II by the great British surgeon Sir Heneage Ogilvie. 11 But typically, the destiny of lone prophets—however truthful they are—is to be ridiculed and ignored. And such was Baggot’s fate.

Dawn

Early sunrays, heralding the dawn, pierced the dark horizon in 1970 when Sönderberg and Westin correlated IAP directly measured during laparoscopy, to that measured through the urinary bladder. 12  In 1972 Shenansky and Gillenwater showed how increased IAP generated by applying abdominal counterpressure (i.e. the MAST suit) depresses cardiac and renal function. 13

Early experience with laparoscopy led to recognition of the adverse effects of pneumoperitroneum-associated increase in IAP: Ivankovich et at described cardiovascular collapse during gynecological laparoscopy 14 and studied the physiology of the phenomenon. 15  Then in 1976, Lenz et al, studying cardiovascular changes during laparoscopy, pointed out the dangers of pneumoperitoneum in patients with cardiovascular dysfunction, anemia or hypovolemia. 16  Simultaneously, (1976), Richardson and Trinkle studied hemodynamic and respiratory alterations with increased intra-abdominal pressure. 17

Even earlier, during the 1960’s and later in the 1970’s, supporting evidence to the clinical significance of elevated IAP was provided in studies in  patients with ascites, the amount of which correlated with cardiorespiratory morbidity –the later reversed by paracentesis.  18,19,20,21 The same was true by the growing number of papers supporting leaving the abdomen open in newborns with omphalocele and gastroschisis. 22,23

Thus the sun has slowly risen to melt the frozen brains –at least the few which were susceptible and welcoming its warm rays.

Sunrise

The early 1980’s produced a few key studies: Kashtan et al (1981) rediscovered the hemodynamic effects of increased IAP 24 ; Harman et al (1982) 25 , as well as Richards et al (1983) 26 demonstrated how elevated IAP adversely affects renal function and how abdominal decompression improves it, and Le Roith et al (1982) studied the effects of increased IAP on plasma antidiuretic hormone levels. 27

It was however the paper by Kron, Harman and Nolan (1984) which is considered by many as a “benchmark” in the clinical perception of intra-abdominal hypertension.  In this combined clinical and experimental study the authors showed that IAP could be used as a criterion for life-saving abdominal re-exploration and decompression. 28  Interestingly, many claim that the term Abdominal Compartment Syndrome (ACS) was first used by Kron et al. 28  However, I could not find such term used within their paper.  This reflects the dangers of citing from secondary sources rather than reading the primary, original ones. 

Sporadic communications continued to appear: Smith et al (1985) reported reversal of postoperative anuria by decompressive laparotomy 29 ;Barnes et al (1985) studied cardiovascular responses to elevated IAP 30 ;Caldwell and Ricotta (1987) measured such changes in visceral blood flow 31 ;Jacques and Lee (1988) reported improvement in renal function after relief of raised IAP due to retroperitoneal hematoma 32 ;Cullen et al (1989) reported on surgical decompression of the abdomen in critically ill patients to reverse cardiovascular, renal and respiratory compromise. 33  Around the same time people started measuring IAP through the urinary catheter in their intensive care units 34 –re-inventing a method reported by Oderbrecht more than 100 years earlier. 2

Then in 1989 the term abdominal compartment syndrome wad finally coined.  It may well be that different people begun to use such term before but the first publication mentioning it was that by Fietsam et al from the William Beaumont Hospital, Royal Oak, Michigan. 35  The authors wrote:

“In four patients with ruptured abdominal aortic aneurysms increased intra-abdominal pressure developed after repair. It was manifested by increased ventilatory pressure, increased central venous pressure, and decreased urinary output associated with massive abdominal distension not due to bleeding. This set of findings constitutes an intra-abdominal compartment syndrome caused by massive interstitial and retroperitoneal swelling…four patients received more than 25 liters of fluid resuscitation (electrolyte and blood) during and within 16 hours after operation and had massive abdominal distension. Decompressive laparotomies were performed in the Intensive Care…Opening the abdominal incision was associated with dramatic improvements in central venous pressure, urinary output, ventilatory pressure, arterial carbon dioxide tension, and oxygenation.”

Thus, by the end of the 1980’s people new how to measure IAP, what damage elevated IAP can produce and how to treat it.  They also defined the clinical syndrome and named it.  But commonly people look at truth but refuse to acknowledge it and so it took a few more years for the concept to penetrate our surgical minds.

Morning

The 1990’s brought with it a plethora of studies –reflecting a growing recognition of IAHT and ACS.  As most studies published during this decade will be cited elsewhere in this book I will only mention key developments. 

  • The introduction of laparoscopic surgery produced numerous studies on the physiology of penumoperitoneum –demonstrating and emphasizing the dangers of increased IAP on various organs and systems.
  • Growing popularity of “damage control” strategies in abdominal trauma increased surgeons’ and intensivists’ awareness of IAHT/ACS and the benefits of leaving the abdomen open and/or its decompression.
  • Cautious enthusiasm with the use of “laparostomy” in severe abdominal infections led to the recognition that various non-traumatic abdominal catastrophes maybe associated with IAHT/ACS and could benefit of abdominal non-closure.
  • Two “collective reviews” of ACS appeared in 1995 36 and 1996 37 --opening the gate to numerous publications, recognizing IAHT/ACS in a large number of surgical-- abdominal and extra-abdominal, traumatic and non-traumatic scenarios—and providing an ever growing list of complications and consequences.

High noon

It is my understanding that high noon is yet to come and it will come only when the majority of clinicians will understand and recognize the clinical significance of IAHT and ACS.  But looking around me I still see surgeons closing distended and tense abdomens with retention sutures under excessive tension, I see surgeons closing hugely swollen abdomens after repair of ruptured AAA, I see abdomens ballooning in the intensive care unit with surgeons and intensivist ignoring the potential benefits of abdominal decompression.  Typically, a while ago, when we submitted for publication ours observations of IAHT/ACS in early severe pancreatitis it has been rejected by reputable surgical journal:  the distinguished journal-reviewers commented that the existence of such syndrome is “controversial and unproven.”  (The manuscript eventually appeared elsewhere. 38 )

The brief history of IAHT and ACS are characteristic of any medical innovation: described, forgotten, re-discovered, and faced with skepticisms and ridicule.  Eventually, after being scientifically proven and re-proven and supported by “clinical leaders” and widely published in reputable journals—it is accepted as “truth.”  But it takes a few generations.

“New ideas seldom have the simplicity of a switched on light bulb.” (--Thomas Starzl).

References

  1. Thorek M. surgical errors and safeguards. J.B Lippincott Comoany, Philadelphia, 1934, p-370
  2. 2. Emerson H. Intra-abdominal pressures. Arch Intern Med 1911;7:754-784
  3. 3. Coombs HC. The mechanisms of the regulation of intra-abdominal pressure. Am J Physiol 1920;61:159-63
  4. Thorington JM, Schmidt CF. A study of urinary output and blood-pressure changes resulting in experimental ascites. Am J Med Sci 1923;165:880-90
  5. Overholt RH. Intraperitoneal pressure. Arch Surg 1931;22:691-703
  6. Bellis CJ, Wangensteen OH.  Venous circulatory changes in the abdomen and lower extremities attending abdominal distention. Proc Soc Exp Biol Med 1939;4:490-498 6
  7. Bradely SE, Bradely GP. The effect of increased intra-abdominal pressure on renal function in man. J Clin Invest 1947;26:1010-1015
  8. Gross RE. A new method for surgical treatment of large omphaloceles. Surgery 1948;24:277-292
  9. Olerud S. Experimental studies on portal circulation at increased intra-abdomioanl pressure. ACTA Physio Scand 1953;30(Supp 109):4-93
  10. Baggot MG. Abdominal blow-out: a concept. Current Research Anesthesia Analgesia 1951;30:295-8
  11. Ogilvie WH. The late complications of abdominal wae wounds. Lancet 1940;2:253-256
  12. Sönderberg G, Westin B. Transmission of rapid pressure increase from the peritoneal cavity to the bladder. Scan J Urol Nephrol 1970;4:155-165
  13. Shenansky JH, Gillenwater JY. The renal hemodynamic and functional effects of external counterpressure. Surg Gynecol Obstet 1972;134:253-258
  14. Ivankovich AS, Albrecht RF, Zahed B et al. Cardiovascular collapse during gynecological laparoscopy. Ill Med J 1974;145:58-61
  15. Motev M, Ivankovich AD, Bieniarz J et al. Cardiovascular effects and acid base and blood gas changes during laparoscopy. Amer J Obstet Gynecol 1973;116:1002-1012
  16. Lenz RJ, Thomas TA, Wilkins DG. Cardiovascular changes during laparoscopy. Anaesthesia 1976;31:4-12
  17. Richardson JD, Trinkle JK. Hemodynamic and respiratory alterations with increased intra-abdominal pressure. J Surg Res 1976;20:401-404
  18. Gordon ME. The acute effects of abdominal paracentesis in Laennec’s cirrhosis upon changes of electrolytes and eater, renal function and hemodynamics. Am J Gastroenterol 1960;33:15-37
  19. Suazzi M, Polese A, Magrini F, et al.  Negative influence of ascites in the cardiac function of cirrhotic patients, Am J Med 1975;59:165-170
  20. Cruikshank DP, Buschsbalm HJ. Effects of rapid paracentesis, cardiovascular dynamics and body fluid composition. JAMA 1973;225:1361-1362
  21. Knauer CM, Love HM. Hemodynamics in cirrhotic patient during paracentesis. N Engl J Med 1967;276:491-496
  22. Ravitch MM. Omphalocle: secondary repair with the aid of pneumoperitoneum. Arch Surg 1969;99:166-170
  23. Allen RG, Wrenn EL, Jr. Silo as a sac in the treatment of omphalocele and gastroschisis. J Ped Surg 1969;4:3-8
  24. Kashtan J, Green JF, Parson EQ et al. hemodynamic effects of increased abdominal pressure. J Surg Res 1981;30:249-255
  25. Harman PK, Kron IL, McLachan DH et al. Elevated intra-abdomial pressure and renal function. Ann Surg 1982;196:594-597
  26. Richards WO, Scovill W, Shin B et al. Acute renal failire associated with increased intra-abdominal pressure. Ann Surg 1983;197:183-187
  27. Le Roith D, Bark H, Nyska M et al. The effect of abdominal pressure on plasma antidiuretic hormone levels. J Surg Res 1982;32:65-69
  28. Kron IL, Harman PK, Nolan SP. The measurement of intra-abdominal pressures a criterion for abdominal re-exploration. Ann Surg 1984;199:28-30
  29. Smith JH, Merrell RC, Raffin TA. Reversal of postoperative anuria by decompressive celiotomy. Arch Intern Med. 1985;145:553-4.
  30. Barnes GE, Laine GA, Giam PY et al. Cardiovascular responses to elevation of intra-abdominal hydrostatic pressure. Am J Physiol. 1985;248:R208-13.
  31. Caldwell CB, Ricotta JJ. Changes in visceral blood flow with elevated intraabdominal pressure. J Surg Res. 1987;43:14-20.
  32. Jacques T, Lee R. Improvement of renal function after relief of raised intra-abdominal pressure due to traumatic retroperitoneal haematoma.  Anaesth Intensive Care. 1988;16:478-82.
  33. Cullen DJ, Coyle JP, Teplick R, Long MC. Cardiovascular, pulmonary, and renal effects of massively increased intra-abdominal pressure in critically ill patients. Crit Care Med. 1989;17:118-21
  34. Iberti TJ, Lieber CE, Benjamin E. Determination of intra-abdominal pressure using a transurethral bladder catheter: clinical validation of the technique. Anesthesiology. 1989;70:47-50.
  35. Fietsam R Jr, Villalba M, Glover JL, Clark K. Intra-abdominal compartment syndrome as a complication of ruptured abdominal aortic aneurysm repair. Am Surg. 1989;55:396-402
  36. Schein M, Wittmann DH, Aprahamian CC, Condon RE. The abdominal compartment syndrome: the physiological and clinical consequences of elevated intra-abdominal pressure. J Am Coll Surg. 1995;180:745-53
  37. Burch JM, Moore EE, Moore FA, Franciose R. The abdominal compartment syndrome.  Surg Clin North Am. 1996;76:833-42.
  38. Gecelter G, Fahoum B, Gardezi S, Schein M. Abdominal compartment syndrome in severe acute pancreatitis: an indication for a decompressing laparotomy? Dig Surg. 2002;19:402-4