Key Clinical Questions
What are the criteria for the diagnosis of acute pancreatitis?
What efforts should be made to determine the etiology during hospitalization, and what is the optimal timing of diagnostic and/or intervention studies in acute pancreatitis?
What are the key components of early management?
What is the management of late complications?
When should consultation with gastroenterology, surgery, or interventional radiology be considered?
When are specific interventions such as endoscopic retrograde cholangiopancreatography, fine-needle aspiration, or antibiotics indicated?
Acute pancreatitis is a common cause for hospitalization in the United States. Recent data from the National Center for Health Statistics have indicated a rising frequency of admissions for acute pancreatitis attributed to the increase in gallstone-related disease. Annually, more than 300,000 hospital admissions for acute pancreatitis present in the United States at a direct cost of more than $2 billion. Although acute pancreatitis is typically a mild, self-limited disease, a wide range of severity exists. Fifteen to twenty percent of patients experience a more severe form of disease with overall in-hospital mortality estimated to range between 2% and 5% of cases.
Risk factors for acute pancreatitis include both genetic susceptibility and environmental exposures. Genes involving mutation in the cystic fibrosis transmembrane conductance regulator, cationic trypsinogen gene (PRSS1), and secretory trypsin inhibitor (SPINK1) have been identified in patients with recurrent acute pancreatitis. Other patient-related factors such as obesity have also been demonstrated to be associated with increased severity of disease.
The most common etiology for acute pancreatitis is now gallstone-related disease, followed by alcohol and idiopathic pancreatitis (Table 157-1). Additional etiologies include metabolic derangements (hypercalcemia, hypertriglyceridemia) and medications (Table 157-2). Less common etiologies include autoimmune and hereditary forms of pancreatitis. Whether pancreas divisum itself is a cause for acute pancreatitis remains controversial.
TABLE 157-1Etiologies of Acute Pancreatitis |Favorite Table|Download (.pdf) TABLE 157-1 Etiologies of Acute Pancreatitis
| ||Examples |
|Gallstone || |
|Alcohol || |
|Autoimmune || |
|Hereditary ||PRSS1, CFTR, SPINK1, CTRC |
|Iatrogenic ||Post-ERCP, postsurgery |
Mumps, Cytomegalovirus, Coxsackievirus
Legionella, Salmonella, Aspergillus
|Metabolic ||Hypercalcemia, hypertriglyceridemia |
|Medication ||See Table 157-2 |
|Obstructive ||Pancreatic or ampullary tumors, pancreas divisum |
|Toxic ||Scorpion venom, organophosphate poisoning |
|Trauma ||Abdominal injury |
|Vascular ||Vasculitis, ischemia, embolism |
|Idiopathic || |
TABLE 157-2Drug-Induced Pancreatitis |Favorite Table|Download (.pdf) TABLE 157-2 Drug-Induced Pancreatitis
|Class I ||Class II |
|Amiodarone ||Didanosine |
|Azathioprine ||Acetaminophen |
|Cannabis ||Clozapine |
|Valproic acid ||Estrogen |
|Mercaptopurine ||Propofol |
|Mesalamine ||Hydrochlorothiazide |
|Omeprazole ||Tamoxifene |
|Metronidazole || |
|Lamivudine || |
|Furosemide || |
|Simvastatin || |
|Dexamethasone || |
|Sulindac || |