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Emphysematous Pancreatitis

Contrast-enhanced axial slice abdominal computed tomography showing extensive peripancreatic phlegmon with abundant gas (arrows) replacing the necrotizing nonenhancing pancreatic tail. Note the normal enhancement of the pancreatic parenchyma medial to the tail.

Contrast-enhanced axial slice abdominal computed tomography showing extensive peripancreatic phlegmon with abundant gas (arrows) replacing the necrotizing nonenhancing pancreatic tail. Note the normal enhancement of the pancreatic parenchyma medial to the tail.

A 63-year-old woman with a history of severe alcohol abuse presented with persistent abdominal pain radiating to the back, vomiting, and lassitude over a week. Examination showed tachycardia, abdominal tenderness, and bipedal edema. Abdominal ultrasound demonstrated only fatty liver. Laboratory tests were notable for white blood cell count of 16.1 × 109/L, serum albumin 1.8 g/dL, and increased liver enzymes (X2-4) with normal bilirubin. Serum amylase 18 U/mL (N 28-100), lipase 9.4 U/L (N 13-60), and urinary amylase were normal. Computed tomography (CT) demonstrated emphysematous pancreatitis with left para-colonic collection and adjacent pleural effusion (Figure 1Figure 2). Intravenous saline, ertapenem, and metronidazole were administered while the patient was being prepared for surgery. Surgical specimen cultures during drainage and debridement identified Enterococcus faeciumKlebsiella pneumoniae, and Candida tropicalis. The patient survived, after a prolonged course in intensive care.

Emphysematous pancreatitis is an unusual occurrence, with just 16 PubMed citations in English.

Polymicrobial infection with gas-forming organisms and possibly an enteropancreatic fistula in the context of severe, often necrotizing, pancreatitis are the main causes of this severe complication of acute pancreatitis, best demonstrated by contrast-enhanced CT, which identifies gas in the retroperitoneum within the necrotic pancreatic parenchyma, a striking image.1

Our first diagnosis was alcoholic hepatitis, but as the CT proved, the normal pancreatic enzymes were misleading. Although serum amylase is highly sensitive in acute pancreatitis, false-negative values occur in hyperlipemic pancreatitis, delayed sampling, and in ~32% of alcoholic pancreatitis, where accrued pancreatic parenchymal damage or extensive necrosis may cease amylase production.2 Cytokine-driven suppression of albumin synthesis (≤3.0 g/dL) is, arguably, the strongest laboratory predictor (odds ratio 7.22) of mortality risk,3but there are several useful predictors of prognosis in acute pancreatitis.4

Management warrants early antibiotic coverage and often drainage and resection of infected necrotic tissue with fistula closure, if present. Selected patients may be managed nonoperatively. Despite the striking presentation, prognosis is variable: based on small case series, it is similar to that of necrotizing pancreatitis,1 with one report suggesting it was a favorable sub-type.

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-Ami Schattner, MD, Yosef Drahy, MD, Ina Dubin, MD

This article originally appeared in the November 2017 issue of The American Journal of Medicine.

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