Pathophysiology of local complications of severe acute pancreatitis

Over 50 per cent of patients with severe acute pancreatitis proceed to a spontaneous and uneventful resolution.

With necrotizing pancreatitis, 40 to 60 per cent develop infection of the necrosis. This is more common in biliary pancreatitis. The risk of pancreatic sepsis is maximum in the third week, although bacterial invasion has been documented in 30 to 50 per cent of patients within 14 days of the onset of symptoms. The earlier infection occurs, the higher is the mortality, as early mixing of bacteria with ongoing enzymatic and necrotizing processes appears to generate a highly toxemic course and amplifies distant tissue injuries. In these early infected cases, culture usually yields a single organism of a Gram-negative species (75 per cent) originating from the digestive tract by translocation, perforation of a hollow viscus, infected bile, or following retrograde cholangiopancreatography, or via hematogenous or lymphatic spread. Anaerobic organisms are present in only 10 per cent of cultures. Infected pancreatic necrosis, where necrotic tissue is the dominant element, differs from pancreatic abscess by the absence of a well-loculated collection of pus, an earlier presentation, and a much higher mortality ( Begerefa/ 1988).

Pancreatic abscess consists of a collection of pus, enclosed by inflammatory walls, resulting from liquefaction of necrotic areas inside or outside the pancreas that have become secondarily infected. Over 50 per cent are polymicrobial with a predominance of enteric bacteria. Candida albicans is often cultured in those previously treated with broad-spectrum antibiotics. In contrast with infected pancreatic necrosis, pancreatic abscess occurs when the active phase of pancreatitis is over and it tends to present with a more indolent process. Remote complications are less frequent, mortality is lower, and sometimes a state of relative well being interplays between the toxemic phase and the clinical emergence of abdominal sepsis.

Acute pseudocyst develops in 10 to 20 per cent of patients with severe acute pancreatitis. It is more common in alcoholic pancreatitis, but hemorrhage and infection are more likely to complicate cysts associated with gallstones. In contrast with pancreatic fluid, collections which represent a mixture of inflammatory exudate, necrotic tissue, and blood, an acute pseudocyst consists of an effusion of pancreatic juice rich in amylase that lacks an epithelial lining and has gradually become enclosed by fibrous walls over a period of 4 to 6 weeks. About 50 per cent disappear spontaneously within 1 to 2 months. Pancreaticopleural or pancreaticopericardial fistula or, more commonly, pancreatic ascites may ensue if rupture occurs. This peritoneal exudate is a major pool of pancreatic enzymes and a potential source of toxic substances. About 30 to 50 per cent become secondarily symptomatic via infection, adjacent extrinsic organ compression, or bleeding.

Serious gastrointestinal complications include bleeding, mechanical obstruction, colonic necrosis, and/or development of perforation or fistula. Persistent abdominal sepsis and fecal fistula are usual presenting features. Vascular thrombosis may manifest as gastrointestinal bleeding, perforation, fistulas, or late stricture. Obstructive jaundice is usually due to biliary stricture and fibrosis, and not to extrinsic compression by a pseudocyst.

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