Pancreatitis may be the ultimate medical disease to cause intra-abdominal hypertension. It involves both of the major processes that can cause IAH – direct injury to the peritoneal or retroperitoneal space and a massive systemic inflammatory response. Initially, severe acute pancreatitis causes inflammation and fluid sequestration in the retroperitoneal space leading to local vascular permeability and edema formation. As this progresses pro-inflammatory cytokines are released and a systemic inflammatory response occurs, leading to system wide vascular leak with massive amounts of fluid sequestration in the mesentery and bowel wall. The current estimate of the prevalence of intra-abdominal hypertension in severe acute pancreatitis is about 40%, with about 10% overall developing abdominal compartment syndrome.[1] In addition, multiple organ dysfunction, ICU length of stay and mortality are all significantly increased in those pancreatitis patients who develop IAH.[1,2]

Treatment of IAH in pancreatitis is dependent first on early detection. Numerous authors strongly emphasize the need to monitor IAP in all severe pancreatitis patients to allow early detection and early intervention to reduce intra-abdominal pressure.[2–4] Once IAH is detected an established treatment algorithm should be used to guide therapy based on the pressure and the unique characteristics of the patient (see treatment algorithm provided). Specific therapies found to be helpful in pancreatis include percutaneous drainage of any fluid pocket present in the retroperitoneal space[5], placement of a paracentesis catheter which is allowed to continually drain small amounts of cytokine rich peritoneal fluid[6] early hemofiltration to remove pro-inflammatory cytokines as well as excess interstitial fluid[7, 8] and decompressive laparotomy without pancreatic exploration when ACS develops.[1,3,4,9,10]

Outcomes have been dramatically improved in studies that utilized these approaches.[3,6,7] In their retrospective review of patients with full blown ACS, Tao et al found early decompressive laparotomy resulted in survival rates of 83% whereas patients who did not undergo decompression had an 80% mortality.[3] Oda et al recognized that by waiting for abdominal compartment syndrome to develop the patient already would be suffering from prolonged ischemia.[7] They therefore frequently monitored all their severe pancreatitis patients intra-abdominal pressures from the time they were admitted to the ICU and intervened well before the onset of ACS. They instituted aggressive hemodialysis on all who developed grade II intra-abdominal hypertension (IAP≥15 mm Hg) and compared their survival rates to historical controls. Early intervention led to a decrease in mortality from the traditional 30% to only 6%. They conclude that early continuous hemofiltration is an effective method to reduce intra-abdominal pressure and reduce mortality in patients suffering from severe pancreatitis.[7] Most recently Sun et al conducted a randomized controlled trial comparing intra-abdominal pressure monitoring plus early continuous paracentesis to standard therapy in their critically ill pancreatitis patient population.[6] They found that early monitoring and intervention for IAH in this patient population resulted in dramatic improvements: Length of hospital stay was reduced from 28 days to 15 days and mortality dropped in half, from 20% to 10%.

In summary, pancreatitis patients who become critically ill have a very high probability of developing intra-abdominal hypertension, which often progresses to life threatening abdominal compartment syndrome. All these patients should have early intra-abdominal pressure monitoring instituted so that medical interventions can be instituted in those patients who progress to intra-abdominal hypertension. By doing this many will not progress to the abdominal compartment syndrome and survival and length of stay times are greatly improved.[1,6,7] Should a patient progress to ACS, early decompressive laparotomy is indicated.[3]

1. Leppaniemi, A. and E. Kemppainen, Recent advances in the surgical management of necrotizing pancreatitis. Curr Opin Crit Care, 2005. 11(4): p. 349-52.
2. Pupelis, G., et al., Clinical significance of increased intraabdominal pressure in severe acute pancreatitis. Acta Chir Belg, 2002. 102(2): p. 71-4.
3. Tao, J., et al., Diagnosis and management of severe acute pancreatitis complicated with abdominal compartment syndrome. J Huazhong Univ Sci Technolog Med Sci, 2003. 23(4): p. 399-402.
4. Gecelter, G., et al., Abdominal compartment syndrome in severe acute pancreatitis: an indication for a decompressing laparotomy? Dig Surg, 2002. 19(5): p. 402-4; discussion 404-5.
5. Reckard, J.M., et al., Management of intraabdominal hypertension by percutaneous catheter drainage. J Vasc Interv Radiol, 2005. 16(7): p. 1019-21.
Sun, Z.X., H.R. Huang, and H. Zhou, Indwelling catheter and conservative measures in the treatment of abdominal compartment syndrome in fulminant acute pancreatitis. World J Gastroenterol, 2006. 12(31): p. 5068-70.
6. Oda, S., et al., Management of intra-abdominal hypertension in patients with severe acute pancreatitis with continuous hemodiafiltration using a polymethyl methacrylate membrane hemofilter. Ther Apher Dial, 2005. 9(4): p. 355-61.
7. Maslovsky, O.P. and V.V. Zagorujko, Acute pancreatitis with multiple organ dysfunction syndrome - is high volume hemofiltration helpful? Intensive Care Medicine, 2005. 31, Supplement 1(134): p. S185, Abstract 710.
8. DeWaele, J.J. and U.J. Hesse, Life saving abdominal decompression in a patient with severe acute pancreatitis. Acta Chir Belg, 2005. 105(1): p. 96-8.
9. Leppaniemi, A.K., et al., Treatment of Abdominal Compartment Syndrome with Subcutaneous Anterior Abdominal Fasciotomy in Severe Acute Pancreatitis. World J Surg, 2006.