What are the criteria for the diagnosis of acute pancreatitis?
What efforts should be made to determine 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 ERCP, fine-needle aspiration, or prophylactic antibiotics indicated?
Acute pancreatitis is a common cause for hospitalization in the United States. Recent data from the National Center for Health Statistics has 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 20% of patients experience a more severe form of disease with overall inhospital mortality estimated to range between 3–5% of cases.
Risk factors for acute pancreatitis include both genetic susceptibility and environmental exposures. Genes involving mutation in the cystic fibrosis transmembrane conductance regulator (CFTR), 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 post-ERCP (endoscopic retrograde cholangiopancreatography) pancreatitis (Table 156-1). Additional etiologies include metabolic derangements (hypercalcemia, hypertriglyceridemia) and medications (Table 156-2). Less common etiologies include autoimmune and hereditary forms of pancreatitis. Whether pancreas divisum itself is a cause for acute pancreatitis remains controversial.
Table 156-1 Etiologies of Acute Pancreatitis ||Download (.pdf)
Table 156-1 Etiologies of Acute Pancreatitis
Most common cause. Combined use of abdominal ultrasound and liver tests enhances diagnosis.
Usually in setting of long-standing alcohol history.
Placement of prophylactic pancreatic duct stent associated with reduced incidence.
Recent classification system based on level of evidence for potentially offending medications.
Should prompt evaluation for underlying cause.
Triglyceride levels can be falsely elevated during an acute episode; levels > 1000 mg/dL are fairly specific.
US and Asian criteria differ. Usually associated with classic radiologic findings. IgG4 is specific but has only ˜50% sensitivity.
Controversial. Anatomic anomaly of pancreatic ducts. Should only be considered if alternative etiologies have been excluded.
Most commonly associated with mutation in cationic trypsinogen (PRSS1) gene.
Despite thorough evaluation, a cause for pancreatitis is unable to be identified in 15–20% of cases.
Table 156-2 Drug-Induced Pancreatitis ||Download (.pdf)
Table 156-2 Drug-Induced Pancreatitis
Class I Medications (Implicated in > 20 reported cases of acute pancreatitis with at least one documented ...