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Mortality rates for acute pancreatitis have declined from at least 10% to around 5% since the 1980s, but the mortality rate for severe acute pancreatitis (more than three Ranson criteria) remains at least 20% Half of the deaths occur within the first 2 weeks, usually from multiorgan failure Multiorgan failure that persists beyond the first 48 hours is associated with a mortality rate of over 50% Later deaths occur because of complications of infected necrosis Recurrences are common in alcoholic pancreatitis
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Banks PA et al Practice guidelines in acute pancreatitis Am J Gastroenterol 2006 Oct;101(10):2379 400 [PMID: 17032204] Mazaki T et al Meta-analysis of prophylactic antibiotic use in acute necrotizing pancreatitis Br J Surg 2006 Jun;93(6):674 84 [PMID: 16703633] Whitcomb DC Clinical practice Acute pancreatitis N Engl J Med 2006 May 18;354(20):2142 50 [PMID: 16707751] Wilcox CM et al Role of endoscopic evaluation in idiopathic pancreatitis: a systematic review Gastrointest Endosc 2006 Jun;63(7):1037 45 [PMID: 16733122]
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B Treatment of Complications and Follow-Up
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A surgeon should be consulted in all cases of severe acute pancreatitis If the diagnosis is in doubt and investigations indicate a strong possibility of a serious surgically correctable lesion (eg, perforated peptic ulcer), exploration is indicated When acute pancreatitis is unexpectedly found on exploratory laparotomy, it is usually wise to close without intervention If the pancreatitis appears mild and cholelithiasis or microlithiasis is present, cholecystectomy or cholecystostomy may be justified When severe pancreatitis results from choledocholithiasis particularly if jaundice (serum total bilirubin > 5 mg/dL) or cholangitis is present ERCP with endoscopic sphincterotomy and stone extraction is indicated MRCP may be useful in selecting patients for therapeutic ERCP Operation may improve survival in patients with necrotizing pancreatitis and clinical deterioration with multiorgan failure or lack of resolution by 4 weeks Surgery is nearly always indicated for infected necrosis The goal of surgery is to debride necrotic pancreas and surrounding tissue and establish adequate drainage Outcomes are best if surgery is delayed until the necrosis has organized, usually about 4 weeks after disease onset In selected cases, nonsurgical drainage of necrotizing pancreatitis under radiologic or endoscopic guidance may be feasible, at least as a temporizing measure, depending on local expertise Peritoneal lavage has not been shown to
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CHRONIC PANCREATITIS
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Chronic or intermittent epigastric pain, steatorrhea, weight loss, abnormal pancreatic imaging A mnemonic for the predisposing factors of chronic pancreatitis is TIGAR-O: toxic-metabolic, idiopathic, genetic; autoimmune, recurrent and severe acute pancreatitis, or obstructive
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Chronic pancreatitis occurs most often in patients with alcoholism (70 80% of all cases) The risk of chronic pancreatitis increases with the duration and amount of alcohol consumed, but pancreatitis develops in only 5 10% of heavy drinkers Tobacco smoking has been reported to accelerate progression of alcoholic chronic pancreatitis About 2% of patients with hyperparathyroidism develop pancreatitis In tropical Africa and Asia, tropical pancreatitis, related in part to malnutrition, is the most common cause of chronic pancreatitis A stricture,
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CMDT 2008
ferrin and carbonic anhydrase II are often found in patients with autoimmune pancreatitis
stone, or tumor obstructing the pancreas can lead to obstructive chronic pancreatitis Autoimmune pancreatitis is associated with hypergammaglobulinemia (IgG4 in particular) and often with autoantibodies and is responsive to corticosteroids About 10 20% of cases are idiopathic Genetic factors may predispose to chronic pancreatitis in some of these cases, including mutations of the cystic fibrosis transmembrane conductance regulator (CFTR) gene, the pancreatic secretory trypsin inhibitory gene (PSTI, serine protease inhibitor, SPINK1), and possibly the gene for uridine 5'-diphosphate glucuronosyltransferase Mutation of the trypsinogen gene on chromosome 7 (PRSS1) is associated with hereditary pancreatitis, transmitted as an autosomal dominant trait with variable penetrance A useful mnemonic for the predisposing factors to chronic pancreatitis is TIGAR-O: toxic-metabolic, idiopathic, genetic; autoimmune, recurrent and severe acute pancreatitis, or obstructive The pathogenesis of chronic pancreatitis may be explained by the SAPE (sentinel acute pancreatitis event) hypothesis by which the first (sentinel) acute pancreatitis event initiates an inflammatory process that results in both injury and later fibrosis In many cases, chronic pancreatitis is a self-perpetuating disease characterized by chronic pain or recurrent episodes of acute pancreatitis and ultimately by pancreatic exocrine or endocrine insufficiency After many years, chronic pain may resolve spontaneously or as a result of surgery tailored to the cause of pain Over 80% of adults develop diabetes 25 years after the clinical onset of chronic pancreatitis
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