
Intra-abdominal hypertension and acute pancreatitis
Author(s) -
A Mifkovič,
J Škultéty,
P. Sýkora,
A Prochotský,
R Okoličány
Publication year - 2013
Publication title -
bratislavské lekárske listy/bratislava medical journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.387
H-Index - 32
eISSN - 1336-0345
pISSN - 0006-9248
DOI - 10.4149/bll_2013_036
Subject(s) - medicine , abdominal compartment syndrome , acute pancreatitis , pancreatitis , shock (circulatory) , gastroenterology , perfusion , systemic inflammatory response syndrome , multiple organ dysfunction syndrome , cardiology , surgery , sepsis , abdomen
Intra-abdominal hypertension (IAH) contributes to organ dysfunction and leads to the development of the abdominal compartment syndrome (ACS). IAH and ACS are relatively frequent findings in patiens with severe acute pancreatitis (SAP) and are associated with deterioration in organ functions. The most affected are cardiovascular, respiratory and renal functions. The incidence of IAH in patients with SAP is approximately 60-80%. There is an accumulating evidence in human and animal studies that changes of perfusion, particularly to the microvasculature, are crucial events in the progression of acute pancreatitis (AP). The perfusion of the small and large intestine is impaired due to reduced arterial pressure, increased vascular resistence and diminished portal blood flow. Bacterial translocation has been described in patients with ACS, and this may apply to patients with SAP. Approximately 30-40% of SAP patients develop ACS because of pancreatic (retroperitoneal) inflammation, peripancreatic tissue edema, formation of fluid collections or abdominal distension. Surgical debridement was the preferred treatment to control necrotizing pancreatitis in the past. However, the management of necrotizing pancreatitis has changed over the last decade. The main objective of this article is to describe the association between IAH and AP and to emphasize this situation in clinical praxis as well (Fig. 1, Ref. 38).