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194
Abdominal Compartment Syndrome
ileal pouch-anal anastomosis (IPAA) for ulcerative colitis.39 Among the gastric bypass patients,
20% subsequently developed incisional hernia, compared to 4% of the IPAA patients (p<0.001).
Five out of 7 IPAA patients with incisional hernia were obese (BMI = 30 kg/m
2
). In contrast,
only 1% of the nonobese IPAA patients developed an incisional hernia. In a study of 50 patients undergoing laparoscopic ventral hernia repair, Raftopoulos et al stratified the patients
according to BMI.
Following incisional herniorrhaphy, obesity is an important predictor of hernia recur-
39,41,42
rence.
study of 160 patients undergoing open incisional herniorrhaphy.
In Sugerman’s hernia study, the rate of recurrent hernia was 41% among the gastric bypass
patients.
39
40
The surface area of the hernia correlated with BMI.
Sauerland et al found a recurrence rate increase of 1.10% per unit of BMI in a
43
Conclusion
The comorbid illnesses of obesity adversely affect virtually every organ system. The pathogenesis of many of these conditions may be related to intra-abdominal hypertension. Weight
loss results in resolution of the majority of these comorbidities.
Commentary
Michael L. Cheatham
Intra-abdominal hypertension (IAH) has been increasingly documented in recent years to
occur in a wide-variety of critically ill patient populations. In this chapter, Drs. Hamad and
Peitzman identify and describe a clinical scenario in which IAH may develop in a nonacute,
chronic setting: the morbidly obese patient. As with IAH in the critically ill, elevated
intra-abdominal pressure (IAP) in the morbidly obese patient can have far reaching effects on
cerebral, cardiac, pulmonary, and renal physiology and function. As illustrated by the authors,
disease processes common to the morbidly obese such as pseudotumor cerebri, obesity
hypoventilation syndrome, gastroesophageal reflux, and stress urinary incontinence are now
recognized as being caused, in large part, by the IAH incurred with an elevated body mass
index (BMI). Further, the propensity to poor fascial healing and increased incisional hernia
rates among the obese has been established as being due to IAH-induced reductions in abdominal wall and rectus sheath blood flow, pathophysiologic changes that, once recognized,
can lead to outcome-altering therapeutic interventions.
This chapter raises three crucial points. First, the IAH-related complications of morbid
obesity as outlined above generally respond to weight loss with resolution of patient symptoms
and improved quality of life. Second, the morbidly obese are potentially at increased risk for
developing symptomatic IAH and even abdominal compartment syndrome (ACS) as a result
of preexisting baseline IAH and organ dysfunction. The morbidly obese patient may well develop IAH / ACS either earlier in a given disease process or following a physiologic insult of
reduced severity compared to their nonobese counterpart. Clinicians should have a low threshold for measuring IAP in the obese patient in order to detect what could well be termed “silent
IAH”. Failure to recognize such elevations in IAP may lead to potentially preventable organ
dysfunction and failure in such patients. Third, and perhaps most importantly, just as IAH/
ACS was originally erroneously considered to be a disease process afflicting only the traumatically injured, IAH/ACS can no longer be regarded as solely a disease of the critically ill. As
illustrated in the case of the morbidly obese, IAH clearly occurs outside of the intensive care
unit and even the hospital setting. As a result, the list of accepted risk factors for IAH must be
reconsidered. Just as our understanding of the critically ill patient populations vulnerable to
elevated IAP has evolved, so must our recognition of nontraditional patient populations such
as the morbidly obese. These nonacute patients with silent IAH may well stand to gain as much
from our diagnosis of their elevated IAP as have our critically ill patients.
References
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2. Finkelstein EA, Fiebelkorn IC, Wang G. State-level estimates of annual medical expenditures attributable to obesity. Obes Res 2004; 12:18-24.
3. Sugerman HJ. Effects of increased intra-abdominal pressure in severe obesity. Surg Clin North Am
2001; 81:1063-1075.
4. Carr DB, Utzschneider KM, Hull RL et al. Intra-abdominal fat is a major determinant of the
National Cholesterol Education Program Adult Treatment Panel III criteria for the metabolic syndrome. Diabetes 2004; 53:2087-2094.
5. Janssen I, Katzmarzyk PT, Ross R. Waist circumference and not body mass index explains
obesity-related health risk. Am J Clin Nutr 2004; 79:379-384.
6. Sugerman H, Windsor A, Bessos M et al. Intra-abdominal pressure, sagittal abdominal diameter
and obesity comorbidity. J Intern Med 1997; 241:71-79.
7. Sanchez NC, Tenofsky PL, Dort JM et al. What is normal intra-abdominal pressure? Am Surg
2001; 67:243-248.
8. Noblett KL, Jensen JK, Ostergard DR. The relationship of body mass index to intra-abdominal
pressure as measured by multichannel cystometry. Int Urogynecol J Pelvic Floor Dysfunct 1997;
8:323-326.
9. McIntosh S, Drinnan M, Griffiths C et al. Relationship of abdominal pressure and body mass
index in men with LUTS. Neurourol Urodyn 2003; 22:602-605.
10. Sugerman H, Windsor A, Bessos M et al. Effects of surgically induced weight loss on urinary
bladder pressure, sagittal abdominal diameter and obesity comorbidity. Int J Obes Relat Metab
Disord 1998; 22:230-235.
11. Bloomfield GL, Sugerman HJ, Blocher CR et al. Chronically increased intra-abdominal pressure
produces systemic hypertension in dogs. Int J Obes Relat Metab Disord 2000; 24:819-824.
12. Bloomfield GL, Ridings PC, Blocher CR et al. A proposed relationship between increased
intra-abdominal, intrathoracic, and intracranial pressure. Crit Care Med 1997; 25:496-503.
13. Kanai H, Matsuzawa Y, Kotani K et al. Close correlation of intra-abdominal fat accumulation to
hypertension in obese women. Hypertension 1990; 16:484-490.
14. Hayashi T, Boyko EJ, Leonetti DL et al. Visceral adiposity and the prevalence of hypertension in
Japanese-Americans. Circulation 2003; 108:1718-1723.
15. Kanai H, Tokunaga K, Fujioka S et al. Decrease in intra-abdominal visceral fat may reduce blood
pressure in obese hypertensive women. Hypertension 1996; 27:125-129.
16. Prior DL, Sprung J, Thomas JD et al. Echocardiographic and hemodynamic evaluation of cardiovascular performance during laparoscopy of morbidly obese patients. Obes Surg 2003; 13:761-767.
17. Sugerman HJ, DeMaria EJ, Felton III WL et al. Increased intra-abdominal pressure and cardiac
filling pressures in obesity-associated pseudotumor cerebri. Neurology 1997; 49:507-511.
18. Sugerman HJ, Felton 3rd WL, Sismanis A et al. Continuous negative abdominal pressure device to
treat pseudotumor cerebri. Int J Obes Relat Metab Disord 2001; 25:486-490.
19. Sugerman HJ, Felton 3rd WL, Sismanis A et al. Gastric surgery for pseudotumor cerebri associated
with severe obesity. Ann Surg 1999; 229:634-640; discussion 640-642.
20. Pelosi P, Croci M, Ravagnan I et al. Respiratory system mechanics in sedated, paralyzed, morbidly
obese patients. J Appl Physiol 1997; 82:811-818.
21. D’Angelo E, Calderini E, Torri G et al. Respiratory mechanics in anesthetized paralyzed humans:
Effects of flow, volume, and time. J Appl Physiol 1989; 67:2556-2564.
22. Sugerman HJ, Baron PL, Fairman RP et al. Hemodynamic dysfunction in obesity hypoventilation
syndrome and the effects of treatment with surgically induced weight loss. Ann Surg 1988; 207:604-
613.
23. Zacchi P, Mearin F, Humbert P et al. Effect of obesity on gastroesophageal resistance to flow in
man. Dig Dis Sci 1991; 36:1473-1480.
24. Mercer CD, Wren SF, DaCosta LR et al. Lower esophageal sphincter pressure and gastroesophageal pressure gradients in excessively obese patients. J Med 1987; 18:135-146.
25. Barak N, Ehrenpreis ED, Harrison JR et al. Gastro-oesophageal reflux disease in obesity: Pathophysiological and therapeutic considerations. Obes Rev 2002; 3:9-15.
26. Suter M, Dorta G, Giusti V et al. Gastro-esophageal Reflux and esophageal motility disorders in
morbidly obese patients. Obes Surg 2004; 14:959-966.
27. Ruhl CE, Everhart CE. Overweight, but not high dietary fat intake, increases risk of gastroesophageal reflux disease hospitalization: The NHANES i epidemiologic followup study. First national
health and nutrition examination survey. Ann Epidemiol 1999; 9:424-435.
195Morbid Obesity and Chronic Intra-Abdominal Hypertension
196
28. Perez AR, Moncure AC, Rattner DW. Obesity adversely affects the outcome of antireflux operations. Surg Endosc 2001; 15:986-989.
29. Jones Jr KB. Roux-en-Y gastric bypass: An effective antireflux procedure in the less than morbidly
obese. Obes Surg 1998; 8:35-38.
30. Smith SC, Edwards CB, Goodman GN. Symptomatic and clinical improvement in morbidly obese
patients with gastroesophageal reflux disease following Roux-en-Y gastric bypass. Obes Surg 1997;
7:479-484.
31. Di Francesco V, Baggio E, Mastromauro M et al. Obesity and gastro-esophageal acid reflux: Physiopathological mechanisms and Role of gastric bariatric surgery. Obes Surg 2004; 14:1095-1102.
32. Ortega J, Escudero MD, Mora F et al. Outcome of esophageal function and 24-hour esophageal
pH monitoring after vertical banded gastroplasty and roux-en-Y gastric bypass. Obes Surg 2004;
14:1086-1094.
33. Schauer P, Hamad G, Ikramuddin S. Surgical management of gastroesophageal reflux disease in
obese patients. Semin Laparosc Surg 2001; 8:256-264.
34. Bloomfield GL, Blocher CR, Fakhry IF et al. Elevated intra-abdominal pressure increases plasma
renin activity and aldosterone levels. J Trauma Inf Crit Care 1997; 42:997-1005.
35. Dwyer PL, Lee ETC, Hay DM. Obesity and urinary incontinence in women. Br J Obstet Gynecol
1998; 95:91-96.
36. Bai SW, Kang JY, Rha KH et al. Relationship of urodynamic parameters and obesity in women
with stress urinary incontinence. J Reprod Med 2002; 47:559-563.
37. Noblett KL, Jensen JK, Ostergard DR. The relationship of body mass index to intra-abdominal
pressure as measured by multichannel cystometry. Int Urogynecol J Pelvic Floor Dysfunct 1997;
8:323-326.
38. Bump RC, Sugerman H, Fantl JA et al. Obesity and lower urinary tract function in women: Effect
of surgically induced weight loss. Am J Obstet Gynecol 1992; 166:392-399.
39. Sugerman HJ, Kellum Jr JM, Reines HD. Greater risk of incisional hernia with morbidly obese
than steroid-dependent patients and low recurrence with prefascial polypropylene mesh. Am J Surg
1996; 171:80-84.
40. Raftopoulos I, Vanuno D, Khorsand J et al. Outcome of laparoscopic ventral hernia repair in
correlation with obesity, type of hernia, and hernia size. J Laparoendosc Adv Surg Tech 2002;
12:425-429.
41. Anthony T, Bergen PC, Kim LT et al. Factors affecting recurrence following incisional herniorrhaphy. World J Surg 2000; 24:95-101.
42. Langer C, Schaper A, Liersch T. Prognosis factors in incisional hernia surgery: 25 years of experience. Hernia 2004, [Epub ahead of print].
43. Sauerland S, Korenkov M, Kleinen T et al. Obesity is a risk factor for recurrence after incisional
hernia repair. Hernia 2004; 8:42-46.
Abdominal Compartment Syndrome
CHAPTER 16
Miscellaneous Conditions
and Intra-Abdominal Hypertension
197Miscellaneous Conditions and Intra-Abdominal Hypertension
Ari Leppäniemi, Andrew Kirkpatrick, Anastazia Salazar, Davis Elliot,
Savvas Nicolaou
ntra-abdominal hypertension and the abdominal compartment syndrome are increasingly
recognized in non-traumatic conditions in the critically ill patient. This chapter deals with
three of those situations: acute pancreatitis, renal transplant and abdominal aortic aneu-
I
rysm (the condition in which some of the very early cases of ACS were described).
and Martin Björck
Part A: Severe Acute Pancreatitis
Ari Leppäniemi*
Abstract
Under-diagnosed and untreated abdominal compartment syndrome (ACS) is a potential
contributing factor to the development of early organ failure seen in patients with severe acute
pancreatitis, and warrants routine measurement of intra-abdominal pressure in all patients
treated for severe pancreatitis. The current estimate of the prevalence of intra-abdominal hypertension (IAH) in severe acute pancreatitis is about 40%, with about 10% overall progressing to ACS associated with increased hospital mortality rates. In the majority of cases, the
development of IAH is rapid and mainly due to the combined effects of aggressive fluid resuscitation and the inflammatory process in the retroperitoneum leading to the development of
visceral edema and pancreatic ascites within days or even hours from admission, although in
some cases a delayed form of ACS has been associated with the emergence of infected
peripancreatic necrosis. Percutaneous drainage of large amounts of pancreatic ascites may decrease the intra-abdominal pressure considerably and is the first line treatment if appropriate.
In most cases, however, surgical decompression through a vertical midline incision without
exploring the pancreas further is the most effective and safest procedure. Decompression performed 2-3 weeks after the onset of the disease can be combined with necrosectomy. Primary
fascial closure of the abdominal wall following abdominal decompression can be attempted,
but in most cases the prolonged inflammatory process in the abdomen and the risk of recurrent
ACS favors the use of gradual closure or delayed reconstruction of the abdominal wall.
*Ari Leppäniemi—Department of Surgery, Meilahti Hospital, University of Helsinki, Finland.
Email: ari.leppaniemi@hus.fi
Abdominal Compartment Syndrome, edited by Rao R. Ivatury, Michael L. Cheatham,
Manu L. N. G. Malbrain and Michael Sugrue. ©2006 Landes Bioscience.
198
Figure A1. Hospital mortality rate (%) in patients treated for severe acute pancreatitis at the Meilahti
Hospital, University of Helsinki, Finland in 1967-2003. (Halonen and Leppäniemi 2004, unpublished data.)
Abdominal Compartment Syndrome
Introduction
The mortality rates for severe acute pancreatitis have shown steady decrease from 50-58%
in 1978-1982 to 12-18% in 1993-1997.
prophylactic antibiotic treatment, more accurate indications and timing of surgical intervention,
advances in the monitoring and management of organ dysfunctions, increased use of enteral
nutrition and early endoscopic sphincterotomy in patients with common bile duct stone-induced
pancreatitis have been major factors contributing to improved survival. In addition to factors
characterizing patient reserves, such as age or previous cardiovascular medication, the development of multiple organ dysfunction or failure is the major determinant of poor outcome.
Recent data from the Meilahti Hospital, University of Helsinki, Finland show that although
the mortality rates in patients with severe acute pancreatitis and multiple organ failure (MOF)
have improved considerably in the last 15 years (Fig. A1), the cumulative mortality charts (Fig.
A2) show that there is little improvement in the early (within 14 days) mortality rate (Halonen
and Leppäniemi, unpublished data, 2004). There is increasing clinical evidence that a major
part of the deaths in the early phase of the disease, previously thought to be caused by an
overwhelming acute inflammatory reaction leading to “early MOF”, is associated with undiagnosed and untreated abdominal compartment syndrome (ACS).
The presence of intra-abdominal hypertension (IAH) can also be used as a predictor of the
severity of acute pancreatitis. In a study of 45 patients with acute pancreatitis using
intra-abdominal pressure (IAP) levels higher than 16 mm Hg as a cut off point, there was a
correlation with the increased IAP and severity of pancreatitis, mortality, peripancreatic infection rate, and need for surgical intervention.
In 2002, the International Association of Pancreatology developed evidence-based guidelines for the surgical management of acute pancreatitis.
grade B and one was grade A. The essence of the recommendations involved the indications for
drainage and/or necrosectomy more than 2 weeks after the onset of the disease in patients with
fine-needle aspiration biopsy proven infected necrosis in patients with sepsis syndrome. Although there was no mention of abdominal compartment syndrome, recommendation six
encompasses all indications indicating early surgery, such as major hemorrhage, intestinal necrosis or perforation: “Early surgery within 14 days after onset of disease is not recommended
in patients with necrotizing pancreatitis unless there are specific indications (recommendation
1
Aggressive fluid resuscitation in the early phase,
3
4
5
Of the 11 recommendations, 10 were
2
199Miscellaneous Conditions and Intra-Abdominal Hypertension
Figure A2. Cumulative mortality rate (%) at 14, 30, 60 and 180 days post-admission in patients treated for
severe acute pancreatitis at the Meilahti Hospital, University of Helsinki, Finland in 1989-2003. (Halonen
and Leppäniemi 2004, unpublished data.)
grade B)”. Rapidly accumulating evidence supports the inclusion of early monitoring and treatment of abdominal compartment syndrome in the management algorithms of patients with
severe acute pancreatitis.
Prevalence
The true prevalence of IAH in patients with severe acute pancreatitis is not known. In a
study of 41 patients with severe acute pancreatitis, 44% of the patients had IAP levels higher
than 12 mm Hg, and 4 patients (10%) had IAP levels higher than 25 mm Hg with severe organ
dysfunction and undergoing abdominal decompression.
6
In another study of 37 patients treated
in the ICU for severe acute pancreatitis, 10 patients (27%) had IAP levels higher than 25 mm
Hg, with an overall frequency of 10/120 (8%) if all patients with severe acute pancreatitis
treated in other units (surgical ICU, high dependency unit) were included.
patients treated for severe acute pancreatitis in China showed that the overall incidence of IAH
(defined as IAP higher than 15 mm Hg) was 36%.
3
7
A study of 297
Thus, it can be estimated that the overall prevalence of IAH in patients with severe acute
pancreatitis is about 40%, and the frequency of ACS requiring surgical decompression
about 10%.
Due to the more aggressive fluid resuscitation policy in the early phase of severe acute
pancreatitis, and the decreasing proportion of patients requiring necrosectomy, it is likely that
the incidences of both early and late onset ACS, respectively, are higher today than in the past.
Severe acute pancreatitis is one of the most common diseases associated with IAH in the
ICU-environment. Among 18 patients treated in a surgical ICU in New York with documented ACS, the underlying condition was severe acute pancreatitis in 3 patients (17%).
8
Time of the Development of ACS
The development of ACS in patients with severe acute pancreatitis occurs most commonly
in the early course of the disease and is probably caused by the combined effects of the aggressive fluid resuscitation and inflammatory process in the retroperitoneum leading to the development of visceral edema and pancreatic ascites.
those who developed organ dysfunction within 72 hours after the onset of symptoms had
a 78% incidence of IAH (>15 mm Hg) compared to 23% in patients with severe acute
9,10
Among 297 patients treated in China,
200
Abdominal Compartment Syndrome
pancreatitis without early organ dysfunction.3 Another study from China with 23 patients
with severe acute pancreatitis complicated with ACS showed that in 6 cases (26%) the ACS
developed at a later stage of the disease and was associated with the presence of infected peripancreatic
11
necrosis.
ACS and Organ Dysfunction
Several studies show the association between IAH and development of organ dysfunction in
severe acute pancreatitis.
ratory failure, 94% cardiovascular and 89% renal failure rate in patients with IAP higher than
12 mm Hg.
Because the pathophysiological responses to the cellular events early in the course of the
disease have the ability to induce organ dysfunction even without the presence of ACS, more
studies are needed to characterize the exact mechanisms, role and magnitude of ACS leading to
early organ failure in severe acute pancreatitis.
6,7,12
De Waele et al6 showed that there was a 94% incidence of respi-
Diagnosis
Currently, there is no evidence suggesting that the standard measurement techniques for
IAP could not be applicable and reliable in patients with severe acute pancreatitis. The most
commonly used technique is the bladder pressure measurement through a Foley catheter.
7,12
Due to the nature of the development of ACS in patients with severe acute pancreatitis
with other potential causes for organ dysfunctions, the routine measurement of IAP in all
patients with severe acute pancreatitis is warranted.
Treatment
The treatment of ACS in patients with severe acute pancreatitis is based on the recognition
of the principal cause of the IAH. If an ultrasound examination confirms the presence of large
volumes of pancreatic ascites, the first line treatment would be the percutaneous drainage of
the intraperitoneal exudate which can lead to a significant drop in IAP (Lisi et al 2004, abstract). In most cases, however, visceral edema is the principal factor contributing to the development of ACS, and decompressive laparotomy and temporary abdominal closure with a Bogota
bag or equivalent is the most effective way of decreasing the IAP.
During the last 10 years, the proportion of patients with infected necrosis or other indications for surgical necrosectomy in severe acute pancreatitis has dropped from 30% to about
15% at the Meilahti Hospital, University of Helsinki, Finland (Fig. A3) (Halonen and
Leppäniemi, unpublished data 2004). When needed, the necrosectomy is performed through
a bilateral subcostal incision. Considering the small proportion of patients eventually requiring
necrosectomy and the (intuitively) inadequate decompression provided by a transverse incision, it is probably better to perform the early decompressive laparotomy through a long, vertical midline incision. Because of the unripe nature of the (sterile) necrosis and the risk of
introducing infection to the peripancreatic space, there are no indications to explore the pancreas further or open the gastrocolic ligament at this stage but limit the operation to decompression and drainage of ascites only (Gonzales Santamaria et al 2004, abstract). Moreover,
premature exploration can lead to fatal retroperitoneal bleeding.
If the decompression is done more than 2-3 weeks after the onset of the disease and there is
evidence of extensive necrosis on a CT scan or established infection of the peripancreatic necrosis, it is the policy of the author to perform a necrosectomy in conjunction with the decompressive laparotomy.
The management of the open abdomen following decompression in severe acute pancreatitis is a challenge. There are some isolated reports of primary closure of the abdominal wall
within a week from decompression, and that should be the aim in all cases.
in most cases with abdominal trauma, especially following damage control surgery with
intra-abdominal packing, or other conditions where the initial event leading to ACS can be
3,6,9,11,13
6
9,11
However, unlike
201Miscellaneous Conditions and Intra-Abdominal Hypertension
Figure A3. Proportion of patients undergoing operative or nonoperative treatment for severe acute pancreatitis at the Meilahti Hospital, University of Helsinki, Finland in 1989-2003. (Halonen and Leppäniemi
2004, unpublished data.)
rapidly reversed with aggressive management of the fluid balance, the inflammatory process in
severe acute pancreatitis usually continues for several weeks prohibiting the early closure of the
abdominal wall due to the risk of developing recurrent ACS. The best currently available technique and the one used by the author is the utilization of the vacuum-assisted closure technique aiming for gradual closure of the abdominal wall. If not possible, skin grafting over the
bowel and late abdominal wall plastic surgical reconstruction 9-12 months later is the safest
option, although associated with considerable morbidity and discomfort to the patient.
Mortality
In a study comparing patients with or without ACS (IAP>25 mm Hg) treated in the ICU
for severe acute pancreatitis, the hospital mortality rate for patients with ACS was 50% compared with 15% in patients without ACS.
mum IAP value within the first 2 weeks and the mortality rate (Fig. A4). In a logistic regression
analysis, however, only the maximal SOFA (Sequential Organ Failure Assessment) score was an
independent risk factor for hospital mortality.
Although some of the reported survival rates of patients undergoing abdominal decompression for ACS in severe acute pancreatitis are low, 1/3,
is associated with better outcome than delayed decompression or none at all. Among 23 patients with ACS and severe acute pancreatitis, 18 patients underwent decompression with a
mortality rate of 3/18 (17%), whereas 4/5 (80%) of the nonoperatively treated patients died.
Moreover, there were no deaths among patients who underwent emergency abdominal decompression within 5 hours after the confirmation of the presence of ACS.
References
1. Bank S, Singh P, Pooran N et al. Evaluation of factors that have reduced mortality from acute
pancreatitis over the past 20 years. J Clin Gastroenterol 2002; 35:50-60.
2. Halonen K, Leppäniemi A, Puolakkainen P et al. Severe acute pancreatitis – prognostic factors in
270 consecutive patients. Pancreas 2000; 21:266-271.
7
There was a clear correlation between the maxi-
13
1/4,6 respectively, early decompression
11
202
Abdominal Compartment Syndrome
Figure A4. Maximum IAP value and mortality rate in 37 patients treated in the ICU for severe acute
pancreatitis.
3. Tao H-Q, Zhang J-X, Zou S-C. Clinical characteristics and management of patients with early
4. Navarro S, Hidalgo JM, Bejarano N et al. Intra-abdominal pressure (IAP) as an indicator of sever-
5. Uhl W, Warshaw A, Imrie C et al. IAP Guidelines for the surgical management of acute pancreati-
6. De Waele J, Hoste E, Blot S et al. Intraabdominal hypertension and severe acute pancreatitis.
7. Keskinen P, Leppäniemi A, Pettilä V et al. Intra-abdominal pressure in acute necrotizing pancreati-
8. Mcnelis J, Soffer S, Marini CP et al. Abdominal compartment syndrome in the surgical intensive
9. Gonzales Santamaria JR, Perez Garcia R, Navarro Ramirez J et al. Handling of the abdominal
10. Lisi M, Sne B, Baillie F et al. Computed tomography guided percutaneous drainage of the ab-
11. Ao J, Wang C, Chen L et al. Diagnosis and management of severe acute pancreatitis complicated
12. Snippe K, Plaudis H, Pupelis G. Increased intra-abdominal pressure, is it of any consequence in
13. Gecelter G, Fahoum B, Gardezi S et al. Abdominal compartment syndrome in severe acute pancre-
7
acute severe pancreatitis: Experience from a medical center in China. World J Gastroenterol 2004;
10:919-921.
ity in acute pancreatitis. Inaugural World Congress Abdominal Compartment Syndrome, Noosa,
Australia, 2004.
tis. Pancreatology 2002; 2:565-573.
Inaugural World Congress Abdominal Compartment Syndrome, Noosa, Australia, 2004.
tis. Inaugural World Congress Abdominal Compartment Syndrome, Noosa, Australia, 2004.
care unit. Am Surg 2002; 68:18-23.
compartmental syndrome in a patient with serious acute pancreatitis of alcohol etiology: report of
a case. Inaugural World Congress Abdominal Compartment Syndrome, Noosa, Australia 2004.
dominal cavity is a safe alternative to celiotomy in patients with abdominal compartment syndrome due to severe phlegmonous pancreatitis: a case report. Inaugural World Congress Abdominal Compartment Syndrome, Noosa, Australia, 2004.
with abdominal compartment syndrome. Journal of Huazhong University of Science and Technology. Medical Sciences 2003; 23:399-402.
severe acute pancreatitis? Inaugural World Congress Abdominal Compartment Syndrome, Noosa,
Australia, 2004.
atitis: an indication for a decompressive laparotomy? Dig Surg 2002; 19:402-4.
203Miscellaneous Conditions and Intra-Abdominal Hypertension
Part B: The Renal Allograft Compartment Syndrome
in Perspective: An Organ Specific Compartment Syndrome
with Illustrative Pathophysiology
Andrew Kirkpatrick,* Anastazia Salazar, Davis Elliot and Savvas Nicolaou
Abstract
Renal allograft compartment syndrome (RACS) is a specific entity described in the transplanted kidney due to closure of fascia with excessive force and may be predisposed to by large
donors and small recipients, and adult kidneys transplanted in children. It is often relieved by
opening the compartment. Diagnosis is by sonography of the allograft. This section will discuss this special variant of abdominal compartment syndrome.
Introduction
Abdominal compartment syndrome (ACS) affects every human organ system, but is recognized clinically as cardiac, respiratory, and renal dysfunction.
100 years ago, these adverse effects, to which the kidneys are particularly susceptible, have only
recently been widely appreciated, in no small measure due to the works
one of the editors of this volume. IAH has been statistically associated with increased renal
dysfunction, multi-system organ failure, and death.
death in it’s fully developed form,
8
and it is assumed that either prophylaxis or earlier interven-
5,7
tion to reduce IAH might improve the previously dismal outcomes of the established ACS.
Routine IAP measurements are now easily obtained and should be performed in all critically ill
patients.
3,11
Raised intra-abdominal pressure (IAP) may begin to affect renal function at only
10 mm Hg and markedly impairs renal function at pressures as low as 20 mm Hg.
cally ill populations may have a 50% incidence of raised IAH (IAP > 12 mm Hg) though.
renal function has not been shown to improve with decompression of the hypertensive peritoneal cavity,
6
other markers are needed to identify which patients with borderline IAH will go
on to develop the ACS from those who will not, and thus could be spared the open abdomen.
1-3
Although first described over
4-7
of Michael Sugrue,
Untreated, the ACS invariably leads to
9-10
12,13
Criti-
14
As
The Renal Allograft Compartment Syndrome
A specific renal allograft compartment syndrome (RACS) has recently been recognized,
adding another specific syndrome to our ever increasing knowledge of IAH and ACS.
suspected intra-operatively during renal transplant if the fascial closure requires excessive force,
or results in graft turgor/color change or diminished renal artery pulsation. All cases diagnosed
postoperatively have been on the basis of poor physiologic function (urine production) and
abnormal Doppler US examinations rather than thorough measurement of intraperitoneal or
compartment pressures. Without early recognition and reexploration, graft loss is felt inevi-
17
table.
It may be predisposed to by large donors and small recipients, and especially when an
adult kidney is donated to a child.
15-18
In the absence of pressure measurements, the basis for
classifying these cases as true compartment syndromes rather than cases of renal vein thrombosis or vascular kinking has been the absence of these findings on re-exploration. In addtion,
vascular normalization has ensued upon opening of the compartment.
15,17
Further study will
be needed to clarify whether the RACS is a localized ACS syndrome or a true generalized
intra-abdominal phenomenon. If determined to be truly intra-abdominal the condition should
be classified as either a specific secondary ACS syndrome, as the site of the raised pressure is
*Corresponding Author: Andrew Kirkpatrick—Departments of Surgery, Critical Care Medicine,
Radiology, Vancouver Hospital & Health Sciences Centre, Vancouver, British Columbia,
Canada. Email: andrew.kirkpatrick@calgaryhealthregion.ca
15-18
It is
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